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Patologas.

Facultad de Odontologa.

Asignatura: Ciclo de integracin bsico clnico II.

Docente: Michael de la Torre S.

Integrantes:

- Reinaldo Arias F.
- Osvaldo Muoz V.
- Adelainne Varela S.
- Patricia Vejar R.
- Patricio Venegas S.

Fecha: 27.Marzo.2017

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ndice.

Introduccin.. 3
Discapacidad intelectual y escala de medicin
- Antecedentes, causas, sntomas y relacin odontolgica...4-6
- Cuidado bucal practico para personas con discapacidad intelectual.7-17
Trastorno espectro autista
- Antecedentes, causas, sntomas y relacin odontolgica..18-20
- La experiencia de las caries y el comportamiento de los pacientes dentales con
trastornos del especto autista21-22
Parlisis cerebral
- Antecedentes, causas, sntomas y relacin odontolgica..23-25
- Efecto de los reflejos orales anormales en la articulacin del habla con paralisis
cerebral espstica 26-32
Esclerosis mltiple
- Antecedentes, causas, sntomas y relacin odontolgica.33-35
- Virus de Epstein Bar en el desprendimiento oral de nios con EM.36-46
Ela
- Antecedentes causas, sntomas y relacin odontolgica..47-49
- Lengua negra y peluda en pacientes con ELA...50-54
Alzaimer
- Antecedentes, causas, sntomas y relacin odontologica .....................55-57
- Periodonitis y declinacin cognitiva en la enfermedad del Alzheimer...58-66
Displaca ectodrmica
- Antecedentes, causas, sntomas y relacin odontolgica..67-69
- Rehabilitacin oral con displacia ectodrmica..70-74
Radio terapia
- Antecedentes, causas, sntomas y relacin odontolgica.75-77
- La radioterapia modulada con intensidad de cabeza y cuello conduce a un aumento
de patgenos orales oportunistas..78-79
Artritis reumatoide
- Antecedentes, causas, sntomas y relacin odontolgica...80-82
- Estatus oral en pacientes con artritis reumatoide temprana: un estudio prospectivo
de casos y controles..83-90
Hemofilia
- Antecedentes, causas, sntomas y relacin odontolgica..91-93
- Salud bucal en pacientes adultos con problemas de coagulacin congnita, estudio de
casos y controles..94-101
Conclusin...102
Referencias.103-105

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Introduccin

Bien sabemos que en el diario vivir nos podemos encontrar con distintas enfermedades en nuestro
alrededor. Sabemos bien que cualquier persona, puede tener o adquirir cierta patologa, y que
nadie est a salvo de estas.

La intencin de este informe es dar a conocer informacin bsica de las diferentes enfermedades
que se pueden presentar en nuestro mbito profesional, para tener conocimiento previo de estas
mismas.

Otro punto es que ya sabiendo la informacin bsica de cada uno, as tener la facilidad de dar un
tratamiento especfico para cada paciente que puede manifestar una o ms patologas que
pueden afectar un tratamiento tradicional que puede efectuar un odontlogo con cierto tipo de
pacientes.

Teniendo eso en cuenta, el conocimiento de tales patologas (como pueden ser de ejemplos,
diabetes, alzhimer, hemofilia, entre otros) son tratadas de diferentes maneras y cada una puede
atraer una complicacin al fallar o el no informarse adecuadamente le la ficha y pasado clnico del
paciente que podemos estar atendiendo.

Hay que tener en cuenta adems que las patologas que puede tener una persona no tan solo
puede afectar de forma fsica al paciente, sino que tambin de una manera psicolgica, por lo que
el profesional de la salud, en este caso el odontlogo debe usar medidas respectivas y mantener
una fuerte comunicacin con la otra persona o paciente, que no les aflija o mentalmente los deje
mal.

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Discapacidad intelectual

Definicin:

Antes conocido como retraso mental pero por cuestiones peyorativas y porque este nombre
limitaba a evaluar solo el coeficiente intelectual se dej

de usar y se cambi a discapacidad intelectual ,esta se define como la limitacin en las


capacidades tanto intelectuales , como conducta adaptativa ,habilidades y prcticas
socio/culturales antes de los 18 aos de edad, el hecho de tener esta discapacidad no implica que
el individuo no sea capaz de aprender

las habilidades intelectuales estn dadas por la capacidad de razonamiento ante situaciones , as
como la solucin de problemas y el aprendizaje por experiencia , pero al hacer una evaluacin
acerca de esto no es suficiente para el diagnstico si no que se tambin se necesita observar la
conducta adaptativa,es decir la lectura , escritura , socialmente la responsabilidad , autoestima y
credulidad , y en la parte prctica ver el autoaseo ,la medicina , la comida entre otros

socialmente se ven los roles de la persona con discapacidad intelectual es decir como se comporta
frente a personas extraas o ya sea en el colegio o trabajo dependiendo del caso y finalmente
pero no menos importante se ve en cuanto a la salud , es decir la capacidad de la persona en
comunicar sntomas y sentimientos.

Epidemiologa:

Gracias a la encuesta nacional de discapacidad en el ao 2004 y ENDISC (estudio nacional de


discapacidad en chile ) alrededor de 2 millones de personas , es decir un 12,9 % de la poblacin
total poseen alguna discapacidad , siendo ms especficos aproximadamente 292.720 personas
tienen alguna discapacidad intelectual y un 2,5 % posee discapacidades mltiples

Etiologa:

Las causas son mltiples, habiendo distintos factores tales como biomdicos, ,sociales y
conductuales

En los biomdicos nos referimos a anomalas genticas ,hereditarias, enfermedades infecciosas ,


trastornos metablicos, entre otros, esto se puede diagnosticar cuando el beb est dentro del
tero de la madre . Una de las enfermedades con mayor prevalencia es el sndrome de down , as
como tambin el X frgil.

sndrome de down : tres cromosomas en el par 21

x frgil : va de generacion en generacion que es la migracin de un pedazo del cromosoma

esto se puede prevenir durante el embarazo para as preparar a la madre para lo que viene y as
hacer mejor la vida del individuo afectado

Factor social se refiere a pobreza , malnutricin de la madre durante la gestacin, violencia , mal
cuidado por parte de los padres

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Factor conductual como consumo de drogas , tabaco, alcohol durante el embarazo e inmadurez
parental , esto se puede prevenir enseando a la mujer los riesgos que trae consigo el alcohol , la
exposicin al mercurio entre otros y as reducir el riesgo

Los sntomas son : la falta o dificultad para el desarrollo motor tal como escribir , en el lenguaje ,
en acatar rdenes y adaptarse con las personas que lo rodean, no crecer intelectualmente y tener
una conducta infantil para su edad.

A pesar de que no haya cura para la discapacidad intelectual, hay avances y

mejoras por parte del paciente ,siempre y cuando haya un apoyo tanto profesional como de las
personas que lo rodean

Clasificacin y escalas de medicin :

Existen diversas escalas de medicin entre las que mas destacan son :

Escala integral: mide la calidad de vida a personas mayores de 18 aos

Esta est planificada y centrada en la persona discapacitada y tiene 2 escalas , una objetiva
respecto a lo que se observa , una encuesta con respuestas si o no y a dems una valorizacin por
parte de alguien externo .

Y luego est la escala subjetiva que se le hace una encuesta con el sistema likert y se refleja la
valoracin propia de la persona con discapacidad

En total esta encuesta dura 27-40 minutos que debe hacer un profesional

Por otro lado est la Escala de la limitacin de la inteligencia la cual tiene una media de 100
puntos, obteniendo 75-70 o inferior la persona con discapacidad, esto se mide con diferentes
escalas , la de wechsler la ms utilizada y esta se divide en varias dependiendo la edad ,con un
autoinforme y una evaluacin por un profesional (INICO) instituto universitario de integracin a la
comunidad

Como el coeficiente intelectual no lo es todo tambin se evala la funcin adaptativa del individuo
y conducta psicoemocional.

para hacer una correcta evaluacin se debe considerar la diversidad cultural y lingstica del
evaluado para no discriminar a las minoras con caracteres especiales en su comunicacin

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Manejo odontolgico:

Entre los problemas habituales de personas con discapacidad intelectual encontramos como
mayor problema la enfermedad de caries e higiene bucal , ya sea por las limitaciones de sus
habilidades motrices ,por la medicacin con un alto ndice cariognico, por problemas tanto
nutricionales como mala deglucin y en algunos casos macroglosia mayoritariamente en personas
con sndrome de down ,estas personas pueden llegar a gingivitis ,periodontitis y en el peor de los
casos prdida de piezas dentales ya que su limitacin en cuanto a comunicarse con otros,la
mayora de los pacientes con discapacidad no comunican el dolor que sienten

El tratamiento con respecto a cad paciente va a ser distinto teniendo que tener en cuenta para el
odontlogo una revisin al historial clnico para as hacer para el paciente una visita mas comoda ,
ya que este tipo de pacientes son muy sensibles sobre todo ante personas extraas, por lo que hay
que instruir a cerca de la higiene asi como de la dieta cariognica tanto al paciente como a los
padres y en caso de que se tenga que realizar algn tratamiento lo mejor es explicar el
procedimiento para que el paciente entienda y asi reducir la ansiedad y falta de cooperacin,
tambin evitar cualquier tipo de distraccin para que el paciente no este en constante movimiento
pudiendo ocscionar alguna lesion iatrogenica por parte del odontologo

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Providing oral care to people with intellectual disability requires adaptation of the skills you use
every day. In fact, most people with mild or moderate intellectual disability can be treated
successfully in the general practice setting. This booklet will help you make a difference in the
lives of people who need professional oral care.

Intellectual disability is a disorder of mental and adaptive functioning, meaning that people who
are affected are challenged by the skills they use in everyday life. Intellectual disability is not a
disease or a mental illness; it is a developmental disability that varies in severity and is usually
associated with physical problems. While one person with intellectual disability may have slight
difficulty thinking and communicating, another may face major challenges with basic self-care and
physical mobility. Data indicate that people with intellectual disability have more untreated caries
and a higher prevalence of gingivitis and other periodontal diseases than the general population.

Health Challenges in Intellectual disability and strategies for Care Many people with intellectual
disability also have other conditions such as cerebral palsy, seizure or psychiatric disorders,
attention deficit/hyperactivity disorder, or problems with vision, communication, and eating.
Though language and communication problems are common in anyone with intellectual disability,
motor skills are typically more affected when a person has

coexisting conditions. Before the appointment, obtain and review the patients medical history.
Consultation with physicians, family, and caregivers is essential to assembling an accurate medical
history. Also, determine who can legally provide informed consent for treatment.

MENTAL CHALLENgES. People with intellectual disability learn slowly and often with difficulty.
Ordinary activities of daily living, such as brushing teeth and getting dressed, and understanding
the behavior of others as well as their own, can all

present challenges to a person with intellectual disability. Set the stage for a successful visit by
involving the entire dental teamfrom the receptionists friendly greeting to the caring attitude of
the dental assistant in the operatory. All should be aware of your patients mental challenges.

Reduce distractions in the operatory, such as unnecessary sights, sounds, or other stimuli, to
compensate for the short attention spans commonly observed in people with intellectual
disability. Talk with the parent or caregiver to determine your patients intellectual and functional
abilities, then explain each procedure at a level the patient can understand. Allow extra time to
explain oral health issues or instructions and demonstrate the instruments you will use. Address
your patient directly and with respect to establish a rapport. Even if the caregiver is in the room,
direct all questions and comments to your patient. Use simple, concrete instructions and repeat
them often to compensate for any short-term memory problems. Speak slowly and give only one
direction at a time. Be consistent in all aspects of oral care, since long-term memory is usually
unaffected. Use the same staff and dental operatory each time to help sustain familiarity. The
more consistency you provide for your patients, the more likely they will cooperate. Listen
actively, since communicating clearly is often difficult for people with intellectual disability. Show
your patient whether you understand. Be sensitive to the methods he or she uses to
communicate, including gestures and verbal or nonverbal requests.

intellectual disability

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BEHAVIOR CHALLENgES. While most people with intellectual disability do not pose significant
behavior problems that complicate oral care, anxiety about dental treatment occurs frequently.
People unfamiliar with a dental office and its equipment and instruments may exhibit fear. Some
react to fear with uncooperative behavior, such as crying, wiggling, kicking, aggressive language,
or anything that will help them avoid treatment. You can make oral health care a better
experience by comforting your patients and acknowledging their anxiety. Talk to the caregiver or
physician about techniques they have found to be effective in managing the patients behavior.
Schedule patients with intellectual disability early in the day if possible. Early appointments can
help ensure that everyone is alert and attentive and that waiting time is reduced. Keep
appointments short and postpone difficult procedures until after your patient is familiar with you
and your staff. Allow extra time for your patients to get comfortable with you, your office, and the
entire oral health care team. Invite patients and their families to visit your office before beginning
treatment. Permit the parents or caregiver to come into the treatment setting to provide
familiarity, help with communication, and offer a calming influence by holding your patients hand
during treatment. Some patients behavior may improve if they bring comfort items such as a
stuffed animal or blanket.

Reward cooperative behavior with compliments throughout the appointment. Consider nitrous
oxide/oxygen sedation to reduce anxiety and fear and improve cooperation. Obtain informed
consent from the legal guardian before admin istering any kind of sedation. Use immobilization
techniques only when absolutely necessary to protect the patient and staff during dental
treatmentnot as a convenience. There are no universal guidelines on immobilization that apply
to all treatment settings. Before employing any kind of immobilization, it may help to consult
available guidelines on federally funded care, your State department of mental health/ disabilities,
and your State Dental Practice Act. Guidelines on behavior management published by the
American Academy of Pediatric Dentistry (http://www.aapd.org) may also be useful. Obtain
consent from your patients legal guardian and choose the least restrictive technique that will
allow you to provide care safely. Immobilization should not cause

physical injury or undue discomfort. People with intellectual disability often engage in
perseveration, a continuous, meaningless repetition of words, phrases, or movements. Your
patient may mimic the sound of the suction, for example, or repeat an instruction over and again.
Avoid demonstrating dental equipment if it triggers perseveration, and note this in the patients
record.

allow extra time for your patient to get comfortable with you, your office, and the entire oral
health care team.

PHySICAL CHALLENgES. Intellectual disabiliy does not always include a specific physical trait,
although many people have distinguishing features such as orofacial abnormalities, scoliosis,
unsteady gait, or hypotonia due to coexisting con ditions. Countering physical challenges requires
attention to detail. Maintain clear paths for movement throughout the treatment setting. Keep
instruments and equipment out of the patients way. Place and maintain your patient in the
center of the dental chair to minimize the risk of injury. Placing pillows on both sides of the
patient can provide stability. If you need to transfer your patient from a wheelchair to the dental
chair, ask the patient or caregiver about special preferences such as padding, pillows, or other
things you can provide to ease the transition. The patient or caregiver can often explain how to
make a smooth transfer. (See Wheelchair Transfer: A Health Care Providers Guide, also part of

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this series.) Some patients cannot be moved into the dental chair but instead must be treated in
their wheelchairs. Some wheelchairs recline or are specially molded to fit peoples bodies. Lock
the wheels, then slip a sliding board (also called a transfer board) behind the patients back to
provide support for the head and neck during care.

CEREBRAL PALSy occurs in one-fourth of those who have intellectual disability and tends to affect
motor skills more than cognitive skills. Un controlled body movements and reflexes associated
with cerebral palsy can make it difficult to provide care.

Place and maintain your patient in the center of the dental chair. Do not force arms and legs into
unnatural positions, but allow your patient to settle into a position that is comfortable and will not
interfere with dental treatment. Observe your patients movements and look for patterns to help
you anticipate direction and intensity. Trying to stop these movements may only intensify the
involuntary response. Try instead to anticipate the movements, blending your movements with
those of your patient or working around them. Softly cradle your patients head during treatment.
Be gentle and slow if you need to turn the patients head. Help minimize the gag reflex by placing
your patients chin in a neutral or downward position. Stay alert and work efficiently in short
appointments. Exert gentle but firm pressure on your patients arm or leg if it begins to shake.
Take frequent breaks or consider prescribing muscle relaxants when long procedures are needed.
People with cerebral palsy may need sedation, general anesthesia, or hospitalization if extensive
dental treatment is required.

CARDIOVASCULAR ANOMALIES such as heart murmurs and damaged heart valves occur frequently
in people with intellectual disability, especially those with Down syndrome or multiple disabilities.
Consult the patients physician to determine if antibiotic prophylaxis
(http://www.americanheart.org) is necessary for dental treatment.

intellectual disability

SEIzURES are common in this population but can usually be controlled with anticonvulsant
medications. The mouth is always at risk during a seizure: Patients may chip teeth or bite the
tongue or cheeks. Persons with controlled seizure disorders can easily be treated in the general
dental office. Consult your patients physician. Record information in the chart about the
frequency of seizures and the medications used to control them. Determine before the
appointment whether medications have been taken as directed. Know and avoid any factors that
trigger your patients seizures. Be prepared to manage a seizure. If one occurs during oral care,
remove any instruments from the mouth and clear the area around the dental chair. Attaching
dental floss to rubber dam clamps and mouth props when treatment begins can help you remove
them quickly. Do not attempt to insert any objects between the teeth during a seizure. Stay with
your patient, turn him or her to one side, and monitor the airway to reduce the risk of aspiration.

VISUAL IMPAIRMENTS, most commonly strabismus (crossed or misaligned eyes) and refractive
errors, can be managed with careful planning. Determine the level of assistance your patient
requires to move safely through the dental office. Use your patients other senses to connect with
them, establish trust, and make treatment a good experience. Tactile feedback, such as a warm
handshake, can make your patients feel comfortable.

Face your patients when you speak and keep them apprised of each upcoming step, especially
when water will be used. Rely on clear, descriptive language to explain procedures and

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demonstrate how equipment might feel and sound. Provide written instructions in large print (16
point or larger).

HEARINg LOSS and DEAFNESS can also be accommodated with careful planning. Patients with a
hearing problem may appear to be stubborn because of their seeming lack of response to a
request. Patients may want to adjust their

hearing aids or turn them off, since the sound of some instruments may cause auditory
discomfort. If your patient reads lips, speak in a

normal cadence and tone. If your patient uses a form of sign language, ask the interpreter to
come to the appointment. Speak with this person in advance to discuss dental terms and your
patients needs. Visual feedback is helpful. Maintain eye contact with your patient. Before talking,
eliminate background noise (turn off the radio and the suction). Sometimes people with a hearing
loss simply need you to speak clearly in a slightly louder voice than normal. Remember to remove
your facemask first or wear a clear face shield.

Record in the patients chart strategies that were successful in providing care. Note your patients
preferences and other unique details that will facilitate treatment, such as music, comfort items,
and flavor choices.

oral Health Problems in Intellectual disability and strategies for Care In general, people with
intellectual disability have poorer oral health and oral hygiene than those without this condition.
Data indicate that people who have intellectual disability have more untreated caries and a higher
prevalence of gingivitis and other periodontal diseases than the general population.

PERIODONTAL DISEASE. Medications, malocclusion, multiple disabilities, and poor oral hygiene
combine to increase the risk of periodontal disease in people with intellectual disability.
Encourage independence in daily oral hygiene. Ask patients to show you how they brush, and
follow up with specific recommendations on brushing methods or toothbrush adaptations.
Involve your patients in hands-on demonstrations of brushing and flossing. Some patients cannot
brush and floss independently due to impaired physical coordination or cognitive skills. Talk to
their caregivers about daily oral hygiene. Do not assume that all caregivers know the basics;
demonstrate proper brushing and flossing techniques. A power toothbrush or a floss holder can
simplify oral care. Also, use your experiences with each patient to demonstrate sitting or standing
positions for the caregiver. Emphasize that a consistent approach to oral hygiene is important
caregivers should try to use the same location, timing, and positioning. Some patients benefit from
the daily use of an antimicrobial agent such as chlorhexidine. Recommend an

ap pro priate delivery method based on your patients abilities. Rinsing, for example, may not
work for a patient who has swallowing difficulties or one who cannot expectorate. Chlorhexidine
applied using a spray bottle or toothbrush is equally efficacious. If use of particular medications
has led to gingival hyperplasia, emphasize the importance of daily oral hygiene and frequent
professional cleanings.

DENTAL CARIES. People with intellectual disability develop caries at the same rate as the general
population. The prevalence of untreated dental caries, however, is higher among people with
intellectual disability, particularly those living in noninstitutional settings. Emphasize
noncariogenic foods and

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beverages as snacks. Advise caregivers to avoid using sweets as incentives or rewards. Advise
patients taking medicines that cause xerostomia to drink water often. Suggest sugar-free
medicine if available and stress the importance of rinsing with water after dosing. Recommend
preventive measures such as fluorides and sealants.

MALOCCLUSION. The prevalence of malocclusion in people with intellectual disability is similar to


that found in the general population, except for those with coexisting conditions such as cerebral
palsy or Down syndrome. A developmental disability in and of itself should not be perceived as a
barrier to orthodontic treatment. The ability of the patient or caregiver to maintain good daily
oral hygiene is critical to the feasibility and success of treatment.

tIPs for CaregIvers are avaIlable In tHe booklet Dental Care every Day: a Caregivers guiDe, also
Part of tHIs serIes.

a developmental disability in and of itself should not be perceived as a barrier to orthodontic


treatment.

intellectual disability

MISSINg PERMANENT TEETH, DELAyED ERUPTION, and ENAMEL HyPOPLASIA are more common in
people with intellectual disability and coexisting conditions than in people with

intellectual disability alone. Examine a child by his or her first birthday and regularly thereafter to
help identify unusual tooth formation and patterns of eruption. Consider using a panoramic
radiograph to determine whether teeth are congenitally missing. Patients often find this
technique less threatening than individual films. Take appropriate steps to reduce sensitivity and
risk of caries in your patients with enamel hypoplasia.

DAMAgINg ORAL HABITS are a problem for some people with intellectual disability. Common
habits include bruxism; mouth breathing; tongue thrusting; self-injurious behavior such as picking
at the gingiva or biting the lips; and picaeating objects and substances such as gravel, cigarette
butts, or pens. If a mouth guard can be tolerated, prescribe one for patients who have problems
with self-injurious behavior or bruxism.

TRAUMA and INJURy to the mouth from falls or accidents occur in people with intellectual
disability. Suggest a tooth-saving kit for group homes. Emphasize to caregivers that traumas
require immediate professional attention and explain the procedures to follow if a permanent
tooth is knocked out. Also, instruct caregivers to locate any missing pieces of a fractured tooth,
and explain that radiographs of the patients chest may be necessary to determine whether any
fragments have been aspirated. Physical abuse often presents as oral trauma. Abuse is reported
more frequently in people with developmental disabilities than in the general population. If you
suspect that a child is being abused or neglected, State laws require that you call your Child
Protective Services agency. Assistance is also available from the Childhelp National Child Abuse
Hotline at (800) 4224453 or the Child Welfare Information Gateway
(http://www.childwelfare.gov).

Making a difference in the oral health of a

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person with intellectual disability may go slowly at first, but determination can bring positive
resultsand invaluable rewards. By adopting the strategies discussed in this booklet, you can
have a significant impact not only on your patients oral health, but on their quality of life as well.

Paper : Cuidado bucal prctico para personas con discapacidad intelectual

Proporcionar atencin oral a las personas con discapacidad intelectual requiere la adaptacin de
las habilidades que utiliza todos los das. De hecho, la mayora de las personas con discapacidad
intelectual leve o moderada pueden ser tratadas con xito en el entorno de la prctica general.
Este folleto le ayudar a hacer una diferencia en las vidas de las personas que necesitan atencin
oral profesional.

La discapacidad intelectual es un trastorno del funcionamiento mental y adaptativo, lo que


significa que las personas afectadas son desafiadas por las habilidades que usan en la vida
cotidiana. La discapacidad intelectual no es una enfermedad o una enfermedad mental; Es una
discapacidad de desarrollo que vara en gravedad y suele asociarse con problemas fsicos.
Mientras que una persona con discapacidad intelectual puede tener una leve dificultad para
pensar y comunicarse, otra persona puede enfrentar grandes desafos con el autocuidado bsico y
la movilidad fsica.

Los datos indican que las personas con discapacidad intelectual tienen ms caries no tratadas y
una mayor prevalencia de gingivitis y otras enfermedades periodontales que la poblacin general.

Muchas personas con discapacidad intelectual tambin tienen otras afecciones como parlisis
cerebral, convulsiones o trastornos psiquitricos, trastorno por dficit de atencin / hiperactividad
o problemas con la visin, la comunicacin y la alimentacin. Aunque los problemas de lenguaje y
comunicacin son comunes en cualquier persona con discapacidad intelectual, las habilidades
motoras suelen ser ms afectadas cuando una persona tiene condiciones coexistentes.

Antes de la cita, obtenga y revise la historia clnica del paciente. La consulta con los mdicos, la
familia y los cuidadores es esencial para el montaje de una historia clnica precisa. Adems,
determine quin puede proporcionar legalmente el consentimiento informado para el
tratamiento.

DESAFOS MENTALES. Las personas con discapacidad intelectual aprenden lentamente ya menudo
con dificultad. Las actividades ordinarias de la vida cotidiana, como cepillarse los dientes y
vestirse, y comprender el comportamiento de los dems, as como la suya propia, pueden
presentar desafos a una persona con discapacidad intelectual.

Establezca el escenario para una visita exitosa mediante la participacin de todo el equipo dental -
desde el saludo amistoso de la recepcionista a la actitud de cuidado de la asistente dental en el
operatorio. Todos deben ser conscientes de los desafos mentales de su paciente.

Reduzca las distracciones en el operatorio, como visiones, sonidos u otros estmulos innecesarios,
para compensar los intervalos cortos de atencin comnmente observados en las personas con
discapacidad intelectual.

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Hable con el padre o cuidador para determinar las habilidades intelectuales y funcionales de su
paciente, luego explique cada procedimiento a un nivel que el paciente pueda entender. Permita
tiempo extra para explicar problemas de salud oral o instrucciones y demuestre los instrumentos
que usar.

Dirija a su paciente directamente y con respecto a establecer una relacin. Incluso si el cuidador
est en la sala, dirija todas las preguntas y comentarios a su paciente.

Utilice instrucciones simples y concretas y reptalas con frecuencia para compensar cualquier
problema de memoria a corto plazo. Hable lentamente y d una sola direccin a la vez.

Sea consistente en todos los aspectos de la atencin bucal, ya que la memoria a largo plazo por lo
general no se ve afectada. Use el mismo personal y el operatorio dental cada vez para ayudar a
mantener la familiaridad. Cuanto ms consistencia proporcione a sus pacientes, ms
probabilidades de que cooperen.

Escuche activamente, ya que comunicarse claramente es a menudo difcil para las personas con
discapacidad intelectual. Muestre a su paciente si usted entiende. Sea sensible a los mtodos que
l o ella usa para comunicarse, incluyendo gestos y peticiones verbales o no verbales.

conducta desafos. ansiedad acerca del tratamiento dental se produce frecuentemente , la gente
desconocida una oficina dental y su equipo de instrumentos exponen miedo. algunos reaccionan
con miedo o no coopera con su conducta, como llorando, meneando, patadas, agresivo ,saca la
lengua, o algo que los ayude a evitar el tratamiento. usted puede hacer salud oral dando una
buena experiencia a los pacientes. hablar a el mdico o mdico acerca de tcnicas ellos tener
fundar a ser eficaz en la gestin de la conducta de el paciente. horario en pacientes con
discapacidad intelectual temprano en el da si es posible. citzas temprano ayuda a asegurar que
todo el mundo este alerta y atento y que el tiempo de espera es reducido. mantener citas cortas y
aplazar procedimientos dificiles hasta que despus de tu paciente se familiarice contigo y tu
personal. permitir tiempo extra para que tu paciente este cmodo contigo, tu oficina, y el.

invitar a pacientes y su familias a visitar tu oficina antes del comienzo del tratamiento. permitir a
padres o mdico a venir al tratamiento en el establecimiento y asi proporcionar familiaridad,
ayuda con comunicacin, y ofrecer un calmante para que no se desespere durante tratamiento.
algunos pacientes 'mejoran su conducta si llevan artculos tal como un relleno animal o manta. o
recompensa cooperativa es decir conducta con felicitaciones en toda la cita. considerar nitroso
xido / oxgeno sedacin a reducir ansiedad y miedo y as mejorar la cooperacin. obtener
consentimiento informado en inmovilizacin en caso de aplicar a todo tratamiento. antes del
empleo a cualquier clase de inmovilizacin, se necesitara consultar en el gobierno federal
financiado cuidado,estado departamento de salud mental / discapacidad, y estado dental prctica
acto. para as obtener consentimiento de tu paciente legal guardin y elegir el menos restrictivo,
tcnica quele permitir usted a proporcionar cuidado y seguridad. inmovilizacin debera no
causar lesin fisica o indebidas molestias. gente con intelectual discapacidad a menudo participar
en un continuo y sin sentido repeticin de palabras, frases, o movimientos. tu paciente imitar el
sonido de el succinador, por ejemplo, o repetir un instruccin ms y de nuevo. evitar usar este si
nota en el paciente este registro.Desafios fisicos.no siempre incluir un especfico rasgo fsico,
aunque mucha gente distingue caractersticas tal como anomalias orofaciales , escoliosis, o

~ 13 ~
hipotona debido a sus condiciones. lucha contra fsicos desafos requiere atencin a detalles.
mantener claro caminos para movimientos en todo el establecimiento. mantener instrumentos y
equipo lejos de el camino del paciente. y mantener a tu paciente en el centro de silla dental a
minimizar el riesgo de lesin. colocar almohadas en ambos lados para proporcionar estabilidad. si
que necesita a transferencia tu paciente de un silla de ruedas a la silla dental , preguntar el
paciente o mdico acerca de preferencias tal como relleno, almohadas, o otro cosas usted puede
proporcionar a facilidad el transicin. el paciente o mdico lata a menudo explicar cmo a hacer
un liso transferencia. algunos pacientes no puede ser movidos en el sillon dental en su lugar deben
ser tratados en su sillas de ruedas. algunos sillas de ruedas.recordar cerradura el ruedas, entonces
deslizar un corredizo bordo (tambin llamado un transferencia bordo) detrs el paciente atrs a
proporcionar apoyo para el cabeza y cuello durante cuidado. atrs a topback a superior cerebral
parlisis se produce en de aquellos quin tener intelectual discapacidad y tiende a afectar
habilidades motoras ms que cognitivos. incontrolados movimientos del cuerpo y reflejos
asociados con paralisis cerebral hace difcil proporcionar un cuidado, debes mantener a tu
paciente en el centro de el dental silla. no hacer fuerzas en brazos y piernas en posiciones
antinaturales, pero permitir tu paciente a establecerse en un posicin es decir cmodo y a su
voluntad no interferir con dental tratamiento. observar movimientos de tu paciente y buscar
patrones ayuda a usted a prever direccin y intensidad. intentr parar estos movimientos slo
intensifica una respuesta involuntaria. intentar en lugar a prever el movimientos, mezcla tu
movimientos con aquellos de tu paciente . ser suave y lento si que necesita a turno el paciente
ayuda minimizar el reflejo por colocar tu paciente barbilla en un neutral o hacia abajo. quedarse
alerta y trabajar eficientemente en citas cortas. ejercer suave pero firme presin en tu paciente
brazo o pierna si lo comienza a batido. gente con cerebral parlisis tienen mayor necesidad de
sedacin, anestesia general, o hospitalizacin si es un tratamiento extenso es necesario. anomalas
tal como corazn murmura y daadas las valvulas del corazn puede ocurrir frecuentemente en
gente con discapacidad intelectual, especialmente aquellos con sndromes o mltiple
discapacidad. consultar el paciente mdico a determinar uso de antibiticos, es necesario para
dental tratamiento. ser controlado con medicamentos anticonvulsivante

siempre hay riesgo durante un embargo: pacientes que se muerden la lengua o mejillas. personas
con controlado embargo trastornos lata fcilmente ser tratados en el general dental oficina.
consultar tu paciente mdico. antes de la cita ver si usa medicamentos y si han sido tomados como
dirigido. saber y evitar cualquier factores que desencadenar tu paciente incautaciones. preprese
a administrar un embargo. si uno se produce durante oral cuidado, eliminar cualquier
instrumentos de el boca y claro el rea alrededor el dental silla. adjuntando seda dental floja a
caucho y accesorios . no hacer intento de introducir cualquier objetos entre el dientes durante un
embargo. quedarse con tu paciente, a su lado, y controlar el va area a reducir el riesgo de
aspiracin.. determinar el nivel de ayuda que tu paciente requiere a avanzar con seguridad por la
ofiicina dental. uso tu pacientes' con otros sentidos a conectarles, establecer confianza, y hacer del
tratamiento una buena experiencia. tctil , tal como un caliente apretn de manos, para hacer
sentir a tus pacientes cmodos. caras cuando usted habla y mantener les informado de cada
prximo paso, especialmente cuando se ultiliza agua, explicar procedimientos y demostrar cmo
equipo podra sentir y escuchar. proporcionar escrito instrucciones en grande imprimir (16 punto o
mayor). atrs a topback a superior perdida de odo y sordera tambin debe ser con cuidadoso y
con planificacin. pacientes con un problema de odo parecen ser tercos con motivo de su
aparente falta de respuesta a un peticin. pacientes con deseo de ajustar su audfonos o listos
para retirarse, hasta el sonido de algunos instrumentos causa molestias auditivas. si tu paciente

~ 14 ~
lee labios, hablar en un normal cadencia y tono. si tu paciente usos un formulario de firmar
lengua, preguntar por el intrprete si va a venir a la cita. hablar con este persona en avance a
discutir condiciones dentales y las necesidades de tu paciente. mantener ojo contacto con tu
paciente. antes de hablar, eliminar fondo ruido (apagar el radio y el succin).a veces la gente con
perdida auditiva necesita escucharte mas claro,. recordar a eliminar tu mascarilla primero. detalles
que facilitarn el tratamiento, tal como msica, sabor y opciones.

Problemas de Salud Bucal en Discapacidad Intelectual y Estrategias para el Cuidado

En general, las personas con discapacidad intelectual tienen una salud bucal y una higiene bucal
ms pobres que las que no tienen esta condicin. Los datos indican que las personas con
discapacidad intelectual tienen ms caries no tratadas y una mayor prevalencia de gingivitis y otras
enfermedades periodontales que la poblacin general.

ENFERMEDAD PERIODONTAL. Los medicamentos, la maloclusin, las discapacidades mltiples y la


mala higiene bucal se combinan para aumentar el riesgo de enfermedad periodontal en personas
con discapacidad intelectual.

Fomentar la independencia en la higiene oral diaria. Pida a los pacientes que le muestren cmo se
cepillan y haga un seguimiento con recomendaciones especficas sobre los mtodos de cepillado o
las adaptaciones del cepillo de dientes. Involucre a sus pacientes en demostraciones prcticas de
cepillado y uso del hilo dental.

Algunos pacientes no pueden cepillarse y usar hilo dental independientemente debido a la


coordinacin fsica o habilidades cognitivas. Hable con sus cuidadores sobre la higiene oral diaria.
No asuma que todos los cuidadores conocen los conceptos bsicos; Demostrar el cepillado
adecuado y las tcnicas de hilo dental. Un cepillo de dientes de poder o un sostenedor de la seda
puede simplificar el cuidado oral. Tambin, use sus experiencias con cada paciente para demostrar
posiciones sentadas o de pie para el cuidador. Enfatice que un acercamiento consistente a la
higiene bucal es importante - los cuidadores deben tratar de usar la misma ubicacin, tiempo y
posicionamiento.

Algunos pacientes se benefician del uso diario de un agente antimicrobiano tal como la
clorhexidina. Recomiende un mtodo de entrega apropiado basado en las habilidades de su
paciente. El enjuague, por ejemplo, puede no funcionar para un paciente que tiene problemas de
deglucin o uno que no puede expectorar. La clorhexidina aplicada con una botella de spray o un
cepillo de dientes es igualmente eficaz.

Si el uso de determinados medicamentos ha conducido a la hiperplasia gingival, destacar la


importancia de la higiene bucal diaria y limpiezas profesionales frecuentes.

Los consejos para los cuidadores estn disponibles en el folleto Cuidado dental todos los das: Gua
del cuidador, tambin parte de esta serie.

CARIES DENTAL. Las personas con discapacidad intelectual desarrollan caries al mismo ritmo que
la poblacin general. Sin embargo, la prevalencia de caries dentales no tratadas es mayor entre las
personas con discapacidad intelectual, en particular las que viven en entornos no institucionales.

~ 15 ~
Enfatizar los alimentos y bebidas no cariognicos como bocadillos. Aconseje a los cuidadores que
eviten el uso de dulces como incentivos o recompensas.

Informe a los pacientes que toman medicamentos que causan xerostoma que beben agua con
frecuencia. Sugiera un medicamento sin azcar si est disponible y destaque la importancia de
enjuagar con agua despus de la dosificacin.

Recomendar medidas preventivas como fluoruros y sellantes.

MALOCCLUSIN. La prevalencia de maloclusin en personas con discapacidad intelectual es


similar a la encontrada en la poblacin general, excepto en aquellos con afecciones coexistentes
como la parlisis cerebral o el sndrome de Down. Una discapacidad del desarrollo en s misma no
debe ser percibida como una barrera para el tratamiento ortodncico. La capacidad del paciente o
cuidador para mantener una buena higiene bucal diaria es fundamental para la viabilidad y el xito
del tratamiento.

LOS DIENTES PERMANENTES QUE FALTAN, LA ERUPCIN RETARDADA y la HIPOPLASIA


ESMALTICA son ms comunes en personas con discapacidad intelectual y condiciones
coexistentes que en personas con discapacidad intelectual por s solas.

Examine a un nio para su primer cumpleaos y con regularidad a partir de entonces para ayudar
a identificar la formacin inusual de los dientes y los patrones de erupcin.

Considere la posibilidad de utilizar una radiografa panormica para determinar si los dientes estn
desaparecidos congnitamente. Los pacientes a menudo encuentran esta tcnica menos
amenazante que las pelculas individuales.

Tome las medidas apropiadas para reducir la sensibilidad y el riesgo de caries en sus pacientes con
hipoplasia del esmalte.

HBITOS ORALES DAINOS son un problema para algunas personas con discapacidad intelectual.
Los hbitos comunes incluyen el bruxismo; respiracin por la boca; Empuje de la lengua;
Comportamiento auto-perjudicial, como la cosquilleo en la enca o mordiendo los labios; Y pica,
comiendo objetos y sustancias tales como grava, colillas de cigarrillos, o plumas. Si se puede
tolerar un protector bucal, prescriba uno para los pacientes que tienen problemas con el
comportamiento auto-perjudicial o el bruxismo.

TRAUMA y LESIONES a la boca por cadas o accidentes ocurren en personas con discapacidad
intelectual. Sugiera un kit de ahorro de dientes para las casas de grupo. Enfatizar a los cuidadores
que los traumas requieren atencin profesional inmediata y explicar los procedimientos a seguir si
un diente permanente es eliminado. Tambin, instruya a los cuidadores para localizar cualquier
pieza faltante de un diente fracturado y explique que radiografas del trax del paciente pueden
ser necesarias para determinar si se han aspirado fragmentos.

~ 16 ~
El abuso fsico a menudo se presenta como un trauma oral. El abuso se informa ms
frecuentemente en personas con discapacidades del desarrollo que en la poblacin general. Si
sospecha que un nio ha sido abusado o descuidado, las leyes estatales requieren que llame a su
agencia de Servicios de Proteccin Infantil. La asistencia tambin est disponible en la lnea directa
de Childhelp National Child Abuse al (800) 422-4453 o en la pasarela de informacin sobre
bienestar infantil (http://www.childwelfare.gov/).

Hacer una diferencia en la salud bucal de una persona con discapacidad intelectual puede ir
lentamente al principio, pero la determinacin puede traer resultados positivos - y recompensas
invaluables. Al adoptar las estrategias discutidas en este folleto, puede tener un impacto
significativo no slo en la salud bucal de sus pacientes, sino tambin en su calidad de vida.

Batshaw ML, Shapiro B, Farber MLZ. Developmental Delay & Intellectual Disability. In Batshaw ML,
Pellegrino L, Roizen NJ (eds.). Children With Disabilities (6th ed.). Baltimore, MD: Paul H. Brookes
Publishing Co., 2007.

Horwitz SM, Kerker BD, Owens PL, Zigler E. Dental health among individuals with mental
retardation. In The Health Status and Needs of Individuals With Mental Retardation. New Haven,
CT: Yale University School of Medicine, 2000. pp. 119-134.

U.S. Public Health Service. Closing the Gap: A National Blueprint for Improving the Health of
Individuals With Mental Retardation. Report of the Surgeon General's Conference on Health
Disparities and Mental Retardation. Washington, DC, February 2001.

Weddell JA, Sanders BJ, Jones JE. Dental problems of children with disabilities. In McDonald RE,
Avery DR, Dean JA. Dentistry for the Child and Adolescent (8th ed.). St. Louis, MO: Mosby, 2004.
pp. 524-556.

~ 17 ~
Trastorno espectro autista:

Definicin:

Condicin de origen cerebral que implica una deficiencia en la interaccin social y en la


comunicacin afectando el actuar, el aprendizaje y la comunicacin con el medio , tambin se
relaciona con la epilepsia en un 30% ya que las neuronas y ncleos son mas pequeos adems se
presencia en algunos casos el aumento de sustancia blanca en lbulos frontales provocando una
macrocefalia.

esta condicin se desarrolla en la niez y dura toda la vida

Se le denomina espectro por la gran cantidad de sntomas diferentes

este incluye al sndrome de asperger

no hay genes especificos para el TEA pero si se sabe que este es hereditario , se relaciona a mal
funcionamiento en genes que codifican proteinas y transmiten seales en sistemas relacionados
con la proliferacion , crecimiento y sobrevivencia celular , gracias a investigaciones se encontro
relacion en el gen MET de cromosoma 7q31 que es mas angosto respecto del desarrollo normal
neocortical y cerebeloso. por lo que se dice que el organo de origen del autismo es la corteza
cerebral

un test de CI muestra que los nios con TEA poseen un mimo resultado con los que no lo padecen ,
solo que en los nios con TEA no tienen sincronizacion neuronal es decir un desbalance en celulas
inhibitoria y exitatorias , provocando deficiencia socioemocional

Epidemiologia:

Afecta a 1 persona en 10000 mundialmente , pero 1 en 150 son portadoras del TEA

Segn encuesta nacional de discapacidad en el ao 2004 del total de la poblacin chilena, 1 de


cada 1000 chilenos presenta discapacidad por trastornos severos de la comunicacin

ENANTE(encuesta nacional sobre el espectro del autismo) dice que en santigo hay 48.000
personas con TEA y los hombres son mas suceptibles que las mujeres

Causas:

no se conocen las causas se cree que esta dado por factores tanto geneticod como ambientales y
esta relacionada con distintas patologias de las cuales solo se da en el 10 a 20% de los casos

Signos y sntomas:

Problemas sociales principalmente en cuanto a comunicacin , las personas que padecen TEA no
tienen interes por las demas personas , cuando estas les hablan no mantienen contacto visual y
parecen no escucharte ni responden a su nombre , tampoco les gusta cambiar su rutina diaria, son
muy sensibles al ruido, repiten o imitan frases y acciones

Poseen una desarrollada imaginacion y un apego hacia algun objeto

~ 18 ~
Diagnstico:

Este es deductivo de parte de los profesionales pero se realiza una serie de pruebas para no caer
en el error DIM IV TR clasifican y caracterizan el comportamiento del paciente pero para esto se
necesita participacin multidisciplinaria, el paciente debe tener aproximadamente un minimo de 3
a 4 aos de edad para que este pueda colaborar con la informacin y no sea inespecifico el
diagnstico

La profundizacin se basa en la deficiencia en la interaccin social, alteracin en la comunicacin y


los patrones restringidos de comportamiento .

No hay cura para esta condicin pero si se logra una intervencin temprana el paciente puede
desarrollar habilidades, para esto se ha probado distintas terapias , como por ejemplo :
musicoterapia , zooterapia , arteterapia pero estos solo han funcionado en algunos casos y por
algn periodo de tiempo

~ 19 ~
Trastorno espectro autista y la odontologa:

Estos pacientes no presentan manifestaciones bucales por su condicin pero si hay pacientes que
les molesta tener la cara mojada , o el sabor y textura de la pasta de dientes asi como tambin hay
otros que no saben escupir todo va a depender del tipo de paciente , por lo mismo hay que seguir
un protocolo el cual consiste en hablar con los padres para asi tener en cuenta como se comporta
el paciente , tambin se necesitara mostrarle los implementos, as como un paseo por la consulta
ya que este tipo de pacientes necesitan uniformidad y continuidad en su entorno , por lo que
mostrarle los implementos reduce la ansiedad, as como tambin el tono de voz el cual debe ser
calmado y amistoso con palabras directas y cortas

Al momento de realizar cualquier movimiento desde el encendido de la luz este debe ser
advertido asi como el ruido ya que pueden provocar alteraciones en la conducta del paciente.

~ 20 ~
The Caries Experience and Behavior of Dental Patients With Autism Spectrum Disorder

ABSTRACT Inline Image fx1

Background

Autism spectrum disorder (ASD) is a lifelong neurodevelopmental disorder. The authors conducted
a study to evaluate the demographics, caries experience and behavior of patients with ASD and
compare these characteristics with those of patients without ASD (unaffected patients).

Methods

The authors reviewed patients' charts and identified a group of 395 patients with ASD and a group
of 386 unaffected patients. They obtained the following patient data for analysis: primary
diagnosis, age, sex, residence (home versus institution or group home), presence of seizure
disorder, additional diagnosis (mental retardation, cerebral palsy, self-injurious behavior or pica),
medications, caries prevalence, caries severity and behavior.

Results

The ASD group had a male:female ratio of 4:1, and patients had a diagnosis of autism, pervasive
developmental disordernot otherwise specified or Asperger syndrome. Sex distribution was equal
in the unaffected group, which was younger and had a higher decayed, missing and filled teeth
(DMFT) score than did the ASD group. When the authors controlled for age and sex, they noted a
statistically significant association between ASD and dental caries prevalence. A significantly higher
percentage of patients with ASD than unaffected patients were uncooperative and required dental
treatment to take place under general anesthesia. Caries prevalence and severity in patients with
ASD were not associated with institutionalization, presence of seizure disorder or additional
diagnosis.

Conclusions

People with ASD were more likely to be caries-free and had lower DMFT scores than did their
unaffected peers. Significantly more patients with ASD than unaffected patients were
uncooperative and required general anesthesia to undergo dental treatment.

~ 21 ~
Paper: La experiencia de la caries y el comportamiento de los pacientes dentales con trastorno del
espectro autista

ABSTRACTO

Fondo

El trastorno del espectro autista (TEA) es un trastorno del desarrollo neurolgico de por vida. Los
autores realizaron un estudio para evaluar la demografa, la experiencia de caries y el
comportamiento de los pacientes con TEA y comparar estas caractersticas con las de los pacientes
sin TEA (pacientes no afectados).

Mtodos

Los autores revisaron los pronsticos de los pacientes e identificaron un grupo de 395 pacientes
con TEA y un grupo de 386 pacientes no afectados. Se obtuvieron los siguientes datos del paciente
para su anlisis: diagnstico primario, edad, sexo, residencia (hogar versus institucin o grupo de
hogar), presencia de trastorno convulsivo, diagnstico adicional (retraso mental, parlisis cerebral,
comportamiento auto-perjudicial ) Prevalencia de caries, gravedad de la caries y comportamiento.

Resultados

El grupo ASD tena una relacin hombre-mujer de 4: 1, y los pacientes tenan un diagnstico de
autismo, trastorno generalizado del desarrollo, no especificado de otro modo o sndrome de
Asperger. La distribucin del sexo fue igual en el grupo no afectado, que era ms joven y tena una
puntuacin ms alta cariada, faltante y llena de dientes (DMFT) que en el grupo ASD. Cuando los
autores controlaron la edad y el sexo, observaron una asociacin estadsticamente significativa
entre el ASD y la prevalencia de caries dental. Un porcentaje significativamente mayor de
pacientes con TEA que los pacientes no afectados no cooperaron y requirieron tratamiento dental
bajo anestesia general. La prevalencia de caries y la gravedad en pacientes con TEA no se
asociaron con la institucionalizacin, la presencia de trastorno convulsivo o un diagnstico
adicional.

Conclusiones

Las personas con TEA tenan ms probabilidades de caries y tenan menores puntuaciones de
DMFT(dientes definitivos cariados) que sus pares no afectados. Significativamente ms pacientes
con TEA que los pacientes no afectados no cooperaron y requirieron anestesia general para
someterse a tratamiento dental.

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Parlisis Cerebral.

Antecedentes.

La parlisis cerebral como su nombre lo dice donde parlisis significa una debilidad o problema
cuando se posiciona el cuerpo y cerebral de cerebro. Adems este se genera cuando el sistema
nervioso no ha terminado de madurar (antes de los cinco aos)

Este es un trastorno que compromete funciones del cerebro y sistema nervioso, este no empeora
con el tiempo, ni se puede traspasar de una generacin a otra. Esta no es una enfermedad
especfica, sino un grupo de trastornos de causas variables ya que depende de donde se localiza la
lesin en el cerebro y la gravedad de una persona. Es crnico no progresivo, secundario a lesin
cerebral producida durante el crecimiento intrauterino o en el momento del parto por falta de
oxgeno (hipoxia) durante el periodo de expulsin o cuando su cerebro este en desarrollo.

Epidemiologia.

Su incidencia es de 2-2.5 por 1000 nacidos vivos y la prevalencia se ha reportado hasta 5 por 1000
habitantes.

Por estudios internacionales, se dice que la prevalencia es mucho mayor en pases en desarrollo
que con los industrializados.

Causas.

Esta parlisis es causada por irregularidades al cerebro. Las complicaciones del nacimiento son
responsable de solo una parte de las causas ya que los bebes nacidos con parlisis congnita (se le
llama as cuando nace con ella, aunque los sntomas se pueden observar hasta meses o aos
despus), otra parte proviene de la parlisis cerebral adquirida lo que significa que comienza
despus del nacimiento por algn motivo especifico como:

- Sangrado del cerebro


- Infecciones cerebrales
- Lesin craneana debido a accidente o cada.

Por ultimo este puede ocurrir durante el desarrollo fetal tanto antes, durante y despus del
embarazo que da desarrollo a particulares causas:

- Dao materia blanca del cerebro donde esta es responsable de transmitir seales dentro
del cerebro y el resto del cuerpo.
- Desarrollo anormal del cerebro donde cualquier interrupcin del proceso normal va causar
una mal formacin interrumpiendo seales.
- Hemorragia cerebral donde puede ocurrir un coagulo sanguneo en la placenta
bloqueando el flujo sanguneo. La alta presin maternal puede llegar a causar un
accidente cerebrovascular.
- Hipoxia, la falta de oxgeno al momento de expulsin del bebe.
- Incompatibilidad entre madre y feto.
- Ictericia severa coloracin amarillenta de la piel y la parte blanca de los ojos causada por
acumulacin de pigmento.

~ 23 ~
Signos y Sntomas.

Los signos aparecen generalmente antes que el nio alcance los tres aos, cuando encontramos
un bebe va tener retraso del desarrollo (se logra observar porque son lentos para aprender a
sentarse, gatear, sonrer o caminar), generalmente favorecen a un solo lado y adoptan una mal
postura, adems en su tono muscular pueden tener hipotona, una disminucin del tono muscular;
hipertona, un aumento de tono muscular; variable, variacin del tono muscular.

Los sntomas van a variar dependiendo el/la paciente, podemos observar diversos sntomas
dependiendo que grado y lugar ha sido daado en el cerebro.

- Agnosia: alteracin de la sensibilidad del tacto.


- Apraxias: incapacidad de realizar movimientos adecuados.
- Alteracin de la atencin, deshidratacin frecuente.
- Contracturas musculares, dislocaciones.
- Dficit intelectual
- Problemas de comunicacin: no tienen capacidad de controlar msculos fonatorios.
- Problemas de crecimiento: interrupcin en su desarrollo en la adolescencia.
- Incontinencia a la vejiga: debido a la falta de control de musculatura.

Adems estos los podemos clasificar dependiendo el tipo de parlisis que contenga:

Parlisis cerebral espstica, sus msculos muy tensos, no se estiran, marcha anormal,
articulaciones rgidas. Estos pueden afectar un lado del cuerpo, o una pierna, o brazo
dependiendo de la lesin y
1. Hemiparesia: afecta solo un lado del cuerpo.
2. Diparesia: afecta las cuatro extremidades del cuerpo con predominio las
extremidades inferiores.
3. Cuadriparesia: afecta las cuatro extremidades del cuerpo.
4. Hemiparesia doble: afecta las cuatro extremidades con predominio extremidades
superiores
5. Monoparesia: afecta mayor grado a solo una extremidad.
Parlisis cerebral disquinetica o atetosis, son mayormente movimientos involuntarios,
reflejos primitivos, posturas anormales, trastornos en los movimientos. Tienen afectados
msculos buco-farngeo.
Parlisis cerebral atxica, se caracteriza por la dificultad de controlar el equilibrio, falta de
coordinacin del movimiento, poseen temblores y marchas atxica pero a partir del
segundo ao de vida.

~ 24 ~
Relacin odontolgica.

La parlisis cerebral compromete habilidades motoras como cognitiva en las personas lo que esto
va a desencadenar una mala higiene bucal, y problemas en su salud oral.

Ahora si bien los problemas se pueden clasificar dependiendo el tipo de parlisis que tenga no
significa que sea exclusivamente de esta. Este trastorno dificulta mucho ms el control y la
prevencin de algunas patologas, ya que se bien el tratamiento se logra hacer con ayuda del
odontlogo, debe a ver una ayuda de los padres ya que los que padezcan parlisis mental no
tienen la misma capacidad de poder mantener su higiene como una persona que no tenga parlisis

Existen distintos tipos de grado de incidencia dependiendo el problema que tenga en la cavidad
oral, podemos diferenciar algunos como:

Caries: el grado es estadsticamente similar al resto, lo que se produce diferente es que las
lesiones pueden ser de mayor tamao, gravedad o profundidad.
Enfermedad periodontal: el grado es medianamente alto, ya que la higiene bucal tiene
limitaciones fsico-motoras, por lo que depende de un tutor para que este se realice bien.
Mal oclusiones: presentan un 50% ms que las personas que no contienen parlisis
cerebral, ya que contienen una mala armona entre los msculos oro faciales con los
movimientos de este.
Hipoplasia al esmalte: esto se debe a que hay una malformacin del cerebro, el proceso de
formacin de diente se ve alterado.
Interposicin lingual: donde los msculos estn contrados hacen que all una mayor
secrecin salival.

Ya sabiendo el grado de incidencia de algunos problemas de la sanidad bucal y el estado de este


todo va a depender de que parlisis va a contener el paciente, por lo que el personal odontolgico
debe identificar tempranamente el compromiso que este conlleva teniendo en cuenta la posicin,
puede ocurrir una disfagia, movimiento impredecibles, buena comunicacin, y una buena
concentracin.

- Parlisis Espstica: la rigidez de los msculos va a provocar que exista una mordida
cruzada o submordida, problemas deglutorios, el alimento no se degrada de inmediato
por lo que se tiene mucho tiempo en la boca haciendo que la placa bacteriana
desmineralice el esmalte. Los cepillos de dientes convencionales no sirven por lo que debe
a ver un manejo odontolgico adaptando el mango del cepillo para que se pueda tomar
bien. Aun as no se asegura una correcta higiene, por lo que debe ser complementada con
los padres.
- Parlisis Atetosis: tienen problema de deglucin e incontinencia salival. El mal control de
los msculos se produce el babeo que tiene otras consecuencias como irritacin a la piel,
lesiones en los labios. Para poder controlar esto el odontlogo debe indicar frmacos que
van a disminuir el flujo salival por lo que puede conllevar a otras consecuencias como la
aparicin de caries que debern ser tratadas constantemente.
- Parlisis Atxica: debido a su desequilibrio y los temblores pueden llegar a causar
traumatismo en los dientes anteriores, o pueden desarrollar bruxismo gastando ms de lo
normal los dientes ya que los temblores son muchos. Esto se maneja a travs de placas de
relajacin, que el odontlogo deber cambiar constantemente durante meses, para as ir
disminuyendo lo mximo posible esta friccin entre dientes.
~ 25 ~
Effects of Abnormal Oral Reflexes on Speech Articulation in Persian Speaking Children with
Spastic Cerebral Palsy

Abstract

Objective

The purpose of this study was to investigate the relationship between the presence of
abnormal oral reflexes and speech sound production in children with severe cerebral palsy.

Materials & Methods

Seven oral reflexes such as, rooting, mouth-opening, biting, chewing, lip, tongue, and suckling
were examined in 52Persian-speaking monolingual children with spastic cerebral palsy (ages 5-
10 yr).Phonetic information tests were administered to investigate their ability for articulation
of the speech sounds.

Results

A significant relationship between three (i.e. the chewing, lip, and biting reflexes) out of the
seven abnormal oral reflexes and the speech articulation was noticed. The presence of the
chewing reflex was associated with deficits in production of /s, z, ,/ sounds. The lip reflex
was associated with deficits in the production of /p, m, r, j, f, / sounds. The biting reflex was
associated with deficits in the production of /z, l, y and / sounds. No significant relationship
was found between the rooting, mouth-opening, tongue, and suckling reflexes and sound
articulation.

Conclusion

The presence of abnormal reflexes in the children with spastic cerebral palsy would suggest a
correlation between these reflexes and sound articulation in Iranian children with spastic
cerebral palsy. Hence, these observations might suggest some disturbances in normal speech
development.

Key Words: Cerebral palsy, Abnormal oral reflexes, Sound articulation, Persian

Introduction

There are three different types of Cerebral palsy (CP) as spastic, ataxic, and athetosis (1-3). It is
mainly a movement disorder caused by non-progressive brain damage which occurs during the
fetal development and birth. The prevalence of CP in children between 3-10 yr is 2.4/1000
live-born children (4-6). Classification of CP has also been made by the numbers of limbs that
are affected (5, 7, 8) and the most common type is spastic CP (3, 4,7). CP is commonly
associated with the disorders of vision, hearing, speech, receptive and expressive language
function, swallowing/feeding, and oral motor function (9, 10). Oral motor disorders in CP
include jaw instability, tongue thrusting, poor tongue movement, poor lip closure,and
excessive drooling. Abnormal oral reflexes have also been observed in children with CP (11).
Clinically, the oral reflexes are not usually observed in children after 18 months (12);
therefore, their developments are quite critical for normal feeding, nutrition, and speech. The
persistence of these reflexes after 18 months in children with CP is considered abnormal and
may have negative effects on the oral motor functions. There are few studies regarding the
~ 26 ~
abnormal oral reflexes in children with CP and their association with speech problems (12, 13).
Accordingly, Sheppard (1964) reported a relation between the primitive craniooropharyngeal
motor patterns and speech performance in athetosis and spastic types of CP (14). Seven
abnormal oral reflexes or deviant oral behavior characteristics have been reported in children
with CP as follows: rooting, mouth-opening, biting, chewing, lip, tongue, and suckling (12-14).
Some speech and language pathologists argue that the presence of abnormaloral reflexes in
children older than 2 yr with CP may indicate the immature or pharyngeal functions. Poor oral
function can contribute to some problems in speech articulation. The main object of this study
was to investigate the relationship between the presence of abnormal oral reflexes and
articulation in Iranian children with spastic CP.

Materials & Methods

Participants

In this non-interventional study, 52 children with spastic CP (5 to 10 yr, 8.5 - SD 0.0565)


referred for rehabilitation services to the clinic of the Faculty of Rehabilitation (Tehran
University of Medical Sciences, Tehran, Iran) enrolled in the study. Inclusion criteria were
based on medical and rehabilitation records and also by the assessments of speech and
language pathologist. The participant had to have no prior records for language deficit,
intellectual deficit, auditory or visual problems, or craniofacial deformities such as a cleft
palate. All participants were monolingual native speakers of Persian. The ethical committee of
Tehran University of Medical Sciences approved the study and a written informed consent
formed was obtained from all parents.

Procedures

Oral reflexes such as rooting, opening of the mouth, lip, tongue, and biting, chewing and
suckling reflexes were evaluated through direct observations and assessments of the children
by a speech and language pathologist. Assessments were based on the presence or absence of
reflexes through the reactions of children to stimuli as described by Mysak (12, 13; Table 1).

The Persian language comprise of twenty-three consonants and six vowels. According to the
manner of articulation, Persian consonants contain the seven plosives/ p, b, g, k, t, d,q/,eight
fricatives/f, v, s, z, h, x, , /, three nasals/m,, n/, two affricates/ , j /one trill /r/, one sound
that is an approximant/y/, and one lateral approximant/l/(15). Most Persian children can
correctly produce all consonants by the age of 5 yr (16). Sixty-eight pictures were presented as
a phonetic test to make assessments for articulation. The test consisted of Persian consonants
being placed at initial, middle and final positions in words. Children were asked to name these
words and then, any error in articulation was recorded on a tape by a speech and language
pathologist. A speech sound was considered as an error if it was misarticulated in at least one
word position and in at least one word. Substitutions, omissions and distortions were
considered as errors. A speech-recorded sample from each child was transcribed using the
International Phonetic Alphabet (IPA). The numbers of incorrect phonemes (extracted from
the transcriptions) were determined for each child. All of the oral reflexes were assessed and
those reflexes contributed to the articulation of the specific sounds such as the lip reflex for
labial and labiodental sounds such as p and fare characterized in Table 2.

~ 27 ~
The Chi-squared test was used for statistical analysis in order to compare the relationship
between the abnormal oral reflexes and articulations for speech sounds. Fishers Exact was
employed for small expected values (less than 5) and the significance value was set at P<0.05.

Results

Fifty-two children aged 5-10 yr with spastic CP participated in this study; comprising of 24
quadriplegia, 19 diplopia, 5 hemiplegia and 4 paraplegia. Evaluation for the presence of
abnormal oral reflexes in children is shown in Figure1. The status of articulation according to
the place and manner of articulations is shown in Figure2. The relationship between the
presence of lip reflex and the articulation of sounds /p, m, r, y, f, /is shown in Table 2. The
presence of a chewing reflexing relationto the articulations of/z, / was significant (P<0.05;
Table 3). There was no significant relationship between the presence of tongue and rooting
reflexes with the articulation of any sound.

Discussion

The purpose of this study was to evaluate the presence of abnormal oral reflexes and their
possible effects on the ability of producing speech sounds in children with spastic CP. The
results of this study showed that abnormal oral reflexes were common in older children with
spastic CP in agreement with previous studies (12-14, 17).Our study also showed that the
chewing reflex was the most common reflex observed in these children. However, the biting
reflex was the most frequent abnormal reflex (18). Reflexes of suckling and rooting were the
least frequent reflexes; in agreement with Love et al. study (18). In terms of the manner of
articulation, the articulation of fricatives was relatively more difficult in children participated in
this study; similar to Platt et al. results (19). Similarly, linguo-alveolar fricatives were closely
linked with oral reflexes (20). However, dental and glottal sounds were the most problematic
for these children during articulation (21). Our results revealed that the accuracy of
articulation was the greatest for bilabial and nasal sounds; which were similar to the findings
in normal children (22). There was a significant relationship between the presence of lip reflex
and the articulation of sounds /p, m/;this could be explained by the variety of involuntary lip
movements displayed by children with spastic CP. As the lip reflex might also trigger other oral
movements such as tongue movement, misarticulation of the sounds i /r, y, f, / might also be
observed in these children. Similar results were also reported by Mysak regarding the
abnormal lip reflex and the possible interference with articulation of /p, m, f/ sounds (12).
However, no relationship was reported between the oral reflexes and articulation proficiency
in older CP children in another study (18). We saw a relationship between the biting and
chewingreflexes and misarticulation of the sounds /z, /. These observations might be due to
the unregulated closing or opening of the jaw following the biting and chewing reflexes that
could effect on tongue movements and this in turn could lead to the misarticulation of the
sounds /z, /. Some researchers have acclaimed this suggestion (12-14, 23); whereas others
believed that the levels of oral reflexes and motor control in speech in the nervous system
were separate mechanisms (24, 25). Therefore, suggested that the abnormal (primitive) oral
reflexes had no effects on speech development. Our data showed an interrelation between
the oral reflexes and sound articulation in older CP children. In addition, normal oral reflexes
in CP play a primary role in feeding skills (12-14). Therefore, a possible relationship could be
presumed between the development of oral reflexes and misarticulation of sounds in CP
children. However, considering some controversies in studies, further studies are needed to

~ 28 ~
elucidate these points. In addition, future studies could be carried out in order to investigate
the presence of oral reflexes in different types of CP and also to determine the results of
treatment of abnormal oral reflexes and their effects on sound articulation.

In conclusion, our results showed the presence of abnormal oral reflexes in children with CP
and the possible effects of these reflexes on sound articulation.

Acknowledgements

This study was supported by Tehran University of Medical Sciences. We would like to
appreciate their generous support.

Author Contribution

HooshangDadgar: Responsible for the study design, collection, and interpretation of the
clinical data and editing in all stages.

Mohammad Reza Hadian: Responsible for the study design, interpretation of the clinical data
and editing in all stages.

Ortega Adriana Lira: involved in first editing of this manuscript. All authors agreed to be
accountable for all aspects of the work in ensuring that questions related to the accuracy or
integrity of any part of the work are appropriately investigated and resolved.

Conflicts of Interest

The Authors declare that there is no conflict of interest

References

1. Surveillance of Cerebral Palsy in Europe (SCPE) Collaborative Group. Surveillance of cerebral


palsy in Europe: a collaboration of cerebral palsy surveys and registers. Dev Med Child Neurol.
2000;42:81624. [PubMed]

2. Karen W Krigger. Cerebral Palsy: An Overview. American Family Physician. 2006;73(1):91


100. [PubMed]

3. OShea Michael T. Cerebral palsy in very preterm infants: New epidemiological insights.
Mental retardation and developmental disabilities research. Reviews. 2002;8:135145.
[PubMed]

4. Krageloh-Mann AIngeborg, Cans B Christine. Cerebral palsy updates. Brain & Development .
2009;31: 537544. [PubMed]

5. Andersen GL, Irgens LM, Haagaas I, Skranes JS, Meberg AE, Vik T. Cerebral palsy in Norway:
Prevalence, subtypes and severity. Eur J Paediatr Neurol. 2008 Jan;12(1):413. [PubMed]

6. Nordmark E, H gglund G, Lagergren J. Cerebral palsy in southern Sweden: Prevalence and


clinical features. ActaPaediatrica . 2001;90:2711276. [PubMed]

~ 29 ~
7. Pfeifer LI, Silva DB, Funayama CA, Santos JL. Classification of CerebralPalsy: Association
between gender, age, motor type, topography and Gross Motor Function. Arq Neuropsiquiatr.
2009;67(4):10571061. [PubMed]

8. Hagberg B. Nosology and classification of cerebral palsy. GiornNeuropsich Eta EvolSuppl.


1989;4:1217.

9. Otapowicz D, Sobaniec W, Kuak W, Sendrowski K. Severity of dysarthric speech in children


with infantile cerebral palsy in correlation with the brain CT and MRI. Adv Med Sci. 2007;52(1)
[PubMed]

10. Selassie GR, Viggedal G, Olsson I, Jennische M. Speech, language, and cognition in
preschool children with epilepsy. Dev Med Child Neurol. 2008;50:432438. [PubMed]

11. Bjornson KF, McLaughlin JF, Loeser JD, Nowak-Cooperman KM, Russel M, Bader KA,
Desmond SA. Oral motor, communication, and nutritional status of children during intrathecal
baclofen therapy: a descriptive pilot study. Arch Phys Med Rehabil. 2003;84:5006. [PubMed]

12. Mysak ED. Neuro speech therapy for the cerebral palsy. 3rd ed. New York: Teacher college
Press; 1980. pp. 878. p.110-112.

13. Sheppard JJ, Mysak ED. Ontogeny of infantile oral reflexes and emerging chewing. Child
Dev. 1984;55:831843. [PubMed]

14. Sheppard JJ. Cranio-oropharyngeal motor patterns in dysarthria associated with cerebral
palsy. J speech Hear Res. 1964;7:373380. [PubMed]

15. International Phonetic Alphabet: Handbook of the International Phonetic Association: A


guide to the use of the International Phonetic AlphabetCambridge. U.K. & New York, NY:
Cambridge University Press; 1999.

16. Damerchi Z, Jalilehvand N, Bakhtiari B, KeyhaniMR Development of Phonetic inventory in


2-to-6 year-old Farsi speaking children. Research in Rehabilitation Sciences. 2010;5:4247. (In
Persian)

17. Dos Santos MT, Nogueira ML. Infantile reflexes and their effects on dental caries and oral
hygiene in cerebral palsy individuals. J Oral Rehabil. 2005;32:880885. [PubMed]

18. Love RJ, Hagerman EL, Taimi EG. Speech performance, dysphagia and oral reflexes in
cerebral palsy. J Speech Hear Disord. 1980;45(1):5975. [PubMed]

19. Platt LJ, Andrews G, Young M, Quinn PT. Dysarthria of adult cerebral palsy: Intelligibility
and articulatory impairment. J Speech Hear Res. 1980;23(1):2840. [PubMed]

20. McFarland DH, Baum SR. Incomplete compensation to articulatory perturbation. J


AcoustSoc Am. 1995;97:18651873. [PubMed]

21. Irwin OC. Communication variables of cerebral palsy and mentally retarded children.
Springfield,IL: C.C. Thomas; 1972.

~ 30 ~
22. Shelley I, Velleman , Marilyn m. In: phonology development in infancy and early childhood:
implications for theories of language learning. Martha C. Pennington., editor. Basingstoke:
Palgrave Macmillan; 2006. p. 34.

23. Ingram TT. Clinical significance of the infantile feeding reflexes. Dev Med Child Neurol.
1992;4:159169.

24. Hixon T, Hardy J. Restricted motility of speech articulation in cerebral palsy. J Speech
Hearing Dis. 1964;29:293306. [PubMed]

25. Dubner R, Sessle BJ, Storey AT. The neural basis of oral and facial function. New York:
Plenum Pres; 1978. p. 483.

Efecto de los reflejos orales anormales en la ariculacion del habla en los nios con paralisis
espstica

Abstracto:

El propsito de este estudio fue investigar la relacin entre la presencia de reflejos orales
anormales y la produccin de sonido del habla en nios con parlisis cerebral severa.

Se observ una relacin significativa entre tres de los siete reflejos orales anormales y la
articulacin del habla (es decir, los reflejos de masticacin, labio y mordida)

Introduccin

Hay tres tipos diferentes de Parlisis Cerebral (CP) como espstica, atxica y atetosis. Es
principalmente un transtorno del movimiento causado por dao cerebral no progresivo que se
produce durante el desarrollo fetal y el nacimiento. La prevalencia de CP en nios entre 3-10 aos
es de 2,4/1000 nios nacidos vivos. La clasificacin de CP tambin se ha hecho por el nmero de
miembros afectados y el tipo ms comn es CP espstica. La CP est comnmente asociada con
trastornos de la visin, audicin, habla, funcin del lenguaje receptivo y expresivo, deglucin /
alimentacin y funcin motora oral. Se han observado reflejos orales anormales en nios con CP.
Clnicamente, los reflejos orales no se observan generalmente en nios despus de 18 meses; Por
lo tanto, sus desarrollos son muy crticos para la alimentacin normal, la nutricin y el habla. La
persistencia de estos reflejos despus de 18 meses puede tener efectos negativos sobre las
funciones motoras orales. En consecuencia, Sheppard (1964) inform de una relacin entre los
patrones primitivos craneofilares y el rendimiento del habla en atetosis y tipos espsticos de CP.
Se han notificado siete reflejos orales anormales o caractersticas de conducta oral desviada en los
nios con CP de la siguiente manera: enraizamiento, apertura bucal, mordida, masticacin, labio,
lengua y lactancia. Algunos patlogos del habla y del lenguaje sostienen que la presencia de
reflejos anormales en nios mayores de 2 aos con CP puede indicar las funciones inmaduras o
farngeas. La mala funcin oral puede contribuir a algunos problemas en la articulacin del habla.
El principal objetivo de este estudio fue investigar la relacin entre la presencia de reflejos orales
anormales y la articulacin en nios iranes con CP espstica.

Discusion

El propsito de este estudio fue evaluar la presencia de reflejos orales anormales y sus posibles
efectos sobre la capacidad de producir sonidos del habla en nios con CP espstica. Los resultados

~ 31 ~
de este estudio demostraron que los reflejos orales anormales eran frecuentes en nios mayores
con CP espstica de acuerdo con estudios previos. Nuestro estudio tambin mostr que el reflejo
masticatorio fue el reflejo ms comn observado en estos nios. Los reflejos de la succin y el
enraizamiento fueron los reflejos menos frecuentes; De acuerdo con Love et al. Estudio. En
trminos de la forma de articulacin, fue relativamente ms difcil en los nios que participaron en
este estudio.

Resultados: De manera similar, las fricativas lingo-alveolares estaban estrechamente


relacionadas con los reflejos orales. Sin embargo, los sonidos dentales y glotales fueron los ms
problemticos para estos nios durante la articulacin. Nuestros resultados revelaron que la
precisin de la articulacin fue mayor para los sonidos bilabiales y nasales; Que fueron similares a
los hallazgos en nios normales. Hubo una relacin significativa entre la presencia de reflejo labial
y la articulacin de los sonidos, lo que podra explicarse por la variedad de movimientos
involuntarios de los labios mostrados por los nios con PC espstica. Como el reflejo labial
tambin puede desencadenar otros movimientos orales tales como el movimiento de la lengua.
Vimos una relacin entre los reflejos mordedores y de masticacin y misarticulacin de los
sonidos. Estas observaciones pueden deberse al cierre o apertura no regulados de la mandbula
despus de los reflejos mordedores y de masticacin que podran afectar a los movimientos de la
lengua, lo que a su vez podra conducir a la misarticulacin de los sonidos. Nuestros datos
mostraron una interrelacin entre los reflejos orales y la articulacin del sonido en los nios
mayores con paralisis cerebral. Adems, los reflejos orales normales en CP desempean un papel
primordial en las habilidades de alimentacin. Por lo tanto, se podra suponer una posible relacin
entre el desarrollo de los reflejos orales y la misarticulacin de los sonidos en los nios Sin
embargo, considerando algunas controversias en los estudios, se necesitan ms estudios para
dilucidar estos puntos. Adems, se podran realizar estudios futuros para investigar la presencia de
reflejos orales en diferentes tipos de PC y tambin para determinar los resultados del tratamiento
de los reflejos orales anormales y sus efectos sobre la articulacin del sonido.

En conclusin, nuestros resultados mostraron la presencia de reflejos orales anormales en nios


con CP y los posibles efectos de estos reflejos en la articulacin del sonido.

~ 32 ~
Esclerosis mltiple.

Antecedentes.

La esclerosis mltiple tambin conocida como Esclerosis en placas, insular o diseminada. Es una
enfermedad inflamatoria autoinmune desmielinizante crnica del sistema nervioso central (SNC),
que predomina en jvenes entre 20 y 40 aos de edad. Lo que significa que afecta al cerebro y la
medula espinal que lesiona la vaina de mielina (material que rodea y protege las clulas nerviosas)
o materia blanca del cerebro y de la medula espinal. Que provoca la aparicin de placas
esclerticas donde hacen que haya un mal funcionamiento ya que se bloquearan los mensajes
entre el cerebro y el cuerpo.

Adems produce anomalas inmunolgicas, esto significa problemas de coordinacin y equilibrio,


una debilidad muscular y alteraciones a la vista. Se caracteriza por episodios muy recurrentes de
fatiga, parestesia, disfuncin vesical.

Epidemiologia.

Si bien esta enfermedad afecta a la gente joven ya que se hizo un estudio donde la mayor
prevalencia es de 27 aos. En chile no hay una informacin que se represente nacionalmente pero
hay estudios que se han hecho en la regin de Magallanes que hay una prevalencia de 13,4 por
100.000 habitantes. Otro estudio en Santiago la prevalencia fue de 11,7 por 100.000 habitantes.
En el ao 2000 haban 1500 personas en chile que lo padecan por lo que se estima que al pasar de
los aos este aumentado entre 2300-2500 personas con esta enfermedad en nuestro pas.

Causas.

La causa se desconoce, vale decir el problema es el Cmo sucede? O Por qu sucede? No se


puede saber an ya que es un antgeno desconocido que desencadena una anomala inmunolgica
que daa a la vaina de mielina y este ya no da impulsos nerviosos o son muy pocos los que hay.

Hay distintos mecanismos en el cual puede haber dao en la vaina de mielina uno de estos es ya
que el sistema inmune activa linfocitos del torrente sanguneo los cuales entran al cerebro y
debilitan los mecanismos de defensa en la barrera sanguneo/cerebro (si esta barrera se rompe,
logra que el cerebro se exponga por primera vez). As el cerebro activa otros sistemas inmunes que
destruyen y atacan la mielina, otra forma que se logre daar es una hiptesis que puede ser una
combinacin de factores genticos y ambientales.

Ahora que desencadena que pase eso, es lo difcil de entender como ya fue nombrado
anteriormente hay algunos factores estudiados que son:

- Susceptibilidad gentica: cuando se hereda la persona tiene mayor susceptibilidad de


contraerlo.
- Factores y virus infecciosos: hay muchos virus que se desarrollan mientras se encuentra la
esclerosis mltiple que puede darse por respuesta a este y se activa el mecanismo.
- Procesos inflamatorios y autoinmunes: los anticuerpos que combaten con los
componentes normales del cuerpo y tejido tienen similitud a los que combaten algunas
enfermedades autoinmunes.

~ 33 ~
Signos y Sntomas.

Los sntoma van variando dependiendo la persona que los experimenta adems dependiendo de
las reas del sistema nervioso central que haya sido afectada y la magnitud que este presenta
donde a su vez va variar la forma que se manifiesta porque puede ser de forma leve o severo
siendo su duracin de das, semanas o meses donde puede reducirse o pueden progresar.

Las fiebres, los baos calientes, la exposicin al sol y al estrs puede desencadenar peor, los
sntomas ms comunes los vamos a clasificar segn qu lugar se ubique el problema:

Musculares, equilibrio y coordinacin:

- Fatiga
- Perdida de equilibrio
- Entumecimiento
- Problemas al caminar (mover brazos y piernas) y su coordinacin
- Temblores.

Vesicales e intestinales:

- Estreimiento
- Incontinencia urinaria

Oculares:

- Visin doble, borrosa.


- Movimientos incontrolables oculares

Cerebrales y neurolgicos:

- Disminucin de atencin, prdida de memoria


- Dificultad al razonar
- Depresin, sentimientos de tristeza

Habla y deglucin:

- Lenguaje mal articulado


- Problemas al masticar y deglutir

Ahora de los sntomas ya nombrados se logra presenciar de forma ms notoria en primera


instancia que el musculo se encuentra dbil, la vista es borrosa, hay mucha torpeza en la persona,
son incapaces de controlar ciertos sentidos. Pero no quiere decir que luego no hayan ms
sntomas, lo contrario pueden avanzar y aparecer ms o disminuir.

~ 34 ~
Relacin odontolgica.

La esclerosis mltiple afecta las partes motoras como sensitivas, donde esto va llevar a tener
mucho ms delicadeza en el tema odontolgico.

Para lograr hacer algn tipo de tratamiento, una revisin de sus dientes debe tener la ficha
biolgica sabiendo de que se trata la enfermedad y el grado en que el paciente la contenga. Ahora
el porqu de esto es que es muy difcil sentar a una persona que padezca esclerosis y que adems
contenga algn tipo de parlisis, agregndole a esto que tampoco tendr la capacidad de
mantener la boca abierta por un tiempo prolongado y no podr controlar los movimientos de su
lengua ni el poder tragar.

Tambin ocurre que al tener esclerosis mltiple puede existir una parlisis de cara donde puede
repercutir en labios, diente, encas, mandbula, donde poder mover la boca ser muy difcil es as
como tendr que trabajar con un neurlogo ya que la deficiencia de higiene bucal es alta llegando
a crearse caries o una enfermedad periodontal.

Aquella persona que tenga de sntoma un mal control muscular tendr problemas al usar el cepillo
dental, hilo dental u otros elementos que pueden ayudar a la higiene por lo que si esto sucede
adems de necesitar una ayuda odontolgica deber necesitar ayuda de la persona que lo est
cuidando para que este logre completar su higiene.

Los frmacos que se consumen para disminuir algunos sntomas de la esclerosis mltiple pueden
causar una resequedad en la boca, o disminuir la cantidad de saliva por lo que pueden provocar
ulceras orales, gingivitis, herpes, infecciones, entre otros.

Adems de todo esto hay que tener en cuenta que una persona con esclerosis mltiple no es
recomendable que usen prtesis por el hecho de que pueden experimentar movimientos
irregulares en su cara, lo que puede provocar que haya dao en la prtesis o que esta se corra del
lugar que se encuentra y cause otro dao aun mayor a los dientes.

Es imposible la utilizacin de dentadura postiza ya que as como las pequeas prtesis pueden ser
expulsadas o tragadas. Por lo que se debe actuar de forma que las citas sean programadas con una
longitud de tiempo explicito, ya que as se evita el estrs y la fatiga, que estas empeoran la
condicin al tener una prtesis.

~ 35 ~
Epstein-Barr virus in oral shedding of children with multiple sclerosis

Abstract

Epstein-Barr virus (EBV) has strong epidemiologic associations and biological plausibility in
multiple sclerosis (MS) pathophysiology.1 Serologic evidence of prior EBV infection is evident in
99% of adult-onset MS patients, exceeding the 95% seropositivity rate in the general adult
populations living in the same temperate regions. 2 The seroprevalence of EBV is also higher in
children with MS (85%99%) than region-, age- and sex-matched healthy children (42%72%).3
5
Elevated EBV-specific antibody titers have been demonstrated in young adults sampled years
before the onset of MS.6,7
EBV establishes lifelong persistence in memory B cells.8 Differentiation of B cells into plasma cells
initiates EBV reactivation from latency resulting in the release of virions into the peripheral blood
and oral mucosa.8Further viral replication occurs in oropharyngeal epithelial cells and the virus is
shed into the saliva.9 EBV reactivation is typically controlled by EBV-specific T-cell responses, which
ensure the EBV replicative (lytic) cycles are brief. 10 EBV gene products, such as viral interleukin (IL)-
10 and latent membrane protein-1 (LMP-1), have been shown to exhibit immunomodulatory
functions.1113
Building on our prior demonstration of a strong association between remote EBV infection and
pediatric MS,3,5 and on the concept that MS may be influenced by host immuneviral interactions,
we compare EBV viral shedding in saliva and genetic variation of BCRF1 and LMP1 genes between
EBV-seropositive children with MS and EBV-seropositive age-matched healthy children. We also
analyze serologic evidence and viral shedding frequency for other common Herpesviruses.

METHODS
Study participants.
Children with relapsing-remitting MS (RRMS)14 were enrolled consecutively from the pediatric MS
clinic at the Hospital for Sick Children, Toronto, Canada, from January 2009 through July 2011. The
healthy control group comprised children with no known neurologic diseases or medical
conditions recruited through community advertisement, frequency matched for age and sex with
the MS participants.
Standard protocol approvals, registrations, and patient consents.
The study was approved by the Research Ethics Board at the Hospital for Sick Children, and written
informed consent was obtained from the parents or guardians and from the participants.
Biological sample collection and processing.
Blood samples were collected from all participants at study entry and also at subsequent
scheduled clinic visits for patients with MS. Blood specimens were processed at the Experimental
Therapeutics Programs at the Montreal Neurological Institute (McGill University, Montreal,
Canada) according to standard operating procedures. Aliquoted sera were stored at 80C until
analysis.
At enrollment, participants were taught oral swab collection techniques, which included swabbing
the inner cheeks, the hard palate, and under the tongue, 3 to 5 times with a sterile nylon swab
(Copan, Murrieta, CA). The swab was placed into a vial containing 1 mL of sterile saline solution
~ 36 ~
and kept in the participants' home freezers until they were returned to our laboratory.
Participants were instructed to collect mouth swabs once a month for 12 consecutive months.
For viral DNA isolation, the specimen tubes were vortexed for 30 seconds, and DNA was extracted
using the QIAamp Blood Mini Kit (Qiagen, Hilden, Germany) according to the manufacturer's
instructions. Extracted DNA was stored at 20C until analyzed.
Serologic analyses.
All serologic determinations were performed blinded to clinical diagnosis in a licensed clinical
microbiology laboratory at the Hospital for Sick Children. Immunoglobulin G (IgG) antibodies
against EBV viral capsid (EBV-VCA), early antigen (EBV-EA), and nuclear antigen1 (EBV-EBNA1)
were measured using commercially available ELISA kits (DiaSorin, Stillwater, MN), per the
manufacturer's instructions. An individual was classified as remotely infected if VCA IgG and
EBNA IgG were detected, recently infected if VCA IgG and EA IgG (but not EBNA) were detected,
and EBV naive if IgG against all 3 EBV antigens were absent.
Serum samples were analyzed for IgG antibodies against herpes simplex virus (HSV; Euroimmun,
Lbeck, Germany), cytomegalovirus (CMV; Zeus Scientific, Raritan, NJ), varicella-zoster virus
(Siemens Healthcare Diagnostics, Marburg, Germany), and human herpesvirus6 (HHV-6; Abnova,
Taiwan), according to manufacturer's instructions.
Detection of viral DNA in mouth swabs.
HHV was detected by PCR in DNA isolated from the mouth swabs of participants with serologic
evidence of prior infection with HSV, EBV, CMV, HHV-6, or HHV-7.15,16 Detailed description of the
PCR methods employed is provided in appendix e-1 and table e-1 on the Neurology Web site
at www.neurology.org.
Identification of EBV BCRF1 and LMP1 variants in mouth swabs.
DNA sequence analyses of the EBV BCRF1 and LMP1 genes were performed with DNA extracted
from mouth swabs collected from all EBV-seropositive participants. Amplification and sequencing
of the full-length EBV BCRF1 gene was performed as described in appendix e-1.
Seven LMP-1 variants have been previously identified based on unique amino acid substitutions
compared with the B95-8 prototype sequence.17 To define the EBV LMP-1 variants present in the
mouth swabs, a matrix-assisted laser desorption/ionizationtime of flight (MALDI-TOF) mass
spectrometry approach, which allows for simultaneous detection of multiple viral genetic variants,
was used.18 The detailed protocol is provided in appendix e-1.
DNA sequence analysis.
DNA sequence chromatograms were inspected and edited using FinchTV version 1.4.0 software
(Geospiza Inc, Seattle, WA). DNA primers were designed using GeneRunner version 3.05 (Hastings
Software Inc., Hastings, NY). Multiple DNA sequence alignments were performed using program
CLUSTAL W19 with default settings.
Statistical analyses.
Sample size calculations were precluded by the paucity of data on EBV shedding. All pediatric
patients with MS identified during the study period were included. Continuous variables were

~ 37 ~
summarized as mean (standard deviation) or median (interquartile range) as appropriate.
Categorical variables were described as frequency (%). Missing data were not imputed. The
proportion of seropositive samples was compared between groups using 2 or Fisher' exact tests.
Continuous variables were compared between groups using Student t test. A p value < 0.05 was
considered to be statistically significant.

RESULTS
Participants.
Twenty-two children aged 1218 years (mean age 16.2 1.7 years) with RRMS and 77 children
with no known neurologic or autoimmune diseases (mean age 14.9 2.5 years; range 818 years)
were enrolled (figure 1). None of the participants had clinically apparent Herpesvirus infection
during the study.
Baseline analyses.
At study entry, 17 out of 22 (77.3%) patients with MS had serologic evidence for remote EBV
infection compared to 35 out of 77 (45.5%) controls (p = 0.008). Fourteen EBV-positive patient
serum samples and 33 EBV-positive control samples were available for quantitative evaluation of
anti-EBNA1 antibody titers. There was a trend for increased average anti-EBNA1 IgG titers among
children with MS compared to healthy controls (p = 0.08; figure e-1). None of the 14 patients with
MS had anti-EBNA1 IgG titers in the lowest quartile, compared to 12 out of 33 (36.4%) healthy
controls (p = 0.009; table 1). Seropositivity rates of HSV, CMV, HHV-6, and HHV-7 did not differ
between children with MS and healthy children (table 1).
Demographic features and baseline seroprevalence of pediatric patients with multiple sclerosis
and matched healthy controls

The presence of Herpesvirus DNA in these specimens was assessed in EBV-seropositive


participants. Ten out of 17 patients (58.8%) had detectable EBV DNA in their mouth swabs
compared to 7 out of 35 (20%) healthy controls (p = 0.007). EBV type 1 was detected more
frequently than EBV type 2 in both the MS (n = 9, 90%) and control groups (n = 6, 85.7%).
Concurrent shedding of EBV type 1 and type 2 was not detected.
To exclude the possibility that pediatric EBV-infected patients with MS have a more generalized
failure of host control of viral infection, we also analyzed viral shedding of HHV-6 and HHV-7 in the
oral mucosa. HHV-6 and HHV-7 have similar biological properties to EBV, namely established
latency in lymphocytes, and periodic lytic reactivation in oropharyngeal epithelial cells, leading to
shedding of virions in the saliva.20We found 1 out of 17 (5.8%) patients with MS had detectable
HHV-6 DNA in their mouth swabs compared to 8 out of 35 (22.9%) healthy children (p = 0.40).
HHV-6 type B was detected in all HHV6-positive participants, with the exception of 1 healthy
control in whom HHV-6 type A was detected. HHV-7 DNA was detected in 16 out of 17 patients
with MS (94%) and 30 out of 35 healthy controls (86%; p = 0.22). None of the participants had
detectable HSV or CMV DNA in their baseline mouth swab samples.
Longitudinal analyses.
To evaluate the frequency of EBV shedding over an extended period of up to 1 year, serial mouth
swabs were requested from all participants, although not all children were compliant with the
monthly protocol. Fifteen EBV-seropositive patients with MS and 22 EBV-seropositive healthy

~ 38 ~
controls provided more than one mouth swab over the 12-month study period. Ninety-nine mouth
swabs were obtained from 15 patients with MS and 160 swabs were obtained from 22 healthy
controls during the follow-up period. The average number of serial samples obtained per patient
with MS was 5.6 (median 4, range 312), and was 6.3 (median 5, range 212) per healthy control.
EBV DNA was detected in the mouth swabs of all EBV-seropositive children with MS at least once
during the study period, with an overall weighted average detection rate of 50.5% (51 EBV-positive
samples out of 99 samples; range 20%100%). In contrast, the weighted average EBV DNA
detection rate among healthy controls was 19.4% (31 EBV-positive samples out of 160 samples;
range 0%83.3%; p = 0.01). Nine healthy controls (who provided 49 samples) did not shed EBV
during the entire study period. Patients with MS demonstrated a consistently higher frequency of
EBV detection in mouth swabs as compared to healthy controls, irrespective of the number of
serial samples provided (
EBV type 1 was shed more often than EBV type 2 in both patients with MS (44 out of 51 EBV-
positive samples; 85%) and healthy children (28 out of 31 EBV-positive samples; 90%), although
one patient with MS (MS-02) and one healthy control (C-02) consistently shed only EBV type 2
throughout the study period. Temporal changes in the predominant EBV subtypes were observed
in 2 patients with MS (MS-01 and MS-08), but in none of the healthy controls.
Figure e-2 summarizes the HHV-6 and HHV-7 shedding frequencies in EBV-seropositive MS and
healthy control participants. The shedding frequencies of HHV-6 and HHV-7 did not differ
significantly between patients with MS and controls. No HSV or CMV DNA was detectable in any of
the serial samples analyzed.
Type I interferons (IFNs), including IFN-, are important for the control of viral infections. To assess
the effect of IFN- on human Herpesvirus oral shedding, we compared HHV oral shedding
frequencies in patients with MS who were undergoing IFN- therapy (n = 7; 49 serial samples) to
patients who were on other immunomodulatory therapies or not on any treatment (n = 8; 50
serial samples) during the study period (table 1). The overall average EBV shedding frequency
among patients with MS treated with IFN- (43.0%) did not differ from the patients with MS who
were not on IFN- treatment (51.0% p = 0.54). There was no difference in the average HHV-6
shedding frequencies between patients on IFN- treatment (17.2%) and patients not on IFN-
treatment (16.7%; p = 0.97). HHV-7 shedding frequency also did not differ between the IFN-
treated (74.2%) and non-IFN-treated (91.6%; p = 0.18) groups.
EBV BCRF1 (ebvIL-10) and LMP-1 genetic variants in children with MS.
Comparison of the full-length BCRF1 (ebvIL-10) gene to the EBV prototype strain B95-8 identified a
total of 6 distinct DNA sequences from B95-8 (figure e-3A). Three amino acid substitutions were
identified (Arg3Gln, Val6Met, Gly23Ser), all of which were located within the signal peptide of
ebvIL-10 (amino acid residues 125), while 4 silent nucleotide changes (a9787g, g9848a, c9980a,
c10020t) were present in the mature ebvIL-10 protein. The most common single nucleotide base
change, c9980a, was present in 4 of the 6 BCRF1 sequence variants, 2 of which also carried at least
1 of the 3 amino acid substitutions. We did not identify any MS-specific nucleotide polymorphism
within the BCRF1 (ebvIL-10 sequence). Five out of 15 (33%) patients with MS and 1 out of 14 (7%)
healthy controls were infected with more than 1 EBV BCRF1 genetic variant.
Distinct LMP-1 variants can be distinguished by amino acid signature patterns at the carboxy
terminus.17Using a MALDI-TOF mass spectrometry approach,18 we identified 4 LMP-1 variants in

~ 39 ~
the mouth swabs of patients with MS and controls (figure e-3B). Two patients with MS, but none
of the controls, had more than 1 LMP-1 variant detected in serial samples.
Go to:

DISCUSSION

Our primary objective was to explore whether pediatric patients with MS differ from healthy
children in relation to EBV-specific biology. First, we confirm a higher seroprevalence for remote
EBV exposure, but not for other common Herpesviruses in pediatric patients with MS relative to
healthy children.3,5 We also demonstrate a difference in the distribution of anti-EBNA1 titers, with
healthy children being more likely to have low titers. Furthermore, we show for the first time that
patients with pediatric-onset MS are more likely to have detectable EBV DNA in their saliva
compared to EBV-seropositive healthy children, and that this is consistently observed on serial
evaluations. The increased frequency of EBV shedding in children with MS does not reflect a more
generalized impairment in control of chronic viral infection, as demonstrated by the similar
shedding frequencies of HHV-6 and HHV-7 in EBV-seropositive patients with MS and healthy
children. Prior reports of a lack of difference in EBV DNA load in the plasma and peripheral blood
mononuclear cells of patients with MS and that of healthy controls also argue against a
generalized impairment of immune control of EBV infection in patients with MS.21
The antiviral nature of IFN- prompted us to evaluate whether treatment of patients with MS
influenced our findings. We observe no difference in EBV, HHV-6, or HHV-7 shedding frequencies
among patients with MS treated with IFN- as compared to patients with MS not exposed to IFN-
. However, given the small sample size, this finding should be interpreted cautiously.
There is very limited data on EBV oral shedding in children. Previous cross-sectional studies have
reported that EBV was detectable in the saliva of 38% of 93 healthy EBV-seropositive children (age
range, 06 years) in Japan,22 and in 50% of healthy pediatric controls in Germany (n = 14; age
range, 1.515.8 years),23compared to our finding of 50% detection rate in patients with MS and
20% detection rate in healthy controls. In healthy individuals, the level of EBV oral shedding does
not appear to be correlated with the level of latently infected memory B cells, 9 but is most likely to
be governed by the efficacy of host immune responses. It was recently suggested that diminished
functional capacity of EBV-specific CD8+ T cells rather than decrease in the number of EBV-specific
CD8+ T cells might facilitate the reactivation of EBV in healthy individuals. 24 Deficits in interferon-
secretion and IL-2 production by human leukocyte antigen (HLA)-B7restricted EBV-specific CD8+
T cells have recently been reported in patients with MS. 21
Impaired host control of EBV lytic cycle is suggested by our finding of higher shedding frequency,
but also by the observation that children with MS shed a broader range of EBV variants over time
compared to controls. Coinfection with EBV type 1 and type 2 was recently shown to be higher in
adult patients with MS (n = 75, 90% coinfected) compared to healthy controls (n = 186; 37%; p <
0.001).25 Our inability to identify MS-associated genetic variations within the BCRF1 (encoding
ebvIL-10) and LMP1 genes in pediatric patients with MS is consistent with findings in studies in
which EBV genetic variation (in the EBNA1, BRRF1, LMP2A, BHRF1, and LMP1 genes specifically)
was evaluated in adult patients with MS, without detection of specific EBV mutations in the MS
cohort.26,27 However, further research may be warranted given evidence that EBV genetic
variations may influence cellular immune responses towards EBV.28 Of interest, ebvIL-10 is a viral
homolog of hIL-10. Structural differences between hIL-10 and ebvIL-10 result in different binding

~ 40 ~
affinities to IL-10 receptors, and altered signaling properties.12 ebvIL-10 modulates hIL-10 activities
in vitro and may downregulate the production of hIL-10,11,12 though the in vivo functional
consequences of ebvIL-10 secretion on human IL-10mediated responses have not been
elucidated. Reduced serum hIL-10 levels have been reported in patients with MS compared to
healthy controls.29,30 Earlier studies showed that amino acid substitutions within the hIL-10 signal
peptide resulted in decreased protein secretion.31 Given the sequence similarity between hIL-10
and ebvIL-10, changes in the signal peptide of ebvIL-10 could also have an effect on ebvIL-10
protein translocation or signal peptide production. Furthermore, the HLA-B27restricted epitope
(RRLVVTLQC; amino acid positions 3-11) is located within the signal peptide sequence of
BCRF1,32 and changes in the epitope sequence, such as the 2 amino acid substitutions that we
identified (Arg3Gln, Val6Met), may impact recognition of EBV-infected cells by cytotoxic T cells.
EBV LMP-1 is another example of an EBV-encoded immunomodulatory protein. LMP-1 functionally
mimics the CD40 receptor that is critical for B-cell activation and proliferation.13 Unlike CD40, LMP-
1 is constitutively activated independent of ligand binding, resulting in enhanced B-cell
activation.13 It has been proposed that LMP-1 may work together with ebvIL-10 to facilitate EBV
replication and reactivation.12 Variations within LMP1 may result in different biological and
signaling properties. For example, several LMP-1 variants demonstrate enhanced NF-B signaling,
which modulates gene expressions mediating the innate and adaptive immune responses in
vitro.33
As we were unable to obtain blood specimens from our study participants on a monthly basis, a
limitation of our study was that we could not assess the relationship between viral DNA in the
mouth swabs and in peripheral blood. Detection of EBV DNA in saliva is positively correlated with
detection in peripheral blood during active replication 34; however, the prevalence of EBV strains
may be different in these 2 sites,35 and may reflect selective tissue tropism of viral strains. 36 With
increasing availability of next-generation sequencing, whole-genome analysis of EBV strains
isolated from patients with MS will likely provide greater insights into whether genetic variation in
the EBV genome is associated with MS, or whether the potential biological impact of EBV in MS is
independent of EBV genetics but perhaps related to host immune responses to EBV.
We show that children with MS are more likely than healthy children to experience frequent
reactivation of EBV but not of other latent Herpesviruses, suggestive of selective impairment in the
immunologic control of EBV lytic cycle in the oral mucosa. Further study of EBV-relevant immune
cell responses in pediatric patients with MS appears warranted.
Go to:

ACKNOWLEDGMENT

The authors thank Lilia Rabinovich (Hospital for Sick Children, Toronto) for technical assistance in
serologic analyses and Carolynn Darrell and Suzanne McGovern (Hospital for Sick Children,
Toronto) for their help with the recruitment of healthy control participants; members of the
Experimental Therapeutics Program at the Montreal Neurological Institute and Hospital for their
help with sample handling; and all participants and their families involved in this study.

AUTHOR CONTRIBUTIONS

Carmen Yea conducted the experiments, analyzed and interpreted the data, performed statistical
analyses, and wrote the manuscript. Raymond Tellier participated in the design of the study,

~ 41 ~
analysis of data, and provided critical revisions of the manuscript. Garrett Westmacott and Patrick
Chong generated and analyzed mass spectrometry data. Ruth Ann Marrie performed statistical
analyses and provided critical revisions of the manuscript. Amit Bar-Or participated in the design
of the study, interpretation of data, and provided critical revisions of the manuscript. Brenda
Banwell participated in the design of the study, interpretation of data, and provided critical
revisions of the manuscript.

STUDY FUNDING

Supported by the Multiple Sclerosis Society of Canada Scientific Research Foundation.

DISCLOSURE

C. Yea reports no disclosures. R. Tellier has received research grants from the Canadian Institutes
of Health Research, The Ministry of Health and Long Term Care of Ontario, the Canadian Liver
Foundation, and the Michael Smith Foundation for Health Research. P. Chong has received funding
from the Genomics R&D Initiative through federal government of Canada. G. Westmacott has
received funding from the Genomics R&D Initiative through federal government of Canada. R.
Marrie receives research funding from Canadian Institutes of Health Research, Public Health
Agency of Canada, Manitoba Health Research Council, Health Sciences Centre Foundation,
Multiple Sclerosis Society of Canada, Multiple Sclerosis Scientific Foundation, and Rx & D Health
Research Foundation, and has conducted clinical trials funded by Sanofi-Aventis. A. Bar-Or receives
research funding from Canadian Institutes of Health Research, Multiple Sclerosis Society of
Canada, Multiple Sclerosis Scientific Foundation, and National Institutes of Health. He has received
speaker, consulting fees, and/or research support from Amplimmune, Aventis, Bayhill
Therapeutics, Berlex/Bayer, Biogen Idec, BioMS, Diogenix, Eli-Lilly, EMD Serono, Genentech,
Genzyme-Sanofi, GSK, Guthy Jackson Greater Good Foundation, Medimmune, Mitsubishi Pharma,
Novartis, Ono Pharmacia, Receptos, Roche, Teva Neuroscience, and Wyeth. B. Banwell receives
research funding from Canadian Institutes of Health Research, Multiple Sclerosis Society of
Canada, Multiple Sclerosis Scientific Foundation, and the Dairy Farmers of Ontario. Dr. Banwell has
received Speaker's Honoraria from Biogen-Idec. Dr. Banwell has provided non-remunerated
consultant input to safety advisory boards for Biogen-Idec, Novartis, and Eli-Lilly. Go
to Neurology.org for full disclosures.

REFERENCES
1. Ramagopalan SV, Dobson R, Meier UC, Giovannoni G. Multiple sclerosis: risk factors, prodromes,
and potential causal pathways. Lancet Neurol 2010;9:727739 [PubMed]

2. Ascherio A, Munger KL. Environmental risk factors for multiple sclerosis: part I: the role of
infection. Ann Neurol 2007;61:288299 [PubMed]

3. Alotaibi S, Kennedy J, Tellier R, Stephens D, Banwell B. Epstein-Barr virus in pediatric multiple


sclerosis. JAMA 2004;291:18751879 [PubMed]

4. Pohl D, Krone B, Rostasy K, et al. High seroprevalence of Epstein-Barr virus in children with
multiple sclerosis. Neurology 2006;67:20632065 [PubMed]

5. Banwell B, Krupp L, Kennedy J, et al. Clinical features and viral serologies in children with
multiple sclerosis: a multinational observational study. Lancet Neurol 2007;6:773781 [PubMed]

~ 42 ~
6. Levin LI, Munger KL, Rubertone MV, et al. Temporal relationship between elevation of Epstein-
Barr virus antibody titers and initial onset of neurological symptoms in multiple
sclerosis. JAMA 2005;293:24962500 [PubMed]

7. DeLorenze GN, Munger KL, Lennette ET, Orentreich N, Vogelman JH, Ascherio A. Epstein-Barr
virus and multiple sclerosis: evidence of association from a prospective study with long-term
follow-up. Arch Neurol 2006;63:839844 [PubMed]

8. Knipe DM, Howley PM, Griffin DE, et al. Fields Virology, 5th ed Philadelphia: Lippincott Williams
& Wilkins; 2007:26032654

9. Hadinoto V, Shapiro M, Sun CC, Thorley-Lawson DA. The dynamics of EBV shedding implicate a
central role for epithelial cells in amplifying viral output. PLoS Pathog 2009;5:e1000496. [PMC free
article][PubMed]

10. Cohen JI. Epstein-Barr virus infection. N Engl J Med 2000;343:481492 [PubMed]

11. Jochum S, Moosmann A, Lang S, Hammerschmidt W, Zeidler R. The EBV immunoevasins vIL-10
and BNLF2a protect newly infected B cells from immune recognition and elimination. PLoS
Pathog2012;8:e1002704. [PMC free article] [PubMed]

12. Yoon SI, Jones BC, Logsdon NJ, Harris BD, Kuruganti S, Walter MR. Epstein-Barr virus IL-10
engages IL-10R1 by a two-step mechanism leading to altered signaling properties. J Biol
Chem 2012;287:2658626595 [PMC free article] [PubMed]

13. Graham JP, Arcipowski KM, Bishop GA. Differential B-lymphocyte regulation by CD40 and its
viral mimic, latent membrane protein 1. Immunol Rev 2010;237:226248 [PubMed]

14. Polman CH, Reingold SC, Edan G, et al. Diagnostic criteria for multiple sclerosis: 2005 revisions
to the McDonald Criteria. Ann Neurol 2005;58:840846 [PubMed]

15. Johnson G, Nelson S, Petric M, Tellier R. Comprehensive PCR-based assay for detection and
species identification of human herpesviruses. J Clin Microbiol 2000;38:32743279 [PMC free
article] [PubMed]

16. Brooks JM, Croom-Carter DS, Leese AM, Tierney RJ, Habeshaw G, Rickinson AB. Cytotoxic T-
lymphocyte responses to a polymorphic Epstein-Barr virus epitope identify healthy carriers with
coresident viral strains. J Virol 2000;74:18011809 [PMC free article] [PubMed]

17. Edwards RH, Seillier-Moiseiwitsch F, Raab-Traub N. Signature amino acid changes in latent
membrane protein 1 distinguish Epstein-Barr virus strains. Virology 1999;261:7995 [PubMed]

18. Ayers M, Siu K, Roberts E, Garvin AM, Tellier R. Characterization of hepatitis C virus
quasispecies by matrix-assisted laser desorption ionization-time of flight (mass spectrometry)
mutation detection. J Clin Microbiol 2002;40:34553462 [PMC free article] [PubMed]

19. Thompson JD, Higgins DG, Gibson TJ. Clustal W: improving the sensitivity of progressive
multiple sequence alignment through sequence weighting, position-specific gap penalties and
weight matrix choice. Nucleic Acids Res 1994;22:46734680 [PMC free article] [PubMed]

~ 43 ~
20. Ward KN. The natural history and laboratory diagnosis of human herpesvirus-6 and -7
infections in the immunocompetent. J Clin Virol 2005;32:183193 [PubMed]

21. Jilek S, Schluep M, Harari A, et al. HLA-B7-restricted EBV-specific CD8+ T cells are dysregulated
in multiple sclerosis. J Immunol 2012;188:46714680 [PubMed]

22. Ikuta K, Satoh Y, Hoshikawa Y, Sairenji T. Detection of Epstein-Barr virus in salivas and throat
washings in healthy adults and children. Microbes Infect 2000;2:115120 [PubMed]

23. Hug M, Dorner M, Frhlich FZ, et al. Pediatric Epstein-Barr virus carriers with or without
tonsillar enlargement may substantially contribute to spreading of the virus. J Infect
Dis 2010;15:11921199[PubMed]

24. Vogl BA, Fagin U, Nerbas L, Schlenke P, Lamprecht P, Jabs WJ. Longitudinal analysis of
frequency and reactivity of Epstein-Barr virus-specific T lymphocytes and their association with
intermittent viral reactivation. J Med Virol 2012;84:119131 [PubMed]

25. Santn A, Cristbal E, Aparicio M, Royuela A, Villar LM, Alvarez-Cermeo JC. High frequency of
co-infection by Epstein-Barr virus types 1 and 2 in patients with multiple sclerosis. Mult
Scler 2011;17:12951300 [PubMed]

26. Brennan RM, Burrows JM, Bell MJ, et al. Strains of Epstein-Barr virus infecting multiple
sclerosis patients. Mult Scler 2010;16:643651 [PubMed]

27. Simon KC, Yang X, Munger KL, Ascherio A. EBNA1 and LMP1 variants in multiple sclerosis cases
and controls. Acta Neurol Scand 2011;124:5358 [PMC free article] [PubMed]

28. Tzellos S, Farrell PJ. Epstein-Barr virus sequence variation: biology and
disease. Pathogens 2012;1:156174 [PMC free article] [PubMed]

29. Salmaggi A, Dufour A, Eoli M, et al. Low serum interleukin-10 levels in multiple sclerosis:
further evidence for decreased systemic immunosuppression? J Neurol 1996;243:1317 [PubMed]

30. Bar-Or A, Fawaz L, Fan B, et al. Abnormal B-cell cytokine responses a trigger of T-cell-mediated
disease in MS? Ann Neurol 2010;67:452461 [PubMed]

31. Whittington HA, Freeburn RW, Godinho SI, Egan J, Haider Y, Millar AB. Analysis of an IL-10
polymorphism in idiopathic pulmonary fibrosis. Genes Immun 2003;4:258264 [PubMed]

32. Kanai K, Satoh Y, Yamanaka H, et al. The vIL-10 gene of the Epstein-Barr virus (EBV) is
conserved in a stable manner except for a few point mutations in various EBV isolates. Virus
Genes 2007;35:563569[PubMed]

33. Mainou BA, Raab-Traub N. LMP1 strain variants: biological and molecular properties. J
Virol2006;80:64586468 [PMC free article] [PubMed]

34. Ling PD, Lednicky JA, Keitel WA, et al. The dynamics of herpesvirus and polyomavirus
reactivation and shedding in healthy adults: a 14-month longitudinal study. J Infect
Dis 2003;187:15711580 [PubMed]

~ 44 ~
35. Sitki-Green D, Covington M, Raab-Traub N. Compartmentalization and transmission of multiple
Epstein-Barr virus strain in asymptomatic carriers. J Virol 2003;77:18401847 [PMC free
article] [PubMed]

36. Huynh GT, Adler FR. Alternating host cell tropism shapes the persistence, evolution and
coexistence of Epstein-Barr virus infections in human. Bull Math Biol 2011;73:1754
1773 [PubMed]

Virus de Epstein Bar en el desprendimiento oral de nios con Esclerosis multiple

Abstracto

Investigar el virus de Epstein-Barr (EBV), la frecuencia oral de desprendimiento y la diversidad


gentica de EBV en pacientes peditricos con esclerosis mltiple (EM).

Se trat de un estudio prospectivo de casos y controles. Se utilizaron ensayos basados en PCR para
detectar el ADN viral en los hisopos bucales mensuales de 22 pacientes peditricos con EM y 77
controles sanos de edad y sexo.

Los nios con EM muestran tasas anormalmente elevadas de reactivacin viral del EBV y un rango
ms amplio de variantes genticas, lo que sugiere un deterioro selectivo en su control
inmunolgico del EBV.

Introduccin

El virus de Epstein-Barr (EBV) tiene fuertes asociaciones epidemiolgicas y plausibilidad biolgica


en la fisiopatologa de la esclerosis mltiple (MS). La evidencia serolgica de infeccin previa por
EBV es evidente en el 99% de los pacientes con EM de adultos, superando el 95% La prevalencia
de EBV es tambin mayor en los nios con EM (85% -99%) que en los nios sanos de la regin,
edad y sexo (42% -72%). Se han demostrado elevadas concentraciones de anticuerpos especficos
de EBV en adultos jvenes, muestreados aos antes de la aparicin de MS.6,7

La replicacin viral ocurre en las clulas epiteliales orofarngeas y el virus se derrama En la saliva.
La reactivacin de EBV se controla tpicamente mediante respuestas de clulas T especficas de
EBV, lo que asegura que los ciclos replicativos de EBV (lticos) son breves. Los productos gnicos de
EBV, tales como la interleucina, se ha demostrado que presentan funciones inmunomoduladoras.

Discusion y resultado

Nuestro objetivo principal era explorar si los pacientes peditricos con EM difieren de los nios
sanos en relacin con la biologa especfica del EBV. En primer lugar, confirmamos una mayor
prevalencia para la exposicin remota de EBV, pero no para otros herpesvirus comunes en
pacientes peditricos con EM en relacin con nios sanos.Adems, se muestra por primera vez
que los pacientes con EM peditrica son ms propensos a tener ADN detectable EBV en su saliva
en comparacin con EBV-seropositivos nios sanos, y que esto se observa constantemente en las
evaluaciones en serie. El aumento de la frecuencia de derrame de EBV en nios con EM no refleja
un deterioro ms generalizado en el control de la infeccin viral crnica. La naturaleza antiviral nos
llev a evaluar si el tratamiento de los pacientes con EM influy en nuestros hallazgos.

Hay muy pocos datos sobre EBV oral derramamiento en los nios. Estudios transversales previos
han informado que el EBV fue detectable en la saliva en el 38% de los 93 nios sanos seropositivos
~ 45 ~
en EBV en Japn 22%, y en el 50% de los controles peditricos sanos en Alemania, en comparacin
con nuestro hallazgo de la tasa de deteccin del 50% en pacientes con EM y 20% de tasa de
deteccin en controles sanos. En individuos sanos, el nivel de desprendimiento oral de EBV no
parece estar correlacionado con el nivel de clulas B de memoria infectadas latentemente, 9 pero
es ms probable que se rija por la eficacia de las respuestas inmunes del husped.

Como no fuimos capaces de obtener muestras de sangre de los participantes en el estudio sobre
una base mensual, una limitacin de nuestro estudio fue que no pudimos evaluar la relacin entre
el ADN viral en los hisopos bucales y en la sangre perifrica. Deteccin de ADN de VEB en saliva se
correlaciona positivamente con la deteccin en la sangre perifrica durante replication34 activa;
Sin embargo, la prevalencia de cepas de EBV puede ser diferente en estos 2 sitios, y puede reflejar
tropismo de tejido selectivo de cepas virales. Con el aumento de la disponibilidad de
secuenciacin de prxima generacin, el anlisis de todo el genoma de las cepas de EBV aisladas
de pacientes con EM probable proporcionar un mejor entendimiento de si la variacin gentica en
el genoma de EBV est asociada con la esclerosis mltiple, o si el potencial impacto biolgico de
EBV en la EM es independiente de la gentica EBV pero tal vez relacionada con respuestas
inmunes del husped a este virus.

Se demuestra que los nios con EM tienen ms probabilidades que los nios sanos de
experimentar la reactivacin frecuente de EBV, pero no de otros herpesvirus latentes, sugestivos
de deficiencia selectiva en el control inmunolgico de VEB ciclo ltico en la mucosa oral.
Continuando el estudio de las respuestas de clulas inmunes con EBV relevante en pacientes
peditricos con EM parece justificado.

~ 46 ~
Esclerosis Lateral Amiotrofia

El ELA es un trastorno que afecta los nervios y msculos del cuerpo. Es espordica del adulto.
Esta enfermedad afecta tanto al cerebro, tronco cerebral y mdula espinal. Esta patologa es
tambin conocida como la enfermedad de Lou Gehrig

Su nombre hace referencia a la afectacin de las fibras nerviosas que se encuentran en la parte
lateral de la medula espinal.

La enfermedad de ELA ocurre en todo el mundo, sin limitaciones raciales, tnicas o


socioeconmicas.

En la esclerosis lateral amiotrofica las clulas nerviosas motoras se desgastan o mueren, por lo
cual, ya no son capaces de mandar mensajes a los msculos.

Podramos decir que principalmente las personas que sufren de esto tienen una edad de entre 40
y 70 aos. Hay una cifra de aproximadamente 50% de personas que llegan a vivir alrededor de
tres aos o ms, con una mortalidad con compromiso respiratorio.
La incidencia reportada es de 2 por cada 100.000 en EE.UU y 2.16 por cada 100.000 habitantes en
Europa.

En Chile no se cuenta con suficiente informacin. Y a nivel mundial, aproximadamente afecta a 5


de cada 100.000 personas.

La enfermedad trae como consecuencia una debilidad muscular progresiva, la que finalmente
termina en una parlisis total. Hay que destacar que no se ven afectados las funciones como la
sensibilidad o la inteligencia, ni tampoco se ven afectados los movimientos oculares (Puesto que
sus moto neuronas son ms resistentes.

Causas: Puede ser causado por un defecto gentico, pero este es un caso de uno cada diez
personas, del resto, la mayora de los casos se desconoce la causa.

Los factores de riesgo sera tener un familiar que posea ELA y otro puede ser el servicio en las
fuerzas armadas.

Los sntomas se presentan ms que nada a mediana edad (aproximadamente a los 50 aos, pero
se pueden manifestar en personas que presentan menos edad), se notan sntomas como cadas,
alteraciones en el habla y/o deglucin. Hay una gran debilidad muscular por lo que es notoria la
dificultad para levantar cosas, subir escaleras o caminar, cada de la cabeza, cambios de voz o
ronquera, dificultad para respirar, dificultad para tragar, asfixia con facilidad, nauseas, vmitos.
Tambin es posible encontrar la depresin, calambres musculares, rigidez muscular, contracciones
musculares y prdida de peso.

Las complicaciones que puede atraer la enfermedad de ELA son la prdida de la capacidad de auto
cuidado, insuficiencia pulmonar, neumona, ulceras de decbito, bajada de peso. Han pasado
aproximadamente 140 aos de su descubrimiento, pero hasta el da de hoy no hay una terapia
que logre ser efectiva para su tratamiento.

~ 47 ~
Hay un tratamiento posible para el ELA, el cual consiste en un medicamento cuyo nombre es
Riluzol, que logra retrasar los sntomas, y le da un plazo ms largo de vida a la persona con aquella
enfermedad.

Hay otros medicamentos que pueden servir el blacofenaco (Diazepam) para controlar la
espasticidad.

Y el Trixhexifenidil (amitriptilina) para las personas con problemas para deglutir su propia saliva.

La fisioterapia, la rehabilitacin y el uso de dispositivos ortopdicos o silla de ruedas, u otras


medidas ortopdicas pueden ser necesarios para maximizar la funcin muscular y la salud en
general.

En caso de depresin hay que usar medicamentos, el ELA puede hacer que la persona se sienta
triste, tampoco olvidar la comunicacin con familiares y personas queridas.

~ 48 ~
ELA y relacin con la odontologa.

La esclerosis lateral amiotrofica genera que las clulas motoras se atrofien, por lo cual afecta a
los msculos en varios de los casos. Esto conlleva a que las personas presenten alteraciones, como
pueden ser la dificultad de deglucin de alimentos, acumulacin de saliva y de babeos, y esto
puede ocasionar asfixias en el paciente.

Debido a estas mismas alteraciones se puede producir una mala higiene bucal debido a que las
personas pierden autonoma, por la poca abertura bucal que pueden ejercer y la capacidad de
auto cuidado que tienen. Por otra parte, hay una gran disminucin de la fuerza lingual. Tambin,
aunque poco comn puede producirse macroglosia en el paciente (que es un aumento del tamao
de la lengua en estado de reposo, o bien, esta al reposar ocupa ms espacio de lo comn).

En la atencin odontolgica, hay varios puntos que un profesional debe tomar en cuenta para
atender a estos tipos de paciente.

Primero que todo, hay que darse cuenta que los pacientes con ELA tienen diferentes grados de
discapacidad fsica y distintos grados de dificultad para de desplazamiento.

Debido a su enfermedad, los pacientes tienden a tener una disminucin de fluidez verbal y
tambin presentan disartria (dificultad de poder articular cierto sonidos y/o palabras) en muchos
casos. As que la comunicacin debe ser con ayuda de los familiares o bien si se requiere con
ayuda de algn fonoaudilogo. Pero hay que considerar, que a pesar de la falta de comunicacin
que ellos pueden ejercer, los pacientes con ELA tienen una gran comprensin, solo se les dificulta
el expresar.

La esclerosis lateral amiotrofica es una enfermedad progresiva, por lo que se debe promover,
prevenir, tratar lo antes posible y tener controles de forma seguida. De esta forma se puede evitar
tratamientos que incomoden al paciente o sean muy invasivos. Para dar instrucciones de una
buena higiene a este tipo de paciente se debe tomar en cuenta los siguientes puntos: Capacidad
de autonoma, cambios en el cepillo dental (en caso de ser necesario), tambin se puede admitir el
uso de cepillo dental elctrico. Se debe incluir un asesoramiento nutricional.

En caso de presentar disfagia (dificultad para deglutir alimentos y/o lquidos), puede indicarse el
uso de colutorios dentales junto con el cepillado en vez de pasta, ya que facilitar la visin del
cuidador y reducir el riesgo de asfixia.

Para la atencin odontolgica, se requiere una visita o consulta con el mdico tratante para poder
conocer el estado en que se encuentra el paciente con ELA.
Durante la atencin, hay que considerar en mantener atenciones cortas y que tengan descanso, si
es necesario, o ms bien usar apoya mordidas. Mantener una posicin del silln o silla
odontolgica con 45, controlar la cantidad de agua que se usa en los procedimientos.

El uso de la anestesia general es segura, pero en caso de tener que sedar al paciente, se debe
consultar a un anestesista, ya que pueden haber algunos riesgos respiratorios que pueden ocurrir
de por medio.

~ 49 ~
Black hairy tongue in a patient with amyotrophic lateral sclerosis

Abstract.

Black hairy tongue (BHT) is a condition characterized by the elongation of filiform papillae
associated with a marked discoloration, from yellowish-brown to black, and a thick lingual coating.
BHT is usually observed in the elderly and in patients with limited self-sufficiency, as a
consequence of poor oral hygiene. In this perspective, the patients affected by amyotrophic lateral
sclerosis (ALS) represent a high-risk category for the occurrence of BHT. The fast and inexorable
loss of their self-sufficiency due to progressive muscle atrophy as well as the impropriate
education of healthcare assistants have demonstrated to have significant reflection on the
maintenance of an adequate standard of oral hygiene. This paper firstly described a case of BHT in
a patient affected by ALS. A case of BHT in a patient (Caucasic, male, 63 years old) affected by ALS
was described. The primary goal of the work was to teach and motivate the patient to the use of
the tongue cleaner in association with the local application of chlorexidine 0.20%. Furthermore, in
order to support the patient with accurate domiciliary oral hygiene, a proper training for his
health-care assistant was provided. The maintenance of the oral health of ALS patient is
fundamental to prevent systemic complications that could jeopardize the already fragile physical
balance of these patients. The dedicated monitoring by a dentist or a dental hygienist would seem
essential in order to achieve this objective.
Keywords: Amyotrophic lateral sclerosis, black hairy tongue, hairy tongue, oral higiene.

Introduction.

Amyotrophic lateral sclerosis (ALS) is a dramatic neurodegenerative disease resulting from the
degeneration of the upper and lower motor neurons in the brain and spinal cord. It is
characterized by progressive functional deficits, including a gradual muscle atrophy and weakness
of limbs, and decreased respiratory functions.[1,2] The quality of life of ALS patients is further
compromised by disorders of speech articulation and intelligibility, which can occur since the
earliest stage of the disease.[3] Due to disturbances in muscular control, dysarthria may also be
correlated with disproportionate tongue impairment and the development of macroglossia.[3,4,5]
Black hairy tongue (BHT) is a benign condition characterized by marked hypertrophy and
elongation of filiform papillae on the dorsal surface of the tongue, consequently to defective
desquamation of the epithelium. The hair-like appearance is generally associated with different
extent of discoloration, varying from yellowish-brown to black, and thickness of tongue coating.
Although the etiopathogenesis of this kind of lesion has not been fully elucidated, several
precipitating factors have been taken into consideration. In particular, prolonged antibiotic
therapy, graft-versus-host-disease (GVHD), bad habits (principally excessive tobacco smoking),
xerostomia, and poor oral hygiene, have been described in literature as predisposing
factors.[6,7,8,9] In addition, the discoloration is thought to be related to the overgrowth of
microorganisms, such as porphyrin-producing chromogenic bacteria or Candida spp.,[10] as well as
to a nonspecific infection.[10,11]
This report firstly describes a clinical case of BHT in a patient affected by ALS. In this circumstance,
the overall rapid progression of muscle weakness, in conjunction with the loss of self-sufficiency,

~ 50 ~
has played a crucial role for its occurrence, as they prevent the patient from the maintenance of
an adequate oral hygiene standard.

Case report.
A 63-year-old Caucasian man was first admitted to the Neurology Department in 2012, with a
diagnosis of ALS with generalized exordium (El Escorial Criteria). Since the early stages, the patient
showed the symptoms, such as limb weakness, fasciculations of the extremities and the tongue, a
marked dysarthria and dysphagia, reduced tongue mobility, sialorrhea that progressed to a
significant weight loss. In addition, the initial involvement of the respiratory muscles, and the
subsequent difficulty in breathing (dyspnea), required noninvasive mechanical ventilation at night.
During a routine checkup in August 2013, the neurologist identified a black lesion on the lingual
dorsum [Figure 1], complicated by the presence of halitosis, which is a major cause of a severe
impairment of interpersonal relationships. Moreover, the partial hypermobility of the tongue and
a reduced self-sufficiency prevailed upon the neurologist to consult the oral pathologist in order to
identify the lesion and to establish an appropriate therapy. The clinical examination conducted to
diagnose BHT is predominantly related to a tragic reduction of the domiciliary oral hygiene of the
patient and the hypofunctional tongue. According to the tongue-coating index by Gmez et
al.,[12] the tongue lesion was therefore classified as a coating score 2 (heavy-thick coating) and
discoloration score 4 (black) of the distal 2/3 of the tongue. Furthermore, the high plaque index
(more than 60%) and a lack of adequate preparation of the health-care assistant to the oral
hygiene procedures specific to the patient's condition were evaluated.
First of all, in order to maintain adequate oral hygienic conditions, the oral hygienist provided the
patient and the health-care assistant with the correct oral hygiene protocols to adopt [Table
1].[13] Specifically, on the basis of the work by Danser et al., the oral clinician focused on and
explained the appropriate approach to brush the tongue.[14] The mechanical removal of the
coating through the use of a tongue scraper, in association with the daily application of a sterile
gauze impregnated with chlorhexidine 0.2%, was crucial.
After 1 month, complete remission of the lesion was achieved, despite the worsening of tongue
mobility and further reduction of the self-sufficiency of the patient

Discussion
BHT represents a relatively uncommon condition, causing great concerns in affected individuals,
due to its clinical presentation. Although the etiology remains unclear and multiple contributing
factors have been considered, the selected individuals have demonstrated to be mainly exposed
to a higher risk of developing BHT. In particular, elderly patients with poor oral hygiene as well as
those with limited self-sufficiency have been recognized as predominately predisposed.[7]
The maintenance of good oral hygiene and the gentle debridement of tongue surface assume a
crucial role in the prevention of local and systemic diseases. In particular, on the basis of the
current knowledge, the effectiveness of the removal of tongue coating represents an essential
prerequisite for preventing bacterial colonization.[14,15]

~ 51 ~
Since an alteration of oral or systemic ecosystem can favourite the development of a pathologic
condition, several studies emphasised the importance of oral hygiene procedures in order to
mantain the microbial equilibrium into the oral niches.[15,16] According to the literature, the
removal of lingual coating can prevent the establishment of periodontal infections[12] as well as
systemic complications. In 2008, Abe et al. investigated the presence of Pneumoniae spp. in the
lingual biofilm, supporting the necessity of interventions to decrease the risk of respiratory
affections in elderly patients.[17] Moreover, in 2013, Santos et al. described how the ventilated
patient can incur more easily into a pulmonary infection in the presence of a bacterial colonization
of the lingual dorsum.[18]
ALS patients represent a high-risk population for such complication, due to the need of mechanical
ventilation for respiratory muscles involvement, and the prevention of lingual pathologies
becomes indispensable to preserve their general health.[17,18] Despite receiving close medical
attention, the critical conditions of ALS patients, especially those with bulbar onset, often divert
the attention from the clinical evaluation of oral health. Furthermore, conditions, such as glossitis,
periodontal diseases, caries, stomatitis, and the development of halitosis, frequently remain
undiagnosed, due to the inability of the patient to communicate discomfort and pain as described
in the literature about the patient affected by other kinds of neurological diseases.[19]
Conclusions.
Since the earliest phases of the ALS, the dedicated support of the oral hygienist would be helpful
for the maintenance of proper oral hygiene, and specifically tongue hygiene, in order to prevent
further local and systemic complications for these patients.[17] In addition, raising awareness
about the risk of developing oral pathologies, that could worsen the prognosis of ALS patients,
would contribute to improve their quality of life.[20] The education of the health-care assistant
about clinical consequences of lacking oral hygiene as well as the standardization of oral health
protocols in critical conditions would provide great benefits to these patients. Throughout the
years, the use of adequate hygiene devices and daily tongue brushing have been proved to be the
best preventive and therapeutic measures, to reduce the amount of pathogenic microorganisms in
the oral niches and, therefore, to prevent the systemic complications related to the decline of the
oral ecological balance.

~ 52 ~
Lengua negra y peluda en pacientes con ELA

Abstracto: EL BTH por su nombre en ingls (Black hairy tongue) ocurre por una elongacin en las
papilas filiformes, principalmente se ve en personas de avanzada edad. Aparece por una poca
higiene bucal. Los pacientes con ELA tienden a tener ms riesgos de aparicin de esta
enfermedad. En el respectivo paper se mostrar un paciente de 63 aos, afectado por ELA. El
principal objetivo fue la enseanza de mtodos de limpieza e higiene para el paciente y
proporcionar informacin adecuada a su asistente de salud.

Introduccin: La lengua peluda negra (BHT) es una infeccin marcada por el alargamiento e
hipertrofia de las papilas filiformes. Se manifiesta con un aspecto similar al del cabello y puede
tener diferentes grados de tincin. Algunos factores que se asocian a esta patologa son el uso de
tratamiento antibitico prolongado, enfermedad del injerto contra el husped, algunas malos
hbitos que pueden ser el cigarro (y su excesivo consumo); xerostoma o la mala higiene dental o
deficiente. La decoloracin est asociada a los microorganismos que all crecen (la cantidad).

Caso: Hombre de 63 aos caucsico, tiene un diagnstico de ELA con exordio generalizado. En las
primeras etapas el paciente present sntomas (debilidad de los miembros, fasciculaciones de las
extremidades y lengua, disartria, disfagia, movilidad reducida de la lengua y sialorrea). Tuvo
tambin una dificultad respiratoria, por lo que necesitaba ventilacin mecnica (No invasiva) en la
noche.

En el agosto del 2013, un neurlogo identific una lesin negra en el dorso de la lengua,
acompaada por la presencia de halitosis. El paciente present lesin de revestimiento 2, capa
gruesa, (segn el ndice de revestimiento de lengua de Gmez) adems de coloracin 4 (negra).
Adems hubo un evalo de placa bacteriana alta (ms del 60%) y falta de preparacin del asistente
sanitario en los procesos de higiene bucal.

Para mantener las condiciones de higiene bucal, el higienista oral proporcion al paciente y al
asistente sanitario los protocolos correspondientes de limpieza bucal a adoptar. Tambin se
enfocaron y el clnico oral explic el enfoque necesario para cepillar la lengua.

Despus de 1 mes, se consigui una remisin completa de la lesin, a pesar del empeoramiento de
la movilidad de la lengua y una reduccin adicional de la autosuficiencia del paciente

Discusin: En particular, se ha reconocido que los pacientes ancianos con una higiene oral
deficiente, as como aquellos con autosuficiencia limitada, estn predispuestos
predominantemente a tener la enfermedad.

El mantenimiento de una buena higiene bucal y el desbridamiento suave de la superficie de la


lengua asumen un papel crucial en la prevencin de enfermedades locales y sistmicas.

Los pacientes con ELA representan una poblacin de alto riesgo para tal complicacin, debido a la
necesidad de ventilacin mecnica para la afectacin de los msculos respiratorios, y la
prevencin de las patologas linguales se hace indispensable para preservar su salud general.
Adems, las condiciones, como la glositis, las enfermedades periodontales, las caries, la
estomatitis y el desarrollo de la halitosis, con frecuencia permanecen sin diagnosticar, debido a la
incapacidad del paciente para comunicar malestar y dolor.

~ 53 ~
Conclusiones: El apoyo del higienista oral sera til para el mantenimiento de una higiene bucal
adecuada (especficamente de la lengua). Adems, la sensibilizacin sobre el riesgo de desarrollar
patologas orales, que podra empeorar el pronstico de los pacientes con ELA, contribuira a
mejorar su calidad de vida. La estandarizacin de protocolos de salud oral (que debe tener en
conocimiento el asistente sanitario) en condiciones crticas proporcionara grandes beneficios a
estos pacientes. Se ha demostrado que el uso de dispositivos adecuados de higiene y el cepillado
de la lengua son las mejores medidas preventivas y teraputicas para reducir la cantidad de
microorganismos patgenos en los nichos bucales y prevenir las complicaciones sistmicas
relacionadas con la disminucin Del equilibrio ecolgico oral.

~ 54 ~
Alzheimer.

El alzhimer es una demencia, es un sndrome adquirido y crnico, que en la mayora de sus casos
es irreversible, es causada por una disfuncin del cerebro. Esta enfermedad afecta la memoria,
comportamiento y el propio pensamiento. Esta es la forma ms comn de demencia.

Es clsico que el alzhimer tenga mayor ndice en las personas mayores a los sesenta aos
aproximadamente y representa una de las diez causas de muertes en este grupo etario. Los
porcentajes son:

1-2% Poblacin de 60 aos.

3-5% Poblacin de 70 aos

15-20% Poblacin de 80 aos.

40-50% Poblacin mayor a 85 aos

Los siguientes factores tambin pueden aumentar el riesgo:

-Pertenecer al sexo femenino

-Tener problemas cardiovasculares debido, por ejemplo, al colesterol alto

-Antecedentes de traumatismo craneal

Hay dos tipos de alzhimer, los cuales son:

Mal de A. de aparicin temprana, en la cual antes de los sesenta aos la persona empieza
presentar sntomas. Tiende a empeorar de manera rpida y es ms extraa que el Alzhimer de
aparicin tarda. Otro detalle, es que est muy ligada a lo que son los genes y puede ser
hereditaria.

Mal de A. de aparicin tarda, hay que mencionar, primero que todo que esta es la forma ms
comn de encontrar la demencia de Alzhimer, puede ser hereditaria, pero aqu los genes no
tienen mucha participacin, y lo principal, que aqu, los sntomas de la enfermedad comienzan a
presentarse arriba de los sesenta aos de edad.

La prevalencia de personas con alzhimer al menos en nuestro pas, se estima que de 1000 adultos
mayores que sobrepasen los 65 aos, 100 de ellos podran presentar la enfermedad.

Las causas que pueden provocar el alzhimer an son desconocidas, pero hay que mencionar que
puede ser debido a un a ciertos cambios que hay en el cerebro humano.

Cabe destacar que una persona tiene ms posibilidades de tener alzhimer si es mayor, tiene un
pariente sanguneo cercano con aquella enfermedad y/o tener ciertos genes ligados al alzhimer.

Los signos que indican la enfermedad de Alzheimer pueden incluir:

Cambios en la personalidad

~ 55 ~
Deterioro en la capacidad de movimiento o al caminar

Dificultad para comunicarse

Bajo nivel de energa

Prdida de memoria

Cambios de estado de nimo

Problemas de atencin y orientacin

Incapacidad de resolver operaciones aritmticas sencillas

El alzhimer cuenta de tres fases, las cuales son:

Fase inicial (se caracteriza por tener algunas fallas en la memoria), Fase intermedia (Disminuye la
memoria reciente y empiezan a producirse cambios de comportamiento), Fase avanzada (el
paciente en esta etapa tiende a depender completamente terceras personas.)

Prevencin:

Aunque no existe una forma comprobada de prevenir el mal de Alzheimer, existen algunas
medidas que pueden ayudar a prevenir o retardar el comienzo de la enfermedad:

-Mantenga una dieta baja en grasa y consuma alimentos ricos en cidos grasos omega-3.

-Haga mucho ejercicio.

-Permanezca activo mental y socialmente.

-Use un casco durante las actividades riesgosas para prevenir las lesiones cerebrales.

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Alzheimer y la odontologa.

EL Alzheimer compromete habilidades tanto cognitivas como motoras en las personas, esto puede
llevar a una falta de higiene e insuficiencia en su salud oral.

De hecho, los pacientes con demencias tienden a presentar ms patologas orales que personas
que no tiene demencia.

La prevalencia de caries aumenta al igual que la prevalencia de Stomatits Subrotsica, disminuye


el flujo salival (Que est asociado a la medicacin del paciente), ocurre con mayor frecuencia la
candidiasis oral, se presenta dificultad para comer, hay alteraciones de gusto y se adquiere glositis.

El tratamiento de una persona con Alzheimer debe ser diseado a que tan avanzada est la
demencia en el paciente. Debemos tener en cuenta que mientras mas avanzada est la
enfermedad, la condicin bucal del paciente empeora progresivamente. Entonces hay que
adelantarse a estos hechos, y si se atiende a una persona es sus primeras etapas de la
enfermedad hay que prevenir inmediatamente y adems tener citas frecuentes con esta persona.

As tambin se debe mantener informado a los familiares y personas que estn a cargo de la
persona sobre las medidas de higiene bucal que hay debe seguir el paciente.

Aqu la persona no debe estar sola, puede ocurrir algo en el trayecto, debe estar siempre
acompaada, por problemas de acceso, movilidad y transporte. Y son ests mismas personas que
deben estar informadas de una higiene bucal adecuada para el paciente.

En el caso que presenten estomatitis sub protsica, se debe considerar en el tratamiento:


Uso del acondicionador de tejidos., correcta remocin y limpieza del aparato protsico: Retirar
prtesis en las noches, realizar limpieza de sta con una escobilla o cepillo diferente con el que se
cepillan los dientes. Se recomienda el uso de cepillo suave. Terapia antifngica: Miconazol 2%
Plastibase (4 veces al da por 20 das).

Hay que tener en cuenta tambin un punto de vista, que es principalmente de tica, hay que tener
consideraciones con estos pacientes por dificultad y la poca autonoma que tienen, tratarles con
amabilidad, ser tolerantes con ellos y en ninguno de los casos tratar de aprovechar esta condicin
a favor para el profesional (tales aprovechamientos pueden ser malos tratos hacia el paciente y
hasta cobros elevados por tratamientos simples).

Y en caso de hacer cualquier tratamiento, si tiene algn acompaador, este debe estar informado
y hacer valer su opinin sobre lo que se deba hacer, puesto que hay una vida que est siendo
tratada, que no tiene un auto cuidado suficiente de s mismo.

A medida que la enfermedad de demencia por alzhimer progresa, la incidencia de muertes por
causadas por neumona se hace mayor, esto se debe por la aspiracin, entonces, los tratamientos
que puedan aumentar el potencial de aspiracin no son recomendables para este tipo de
pacientes, es especial si es muy avanzada la enfermedad.
En general los procedimientos dentales deben ser breves, y en algunos casos se puede considerar
el uso de sedacin, sobre todo en los pacientes con conductas agresivas.

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Periodontitis and cognitive decline in Alzheimers Disease

Abstract.

Periodontitis is common in the elderly and may become more common in Alzheimers disease
because of a reduced ability to take care of oral hygiene as the disease progresses. Elevated
antibodies to periodontal bacteria are associated with an increased systemic pro-inflammatory
state. Elsewhere raised serum pro-inflammatory cytokines have been associated with an increased
rate of cognitive decline in Alzheimers disease. We hypothesized that periodontitis would be
associated with increased dementia severity and a more rapid cognitive decline in Alzheimers
disease. We aimed to determine if periodontitis in Alzheimers disease is associated with both
increased dementia severity and cognitive decline, and an increased systemic pro inflammatory
state. In a six month observational cohort study 60 community dwelling participants with mild to
moderate Alzheimers Disease were cognitively assessed and a blood sample taken for systemic
inflammatory markers. Dental health was assessed by a dental hygienist, blind to cognitive
outcomes. All assessments were repeated at six months. The presence of periodontitis at baseline
was not related to baseline cognitive state but was associated with a six fold increase in the rate of
cognitive decline as assessed by the ADAS-cog over a six month follow up period. Periodontitis at
baseline was associated with a relative increase in the pro-inflammatory state over the six month
follow up period. Our data showed that periodontitis is associated with an increase in cognitive
decline in Alzheimers Disease, independent to baseline cognitive state, which may be mediated
through effects on systemic inflammation.

Introdution.

Periodontal disease is widespread in the UK population and typical of most other westernized
countries including North America[1]. In older age groups it is believed to be a major cause of
tooth loss. In the UK in 1998, only 38% of adults aged over 65 had 21 or more of their original 32
teeth with 50% of these reporting periodontitis before they lost teeth[2]. A number of studies
show that having few teeth, possibly as a consequence of earlier periodontitis, is associated with
an increase risk of developing dementia [3].
Periodontitis has been shown to be associated with a raised serum pro-inflammatory state as
shown by increases in C Reactive Protein (CRP) [4] and pro-inflammatory cytokines (e.g. Tumour
Necrosis Factor (TNF)) with a reduction in anti-inflammatory markers (e.g. interleukin 10 (IL
10)) [5]. Chewing on involved teeth may lead to the introduction of periodontal bacteria shown by
detectable amounts of serum bacterial lipopolysaccharide (LPS) [6,7]. In Alzheimers Disease (AD)
periodontitis may be even more common because of a reduced ability to take care of oral hygiene
as the disease progresses and in AD increased elevation of serum levels of antibodies with
associated increases in TNF have been reported [8]. We have previously shown that chronic
inflammatory diseases are associated with increased systemic pro-inflammatory cytokines and an
increased rate of cognitive decline in AD [9]. We hypothesised that periodontitis would increase
with increasing dementia severity in AD but that periodontitis would be associated with an
increased rate of cognitive decline independent of the degree of dementia severity. We further
hypothesised that periodontitis would be associated with a relative increase in systemic measures
of the pro-inflammatory state and a decrease in anti-inflammatory state.
Materials and methods.

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Study design
60 non smoking community dwelling participants (and their caregivers) with mild to moderate
dementia and a minimum of 10 teeth who had not received treatment for periodontitis in the past
6 months, were recruited during the period August 2012 to August 2013 from clinical referrals to
memory assessment services in Southampton, United Kingdom. All participants in this study had
to have capacity to give consent for themselves following United Kingdom Medical Research
Council guidance http://www.mrc.ac.uk/documents/pdf/medical-research-involving-adults-who-
cannot-consent/. A surrogate consent procedure was not used. As part of the assessment of
capacity a trained psychiatrist explained orally and in writing the nature, duration, and purpose of
the study so that the participant was aware of the potential risks, inconveniences, or adverse
effects that may occur. All participants in this study were considered to understand this
information; to weigh up the information and retain it for long enough to make a decision as to
whether to take part. All participants communicated this decision by signing the participants
information sheet and consent form. The participants capacity to consent was monitored
throughout the study and any participants considered to have lost this capacity were withdrawn.
Participants fulfilled National Institute of Neurological and Communicative Disorders and Stroke-
Alzheimers Disease and Related Disorders Association (NINCDS-ADRDA) criteria for probable or
possible AD [10] with a modified Hachinski Ischaemic Scale score [11] of greater than 4 points and
all had been on a stable cholinesterase inhibitor for at least 6 months. Participants were
cognitively tested using the Alzheimers Disease Assessment Scale (ADAS-cog) [12] as the primary
cognitive outcome and the standardized Mini-Mental State Examination (sMMSE) [13] as a
secondary cognitive outcome. Immediately following cognitive assessment at baseline a venous
blood sample was taken for CRP, the pro-inflammatory cytokine TNF, the anti-inflammatory
cytokine IL10 and for antibodies to P.gingivalis. The participants dental health (number of teeth
and measures of periodontitis including the number of sites (6 sites per tooth) with plaque scores
assessed as grade 2 (plaque identifiable without the need for a dental probe) and grade 1 (plaque
identifiable using a dental probe), pocket depth in millimeters per site and the number of sites
showing bleeding on probing was assessed by an accredited research dental hygienist. These
assessments are all used to determine the presence or absence of periodontitis following
established Centre for Disease Control/American Academy of Periodontology (CDC/AAP) case
definitions [14]. The participants main caregiver, defined as a caregiver spending at least 10 hours
per week with the participant, was interviewed to assess medical and dental history including
treatment for periodontitis and medication use over the previous 6 months. The participant and
main caregiver were reviewed at six months and reassessed in an identical manner.

Standard Protocol Approvals, Registrations, and Patient Consents


This study received approval from the South and West Hampshire Local Research Ethics
Committee (11/SC/0422). Written informed consent was obtained from all patients participating
in the study.

Serum inflammation, antibody and DNA assays


All blood samples were centrifuged and sera aliquotted on ice and stored at -80C within 2 hours.
Levels of CRP, TNF and IL-10 were assayed using sandwich immunoassay multi-plex cytokine
assay (Meso Scale Discovery (MSD). A protocol provided by MSD for custom assays was used with
no major modifications. Serum IgG antibody titre to P.gingivalis was determined by direct binding
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Enzyme Linked Immunosorbent Assay. Heat killed P.gingvalis (Invivogen) was coated onto 96 well
maxisorp plates at a concentration of 108 cells/ml. The plates were washed five times with
Phosphate Buffered Saline (PBS) 0.05% tween, and blocked with 1% PBS Bovine Serum Albumin
(BSA). Patient serum samples were added at a dilution of 1:125 in PBS 1% BSA and incubated for
90 minutes. After washing five times, goat anti-human IgG (Sigma) was added at a dilution of
1:40,000 in PBS 1% BSA, and incubated for 60 minutes. Bound IgG was detected using
Tetramethylbenzidine (Sigma) as a substrate, and the reaction was stopped using 1M H 2SO4 before
reading optical density at 450nm. Blood for DNA (principally APOE genotype) was taken at
baseline. APOE genotypes were determined by Taqman genotyping of SNP rs7412 and KASP
genotyping of SNP rs429358.

Statistical analysis
Assessment of normality of continuous variables was determined by quantile-quantile plots of the
residuals. Baseline ADAS-COG, sMMSE; IL10; TNF; optical density to IgG antibodies
to P. gingivalis and changes in ADAS-COG; sMMSE and TNF were normally distributed. Baseline
serum CRP; and changes in CRP and IL10 levels were not normally distributed. Baseline
comparisons were made using t tests and Mann-Whitney tests for continuous variables,
depending on whether normally distributed or not. For categorical variables, Chi squared tests
were used. Comparisons between the two groups were made using linear regression, with
adjustment for potential confounding factors of age; gender and baseline cognitive score (ADAS-
COG or sMMSE). Previous studies have suggested that around half of participants in this age group
would have periodontitis. Power calculations of 52 participants completing the study were based
on statistical evidence to suggest that a sample size of 26 patients per group is an optimum figure
for a pilot study of this nature [15,16]. Assuming a standard deviation change of 5 points this study
size gave us 80% power to detect a meaningful clinical difference effect size of 4 points change in
the ADAS-COG over a 6 months period ( = 0.05). The unequal ratio between groups found in the
study (1.7) meant that a total of 56 subjects were needed for the same effect size and power.
Allowing for a 1020% drop out rate this required the recruitment of 57 to 65 participants. In this
pilot study we made no explicit allowance for multiplicity of testing, and therefore make no claims
about significance where an adjustment of the type I error rate (e.g. Bonferroni) would lead to a
given p-value no longer reaching statistical significance. Multivariate analysis was used to adjust
for possible confounding effects of age, gender and baseline cognitive status.
Results.

Baseline data
Following consent procedures one participant was found to be an intermittent smoker and was
excluded from further involvement in the study. Of the 59 participants remaining all fulfilled
NINCDS-ADRDA criteria for probable or possible AD and all had a modified. Hachinski Ischaemic
Scale score of greater than four points.

Baseline demographics, dental health measures and cognition


The mean age of the cohort at baseline was 77.7 (s.d. 8.6) years. 30 (51%) participants were men.
89.0 (s.d. 12.5) % participants had detectable plaque of whom 19.9 (s.d. 11.8) % had plaque
identifiable without the need for a dental probe (grade 1) and 69.1 (s.d. 20.6) % participants had

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identifiable plaque using a dental probe (grade 2). The mean probing depth was 2.5 (s.d. 0.4) mm
per participant with 6.7 [IQR 2.5 to 13.6] % of sites probing greater than 3mm. 13.6 [IQR 7.6 to
21.5] % of gingival sites showed bleeding on probing. Examination of the variables for plaque;
probing depth and bleeding sites resulted in the classification of 22 (37.3%) participants fulfilling
CDC/AAP criteria for the presence of periodontitis of whom 15 (25.4)% had moderate and 7
(11.9%) had severe periodontitis. At baseline participants had a mean number of 21.9 (s.d. 5.2)
teeth, ranging from 10 to 32 teeth present.
At baseline participants had a mean ADAS-COG score of 46.2 (s.d. 12.3) points and a mean sMMSE
score of 20.4 (s.d. 5.0) points.

Longitudinal follow up
Fifty two of 59 (88%) participants completed follow up at 6 months. One participant died; 3
participants declined follow up and 3 participants were lost to follow up. At 6 month follow up 15
(75%) of the 20 subjects fulfilling CDC/AAP criteria for periodontitis at baseline still fulfilled these
criteria whilst 30 (94%) of the 32 subjects not fulfilling these criteria at baseline continued to not
fulfil these criteria. The mean change in the ADAS-cog was 2.9 (s.d. 6.6) pts. The mean change in
the sMMSE score was -1.4 (s.d. 3.2) pts.
The relationship between the presence of periodontitis at baseline and cognitive decline over the
six month follow up period is shown in
There was a significant difference in the rate of change in the ADAS-cog score and the presence or
absence of periodontitis at baseline which remained following adjustment for baseline age, gender
and baseline ADAS-cog score. There was also a significant relationship between the presence of
periodontitis and change in sMMSE score but this was not significant when adjusting for baseline
age, gender or baseline sMMSE score.
There was no significant association between the rate of decline on the sMMSE score and with the
number of teeth at baseline (Pearson -0.1 p = 0.4) but there was a significant association with the
rate of decline on the ADAS-cog score (Pearson 0.35 p = 0.01). However, this relationship was no
longer significant when adjusting for the presence of periodontitis at baseline (adjusted
correlation 0.25 p = 0.07).
There was no significant association between baseline serum P. Gingivalis antibody levels and the
rate of decline on the ADAS-cog score (Pearson -0.03 p = 0.9) or rate of decline on the sMMSE
score (Pearson -0.2 p = 0.1).

Systemic inflammatory markers


54 (92%) participants gave consent for blood sampling for peripheral inflammatory markers (CRP,
TNF, IL10) and DNA for ApoE genotyping at baseline.
Baseline serum levels and relationships with baseline demographics and cognitive and dental
measures are shown
There were no significant relationships between baseline systemic inflammatory markers and
demographic; cognitive or dental measures.

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31 (54%) participants carried the ApoE e4 allele. There were no significant relationships between
carriers of the ApoE e4 allele and dental measures including the presence or absence of
periodontitis (32% participants with the e4 allele compared with 43% participants without the e4
allele had periodontitis X2 0.7 p = 0.4).
43 of the 52 (83%) participants who agreed to follow up gave a blood sample for peripheral
inflammatory markers (CRP, TNF, IL10) at six month follow up. Changes in serum levels and
relationships with baseline dental measures are shown in.
No significant relationships were found with number of teeth and changes in serum inflammatory
markers. However, the presence of periodontitis at baseline was associated with a fall in serum
IL10 levels, and serum baseline P. gingivalis antibody levels were also associated with a fall in
serum IL10 levels and an increase in serum TNF levels.
Discussion.

A number of studies have shown that patients with AD have poorer dental health than aged
controls and that the more severe the dementia the worse the dental health [17,18], most likely
reflecting increasing difficulties with self care in more severe dementia [19,20]. We did not find a
clear relationship between severity of dementia and degree of periodontitis, most likely reflecting
the absence of subjects with severe dementia in the study. However, no studies to date have
examined whether, in a longitudinal study, poor dental health correlates with poorer cognitive
outcomes that are independent to baseline cognitive state. This study shows that in AD poor
dental health, and in particular, the presence of periodontitis, is associated with a marked increase
in cognitive decline over a six month follow up period, independent to baseline cognitive state. As
anticipated baseline periodontal state appeared largely stable over the six month period, although
there was some improvement in some participants most likely reflecting heightened awareness of
the potential importance of oral care due to participation in the study.
A number of reasons might be given for the relationship between periodontitis and increased
cognitive decline. Firstly, the small numbers of participants in this study cannot rule out that the
relationship is due to chance and the study needs to be replicated. Secondly, it is possible that
participants with a more precipitous rate of cognitive decline become more susceptible to
periodontitis through an unknown mechanism that is independent to the degree of cognitive
impairment or, thirdly, that periodontitis is a reflection of a confounding factor such as a
compromised or modified inflammatory or immune response that is also a driver of AD
progression. On the other hand, periodontitis may be a direct driver of disease progression. The
presence of periodontitis is determined by the examination of sites around teeth and thus the
positive relationship between periodontitis and higher number of teeth was expected. However,
the lack of relationship between low tooth number, a possible indicator of past periodontitis, and
cognitive decline suggests that active chronic periodontitis is most important in driving cognitive
decline once AD is established. A number of studies have suggested that periodontitis is associated
with higher amyloid precursor protein expression [21] and higher amyloid loads in the elderly [22].
In addition other studies have shown that antibodies to common periodontal microbiota [23,24]
or tooth loss [3,25] caused by chronic periodontitis, might precede the development of AD by
many years. We did not find a significant relationship between serum
baseline P. gingivalis antibody levels and rates of cognitive decline. The relationship may require
the additional role of other periodontal organisms or it may be that in some individuals antibody

~ 62 ~
levels to P. gingivalis reflect exposure to the organism which hasnt resulted in periodontal
disease.
The mechanism for the relationship between periodontitis and cognitive decline is still unclear but
there is increasing evidence to support a role for systemic inflammation. Thus, cross sectional
studies have shown that the presence of periodontitis, or antibodies to common periodontal
bacterial flora, are associated with an increase in a systemic proinflammatory state characterized
by an increase in serum CRP; TNF [8] and TNF/IL10 ratios [26] in participants with AD. We have
previously shown that AD patients with a range of acute and chronic inflammatory conditions have
an increased pro-inflammatory cytokine profile that is associated with an increased rate of
cognitive decline [9]. In this current study we show evidence of a relative increase in the
proinflammatory state and decrease in the anti-inflammatory state over a six month follow up
period in AD participants with periodontitis. A similar association was found between pro-
inflammatory state and the presence of IgG antibodies to P gingivalis, generally associated with
the presence of periodontitis. If, as this current study suggests, there is a direct relationship
between periodontitis and cognitive decline then treatment of periodontitis might be a possible
treatment option in AD. Encouragingly a small study of periodontal treatment [27], in AD
participants suggest that there may be some cognitive benefits to this approach supporting the
need for a randomized trial to test this hypothesis.

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Periodontitis y declinacin cognitive en la enfermedad del Alzheimer
Abstracto: La periodontitis es comn en ancianos, y an mucho ms en aquellos con alzhimer
(por la poca capacidad de cuidar su higiene oral mientras la enfermedad progresa).

El objetivo del paper fue determinar si la periodontitis en la enfermedad de Alzheimer se asocia


con el aumento de la gravedad de la demencia y el deterioro cognitivo, y un aumento del estado
sistmico pro inflamatorio.

Hubo estudio observacional de seis meses a 60 participantes de la comunidad de vivienda con


leve a moderada enfermedad de Alzheimer fueron cognitivamente. La salud dental fue evaluada
por un higienista dental, ciego a los resultados cognitivos. Periodontitis en la lnea de base se
asoci con un aumento relativo en el estado pro-inflamatorio durante el perodo de seguimiento
de seis meses. Nuestros datos mostraron que la periodontitis se asocia con un aumento en el
deterioro cognitivo en la enfermedad de Alzheimer, independiente del estado cognitivo inicial,
que puede estar mediado a travs de los efectos sobre la inflamacin sistmica.

Introduccin: La enfermedad periodontal est muy extendida en la poblacin del Reino Unido y es
tpica de la mayora de los pases occidentalizados. En los grupos de mayor edad se cree que es
una de las principales causas de prdida de dientes. Una serie de estudios muestran que tener
pocos dientes, posiblemente como consecuencia de la periodontitis anterior, se asocia con un
mayor riesgo de desarrollar demencia.

En la enfermedad de Alzheimer (AD) la periodontitis puede ser an ms comn debido a una


capacidad reducida para cuidar la higiene bucal a medida que la enfermedad progresa.

Hemos planteado la hiptesis de que la periodontitis se incrementara con el aumento de la


gravedad de la demencia en la EA, pero que la periodontitis se asociara con un aumento de la tasa
de disminucin cognitiva independiente del grado de gravedad de la demencia.

Materiales y mtodos.

60 participantes de la comunidad no fumadores con demencia leve a moderada y un mnimo de


10 dientes que no haban recibido tratamiento para la periodontitis en los ltimos 6 meses, fueron
reclutados durante el perodo de agosto de 2012 a agosto de 2013. Como parte de la evaluacin
de la capacidad, un psiquiatra entrenado explic oralmente y por escrito la naturaleza, duracin y
propsito del estudio para que el participante fuera consciente de los posibles riesgos.

Se utilizaron evaluaciones para determinar la presencia o ausencia de periodontitis. Se hizo


preguntas a los cuidadores para conocer antecedentes clnicos y dentales, adems de
tratamientos que llevaba a cabo. Adems de muestras de sangre del paciente.

Ensayos de inflamacin srica, anticuerpos y ADN: Todas las muestras de sangre de los pacientes
fueron preparadas y se agregaron sustancias especficas a estas. Se comparaban las muestras de
sangre, entre diferentes grupos, entre otros. Y las pruebas anteriores daban a conocer que la
mitad de los sujetos experimentales ya tena periodontitis. Estas personas fueron sometidas a
diferentes pruebas y exmenes.

Resultados.
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Datos de referencia: Una de las personas era fumadora intermitente y fue excluida de la
investigacin. De los restantes se cumplieron todos los criterios.

89% de participantes tenan placa detectable de los cuales 19,9 % tenan placa identificable sin la
necesidad de una sonda dental. La profundidad media de sondaje fue de 2,5 (0,4) mm por
participante con 6,7 % de sitios que probaron ms de 3 mm. 13,6% de los sitios gingivales
mostraron hemorragia al sondeo. Examen de las variables de la placa; Profundidad de sondaje y
sitios de hemorragia resultaron en la clasificacin de 37,3% participantes que cumplan con los
criterios de CDC / AAP para la presencia de periodontitis, de los cuales 25,4% tenan moderada y
11,9% tenan periodontitis severa. En la lnea de base, los participantes tenan un nmero medio
de 21,9 dientes (10 a 32 dientes presentes).

En la tabla uno, se ve la relacin entre presencia de periodontitis y demografa basal (edad y sexo)

Seguimiento longitudinal: 88% de los participantes completaron el seguimiento a los 6 meses. Un


participante muri; 3 participantes rechazaron el seguimiento y se perdi a 3 participantes para el
seguimiento. A los seis meses de seguimiento, 75% de los 20 sujetos que cumplan los criterios de
los CDC / AAP para la periodontitis en la lnea de base todava cumplan estos criterios, mientras
que el 94% de los 32 sujetos que no cumplan estos criterios.

En la tabla dos se muestra la relacin entre la presencia de periodontitis en la lnea de base y el


cambio cognitivo durante el perodo de seguimiento de seis meses. Hubo una diferencia
significativa en la tasa de cambio en la puntuacin de ADAS-cog y la presencia o ausencia de
periodontitis.

Marcadores inflamatorios sistmicos:

54 (92%) de los participantes dieron su consentimiento para el muestreo de sangre para los
marcadores inflamatorios perifricos y ADN para el genotipo ApoE en la lnea de base.

En la tabla tres se muestra las relaciones entre los marcadores basales de la inflamacin srica y la
demografa basal; Medidas cognitivas y medidas de salud dental. No hubo relaciones significativas
entre los marcadores inflamatorios sistmicos basales y demogrficos; Cognitivas o dentales.

43 de los 52 (83%) participantes que aceptaron dar seguimiento dieron una muestra de sangre
para los marcadores inflamatorios perifricos a los seis meses de seguimiento.

En el cuadro cuatro se presentan las relaciones entre el cambio en los marcadores inflamatorios
sricos de las medidas basales y basales de salud dental. No se encontraron relaciones
significativas con el nmero de dientes y los cambios en los marcadores inflamatorios sricos. Sin
embargo, la presencia de periodontitis en la lnea de base se asoci con una cada en los niveles
sricos de IL10, y los niveles sricos de anticuerpos de P. gingivalis tambin se asociaron con una
cada en los niveles sricos de IL10 y un aumento en los niveles sricos de TNF.

Discusin.

Los pacientes con la enfermedad de AD tienen peor salud dental si aumenta su edad o la gravedad
de su demencia. No se encuentra una clara relacin entre la gravedad de la demencia con el grado
de periodontitis. Este estudio demuestra que en la AD la mala salud dental, y en particular, la
presencia de periodontitis, se asocian con un marcado aumento de la disminucin cognitiva

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durante un perodo de seguimiento de seis meses, independiente del estado cognitivo de
referencia.

Hay varias razones que se pueden dar para la relacin entre la periodontitis y el aumento de
declive cognitivo. el pequeo nmero de participantes en este estudio no puede descartar que la
relacin se deba a la casualidad y el estudio necesita ser replicado, es posible que los participantes
con una tasa ms pronunciada de disminucin cognitiva se vuelvan ms susceptibles a la
periodontitis a travs de un mecanismo desconocido que sea independiente del grado de
deterioro cognitivo, que la periodontitis sea un reflejo de un factor de confusin como un
compromiso O una respuesta inflamatoria o inmunitaria modificada que tambin es un impulsor
de la progresin de la AD. Sin embargo, la falta de relacin entre el nmero de dientes bajos, un
posible indicador de periodontitis pasada y la disminucin cognitiva sugiere que la periodontitis
crnica activa es ms importante en la conduccin de la disminucin cognitiva una vez que se
establece AD. Tampoco se encontr una relacin significativa entre los niveles sricos de A. de P.
Gingivales y las tasas de disminucin cognitiva. El mecanismo para la relacin entre la periodontitis
y el deterioro cognitivo an no est claro, pero hay evidencia creciente para apoyar un papel para
la inflamacin sistmica. Hemos demostrado previamente que los pacientes con AD con una serie
de condiciones inflamatorias agudas y crnicas tienen un perfil de cito quinas pro-inflamatorias
aumentado que se asocia con una mayor tasa de disminucin cognitiva.

Como sugiere este estudio actual, existe una relacin directa entre la periodontitis y el deterioro
cognitivo, entonces el tratamiento de la periodontitis podra ser una opcin de tratamiento
posible en la EA. Alentadoramente un pequeo estudio de tratamiento periodontal , en AD
participantes sugieren que puede haber algunos beneficios cognitivos a este enfoque de apoyo a
la necesidad de un ensayo aleatorio para probar esta hiptesis.

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Displasia ectodrmica

Generalidades:

Forma parte de un amplio grupo enfermedades genticas, las cuales son hereditarias bien de
manera autosmica, dominante o recesiva o ligada al cromosoma X, en las cuales se ve afectado el
ectodermo, que es la capa de clulas ms externa del embrin que dar origen a la parte ms
superficial de la piel, glndulas sudorparas, uas y pelo, tambin en cavidad bucal, dientes y
glndulas salivares.

Cuando un individuo padece de dos o ms alteraciones en el tejido proveniente del ectodermo,


por ejemplo, alteraciones en las glndulas sudorparas y en las piezas dentarias se denomina
sndrome de displasia ectodrmica y cada uno de los diferentes sndromes de D.E representa una
combinacin de diferentes alteraciones.

Los tipos de displasia ectodrmica que se observan ms comnmente son las de tipo anhidrtica o
sndrome de christ-siemens-touraine y la de tipo hipohidrotica. La de tipo anhidrotica es el
trastorno recesivo ligado al cromosoma X, esta afeccin gentica es un trastorno en el gen y sus
alteraciones principales son la hipotricosis, que es la afectacin del cuero cabelludo y vello
corporal como por ejemplo leve pigmentacin en l. La hipohidrosis afectacin en glndulas
sudorparas que se puede manifestar en sudoracin deficiente o nula y por ultima la hipodoncia
que se caracteriza por la erupcin de algunos dientes malformados que aparecen a edad tarda o
incluso estn ausentes en la dintincion permanente. La displacia ectodrmica de tipo hipohidrotico
se caracteriza por la deficiencia en el desarrollo de la estructura derivada del ectodermo, ejemplos
de ella son la hiperqueratosis de palmas de la manos y plantas de los pies, que es el
engrosamiento de la capa externa de la piel y distrofia ungueal que es una alteracin en las uas,
esta condicin por lo general afecta el dedo pulgar.

Los exmenes o pruebas que se pueden realizar para detectar la displasia ectodrmica pueden ser
una biopsia de las membranas mucosa, una biopsia de la piel, pruebas genticas, solo disponible
para algunas de estas anomalas y por ltimo se pude hacer una radiografa de los dientes y
huesos.

La displaca ectodrmica no tiene cura solo un manejo sistemtico para minorizar los efectos de
las malformaciones en la calidad de vida.

Epidemiologia:

La displaca ectodrmica hipohidrotica, la cual es del tipo ms frecuente, se ha reportado en


1:5.000 10.000 nacidos vivos.

Causa:

Las malformaciones de la displasia ectodrmica son genticas, por lo tanto pueden ser
transmitidos o heredados a la descendencia. Sin embargo, puede ser posible que un individuo sea
el primero en una familia en ser afectado. En ese caso, la displasia ectodrmica se ha originado por
una mutacin gentica nueva al formarse el ovulo, el espermatozoide o tras la fecundacin.

~ 67 ~
Principales caractersticas y sntomas:

Estas pueden ser muy variadas debido al amplio grupo de enfermedades que los individuos
pueden padecer, sin embargo algunas de las caractersticas ms comunes de estos padecimientos
pueden ser no sudar o presentar una disminucin de la sudoracin por la falta de glndulas
sudorparas, escaso vello corporal y pelo en el cuero cabelludo, tambin muy fino y poca
pigmentacin en l, ausencia congnita parcial o total de piezas dentarias o malformacin de
estas, la piel muy delgada, con poca pigmentacin, lisa y fcil de irritar, una hiperqueratosis en
palmas de las manos y plantas de los pies, otros sntomas tambin pueden incluir uas anormales,
frente grande, discapacidad del aprendizaje y dificultad de audicin.

~ 68 ~
Relacin odontolgica

Las manifestaciones orales pueden ser de diversos tipos, como, por ejemplo, estructurales,
morfolgicas, numricas, de su posicin o de la composicin de la pieza dentaria.

Las alteraciones numricas pueden manifestarse con hipodoncia que es la ausencia de hasta seis
piezas dentarias o anodoncia que es la ausencia total como parcial de piezas dentarias. Las
principales agenesias dentarias son de los segundos premolares, incisivos laterales superiores e
incisivos inferiores y como consecuencia de la ausencia de piezas dentarias se produce un
desarrollo del hueso maxilar atrfico, observndose clnicamente una protuberancia de los labios.
Una agenesia dentaria es una patologa congnita que derivada de la ausencia de una o ms piezas
dentarias temporales o permanentes, la causa de esta patologa es debido a una malformacin
durante el proceso de formacin de la lmina dentaria

En cuanto a la estructura de las piezas dentarias esta puede estar afectada, presentando coronas
puntiagudas, curvas o cnicas, tambin se puede presentar hipoplasias del esmalte, siendo estas
un esmalte hipoplasico que es un esmalte ms delgado de lo normal, hipo calcificado en el que el
esmalte de las piezas dentarias se encuentra descalcificado o hipo maduro en el que el esmalte
presenta un aumento de porosidad en su superficie, lo que confiere un color opaco.

En algunas manifestaciones se encuentran afectadas las glndulas salivales por lo que se puede
presentar una disminucin de la produccin de saliva llevando a una sequedad de la cavidad bucal,
una xerostoma. Exponiendo a las personas a un mayor riesgo de contraer alguna enfermedad
periodontal debido a que aumenta la susceptibilidad a enfermedades fngicas y bacterianas,
tambin mayor probabilidad de padecer halitosis.

Algunos manejos odontolgicos de estos padecimientos pueden ser, por ejemplo, para el esmalte
hipoplasico, en general restauraciones con resina compuesta estas por lo general tiene un buen
resultado y si esta restauracin es fallida se debe considerar otra opcin que sera el
recubrimiento completo de la pieza dentaria, una corona.

Para la ausencia parcial o total de piezas dentarias las alternativas rehabilitadoras ms exitosas
serian la utilizacin de prtesis parciales o totales, removibles o fijas, sobre dentadura o implantes
dentales.

En nios de etapa de crecimiento se utilizan prtesis removibles las cuales permiten desarrollar
una buena dimensin de hueso maxilar y en adultos se tiene muy buenos resultados con los
implantes.

~ 69 ~
Oral rehabilitation of a hypohldrotic ectodermal dyspiasia patient: A 6-year foilow-up

Anut Itthagarun, DDS, PDipDS, PhDVNigel M. King, BDS, MSc, PhD^

This case report describes the oral rehabilitation of a female chiid wifh hypohldrotic ectodermai
dysplasia over a 6-year fime period, ft demonstrates the need for periodic modification and
repiacement of a prosthesis, an orfhodontic appiiance, and a gingjvopiasty Although the initiai
treafmenf plan was considered to be a compromise due to iimited cooperation, an improvement
was observed in fhe pafient's social behavior as a consequence of her denfai freatment. The
effects of unavoidable changes in the denfai feam over 6 years are aiso discussed. (Quintessence
Int 2000,31:642-648)

Key words; ectodermai dyspiasia, oral rehabilifafion

Ectodermal dysplasia is tnade up of a rare group of inherited disorders characterized by aplasia or


dysplasia of tissues of ectodermal origin, such as skin, hair, teeth, and nails.' The most common,
classic type is hypohidrotic ectodermal dysplasia, also known as Christ-Sicmens-Touraine
syndrome.- This is characterized by the triad of hypohidrosis (lack of sweat glands), hypotricbosis
{skin abnormalities), and bypodontia.^ Clarke suggested an X-linked form of transmission with the
gene carried by the female and manifested in the male.'' However, the anhidrotic variation of
ectoderma! dysplasia may occur in a family without a previous history of this disease, due to gene
mutation.''" In childhood, the diagnosis is often easily made on the basis of a history and clinical
examination. Tbe most common oral characteristic is hypodontia or anodontia, reflecting the
suppression of dental ectoderm.'' A reduced number of teeth present might demonstrate delayed
eruption. Due to the absence of teeth, the volume of alveolar bone and its growtb are decreased,
resulting in a loss of vertical dimension and protuberant lips. Incisors and canines, when present,
often have conical crowns. Some reports have suggested that the rnost cornmon complaint of
affected

'Assistant Professor, Pediatric Dentistry. Faculty of Dentistry, University ot Hong Kong, hlong Korg.

^Professor, Pediatric Dentistry. Faculty of Dentistry, University of Hong Kong, Hong Kong.

Reprint requests: Dr N. M. King, Faculty ot Dentistry, University of Hong Kong, 2/F Prince Philip
Dental Hospital, 34 Hospital Road, Sai Ying Pun, tHong Kong. E-mail: nmking@glink.net.hk

individuals during childhood and adolescence are dental abnormalities and altered facial
appearance.' Children and adolescents with ectodermal dysplasia often require complex
prosthetic treatment to manage the hypodontia. Oral rehabilitation is important frotn functional,
estbetic, and psychologic perspectives.""" Oral rehabilitation involves a number of challenges,
which are further complicated by the growth and development of the child, variation in tooth
development and eruption, the type of age-appropriate prosthesis, and the planning and timing of
treatment. Therefore, a multidisciplinary team approach is recommended for successful treatment
of affected individuals.'^ At the least, this should include a pediatric dentist, an orthodontist, a
prosthodontist, and an oral and tnaxillolacial surgeon. Reports in the literature concerning the
dental treatment of ectodermal dysplasia are often case reports dealing with different types of
removable prostheses.''-" iMost of them have suggested that periodic recall is necessary because
tbere is usually a need to remake the prostbesis and any other oral appliances, due to growth.'=-
''' It has been suggested that this tnay cause difficulties in meeting the demand for treatment.

~ 70 ~
However, only a few reports have actually followed the cases over time.''"* This report describes
the findings over a 6-year follow-up of a 13-year-old female with hypohidrotic ectodermal
dysplasia. When the treatment was being planned and subsequently administered, it was
considered to be a compromise due to tbe patient's behavior. Over time, the patient has
nevertheless enjoyed a much better quality of life. Unfortunately, there were adverse effects due
to the unavoidable cbanges in the composition of the dental team during the follow-up period

CASE REPORT

The proband was born in December 1986, after an uneventful full-term pregnancy. Sbe was tbe
only child of ber normal, healthy Cbinese parents. During infancy, sbe was frequently bospitalized
due to high fevers of unknotvn etiology. During ber second year of life, a dermal biopsy confirmed
hypohidrotic ectodermal dysplasia, Sbe presented with most of the characteristics of hypohidrotic
eetodermal dysplasia, such as deficiency of sweat glands, sparse scalp hair and eyebrows, mild
pbotopbobia, protuberant lips, delayed eruption of teetb, conical anterior teeth, and hypodontia.
No similar cases of ectodermal dysplasia had been detected among her parents or close relatives.
At tbe age of 3 years, she was referred by her pediatrician for an examination of her oral and
dental tissues and possible dental rehabilitation. At that time, only 3 eonieal maxiiiary incisors had
erupted. Because of management problems and a severe gag reflex, only a propbylaxis could be
performed. Arrangements were made to review her every 4 months until she could cooperate
sufficiently to receive dental treatment. Shortly after commencing primary school, she expressed a
desire for an improvement to her appearance. According to the child and her mother, sbe was
often teased by her classmates because of her "pointed" and "missing" teeth. Consequently, she
was considered to be different from others and was treated with prejudice because of her unusual
facial appearance. Extraorally, she had a concave soft tissue profile and protuberant lips.
Intraorally, in the maxillary arch, the primary left lateral incisor and the molar were missing. Five of
her primary maxillary anterior teeth (teeth 53[C], 52[D], 51[E], 6i[F], and 63[Hj) were conical. In
the mandibular arch, all of the anterior teetb were missing (Eigs la and lb). Kadiographically,

Fig 2 Ciinieai pnorograpiT ihO'vmg tine dentition after cementation of ttie mdirec: resin compcs te
vereers and tixed partiai denture in ttie maxiliary arcii and the mandibular prosthesis.

apart from the first and second molars, only 2 of her maxillary tooth buds, the right second
premolar and the permanent left central incisor, and 2 mandibular tootb buds, the left and rigbt
first premolars, were present. In addition, the primary maxillary left central incisor bad a shorter
root compared with its antimere. A mandibular removable partial prostbesis witb Cclasps on tbe
mandibular second molars was fabricated. Eor tbe maxillary arch, a 3-unit laboratory-cured resin
composite xed partial denture from the primary maxillary right central incisor lo the primary left
lateral ineisor and 3 indirect resin composite veneers for the primary tnaxillary right canine,
primary lateral incisor, and primary maxillary left canine were prepared and cemented (Eig 2). The
patient and her mother were pleased with the prosthesis. Regular recalls were scheduled to make
any needed adjustments. Foiiow-up

Dtjring the first 6 months of recall visits, the child was cooperative and appeared to have adapted
well to the dental office environment. Her original complaint had been her lack of teeth and the
embarrassment caused by her appearance. This resulted in her covering her mouth with her hand
while speaking. After implementation of the maxillary veneers and the fixed partial denture and
the mandibular prosthesis, her attitude, self-confidence, and peer group interaction showed signs
of improvement. According to her mother, the patient had changed
~ 71 ~
from being quiet and introspective to being active and cheerful. She would talk and even iaugh
with her mouth widely open (Figs 3a and 3b). Moreover, her hody weight changed from the 10th
percentile at the time of presentation to the 100th percentile after 6 years. During the past 6
years, there has heen a change in the pafient's dental care provider at least every 2 years, which is
inevitable in a teaching institute. Due to erupting teeth and growth of the jaws, the mandibular
prosthesis was modified, adjusted, and reconstructed as necessary. As the patient's tolerance level
improved, the C-ciasps on the tnandibular second molars were replaced by Adams clasps to gain
greater retenfion (Fig 4), The primary denture-bearing mucosa appeared to be healthy. One year
after placement of the resin eomposite veneers, the primary maxillary left central incisor and the
attached pontic were removed because its permanent replacement began to erupt (Figs 5a and
5b). After the permanent tooth had fully erupted, there was a space between it and the primary
right central incisor of about 3 mm. On the advice of the team orthodonfist, a tnaxillary removable
appliance with a finger spring was fabricated (Figs 6a and 6b) to close the space between the 2
teeth. This treatment was not successful because the pafient did not wear the removable
appliance regularly, as instructed. Consequently, a fixed appliance with an open coil spring was
then fitted (Figs 7a and 7b). After the fixed appliance had been active for 6 months, the space
between the permanent left central incisor and the primary right central incisor was closed, and
the positions of all the teeth were favorahle for the fabrication of a resin composite fixed partial
denture. During the space-closing procedure, the oral hygiene of the patient deteriorated,
especiaily in the maxillary anterior region [Fig 8). Plaque removal and oral hygiene instruction was
performed monthiy Even after a professional orai prophyiaxis, the patient returned with gingivai
infiammation and subsequent gingivai hyperplasia. This was eventitaily treated by electrostirgery
to remove the excess gingival tissue. The resin composite fixed partial denture from the
permanent left eentrai ineisor to the primary left canine was postponed until the child eould
demonstrate that she was able to maintain good oral hygiene. In order to encourage the girl, the
permanent left cen

tral incisor was built up with resin composite to further improve her appearance [Figs 9a and 9b).
A maxillary removable appliance with a passive finger spring was fitted as a retainer to prevent the
tooth from drifting (Fig 10). During the 2 weeks after the maxillary removable appliance was
delivered, a 1-mm median diastema occurred. According to the mother, her daughter did not wear
the maxillary removable appliance, and subsequently, she refused to wear the mandibular
prosthesis. Cttrrently, there is generalized spacing in the maxillary anterior region. In the
mandibular arch, the left first premolar is fully erupted and the right first premolar is about to
erupt (Fig 11). Disappointingly, the girl has deelined to wear any removable appliances. Plaeement
of endosseous implants is being considered. This is a long-term option because of her age and
future growth and d DISCUSSION

When treating a child with ectodermai dysplasia, it is important to motivate botb the child and bis
or ber parents toward treatment and tben to work witb them to ensure compliance. At the
present time, the reported child has not expressed a desire for further improvements to be made
to her appearance, probably because she is now rarely teased by her peers and does not feel as
embarrassed by her appearance as she did a few years ago. This is to be expected because primary
school children are strongly influenced by peer groups,-^"^^ while older children are more
sophisticated in their evaluation of responses.^' Also, once a child has been accepted into a peer
group, especially one of girls, the understanding and cooperation among those peer group
members are very salient,--^0 It has been shown that oral bygiene instructions need to be
regularly reinforced if they are to be effective,^' as was graphically illustrated by this girl. It is

~ 72 ~
hoped that the enthusiasm of the dentist who comtnenced her treatment will have a positive
effect on her. The girl and her mother were pleased when they learned that she would be
transferred back to her original dentist. Great care will need to be taken to maintain the girl's oral
hygiene in order for her to benefit from the long-term treatment plan. In addition, the girl and her
parents will be educated and motivated about the dental problems related to her genetic and
psychologic condifions.

CONCLUSION

This case report and follow-up of the oral rehabilitation of a growing chiid with hypohidrotic
ectodermal dysplasia was challenging from the beginning, 6 years ago. Tbe short- and long-term
treatment plan for tbe severe hypodonfia was made using a multidisciplinary team approach. The
patient's initial bebavior was aggressive and uncooperative, yet shortly after commencing primary
school, the reactions of her peers created a desire for her to improve her appearance. Not without
difficulties, the initial treatment, which included veneers, a fixed partial denture, and a removable
prosthesis, was completed. This treatment was considered to be successful for estbetic,
functional, and psychologic reasons. As a consequence, the patient began showing positive
bebavioral changes and became fully cooperative as the dental treatment progressed.
Unfortunately, the changes in the dental team members in the subsequent years bad a negative
impact. Tbis was manifested in her neglect to maintain her oral hygiene, which delayed her future
treatment. Motivation and cotnprehension toward oral hygiene are important factors in the
successful longterm treatment of children with genetic defects such as ectodermal dysplasia. This
case demonstrated that whenever possible, care of the child with ectodermal dysplasia should
ideally be managed by tbe same dental team, in order to ehminate behavioral deviation in the
child. This is especially important in cases in which a trusting relationship between the dental team
and the pafient has been successfully created.

Ouintessenoe international 647

Itthagarun/King

REFERENCES

1. Freire-Maia N. Ectodermal dysplasia revisited. Acta Genet Med Gemellol (Roma) 1977;26:121, 2.
Rimoin DL, Connor JM, Pyeritz R, Emery and Rimoin's Principles and Practice of Medical Genetics,
ed 3. London: Churciiiil Livingstone 1996:1279-1283, 3. Bergendai T, Eckerdal O, Hallotisten AL,
Koch G, Kurol J, Kvint S. Osseointegrated implants in the oral habilitation of a boy with ectodermal
dysplasia; A case report, Int Dent J 1991;41:149-156. 4. Clarke A. Hypohidrotic ectodermal
dysplasia. J Med Genet 1987i24:659-663, 5. Clarke A, Philips Dl, Brown R, Harper PS, Clinical
aspects of X-liriked hypohidrotic ectodermal dysplasia. Arch Dis Child 1987;62:989-996. 6.
Itthagarun A, King NM, Ectodermal dysplasia; A review and case report. Quintessence Int
1997;28:595-602, 7. Siegel MB, Potsic WP, Ectodermal dysplasia: The otolaryngo-logical
manifestations and management. Int ] Pediatr Otorhinolaryngol 1990;19:265-271. 8. Grinberg S,
over P, Quiros L, Diaz LG, Terrn F. Ectodermal dysplasia: Report of two female cases. J Dent Child
19S0;47:193-195, 9. Gegenheimer R, Shaull KL, An overdenture approach o ectodermal dysplasia
in children. Quintessence Dent Technol 1983;7:151-154, 10. O'Dwyer MR, Renner RP, Fergusen FS.
Overdenture treatment-One aspect of the team approach for the EEC syndrome patient. J Pedod
1984;8:192-205, 11. Boi JR, Duran J, Cortada M, Jimenez A. Golobart J, Ccphalometric changes in a
patient with ectodermal dysplasia after placement of dentures. J Clin Pediatr Dent 1993; 17 217-

~ 73 ~
220 12. Farrington FH. The team approach to the management of ectodermal dysplasia. Birth
Defects Orig Artie Ser 1988; 24:237-242. 13. Nortje C, Farman A, Thomas CJ, Watermeyer G X-
linked hypohidrotic ectodermal dysplasia: An unusual prosthetic prohlem, J Prosthet Dent
1978;40:137-142. 14. Herer PD. Treatment of anhidrotic ectodermal dysplasia. Report of case J
Dent Child 1975;42:133-136. 15. Punjabi AP. Oral rehabilitation in two siblings with anhidrotic
ectodermal dysplasia-Prosthetic considerations, J Indian Med Assoc 1983;55:119-123, 16. Hollist
NO, Grillo TA, Kubota K, Okada S, Ono Y, Nakata M, et al, Management of ectodermal dysplasia
bypohydrotic type. Odontostomatol Trop 1984;7(1):9-16.

17 Keng SB. Orofacial manifestation of hypohidrottc ectodermal dysplasia-Case report. Ann Acad
Med Singapore 1984; 13:552-555. 18. Guckes AD, Brahim JS, McCarthy GR, Rudy SF, Cooper LP,
Using endosseous dental implants for patients with ectodermal dysplasia, ) Am Dent Assoc
1991;122:59-e>2, 19. Lekholm U, The use of osseointegrated implants in growing jaws. Int J Oral
Maxillofac Implants 1993;H 243-244, 20. Smith RA, Vargervik K, Kearns G, Bosch C, Koumjian J.
Placement of an endosseous implant in a growing child with ectodermal dyspbasia. Oral Surg Oral
Med Oral Pathol 1993;75:669-673. 21. Cronin RJ Jr, Oesterle LJ, Ranly DM. Mandibular implants
and tbe growing patient. Int j Oral Maxillofac Implants 1994;9:55-62. 22. Pigno MA, Blackman RB,
Cronin RJ Jr, Cavazos E. Prosthodontic management of ectodermal dysplasia: A review ot the
literature. J Prosthet Dent 1996;76:541-545. 23. Roff JD, Wirt RD. Childhood social adjustment,
adolescent status, and young adult mental healtb Am J Orthopsychiatry 1984;54:595'602. 24.
Asher SR, Dodge IA, Identifying children who are rejected by their peers. Dev Psychol
1986;22:444-449, 25. Hymel s, Wagner E. Butler LJ, Reputation bias' View from the peer group. In:
Asher SR, Coie JD (eds). Peer Rejectioti in Childhood. New York: Cambridge 1990:156-186. 26.
Hartup WW. The peer system. In' Hetherington EM (ed). Handbook of Child Psychology: Vol, 4
Socialization, Personality and Social Development, ed 4. New York: Wiley, 1983:103-196, 27.
Feidman E, Dodge KA. Social information processing and sociometric status: Sex, age and situation
effect. J Abnorm Child Psychol 1987;15:2] 1-227 28. Coie JD, Dodge IA, Coppotelli H, Dimensions
and type of social status: A cross-age perspective. Dev Psychol 1982; 18:557-570, 29. Berndt TJ.
Social cognition, social behavior, and children's friendship. In: Higgins ET Ruble DN, Hartup WW
(eds). Social Cognition and Social Development: A Sociocultural Perspective, New York: Cambridge
University Press, 1983: 158-192.

Resumen de paper de displaca ectodrmica

Rehabilitacin oral de una paciente con displasia ectodrmica hipohidrotica: un estudio a lo largo
de 6 aos

En este estudio se relata la rehabilitacin oral de una mujer con displaca ectodrmica
hipohidrotica, a lo largo de un periodo de 6 aos donde se demuestra la necesidad de la
modificacin peridica y el remplazo de una prtesis, un aparato de ortodoncia y una
gingivoplastia. A lo largo del tratamiento se evidencio una mejora en el comportamiento socia de
la paciente debido a sus diversos tratamientos dentales. Tambin se discuten los efectos de
cambios en el equipo dental a lo largo de 6 aos.

~ 74 ~
Radioterapia

Antecedentes Generales

Qu es y para qu se utiliza?

La radioterapia es la utilizacin de radiaciones ionizantes para el tratamiento local o locorregional


(restringido a una regin localizada del cuerpo) de determinados tumores empleando rayos X de
alta energa.

Las radiaciones ionizantes son de naturaleza electromagntica o corpusculares, con suficiente


energa capaces de causar por un mecanismo directo o indirecto, excitacin o ionizacin en los
tomos de la materia con la que interacta.

Se entiende por ionizacin, al proceso o fenmeno por el cual se generan pares de iones, que en
lneas generales no son mas que tomos cargados elctricamente por la prdida o ganancia de
electrones.

Se entiende por excitacin, al fenmeno mediante el cual un electrn de un tomo salta de una
rbita a otra de distinto nivel energtico, regresando inmediatamente despus al nivel original.
Emitiendo energa durante el transcurso del proceso.

Su objetivo es destruir las clulas tumorales causando el menor dao posible a los tejidos
indemnes (sanos) adyacentes (que rodean) a dicho tumor.

La radioterapia produce una serie de cambios en los tejidos irradiados . Es as como en el territorio
bucomaxilofacial se pueden observar mltiples cambios, los cuales pueden ser reversibles o
irreversibles, los cuales condicionan que el paciente requiera de cuidados especiales al momento
de recibir su atencin odontolgica.

En la clnica diaria las radiaciones utilizadas pueden provenir de istopos radiactivos que se
encuentran presentes en la naturaleza, como el Cobalto-60 o bien pueden ser generadas de
manera artificial (radiaciones electromagnticas en forma de Rayos X).

Existen dos tipos bsicos de radioterapia, la teleterapia (irradiacin a distancia) y la braquiterapia


(irradiacin en contacto).

Las clulas tumorales se multiplican ms rpidamente que las clulas normales del cuerpo. Dado
que la radiacin es ms daina para las clulas que se reproducen rpidamente (clulas lbiles), la
radioterapia causa ms dao a las clulas cancergenas que a las normales. Esto impide que estas
aumenten (proliferen) y se dividan, y lleva a que se presente muerte celular (apoptosis/necrosis).

Si nos referimos a las manifestaciones mas comunes de cncer en el territorio estomatogntico,


encontramos el carcinoma de clulas escamosas, para el cual las herramientas teraputicas ms
eficaces son la ciruga y la radioterapia.

Manifestaciones generales de la radioterapia

Entre los efectos secundarios generales encontramos astenia, alopecia, dermatitis aguda y crnica,
trastornos oculares, auditivos, tirodeos, enfermedad de la arteria cartida, entre otros.

~ 75 ~
Manifestaciones Bucomaxilofaciales

Mucositis: complicacin oral ms comn. Se produce como consecuencia de un desequilibrio


entre la perdida de clulas y la proliferacin conducente a la disminucin de clulas epiteliales, por
lo que el epitelio pierde su grosor, lo cual es manifestado como mucositis de la mucosa oral. La
indicacin de tratamiento se realiza segn el grado, va desde medidas de higiene bucal, uso de
colutorio, dieta y antifngicos.

Candidiasis: se caracteriza por la presencia de depsito blanco que se remueven al raspaje. Puede
manifestarse como pseudomembranosa o eritematosa. Las infecciones fngicas de la cavidad oral
pueden tratarse con nistatina y fluconazol.

Disgeusia: se produce porque las papilas gustativas son sensibles a la radiacin ionizante, lo cual
ocasiona una prdida de su estructura histolgica normal y se traduce en alteraciones de la
percepcin del gusto.

Caries por radiacin: si bien su aparicin es de carcter multifactorial, la hiposialia (disminucin


del flujo salival) es el principal factor involucrado.

Osteoradionecrosis: es una necrosis isqumica (debido a la perdida de irrigacin) del tejido seo
producto de la radiacin. Constituye una de las consecuencias ms graves de la radioterapia.

Puede ocurrir espontneamente (menos frecuente) o despus de un trauma (generalmente post


exodntico). En los estadios iniciales se utilizan antispticos locales, analgsicos, AINEs y
esteroides orales para controlar el cuadro clnico y la progresin. La mayora de los pacientes
requerirn el uso de oxigeno hiperbrico (aumenta gradualmente la concentracin de oxgeno en
todos los tejidos corporales, an con el flujo sanguneo reducido u obstruido) y la reseccin
quirrgica de los focos de necrosis.

Necrosis de tejidos blandos: corresponde a una lcera situada en el tejido irradiado, sin presencia
de neoplasia maligna residual. La aparicin esta relacionada con la dosis, tiempo y volumen de la
glndula irradiada (efectos determinsticos).

Trismus: es generalmente visto como resultado de la fibrosis conducente a la prdida de


flexibilidad y extensin. El tratamiento consistir en la administracin de relajantes musculares y
fisioterapia oral (especialista en trastornos temporomandibulares y dolor orofacial).

Xerostoma: las glndulas partidas se caracterizan por sufrir una reduccin significativa en su
volumen durante la radiacin, y estas son responsables de producir entre un 60% a un 65% del
volumen total de saliva. Existen sustitutivos artificiales de saliva con mucina o metilcelulosa que
producen un alivio subjetivo de 5 a 10 minutos, pero que debido a su corta duracin los pacientes
prefieren humedecer su cavidad oral con agua. La pilocarpina es un agonista colinrgico
estimulante salival.

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Precauciones en el manejo odontolgico

Todo paciente oncolgico tiene el deber de acudir al odontlogo antes de ser sometido al
tratamiento de radioterapia, quimioterapia o ambas en conjunto. De todas formas independiente
del momento en que llegue el paciente, el paso inicial consiste en hacer una historia clnica
(anamnesis) detallada en la que se deben constatar todos los datos de la teraputica
antineoplsica y para ello es relevante una estrecha comunicacin odontlogo- mdico onclogo.

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Head and neck intensity modulated radiation therapy leads to an increase of opportunistic oral
pathogens.
Abstract
OBJECTIVES:
The introduction of intensity modulated radiation therapy (IMRT) has led to new possibilities in
the treatment of head and neck cancer (HNC). Limited information is available on how this more
advanced radiation technique affects the oral microflora. In a prospective study we assessed the
effects of various advanced treatments for HNC on the oral microflora, as well as the effects of
elimination of oral foci of infection.
MATERIALS AND METHODS:
All consecutive dentate patients >18years, diagnosed with a primary oral or oropharynx carcinoma
and seen for a pre-treatment dental screening (May 2011-May 2013) were included. Patients were
grouped by oncologic treatment: surgery (SURG), IMRT (IMRT) or IMRT+chemotherapy (CHIMRT).
Dental screening data, demographic data, subgingival biofilm samples, oral lavages and whole
saliva samples were obtained to microbiologically analyze the effects of cancer treatments (1-year
follow-up).
RESULTS:
This study included 82 patients (29 SURG, 26 IMRT and 27 CHIMRT). The trends in changes in
prevalence and proportions of microorganisms were comparable in the IMRT and CHIMRT group.
However, relative to the SURG group, increased prevalence of enteric rods, staphylococci and
Candida species was observed in the IMRT and CHIMRT groups. In these groups, elimination of
oral foci decreased the frequency of detection of pathogens such as Porphyromonas gingivalis,
Tannerella forsythia and Streptococcus mutans.
CONCLUSION:
Different treatments in HNC patients result in different changes in the oral microflora.
Opportunistic pathogens such as staphylococci, enteric rods and Candida sp. tend to increase in
prevalence after IMRT with or without chemotherapy, but not after surgical intervention.
Copyright 2016 Elsevier Ltd. All rights reserved
Radioterapia con intensidad modulada de cabeza y cuello conduce a un aumento de patgenos
orales oportunistas.

ABSTRACT

Objetivos:

La introduccin de la terapia de radiacin de intensidad modulada (IMRT) ha dado lugar a nuevas


posibilidades en el tratamiento del cncer de cabeza y cuello (HNC). Hay poca informacin
disponible sobre cmo esta tcnica de radiacin ms avanzada afecta a la microflora oral. En un
estudio prospectivo se evaluaron los efectos de varios tratamientos avanzados para la HNC en la
microbiota oral, as como los efectos de la eliminacin de focos orales de infeccin.

MATERIALES Y METODOS

Se incluyeron todos los pacientes dentados consecutivos > 18 aos, diagnosticados con un
carcinoma oral u orofarngeo primario y vistos para un cribado dental previo al tratamiento (mayo
de 2011 a mayo de 2013). Los pacientes fueron agrupados por tratamiento oncolgico: ciruga

~ 78 ~
(SURG), IMRT (IMRT) o quimioterapia+IMRT (CHIMRT). Se obtuvieron datos de cribado dental,
datos demogrficos, muestras de biofilm subgingival, lavados orales y muestras de saliva total
para analizar microbiolgicamente los efectos de los tratamientos contra el cncer (seguimiento
de 1 ao).

RESULTADOS

Este estudio incluy 82 pacientes (29 SURG, 26 IMRT y 27 CHIMRT). Las tendencias en los cambios
en la prevalencia y las proporciones de microorganismos fueron comparables en el grupo IMRT y
CHIMRT. Sin embargo, en relacin con el grupo SURG, se observ una mayor prevalencia de
enterobacterias, estafilococos y especies de Candida en los grupos IMRT y CHIMRT. En estos
grupos, la eliminacin de focos orales disminuy la frecuencia de deteccin de patgenos como
Porphyromonas gingivalis, Tannerella forsythia y Streptococcus mutans.

CONCLUSION

Diferentes tratamientos en pacientes con HNC resultan en diferentes cambios en la microflora


oral. Patgenos oportunistas como estafilococos, enterobacterias y Candida sp. Tienden a
aumentar en la prevalencia despus de la IMRT con o sin quimioterapia, pero no despus de la
intervencin quirrgica.

PALABRAS CLAVE

Quimioradioterapia; Neoplasias de cabeza y cuello; Radioterapia de intensidad modulada;


Microbiota; Periodontitis

~ 79 ~
Artritis reumatoide

Generalidades:

Es una enfermedad sistmica autoinmune, inflamatoria, crnica y progresiva. Esta se caracteriza


por la inflacin de articulaciones pequeas, grandes y tejidos circundantes en todo el cuerpo, solo
a excepcin del esqueleto axial, sin contar la columna vertebral, cervical y las articulaciones
temporomandibulares y tambin puede afectar otros rganos. Si en esta enfermedad no se logra
controlar la inflacin de las articulaciones y tejidos circundantes, se produce una destruccin
progresiva de estos afectando no solo a las articulaciones, tambin a los cartlagos y huesos con
deformaciones los cual lleva progresivamente a distintos grados de invalides adems tiene
consecuencias a nivel sistmico.

Esta enfermedad no tiene algn examen para determinar con certeza que se padece de esta, pero
dos pruebas de laboratorio que por lo general ayudan al diagnstico son el factor reumatoideo y
los anticuerpos anti pptidos cclicos cirtrulinados. Tambin otros exmenes que se pueden
realizar son un conteo sanguneo completo, tasa de sedimentacin eritrocitica, radiografas,
ecografas o resonancias magnticas de las articulaciones y anlisis del lquido sinovial.

La artritis reumatoide requiere un tratamiento a lo largo del tiempo, este puede incluir desde
educacin del enfermo, medicamentos, fisioterapia, dieta y hata posiblemente ciruga. Si se aplica
un tratamiento agresivo y oportuno para este tipo de artritis podra ser muy til para frenar la
destruccin de la articulacin y tambin prevenir deformidades.

Epidemiologia:

La prevalencia de la artritis reumatoide a nivel mundial es del 1% y afecta las mujeres con mayor
frecuencia que a los hombres en una razn 3-4: 1, en un rango de edad entre 35 y 45 aos. A nivel
de latino americano se ha estimado con diferentes estudios que la prevalencia es entre 0,2 y 0,5
%. En Chile el nico estudio a nivel poblacional realizado a estimado una prevalencia de esta
enfermedad en un 0,46 %.

Causa:

Esta enfermedad tiene una causa exacta desconocida, siendo una condicin autoinmune lo que
implica que el sistema inmunitario del cuerpo ataque por error al tejido sano. Los lugares
afectados con mayor frecuencia por la artritis reumatoide son las muecas, dedos de las manos,
rodillas, pies y tobillos.

Principales caractersticas de los signos y sntomas:

Esta enfermedad suele comenzar de manera lenta, siendo sus sntomas iniciales prdida de peso,
dolor articular leve, rigidez y fatiga sistemtica. La evolucin de esta enfermedad puede variar de
leves molestias articulares de breve duracin a poli artritis crnica que es dolor y deformacin de
las articulaciones. Los signos y sntomas ms caractersticos pueden incluir de rigidez matinal de un
plazo de por lo menos una hora, aumento de volumen en las muecas, artritis en tres o ms
articulaciones, ndulos reumatoideos estos son subcutneos, tambin alteraciones radiolgicas
caractersticas que pueden ser erosiones u osteoporosis yuxtarticular. Estas alteraciones son
presentadas por el 30% de los pacientes en el primer ao de padecimiento de la enfermedad y al
segundo aumenta al 90 % de los pacientes.

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A nivel sistmico se observan altos niveles de protenas C reactiva, esta es contribuyente al
desarrollo de otras complicaciones, como por ejemplo enfermedades cardiovasculares, tambin
una de las manifestaciones sistmicas ms comunes es la anemia y esta ocurre con mayor
frecuencia en etapas tempranas de la enfermedad. Tambien la osteoporosis debido al aumento de
la actividad de osteoclastos y la formacin sea reducida por la disminucin de la actividad de los
osteoblastos. Con el tiempo las articulaciones pueden perder su rango de movimiento y
deformarse.

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Relacin odontolgica

La artritis reumatoide puede producir manifestaciones a nivel oro facial como por ejemplo
afectaciones a nivel de la articulacin temporomandibular, xerostoma, sndrome de Sjogren
secundario y periodontitis entre otras.

En la articulacin temporomandibular se manifiesta con dolor, hinchazn o limitaciones en el


rango de movimiento. En los nios este padecimiento puede llegar ocasionar la restriccin del
crecimiento de la mandbula.

En cuanto al sndrome de sjorgen secundario cerca de un tercio de las personas que padecen
artritis reumatoides lo padecen y este se manifiesta con la hiposalivacin que es la disminucin
anormal de secrecin de saliva aumentando as la susceptibilidad a enfermedades fngicas y
bacterianas.

La periodontitis se encuentra de formas ms avanzadas en personas que padecen de artritis


reumatoides en comparacin de personas que no la padecen.

Tambin se produce una inmunosupresin por los medicamentos lo que conlleva a la aparicin de
enfermedades oportunistas y manifestaciones atpicas de enfermedades como caries, candidiasis y
periodontitis.

Esta enfermedad tambin est fuertemente ligada a una mala higiene bucal debido al deterioro de
la destreza manual y adems una desmotivacin.

En cuanto al manejo odontolgico las precauciones generales son que es recomendable la


atencin en la maana, posicin cmoda en el silln, dar tiempos de descanso, libertad de
movimientos y evitar la mantencin prolongada de la apertura bucal.

Realizar un examen cuidadoso de la ATM, estado periodontal y evaluacin de xerostoma, estos


exmenes ayudaran a obtener un diagnstico y un tratamiento oportuno.

Si la persona padece de sndrome de sjorgen se debe considerar que presentara xerostoma, por
ende, un mayor riesgo de caries atpicas y enfermedades oportunistas como la candidiasis.

A modo de prevencin a las personas que padece esta enfermedad se le debe recomendar por
ejemplo el uso de cepillo de dientes elctrico o modificado para que se le facilite la sujecin de
este, tambin el uso de enjuagues bucales en base a aloe vera, lantoina y con fluoruro de sodio
con el objetivo de hidratar la cavidad bucal y prevenir caries dentales. Se debe considerar bajo que
tratamiento est el paciente, que otra alteracin o enfermedad sistmica padece y que frmacos
consume para estas y adems el nivel en que se encuentra su artritis.

~ 82 ~
Original article

Oral status in patients with early rheumatoid arthritis: a prospective, casecontrol study

Bjo rn Wolff1, Timo Berger1, Cornelia Frese1, Regina Max2, Norbert Blank2, Hanns-Martin
Lorenz2 and Diana Wolff1

Abstract

Objective. Patients with RA suffer from a higher risk of periodontal attachment loss and increased
oral inflammation. We hypothesize that there are pathogenetic and immunological interactions
between these diseases that go beyond impaired manual dexterity accompanying advanced RA.
The primary objective of the present study was to determine whether a loss of alveolar bone can
be detected in RA patients during the early course of the disease. Methods. In this cross-sectional,
epidemiological casecontrol study, 22 patients with early RA (ERA) were compared with 22
matched healthy controls. Oral and periodontal status, clinical activity, and sociodemographic
parameters were determined. Oral microbiota were analysed using real-time quantitative PCR
specific for leading oral pathogens.

Results. More advanced forms of periodontitis were found in ERA patients compared with
controls. ERA patients had a greater number of missing teeth [ERA 5.7(S.D. 5.0), controls 1.9(S.D.
1.0), P=0.002], deeper periodontal pockets [clinical attachment level: ERA 3.4 (S.D.0.5mm),
controls 2.7 (S.D.0.3mm), P<0.000], and greater bleeding on probing [ERA 18.6% (S.D.9.0%),
controls 10.5% (S.D.5.1%), P=0.001] despite comparable oral hygiene. Tannerella forsythia (6.77-
fold, P=0.033) subgingivally and Streptococcus anginosus (3.56-fold, P=0.028) supragingivally were
the characteristic pathogens in ERA.

Conclusion. Increased loss of periodontal attachment and alveolar bone can be detected in
patients with ERA, therefore we propose that the consulting rheumatologists inform the patients
that they have a higher risk of periodontal disease. It would be beneficial if these patients were
referred directly for intensive dental care.

Key words: periodontal attachment loss, rheumatoid arthritis, casecontrol studies, oral hygiene,
periodontal index, plaque index.

Introduction

RA and periodontal disease (PD) are chronic inflammatory diseases that share striking similarities
[1]. In both entities, proinflammatory cytokines such as IL-1b, IL-6 and TNF-a are up-regulated,
promoting inflammation of soft tissue and destruction of bone. Patients with

established RA have a greater prevalence of PD [25]. Furthermore, patients with PD have a greater
risk of various systemic inflammatory diseases such as atherosclerosis, diabetes mellitus and RA [6,
7]. In recent studies, biologic DMARDs used in the treatment of RA, such as TNF and IL-6 inhibitors,
not only improved signs and symptoms, but also inhibited the radiological progression of both RA
and PD [810]. Whereas infection with the leading periodontal pathogens such as Porphyromonas
gingivalis, Tannerella forsythia and Treponema denticola is believed to cause and perpetuate PD
[11], the aetiology of RA, because of its complexity, is still unclear. Genetic susceptibility and
environmental factors such as smoking and distinct oral and intestinal microflora may act in
concert to modulate the immune

~ 83 ~
RHEUMATOLOGY

Rheumatology 2014;53:526531 doi:10.1093/rheumatology/ket362 Advance Access publication 23


November 2013

CLINICAL SCIENCE

system. P. gingivalis infection of the oral cavity is common in both healthy and PD patients.
Besides its high proteolytic activity and set of virulence factors that promote persistence, P.
gingivalis is the only known periodontal pathogen that expresses bacterial peptidyldeaminase
(PPAD). Recently PPAD has been shown to citrullinate other proteins, driving the generation of
ACPAs as well as citrullinating itself [12, 13]. Thus PPAD, as a bacterial protein, adds to the ACPAs,
possibly helping to break immunological tolerance in RA [14]. The primary objective of the present
study was to determine whether a clinically significant loss of alveolar bone in terms of the clinical
attachment level (CAL) was detectable in patients with early RA (ERA) compared with healthy
controls. The secondary objective was to determine whether distinct oral pathogens were
associated with ERA.

Materials and methods

This cross-sectional epidemiological casecontrol study involved a total of 44 subjects (n=44). All RA
subjects were recruited consecutively from the Division of Rheumatology, University Clinic of
Heidelberg, and a rheumatology outpatient practice. Control subjects were first-time patients who
were recruited consecutively from the Department of Conservative Dentistry, University of
Heidelberg. Medical history (chart review and interview), diet, smoking, alcohol consumption and
current medications were determined. Results of musculoskeletal exams and laboratory
assessments were also documented. Patients with ERA formed the case group (n=22). Healthy
controls (n=22) were statistically matched according to gender, age (3044, 4554, 5564, 6575 years)
and smoking status (smoker, previous smoker, non-smoker). The study was approved by the Ethics
Committee of the Medical Faculty, University of Heidelberg (S-401/2009). Written informed
consent was obtained from all subjects prior to enrolment. All subjects who met the study criteria
were offered enrolment.

Inclusion criteria

RA patients met the 2010 ACR/European League Against Rheumatism (EULAR) criteria for RA [15].
Patients had to have active RA, defined as having a 28-joint DAS (DAS28) >3.2, and ERA, defined as
the onset of symptoms <2 years prior. Patients had to be otherwise healthy. All patients were
Caucasian and were between 30 and 75 years old.

Exclusion criteria

Exclusion criteria were previous or current therapy with biological DMARDs, poor oral hygiene or
disabilities that interfere with adequate oral hygiene, periodontitis as a manifestation of systemic
disease, periodontal therapy within the past 5 years and professional tooth cleaning, intake of
antibiotics, or pregnant or nursing during the past 6 months.

Rheumatologic assessment

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The DAS28 score system based on the ESR was used to assess rheumatoid disease activity in the
RA subjects. Most ERA subjects (63.6%, n=14) were given DMARDs and corticosteroids, one-third
(31.8%, n=7) received corticosteroids alone and one patient received DMARDs alone. Proton pump
inhibitors were used in four patients (18.2%) at the time of enrolment. Control subjects did not
receive any medication.

Oral assessment

Oral examinations were performed at the Department of Conservative Dentistry, University of


Heidelberg. The number of decayed, missing and filled teeth (DMF-T) [16], gingival bleeding index
(GBI) [17] and plaque index (PI) [18] were recorded. Periodontal status, including the CAL, probing
pocket depth (PPD) and bleeding on probing (BOP), was assessed at six sites per tooth by an
experienced examiner who was calibrated and trained prior to the investigation. Disease status
was defined according to Armitage [19] as generalized mild, generalized mild localized moderate,
generalized mild localized severe, generalized moderate, generalized moderate localized severe
and generalized severe periodontitis.

Microbiological assessment

Samples of oral biofilm were assessed from supragingival and subgingival sites. Supragingival
biofilm was swiped off the tooth surfaces with sterile curettes or paper points. Subgingival biofilm
was extracted by inserting a sterile paper point into deep, active periodontal pockets (BOP
positive) for 20s. From each patient three supragingival and three subgingival samples were taken
and pooled, respectively, by transferring them to 1.5ml sterile tubes. Samples were immediately
frozen (25 C) until further analysis. Bacterial DNA was isolated and
amplified following published protocols [20, 21]. Samples were analysed using a quantitative real-
time PCR (RQ-PCR) assay screening for 43 health- and caries-associated bacteria [22]. Additionally,
periodontal PCR primers for nine leading periodontal pathogens [23, 24] were added to the PCR
assay. Bacterial DNA was isolated following published protocols [21, 25] and by using a
modification of the QIAamp DNA Mini Kit (Qiagen, Hilden, Germany). Since the amount of
bacterial DNA from clinical sampling is rarely sufficient for molecular-based analysis, 50ng of DNA
was amplified according to a published protocol [20] and subsequently purified using the Marligen
PCR Purification Kit (Marligen Biosciences, Ijamsville, MD, USA) according to the manufacturers
protocol. The amount of isolated or amplified DNA used as input DNA for RQ-PCR was quantified
spectrophotometrically. RQ-PCR was performed in a reaction volume of 12ml containing
1

SYBR Green PCR Master Mix (ABsolute QPCR SYBR Green Mix, ABgene, Hamburg, Germany),
0.33mm specific primer and 3ng of isolated template DNA on an ABI PRISM 7900 Sequence
Detection System (ABI 7900 HT, SDS 2.2 AbiPrism, Applied Biosystems, Foster City, CA, USA) in
384-well PCR plates (Thermo Scientific,

www.rheumatology.oxfordjournals.org 527

Periodontal attachment loss in ERA

ABgene, Hamburg, Germany). The reaction conditions were 95 C


for 15min, followed by 40 cycles of 95 C for 15s and

~ 85 ~
60 C for 1min. Data analysis was conducted with Sequence
Detection Software version 2.2.2 (Applied Biosystems).

Statistics

All data were analysed using GraphPad InStat version 3.0 (GraphPad, San Diego, CA, USA) and
GraphPad Prism version 5.0 as statistical software. An unpaired t-test with Welch correction and
the MannWhitney U-test were applied for independent samples to test the significance of
quantitative data. The association of categorical variables was assessed by the chi-square test.
Statistical significance was declared if the P-value was <0.05. Analysis of the relative abundance
and hierarchical cluster analysis of oral bacteria were performed using DataAssist 3.0 (Applied
Biosystems, Darmstadt, Germany). Differences of at least 2.5 in the abundance of pathogens in
RQ-PCR were considered relevant.

Results

Advanced forms of periodontitis found in ERA

Of the 22 ERA subjects included in this study, 68% were female, with a mean age of 51.7 years.
The mean disease duration was 5.9 months, the mean DAS28 was 4.55 and the mean of the HAQ
was 0.79. Thirty-seven per cent of the patients were IgM-RF positive, with a mean titre of 60IU/l.
Fourteen per cent of ERA subjects were current smokers (Table 1). All ERA subjects had moderate
to severe forms of PD. Most ERA patients (n=15) had moderate-severe PD. Three ERA patients
displayed severe PD. Therefore, according to Armitage [19], all ERA patients had a diagnosis of PD.
In the healthy controls, the majority (n=15) had mild-moderate or moderate PD (Fig. 1).

Loss of CAL in ERA

Although the DMF-T indexes of the ERA [17.6 (S.D. 6.4)] and control group patients [15.5 (S.D. 4.8)]
were comparable, there was a significantly higher number of missing teeth in the ERA group [5.7
(S.D. 5.0)] compared with the healthy controls [1.9 (S.D. 1.0), P=0.002]. The GBI was significantly
higher in ERA [median 19.5% (95% CI 16.9, 28.7)] compared with controls [12.5% (95% CI 11.3,
21.0), P=0.022]. The PI as a measure of oral hygiene was comparable between ERA [33.6% (S.D.
13.0%)] and controls [30.8% (S.D. 11.1%), P=0.445]. BOP, indicating inflammation of the gingiva
and periodontal attachment, was higher in the ERA group [18.6% (S.D. 9.0%)] than in the control
group [10.5 (S.D. 5.1%), P=0.001]. Also, PPD was significantly higher in the ERA group [2.9 (S.D.
0.4)mm] compared with the control group [2.4 (S.D. 0.3)mm, P<0.0001]. The primary endpoint of
the studywhich was metwas to measure a clinically meaningful difference in the CAL between
the ERA and control group. The difference in the CAL between the ERA group [3.4 (S.D. 0.5)mm]
and the control group [2.7 (S.D.

TABLE 1 Demographic characteristics, data on ERA patients and controls

Parameter

ERA (n=22)

Controls (n=22)

Age, mean (S.D.), yearsa 51.7 (9.7) 51.9 (9.6) Gender, femalea 15 Disease duration, mean (S.D.),
months 5.9 (3.1) DAS28, mean (S.D.) 4.55 (1.1) HAQ, mean (S.D.) 0.78 (0.58) ESR, mean, mm/h
~ 86 ~
22.1 CRP, mean, mg/l 10.8 IgM-RF positive, % 37 ACPA positive, % 41 Smokera Yes 3 No 9 In the
past 10 BMI <25 7 9 2530 10 10 >30 5 3 Educational status Low 2 0 Medium 18 16 High 2 6
Consumption of alcohol Little 19 18 Moderate 2 4 Frequent 1 0

Sub- and supragingival ERA microbiota compared with healthy controls

Subgingival microflora in ERA vs control group T. forsythia (6.77-fold, P=0.033) was the only
enriched bacterium in ERA. Fusobacteria species 1 (0.33-fold, P=0.036), Lactobacillus gasseri (0.19-
fold, P=0.01), Lactobacillus species 4 (0.23-fold, P=0.016), Leptotrichia species (0.34-fold, P=0.041)
and Streptococcus gordonii (0.27-fold, P=0.014) were underrepresented in ERA compared with the
control group (Table 3).

Supragingival microflora in ERA vs control group S. anginosus (3.56-fold, P=0.028) was the only
bacterium more abundant in ERA than in healthy subjects. Rothia dentocariosa (0.15-fold,
P=0.006), Actinomyces species 2 (0.19-fold, P=0.049) and Corynebacterium durum (0.17-fold,
P=0.040) were underrepresented in ERA supragingivally (Table 4).

Discussion

We showed that in a Caucasian ERA cohort with a mean disease duration of <6 months, a clinically
significant loss of CAL is detectable compared with a matched healthy control cohort. All other
important periodontal parameters, such as GBI, BOP, number of missing teeth and PPD, were also
significantly elevated in ERA. With a mean of 5.7, the number of missing teeth in ERA patients was
also considerably greater than in the average German population of comparable age, with a mean
of 2.4 missing teeth (status 2005 [26]). Despite the high prevalence of PD in our healthy control
cohort (90%), more advanced forms of PD were observed in the ERA cohort, leading to a diagnosis
of PD in all ERA patients. A number of epidemiological studies showed higher odds ratios of PD
prevalence in established RA patients [2, 4], however, there are few studies on ERA [27]. Our study
strengthens the association of RA and PD in Caucasians. Results are in line with other recent
casecontrol studies in American and Indian ERA/PD patients [5, 27, 28]. Despite similar baseline
demographics, the prevalence of PD and CALs measured in patients both in our ERA cohort and in
our healthy control cohort were substantially higher than those in the other casecontrol ERA/PD
studies. This might be explained by different methods of measuring, different health care plans or
regional differences. This difference, however, underlines the importance of further studies in
different ethnic groups. Nevertheless, the prevalence of at least moderate forms of PD in our
healthy cohort (90%) was consistent with the expected high prevalence of PD in the age-matched
German population [26]. In our ERA cohort, the prevalence of PD was 100% and more advanced
forms of PD were already present. PD was graded as severe in three ERA patients (none in the
control) and moderate to severe in 16 ERA patients (seven in the control). As people with long-
standing RA often suffer from impaired function of the hands, elbows and shoulders, it was
suggested that this impairment leads to poor oral hygiene, which in turn explains the increased PD
in RA patients [4]. To address this bias, we selected RA patients with short disease duration. Also,
ERA patients had to be naive to biologic DMARDspotent suppressors of inflammatory and
erosive processes that would have suppressed the effects of the underlying

Periodontal attachment loss in ERA

diseases. It was recently shown that anti-IL-6R and antiTNF treatment of RA significantly improved
the main periodontal parameters, such as CAL, compared with anti-rheumatic treatment without

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biologic DMARDs [29]. Because the PI, as a parameter of oral hygiene, was comparable between
the groups, it seems unlikely that manual impairment explains the more advanced forms of PD in
the ERA cohort. It is hypothesized that oral pathogens trigger not only the pathogenesis and
perpetuation of PD, but also RA. Recently it was shown that P. gingivalis peptidyl arginine
deiminase acts not only as an enzyme to citrullinate other proteins to generate ACPAs, but also
serves to autocitrullinate as an antigen itself [12, 13]. We therefore tried to determine whether
the most common oral pathogens were associated with ERA. In subgingival plaque samples of ERA,
there was a trend to enrich P. gingivalis (2-fold, P=0.08); however, P. gingivalis infection was
common in both cohorts. T. forsythia and S. anginosus were the only enriched bacteria in our ERA
cohort. T. forsythia is a strictly anaerobic, gram-negative bacterium belonging to the red complex
of bacteria [30]. It is associated with both severe and chronic periodontitis. The enrichment seen
for these pathogens in ERA might be explained as an effect of either an advanced form of PD seen
in ERA [27], the antirheumatic medication or a different oral milieu caused by RA. Given that in our
study PD predisposed RA, another explanation could be that these pathogens are not only causing
PD, but also acting as environmental factors causing or aggravating RA. The major limitations of
our study are that (i) patients with RA received anti-rheumatic medication that might have
affected the oral microbiota, although current and previous therapy with biologic DMARDs was an
exclusion criterion, and (ii) the limited patient number did not allow analysis of PD severity as a
factor of variance. In conclusion, patients with ERA should be informed by their consulting
rheumatologist that there is a high risk of experiencing PD. Following the diagnosis of ERA, it is
recommended that patients be referred to a dental specialist to provide intensive dental care.
Whether this intensified dental care will also impact the course of RA is currently under
investigation.

Rheumatology key messages

. Increased alveolar bone and periodontal attachment loss can be detected in patients with ERA. .
Intensified dental care might help to minimize mutual inflammatory inducement of periodontal
disease and RA.

Acknowledgements

We thank Dr K. Stucke, Institute of Medical Biometry and Informatics, Ruprecht Karls University,
Heidelberg, for statistical support, Professor P. Lichter of the German Cancer Research Center for
technical support and Dr I. Gao for referring patients.

Disclosure statement: The authors have declared no conflicts of interest.

References

1 Janssen KM, Vissink A, de Smit MJ et al. Lessons to be learned from periodontitis. Curr Opin
Rheumatol 2013;25: 2417. 2 de Pablo P, Dietrich T, McAlindon TE. Association of periodontal
disease and tooth loss with rheumatoid arthritis in the US population. J Rheumatol 2008;35:706. 3
Smit MD, Westra J, Vissink A et al. Periodontitis in established rheumatoid arthritis patients: a
crosssectional clinical, microbiological and serological study. Arthritis Res Ther 2012;14:R222. 4
Pischon N, Pischon T, Kroger J et al. Association among rheumatoid arthritis, oral hygiene, and
periodontitis. J Periodontol 2008;79:97986. 5 Joseph R, Rajappan S, Nath SG et al. Association
between chronic periodontitis and rheumatoid arthritis: a hospital-based case-control study.
Rheumatol Int 2013; 33:1039. 6 Jepsen S, Kebschull M, Deschner J. [Relationship between

~ 88 ~
periodontitis and systemic diseases]. Bundesgesundheitsblatt Gesundheitsforschung
Gesundheitsschutz 2011;54:108996. 7 Detert J, Pischon N, Burmester GR et al. The association
between rheumatoid arthritis and periodontal disease. Arthritis Res Ther 2010;12:218. 8
Kobayashi T, Okada M, Ito S et al. Assessment of interleukin-6 receptor inhibition therapy on
periodontal condition in patients with rheumatoid arthritis and chronic periodontitis. J Periodontol
2013 Advance Access published 14 March 2013, doi: 10.1902/jop.2013.120696. 9 Pers JO, Saraux
A, Pierre R et al. Anti-TNF-alpha immunotherapy is associated with increased gingival inflammation
without clinical attachment loss in subjects with rheumatoid arthritis. J Periodontol
2008;79:164551. 10 Mayer Y, Elimelech R, Balbir-Gurman A et al. Periodontal condition of patients
with autoimmune diseases and the effect of anti-tumor necrosis factor-alpha therapy. J
Periodontol 2013;84:13642. 11 Socransky SS, Haffajee AD. Periodontal microbial ecology.
Periodontol 2000 2005;38:13587. 12 Wegner N, Lundberg K, Kinloch A et al. Autoimmunity to
specific citrullinated proteins gives the first clues to the etiology of rheumatoid arthritis. Immunol
Rev 2010;233: 3454. 13 Wegner N, Wait R, Sroka A et al. Peptidylarginine deiminase from
porphyromonas gingivalis citrullinates human fibrinogen and alpha-enolase: implications for
autoimmunity in rheumatoid arthritis. Arthritis Rheum 2010;62:266272. 14 Quirke AM, Lugli EB,
Wegner N et al. Heightened immune response to autocitrullinated Porphyromonas gingivalis
peptidylarginine deiminase: a potential mechanism for breaching immunologic tolerance in
rheumatoid arthritis. Ann Rheum Dis 2013 Advance Access published 28 March 2013, doi:
10.1136/annrheumdis-2012-202726.

530 www.rheumatology.oxfordjournals.org

Bjo rn Wolff et al.

15 Aletaha D, Neogi T, Silman AJ et al. 2010 rheumatoid arthritis classification criteria: an


American College of Rheumatology/European League Against Rheumatism collaborative initiative.
Ann Rheum Dis 2010;69:15808. 16 Klein H, Palmer CE, Knutson JW. Studies on dental caries.
Dental status and dental needs of elementary school children. Public Health Rep 1938;53:168590.
17 Ainamo J, Bay I. Problems and proposals for recording gingivitis and plaque. Int Dent J 1975;25:
22935. 18 OLeary TJ, Drake RB, Naylor JE. The plaque control record. J Periodontol 1972;43:38. 19
Armitage GC. Development of a classification system for periodontal diseases and conditions. Ann
Periodontol 1999;4:16. 20 Wolff D, Staehle HJ, Wolff B. Amplification of minute amounts of oral
bacterial DNA for real-time quantitative PCR analysis. Caries Res 2010;44:498504. 21 Martin FE,
Nadkarni MA, Jacques NA et al. Quantitative microbiological study of human carious dentine by
culture and real-time PCR: association of anaerobes with histopathological changes in chronic
pulpitis. J Clin Microbiol 2002;40:1698704. 22 Wolff D, Frese C, Maier-Kraus T et al. Bacterial
biofilm composition in caries and caries-free subjects. Caries Res 2013;47:6977. 23 Periasamy S,
Kolenbrander PE. Aggregatibacter actinomycetemcomitans builds mutualistic biofilm communities
with Fusobacterium nucleatum and

Veillonella species in saliva. Infect Immun 2009;77: 354251. 24 Abiko Y, Sato T, Mayanagi G et al.
Profiling of subgingival plaque biofilm microflora from periodontally healthy subjects and from
subjects with periodontitis using quantitative real-time PCR. J Periodontal Res 2010;45: 38995. 25
Nadkarni MA, Martin FE, Jacques NA et al. Determination of bacterial load by real-time PCR using a
broad-range (universal) probe and primers set. Microbiology 2002; 148(Pt 1):25766. 26 Micheelis
W. [Oral health in Germany: an oral epidemiological outline]. Bundesgesundheitsblatt
Gesundheitsforschung Gesundheitsschutz 2011;54(9): 10226. 27 Scher JU, Ubeda C, Equinda M et

~ 89 ~
al. Periodontal disease and the oral microbiota in new-onset rheumatoid arthritis. Arthritis Rheum
2012;64:308394. 28 Potikuri D, Dannana KC, Kanchinadam S et al. Periodontal disease is
significantly higher in non-smoking treatment-naive rheumatoid arthritis patients: results from a
case-control study. Ann Rheum Dis 2012;71: 15414. 29 Mayer Y, Balbir-Gurman A, Machtei EE.
Anti-tumor necrosis factor-alpha therapy and periodontal parameters in patients with rheumatoid
arthritis. J Periodontol 2009; 80:141420. 30 Socransky SS, Haffajee AD, Cugini MA et al. Microbial
complexes in subgingival plaque. J Clin Periodontol 1998; 25:13444.

Resumen de paper de artritis reumatoide

El estado oral en un paciente con enfermedad de artritis reumatoide temprana: un estudio


prospectivo de casos y controles

Se realiz un estudio a 22 pacientes con artritis reumatoides temprana y se compar con 22


pacientes sanos. En este se midi situacin oral y periodontal, actividad clnica situacin
sociodemogrfica, microbiologa oral con el objetivo de verificar si los pacientes que padecen de
artritis reumatoides tienen un mayor riesgo de sufrir perdida de insercin periodontal y aumento
de la inflacin en ella, el principal objetivo de este estudio rea determinar si la perdida de hueso
alveolar se puede detectar en pacientes con artritis reumatoide en el curso temprano de la
enfermedad.

Se obtuvo como resultado que si se puede detectar en pacientes con artritis reumatoides
temprana el aumento de perdida de insercin periodontal y el hueso alveolar

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Hemofilia

Conceptos Generales

La Hemofilia es un trastorno de la coagulacin de origen gentico, de carcter recesivo y ligado al


cromosoma X, en el que se encuentran los genes que codifican los factores hemostticos VIII y IX.
Algunas alteraciones estructurales o moleculares de dichos genes condicionan una deficiencia
cuantitativa del factor VIII en la hemofilia A (HA) y del factor IX en la hemofilia B (HB). La
enfermedad es heredada en el 70% de los casos; en el otro 30% es consecuencia de una mutacin
de novo.

Manifestaciones Generales

Se debera sospechar de esta condicin en pacientes que presenten propensin a la aparicin de


hematomas, hemorragias espontneas, en especial en articulaciones, msculos y tejidos blandos,
sangrado excesivo posterior a un trauma o ciruga. Los exmenes de laboratorio a considerar ante
la sospecha de la enfermedad son:

Tiempo de tromboplastina parcial activado (TTPA) Tiempo de Protrombina (TP)Hemograma con


recuento de plaquetas. El diagnstico definitivo de la hemofilia y su clasificacin se realizan
midiendo el nivel funcional del F(VIII) o F(IX) para la HA o HB, respectivamente. La mayora de los
pacientes tiene < 30% de la funcin del factor en cuestin. Segn el nivel del factor se clasifica en 3
grados de severidad: Hemofilia grave, si hay menos de 1% de nivel del factor; Hemofilia moderada,
si el factor se encuentra entre 1 a 5% y Hemofilia leve, si el factor se encuentra entre 5 a 40%. El
cuadro clnico para Hemofilia A y B es idntico y se caracteriza por hemorragias recurrentes,
especialmente en las articulaciones, pudiendo ocurrir en casos ms graves hemorragias internas y
del SNC.

La mayora de las personas con hemofilia son capaces de llevar vidas relativamente normales. Sin
embargo, algunos pacientes tienen eventos hemorrgicos significativos, con mayor frecuencia
sangrado crnico dentro de los espacios de las articulaciones.

Un pequeo porcentaje de las personas que padecen hemofilia puede morir a causa de un
sangrado severo.

Manifestaciones Bucomaxilofaciales

Pueden ocurrir sangramientos bucales provenientes de muchos lugares. Los procesos incluso
fisiolgicos de erupcin dentaria pueden provocar sangramientos, as como en cualquier proceder
por mnimo que sea como el caso de las tartrectomas en dependencia de la severidad de la
enfermedad. Los sitios afectados pueden ser lengua, mejillas, piso de boca, paladar duro o blando,
mucosa gingival y zona faringoamigdaliana.

Epidemiologa
~ 91 ~
La hemofilia A afecta a uno de cada 5.000-10.000 varones y representa aproximadamente un 85%
de los casos de hemofilia, mientras que la hemofilia B lo hace en uno de cada 30.000 y representa
al 15% restante. Segn datos de la Federacin Mundial de la Hemofilia, el nmero de personas
afectadas en el mundo es aproximadamente 400.000.

En Chile existen 32 centros de atencin que tratan a un total aproximado de 1.200 personas con
hemofilia. Este dato se refiere solamente a los pacientes que han consultado por problemas
agudos y requieren tratamiento de sustitucin. Se desconoce la prevalencia de pacientes leves o
moderados poco sintomticos, que en situaciones especiales (ciruga o trauma) podran tener
complicaciones graves si no se efecta un tratamiento adecuado. La mayora de estos pacientes se
encuentran en la Regin Metropolitana (56%).

Tratamiento mdico general

El tratamiento se realiza con concentrado liofilizado de factor VIII o IX obtenido de donantes o por
medios recombinantes. Si no se dispone de estos se usa crio-precipitado en la hemofilia A o el
plasma fresco en la B y ante procederes quirrgicos y/o extracciones dentales. La evaluacin del
paciente debe hacerse en conjunto hematlogo-odontlogo. A nivel nacional los especialistas
recomiendan la siguiente posologa:

- Hemofilia A: Factor VIII 20-30 U/Kg/dosis 3 veces por semana


- Hemofilia B: Factor IX 30-40 U/Kg/dosis 2 veces por semana.

Los tratamientos alternativos y coadyuvantes son importantes, particularmente donde los


concentrados de factor de coagulacin son limitados o no estn disponibles, ya que podran
disminuir la cantidad de productos de tratamiento requeridos. La desmopresina aumenta los
valores plasmticos de factor VIII, se usa en casos de hemofilia A leve. Los antifibrinolticos, tales
como, el cido tranexmico o el cido psilon aminocaproico son eficaces como tratamiento
coadyuvante para hemorragias en mucosas.

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Precauciones en el manejo odontolgico

Antes de planificar tratamiento odontolgico es vital la interconsulta al hematlogo tratante,


quien evaluar la condicin individual de cada paciente y entregar recomendaciones especiales
de ser necesario.

Los exmenes de rutina y limpiezas no profundas no requieren terapia de reemplazo.

Los procedimientos invasivos en odontologa requieren el uso de factores antihemoflicos, por lo


que se recomienda la atencin el da que se administra la profilaxis, si no la recibe se requiere
dosis de ataque para elevar el factor deficiente.

En caso de anestesia troncular al nervio dentario inferior, pulido radicular, endodoncia en diente
temporal o permanente y exodoncia de diente temporal, se requiere dosis de ataque. Se debe
elevar el Factor a un 20- 30%, una sola dosis y recomendar terapia asociada: Reposo - Rgimen
Blando - cido tranexmico: 30- 50mg/kg/da repartido en tres dosis por 5 a 7 das.

En exodoncia de dientes permanentes, se requiere dosis de ataque, aumentar el factor al menos


en 40%. Una sola dosis diaria y repetir a las 24 horas. Y terapia asociada: Reposo - cido
tranexmico: 30-50mg/ kg/da repartido en tres dosis por 10 das - Sellante de fibrina.

Se recomienda enjuague con cido tranexmico en forma previa y posterior al procedimiento y en


caso de nios pequeos, aplicacin tpica con algodn.

Es necesario contar con medidas locales y sistmicas suficientes para cohibir eventuales
hemorragias y tener la posibilidad de contactarse con hematlogo frente a alguna complicacin.

Todo lo anterior se resume en que el odontlogo debe aplicar la prevencin en cualquier situacin
que est a su alcance y mantener como regla evitar los procedimientos quirrgicos que no sean
esenciales.

~ 93 ~
Oral health in adult patients with congenital coagulation disorders a case control study

D. ZIEBOLZ,* C. STU HMER, E. HORNECKER,* A. ZAPF, R. F. MAUSBERG* and J. F. CHENOT

*Department of Preventive Dentistry, Periodontology and Cariology, University Medical Center


Goettingen, Germany;

Department of Oral and Maxillofacial Surgery, Hannover Medical School, Germany; Department of
Biometry, Hannover

Medical School, Germany; and Department of General Practice, University Medical Center
Goettingen, Germany

Summary. Inflammatory disorders of the periodontium, gingivitis and periodontitis are among the
most prevalent diseases worldwide. A few studies have found poorer oral health in patients with
congenital coagulation disorders (CCD) like haemophilia and von Willebrands disease compared
with non-affected controls. The aim of this study was to investigate the effect of congenital
coagulation disorders on oral health and periodontal (alveolar) bone loss. This is a case control
study comparing oral health and periodontal bone loss of patient with congenital coagulation
disorders with matched healthy subjects. The examination included dental status (DMF-T),
assessment of oral hygiene (modified Quigley-Hein-Index: QHI) and a dental panoramic X-ray for
assessment of alveolar bone loss caused by periodontal disease. A total of 15 patients with CCD
(Haemophilia A: n = 8, von Willebrands disease: n = 7) were matched with 31 non-affected
controls. We observed no clinical relevant difference of oral health (DMF-T, QHI) between patients
with CCD and controls despite better oral hygiene (QHI) of patients with CCD. Moreover, there
was a statistically significant difference in periodontal bone loss, but the observed difference is not
clinically meaningful. Unlike previous studies carried out mainly in children we found no evidence
that oral health or periodontal status in adult patients with CCD is worse than that in healthy
subjects. However, larger studies and longitudinal studies in adults are needed to confirm our
results. Keywords: congenital coagulation disorders, haemophilia, oral health, periodontal
(alveolar) bone loss, von Willebrands disease

Introduction

The management of patients with congenital coagulation disorders (CCD) causes a considerable
number of problems in dental medicine [1,2]. Affected patients require special attention;
however, given the relative rarity of such disorders, most dentists have no experience in dealing
with dental problems in patients with CCD. von Willebrands disease affects about 1% of the
population and is the most common CCD. Most patients have a mild to moderate form of the
condition and are only diagnosed after a significant bleeding episode. [3,4]. Haemophilia affecting
only about 1 in 5000 to 10 000 men is rarely missed [5]. Current recommendations for dental
management of CCD like, e.g. haemophilia and von Willebrands disease focus mainly on
associated coagulation problems [2,6,7]. Only few small studies have examined dental and
periodontal status mostly of children or young adults with haemophilia [810]. The studies found

~ 94 ~
poorer oral health compared with normal controls. One study including three subjects with von
Willebrands disease was inconclusive [9]. Only one case report about aggressive periodontal
disease described a family affected with von Willebrands disease [11]. Inflammatory disorders of
the periodontium, gingivitis and periodontitis are among the most prevalent diseases worldwide.
About 8090% of the population in the western world above age of 35 are affected [12].
Periodontitis leads to irreversible loss of connective tissue and bone around the teeth and is
therefore the most frequent cause for tooth loss in adults [13]. The main cause is bacterial
colonization of the oral cavity building up a biofilm (dental plaque) on the teeth [14]. However, the
cause of disease is influenced by many other factors like smoking, alcohol and genetic factors
Correspondence: Dr. Dirk Ziebolz, MSc, University Medical Center Goettingen, Preventive
Dentistry, Periodontology and Cariology, Robert-Koch Str. 40, D-37075 Goettingen, Germany. Tel.:
+49 551 39 8368; fax: +49 551 39 22037; e-mail: dirk.ziebolz@med.uni-goettingen.de

Accepted after revision 15 September 2010

Haemophilia (2011), 17, 527531 DOI: 10.1111/j.1365-2516.2010.02443.x 2011 Blackwell


Publishing Ltd 527

[13]. Diabetes, HIV and other systemic disease are the associated risk factors [1517]. It is
conceivable that congenital coagulation disorders are risk factors for periodontitis and subsequent
alveolar bone loss. The aim of this case control study was to investigate the effect of congenital
coagulation disorders on oral health and periodontal (alveolar) bone loss. Materials and methods

This is a case control study comparing oral health and periodontal bone loss of patient with
congenital coagulation disorders with matched healthy subjects. The study was reviewed and
approved by the ethics committee of the Hannover Medical School, Germany. Subjects Congenital
coagulation disorder group. Patients between 18 and 60 years suffering from congenital
coagulation disease (haemophilia A/B or von Willebrands disease) who attended the dental clinic
of Hannover Medical School in 2007 were asked to give informed consent to participate in the
study. To avoid confounding with other conditions affecting oral health, the following medical
conditions were considered exclusin criteria: smoking in the last 5 years, heart disease (coronary
artery disease, hypertension), diabetes mellitus, infectious diseases (hepatitis, HIV), seizures, drug
addiction, chronic renal failure, organ transplantation, immunosuppressive medication,
continuous medication and pregnancy. A dental panoramic X-ray (less tan 1 year old) had to be
available. Control group. Healthy patients receiving routine dental check-up were selected
randomly as controls. Patients were matched by age and gender: each CCD patient was matched
with two healthy controls. Inclusion and exclusion criteria were identical. Clinical examination All
subjects were examined once under standardized conditions by an experienced dentist (dentist 1
DZ). The dental examination was performed during a routine dental check-up in the dental office
of the Hannover Medical School (CCD patients) or in the dental practice (control patients). Oral
health. The examination included dental status (DMF-T) and assessment of oral hygiene [modified
Quigley-Hein-Index (QHI)] [1820]. The DMF-T is a caries index used internationally to quantify the
number of decayed teeth, missing teeth and filled teeth with values ranging from 0 to 28. The
modified QHI evaluates oral hygiene by colouring dental plaque with a plaque detector
(erythrosine solution). The plaque extension is graded on a scale from 0 to 5, values below 1 are
considered as good oral hygiene. Radiographic examination Periodontal bone loss. Periodontal
(alveolar) bone loss and the periodontal structures were assessed radiographically with a dental
panoramic X-rays/tomography (DPT). All DPTs were performed under the same conditions (70 kV,

~ 95 ~
0.9 mA) with conventional films. All radiographs were taken with the same X-ray machine using
the same program. The evaluation of bone loss was carried out under standardized conditions.
Each X-ray was examined by one dentist (dentist 2 CS) using identical assessment criteria. The
examiner was blinded to which group patients belonged to. All X-rays were examined with 14 days
between the examinations. The level of alveolar bone loss was evaluated for each tooth: the
distance between the limbus alveolaris and the cemento-enamel junction was examined mesially
as well as distally in millimetre (mm) with an mm-scaled periodontal probe (CP-15UNC, Hu-Friedy,
Chicago, IL, USA) [21]. The level of periodontal status was graded according to recommendations
from Page and Eke for definition of periodontitis [22]:

severe periodontitis: alveolar bone loss >5mm (>30% of the sites)

moderate periodontitis: alveolar bone loss 35mm (>30% of the sites)

no or mild periodontitis: alveolar bone loss 12mm (>70% of the sites)

Statistical evaluation Data were assessed for Normal distribution. Accordingly we used Students t-
test if Normal distribution could be assumed and MannWhitney U-test otherwise. Chi-square test
was used for dichotomous data. For description of alveolar bone loss in the two roups in a first
step the figures obtained of mesial and distal alveolar bone were used to calculate the mean loss
for each tooth. Afterwards the mean (mesial and distal summarized) of all teeth per patients was
used for the Students t-test. A P-value less than 0.05 was considered as significant. Statistical
analysis was performed using SAS 9.2 (SAS Institute Inc., Cary, NC, USA).

Results

Description of the population Congenital coagulation disorders group. A total of 37 patients


(female = 21, male = 16) with CCD were asked to give consent. Five patients declined and another
17528 D. ZIEBOLZ et al. Haemophilia (2011), 17, 527531 2011 Blackwell Publishing Ltd were
excluded because they did not meet the inclusin criteria (mostly smokers). Finally 15 patients
(female = 5; male = 10) could be included (40%); 8 patients with haemophilia A (severe: n = 6,
moderate: n = 2) and 7 patients with von Willebrands disease Typ IIA. The average age was 39.2
(SD 8.3) years. Control group. A total of 81 patients were approached to act as controls, of which
7 declined and 43 were ineligible mostly because of smoking. Finally 31 subjects (male = 21,
female: n = 10) with an average age of 36.4 (SD 9.6) years were included in the study. From one
male patient all data were not collected and therefore one more patient was recruited for a full
data set.

The distribution of age and gender between the two groups was not significantly different
(Table1.). Oral healthThe comparison of patients and healthy controls is shown in Table 1. The
median DMF-T of patients withCCD and healthy controls was not significantly different (P = 0.41).
Moreover, no difference in sub-indices number of missing teeth (MT) (P = 0.12), number of
decayed teeth (DT) (P = 0.5) as well as number of filled teeth (FT) (P = 0.28) was observed. Patients
with CCD had a significantly better oral hygiene (modified QHI) (P = 0.01) (Fig. 1). Periodontal bone
loss Patients with CCD had significantly more alveolar bone loss than controls (DPT) (P = 0.003)
(Fig. 1). We also observed that patients with CCD had significantly more frequently moderate to
severe periodontitis (80%)compared with the controls (48%) based on radiological assessment of
alveolar bone loss (P = 0.04, Table 1). A subgroup analysis comparing alveolar bone loss in patients
with haemophilia to von Willebrands disease did not show a significant difference (P =

~ 96 ~
0.92).Discussion Summary of the main results We observed no clinical relevant difference of oral
health between patients with CCD and healthy controls despite better oral hygiene of patients
with CCD. Moreover, there was a statistically significant difference in periodontal (alveolar) bone
loss, but the observed difference (less than 1 mm) is clinically not meaningful according to our
clinical experience. Comparison with existing literatura An Egyptian study found significantly
higher DMF-T in haemophilic children (average age 78 years, n = 30/ 30) compared with non-
haemophilic controls [23]. Another study in adolescents (average age 16 years) in Pakistan also
observed significantly higher DMF-T in haemophiliacs (n = 52/192) [8]. Our study which was
performed in adults cannot be directly compared with other studies on oral health of patients with
CCD [810,23]. However, the results of the DMF-T in this study (CCD: median = 18; controls:
median = 15) are similar to the findings of the age group 3544 years (mean DMF-T = 14.5) in
German Study on Oral Health (DMS-IV) [24]. A large Polish study (n = 180) in children with
haemophilia and von Willebrands disease from age 418 also found no significant difference in
DMF-T [9]. Despite these non-significant findings, the author concluded that oral health in severe
haemophiliacs is worse. A study in haemophilic children in Northern Ireland also found no
difference [25]. The observed differences might be related to economic wealth and differences in
provision of dental care.

Salud bucal en pacientes adultos con problemas de coagulacin congnita- estudio de casos y
controles

ASBTRACT

Los trastornos inflamatorios del periodonto, la gingivitis y la periodontitis se encuentran


entre las enfermedades ms prevalentes en todo el mundo. Algunos estudios han encontrado
una menor salud oral en pacientes con trastornos congnitos de la coagulacin (CCD) como la
hemofilia y la enfermedad de Von Willebrand en comparacin con los controles no afectados.
El objetivo de este estudio fue investigar el efecto de los trastornos congnitos de la
coagulacin sobre la salud bucodental y la prdida sea periodontal (alveolar). Este es un
estudio de control de casos que compara la salud oral y la prdida sea periodontal de
pacientes con trastornos congnitos de la coagulacin con sujetos sanos pareados. El examen
incluy el estado dental (DMF-T), la evaluacin de higiene oral (Quigley-Hein-Index: QHI
modificado) y una radiografa panormica dental para la evaluacin de la prdida sea
alveolar causada por la enfermedad periodontal. Un total de 15 pacientes con CCD (Hemofilia
A: n = 8, enfermedad de von Willebrand: n = 7) fueron comparados con 31 controles no
afectados. No se observaron diferencias clnicamente relevantes de salud oral (DMF-T, QHI)
entre pacientes con CCD y controles a pesar de una mejor higiene bucal (QHI) de los pacientes
con CCD. Adems, hubo una diferencia estadsticamente significativa en la prdida sea
periodontal, pero la diferencia observada no es clnicamente significativa. A diferencia de los
estudios previos realizados principalmente en nios, no encontramos evidencia de que la
salud oral o el estado periodontal en pacientes adultos con CCD sea peor que en sujetos sanos.
Sin embargo, estudios mayores y estudios longitudinales en adultos son necesarios para
confirmar nuestros resultados.

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MATERIALES Y METODOS

Este es un estudio de control de casos que compara la salud bucal y la prdida sea
periodontal de pacientes con trastornos congnitos de la coagulacin con sujetos sanos
pareados.

El estudio fue revisado y aprobado por el comit de tica de la Escuela de Medicina de


Hannover, Alemania.

Asignaturas

Grupo de trastornos congnitos de la coagulacin. Se pidi a los pacientes entre 18 y 60 aos


que padecan enfermedad de coagulacin congnita (hemofilia A / B o enfermedad de von
Willebrand) que asistieron a la clnica dental de la Escuela de Medicina de Hannover en 2007,
dar su consentimiento informado para participar en el estudio. Para evitar confundir con
otras afecciones que afectan la salud bucal, se consideraron los siguientes criterios de
exclusin: tabaquismo en los ltimos 5 aos, cardiopata (hipertensin), diabetes mellitus,
enfermedades infecciosas (hepatitis, VIH) , Convulsiones, adiccin a las drogas, insuficiencia
renal crnica, trasplante de rganos, medicacin inmunosupresora, medicacin continua y
embarazo. Una radiografa dental panormica (menos de 1 ao de edad) tena que estar
disponible.

Grupo de control. Los pacientes sanos que recibieron un control dental rutinario fueron
seleccionados aleatoriamente como controles. Los pacientes fueron emparejados por edad y
sexo: cada paciente CCD fue emparejado con dos controles sanos. Los criterios de inclusin y
exclusin eran idnticos.

Exmen clinico

Todos los sujetos fueron examinados una vez bajo condiciones estandarizadas por un dentista
experimentado (dentista 1 DZ). El examen dental se realiz durante un chequeo dental de
rutina en el consultorio dental de la Escuela de Medicina de Hannover (CCD) o en la prctica
dental (pacientes de control).

Salud bucal. El examen incluy el estado dental (DMF-T) y la evaluacin de la higiene oral
[modificado Quigley-Hein-Index (QHI)] [18 - 20]. La DMF-T es un ndice de caries usado
internacionalmente para cuantificar el nmero de dientes cariados, dientes faltantes y dientes
rellenos con valores que van de 0 a 28.

El QHI modificado evala la higiene bucal coloreando la placa dental con

Un detector de placa (solucin de eritrosina). La extensin de la placa se clasifica en una


escala de 0 a 5, valores inferiores a 1 se consideran como una buena higiene oral.

Examen radiogrfico

Prdida de hueso periodontal. La prdida sea periodontal (alveolar) y las estructuras

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periodontales se evaluaron radiogrficamente con una radiografa dental panormica /
tomografa (DPT). Todos los DPT se realizaron en las mismas condiciones (70 kV, 0,9 mA) con
pelculas convencionales. Todas las radiografas se tomaron con la misma mquina de rayos X
usando el mismo programa.

La evaluacin de la prdida sea se realiz bajo condiciones estandarizadas. Cada radiografa


fue examinada por un dentista (dentista 2 CS) utilizando criterios de evaluacin idnticos. El
examinador fue cegado a qu grupo de pacientes perteneca. Todos los rayos X fueron
examinados con 14 das entre los exmenes. Se evalu el nivel de prdida sea alveolar para
cada diente: la distancia entre el limbo alveolar y la unin cemento-esmalte fue examinada
mesialmente y distalmente en milmetro (mm) con una sonda periodontal de escala mm (CP-
15UNC, Hu- Friedy, Chicago, IL, EE.UU.) [21].

El nivel de estado periodontal se clasific de acuerdo con las recomendaciones de Page y Eke
para la definicin de periodontitis [22]:

periodontitis severa: prdida sea alveolar > 5 mm (> 30%

De los sitios)

Periodontitis moderada: prdida sea alveolar 3-5mm

(> 30% de los sitios)

no o periodontitis leve: prdida de hueso alveolar 1-2mm

(> 70% de los sitios)

Evaluacin estadstica

Los datos fueron evaluados para la distribucin normal. Por lo tanto, usamos la prueba t -
Student si se poda asumir la distribucin normal y la prueba U de Mann-Whitney. Para los
datos dicotmicos se utiliz la prueba del Chi cuadrado.

Para la descripcin de la prdida sea alveolar en los dos grupos en un primer paso se
utilizaron las cifras obtenidas de hueso alveolar mesial y distal para calcular la prdida media
de cada diente. Posteriormente se utiliz la media (mesial y distal resumida) de todos los
dientes por paciente para la prueba t de Student. Se consider significativo un valor P inferior
a 0,05. El anlisis estadstico se realiz utilizando SAS 9.2 (SAS Institute Inc., Cary, NC, EE.UU.).

Resultados

Descripcin de la poblacin

Grupo de trastornos congnitos de la coagulacin. Un total de 37 pacientes (mujeres = 21,


hombres = 16) con CCD se les pidi dar su consentimiento. Cinco pacientes declinaron y otros 17
fueron excluidos porque no cumplan los criterios de inclusin (en su mayora fumadores).

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Finalmente, 15 pacientes (mujeres = 5, varones = 10) podran ser incluidos (40%); 8 pacientes con
hemofilia A (grave: n = 6, moderado: n = 2) y 7 pacientes con enfermedad de von Willebrand Tipo
IIA. La media de edad fue de 39,2 (SD 8,3) aos.

Grupo de control. Un total de 81 pacientes fueron abordados para actuar como controles, de los
cuales 7 disminuyeron y 43 fueron inelegibles debido principalmente al tabaquismo. Finalmente se
incluyeron en el estudio 31 sujetos (hombres = 21, mujeres: n = 10) con una edad media de 36,4
(SD 9,6) aos. De un paciente varn todos los datos no fueron recogidos y por lo tanto un nuevo
paciente fue reclutado para un conjunto completo de datos.

La distribucin de la edad y el sexo entre los dos grupos no fue significativamente diferente.

Salud bucal

La comparacin entre los pacientes y los controles sanos se muestra en la Tabla 1. La mediana
de la DMF-T de los pacientes con CCD y controles sanos no fue significativamente diferente (P
= 0,41). Por otra parte, no se observaron diferencias en el nmero de subndices de dientes
perdidos (MT) (P = 0,12), nmero de dientes cariados (DT) (P = 0,5) y nmero de dientes
llenos (P = 0,28) . Los pacientes con CCD tenan una higiene bucal significativamente mejor
(QHI modificado) (P = 0,01)

Prdida de hueso periodontal

Los pacientes con CCD tenan significativamente ms prdida de hueso alveolar que los
controles (DP) (P = 0,003) (Fig. 1). Tambin observamos que los pacientes con CCD tenan
significativamente ms frecuentemente de moderada a severa periodontitis (80%) en
comparacin con los controles (48%) sobre la base de la evaluacin radiolgica de la prdida
sea alveolar (P=0.04)

Un anlisis de subgrupos que compar la prdida sea alveolar en pacientes con hemofilia a
enfermedad de von Willebrand no mostr una diferencia significativa (P = 0,92).

Discusin

Resumen de los principales resultados

No se observ ninguna diferencia clnica relevante de salud oral entre los pacientes con CCD y
controles sanos a pesar de una mejor higiene bucal de los pacientes con CCD. Por otra parte,
hubo una diferencia estadsticamente significativa en la prdida de hueso periodontal
(alveolar), pero la diferencia observada (menos de 1 mm) no es clnicamente significativa
segn nuestra experiencia clnica.

Comparacin con la literatura existente

Un estudio egipcio encontr una DMF-T significativamente mayor en los nios hemoflicos
(edad promedio 7-8 aos, n = 30/30) en comparacin con los controles no hemoflico [23].
Otro estudio en adolescentes (edad promedio 16 aos) en Pakistn tambin observ
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significativamente mayor DMF-T en hemoflicos (n = 52/192) [8]. Nuestro estudio que se
realiz en adultos no se puede comparar directamente con otros estudios sobre la salud oral
de los pacientes con CCD [8 - 10, 23]. Sin embargo, los resultados de la DMF-T en este estudio
(CCD: mediana = 18, controles: mediana = 15) son similares a los hallazgos del grupo de edad
35-44 aos (DMF-T media = 14,5) Salud bucal (DMS-IV) [24]. Un gran estudio polaco (n =
180) en nios con hemofilia y enfermedad de von Willebrand de 4-18 aos tampoco encontr
diferencias significativas en la DMF-T [9]. A pesar de estos hallazgos no significativos, el autor
concluy que la salud bucal en las hemoflicas graves es peor. Un estudio en nios hemoflicos
en Irlanda del Norte tampoco encontr diferencias [25]. Las diferencias observadas podran
estar relacionadas con la riqueza econmica y las diferencias en la provisin de atencin
dental.

Este es, a nuestro conocimiento, el primer estudio que examina la prdida de hueso
periodontal (alveolar) en pacientes con CCD. Slo un informe de un caso, basado en una
familia con cuatro miembros, sugiri una posible relacin entre la enfermedad de von Wille-
mark y la periodontitis [11].

La madre afectada (45 aos), as como dos hijos afectados (21 y 19 aos) tenan todos una
periodontitis severa. Slo una hija afectada (15 aos) fue periodontalmente sana. Nuestros
resultados no apoyan esta hiptesis, aunque hemos observado una moderada
estadsticamente significativa pero clnicamente no relevante aumento de la prdida sea en
el grupo CCD.

Fortalezas y limitaciones

Este es el primer estudio que compara la salud oral y el estado periodontal en pacientes con
CCD adultos con controles sanos. Nuestro estudio tiene varias limitaciones. Como resultado de
estrictos criterios de exclusin para evitar confundirse con otras condiciones que afectan la
salud bucal, slo podramos incluir un pequeo nmero de pacientes. Por lo tanto, hemos
agregado pacientes con dos trastornos de coagulacin diferentes en un grupo para
comparacin. Se realiz un anlisis de subgrupos que no mostr diferencias. El examen de la
prdida sea periodontal (alveolar) se bas nicamente en radiografas panormicas; Sin
embargo, para una mejor evaluacin de la situacin clnica, hubieran sido tiles parmetros
adicionales (profundidad de bolsillo, nivel de insercin clnica). Dado que estos
procedimientos invasivos pudieron haber causado sangrado prolongado y / o observacin
prolongada en pacientes con CCD, no examinamos estos parmetros.

Conclusin

La enfermedad periodontal es un problema de salud pblica subestimado. Aunque los


pacientes con CCD requieren una atencin especial para el tratamiento dental invasivo, no
encontramos evidencia de que la salud oral o el estado periodontal sea peor que en sujetos

~ 101 ~
sanos. Sin embargo, estudios mayores y estudios longitudinales en adultos son necesarios
para confirmar nuestros resultados.

Conclusion.

AL ya haver investigado las diversas patologas que se desarrollan a lo largo de este trabajo
podemos concluir que todo va a depender de la patologa que contenga el paciente, ya que van
actuar todos de diferentes formas ya sea por un problema en sus habilidades motoras o sensitivas.

Uno debe acomodarse a la patologa que se nos presente adelante, desarrollar las habilidades
blandas para lograr ayudar a una persona que contiene esto. Quiza puede que hayan muchas
personas que lo contengan pero no asisten al dentista por el hecho de su enfermedad, esto no
debe ser as por el hecho de que la especializacin nos permite poder ayudarlos.

Adems podemos observar que la higiene dental se dificulta mucho ya que no actua su cuerpo al
100% como una persona que no contenga ningn tipo de problema, hay que tener mucha mayor
precaucion con esto ya que puede llevar a desencadenar problemas muchos mas graves. Es muy
importante que estos pacientes sean controlados peridicamente y no fallen el da que le
corresponde.

Esto se debe a que con estas consultas podemos prevenir de ciertos riesgos que pueden existir,
adems hay veces que se debe pedir ayuda externa (persona que lo cuida, algn familiar) por el
echo de que como las patologas limitan tanto musculos o huesos, estos no logran ocupar bien el
cepillo de dientes o el hilo dental o el enguaje bucal.

A su vez para el odontlogo tambin debe ser importante saber detalladamente de que se trata la
enfermedad o el trastono que contenga el paciente, ya que cada paciente se debe tratar de
manera distinta acomodndose a l para lograr desarrollar el trabajo y no causarle algn tipo de
dao al paciente.

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Referencias.

Discapacidad intelectual y escala de medicin:

- Verdugo,M ;Gomez, L ;Martinez,B; Dominguez,M;Clavero,D; Tamarit,J(2013) Escala Inoci-


feaps.Marzo21,2017de universidad se salamanca sitoweb:
http//sid.usal.es/idocs/F8/FDO26363/Herramientas %207_2013.pdf
- Verdugo, M(2002).analisis de la definicin de discapacidad intelectual de la asociacin
americana sobre retraso mental.Siglo Cero, Vol 34(1) , num 205
- Miguel Angel Verdugo. (2001). EVALUACION DE NINOS CON DISCAPACIDADES Y
EVALUACION DEL RETRASO MENTAL. 21 marzo 2017, de SID servicio de informacin de
discapacidad Sitio web: http://sid.usal.es/idocs/F8/8.4.1-5023/8.4.1-5023.PDF
- Dr. Leopoldo Lozano Dentzano. (1997). ODONTOLOGIA Y DISCAPACIDAD. 21 marzo 2017,
de OMS 1997 Sitio web:
https://www.fundacionprevent.com/app/webroot/news/Infounomas/PDFS/odontologia_
discapacidad.pdf
- dr. carlo paolinElli g. (1), dr. milton gonzlEz a. (2). (2014). EpidEmiologa dE la
discapacidad En chilE, nios y adultos EpidEmiology of disability in ChilE, ChildrEn and
adults. 21 Marzo 2017, de [REV. MED. CLIN. CONDES Sitio web:
https://www.clinicalascondes.cl/Dev_CLC/media/Imagenes/PDF%20revista%20mdica/20
14/2%20marzo/1-Dr.Paolinelli.pdf

Trastorno espectro autista:

- A. Dez-Cuervo a, J.A. Muoz-Yunta b, J. Fuentes-Biggi c, R. Canal-Bedia d, M.A. Idiazbal-


Aletxa e, M.J. Ferrari-Arroyo f, F. Mulas g, J. Tamarit h, J.R. Valdizn i, A. Hervs-Ziga j, J.
Artigas-Pallars k, M. Belinchn-Carmona l, J.M. Hernndez m, J. Martos-Prez n, S.
Palacios o, M. Posada-De la Paz p. (2005). Gua de buena prctica para el diagnstico de
los trastornos del espectro autista. Viernes 24 marzo, de Rev-Neurol Sitio web:
http://www.psicomed.net/articulos/diag_autismo.pdf
- Patricio Medina. (Julio 24 2012). ENATEAEncuesta nacional sobre el Espectro del
Autismo.. 21 marzo2017, de AutismoDiario Sitio web:
https://espectroautistaenchile.wordpress.com/tag/estadisticas/
- Eunice kennedy shriver National Institute of Child Health and Human development. (5ta
edition 2013). Cules son los sntomas del trastorno del espectro autista (ASD por sus
siglas en ingls)?. 21 marzo 2017, de Asociacion americana de psiquiatra Washington DC
Sitio web:
https://www.nichd.nih.gov/espanol/salud/temas/autism/informacion/Pages/sintomas.as
px
- Centro Nacional de Defectos Congnitos y Discapacidades del Desarrollo de los CDC,
Centros para el Control y la Prevencin de Enfermedades. (16 de septiembre de 2014).
Trastornos del espectro autista (TEA). 24 marzo 2017, de CDC centros para el control y
prevencin de enfermedades Sitio web: https://www.cdc.gov/Spanish/

~ 103 ~
- Olga Llorente Atienza. (Septiembre 2014). Manejo de pacientes con TEA en odontologa .
Viernes 24 marzo, de GDpracticaclinica Sitio web: http://www.gacetadental.com/wp-
content/uploads/2014/09/261_PRACTICACLINICA_ManejoPacientesTEA.pdf?download=cd
35d7d1dfe951961ebcc1c6093146d4

Paralisis cerebral:

- Campellone, J & Noritz, G. (2015). Paralisis cerebral. 2017, de Medlineplus Sitio web:
https://medlineplus.gov/spanish/ency/article/000716.htm
- Bachrach. S. (Julio, 2012). Paralisis cerebral. 2017, de Nemours Sitio web:
http://kidshealth.org/es/kids/cerebral-palsy-esp.html
- Bethesda, MD. (Septiembre, 2007). Paralisis cerebral, esperanza de investigacion. 2017, de
National institute of neurological disorders and stroke Sitio web:
https://espanol.ninds.nih.gov/trastornos/paralisiscerebral.htm
- Esther, M. (Diciembre, 2016). Paralisis Cerebral. 2017, de Webconsultas Sitio web:
http://www.webconsultas.com/paralisis-cerebral/paralisis-cerebral-2832
- Kleinsteuber, K.., De los Angeles, M & Varela A. (2014). Paralisis Cerebral. 2017, de Revista
pediatria electronica Sitio web:
http://www.revistapediatria.cl/vol11num2/pdf/6_PARALISIS_CEREBRAL.pdf
- Asociacion americana de embarazos. (2003). Paralisis cerebral: causas, el tratamiento y la
prevencion.. 2017, de American pregnancy Sitio web:
http://americanpregnancy.org/es/birth-defects/cerebral-palsy/
- Jara, A & Martiinez A. (2015). Paralisis Cerebral. 2017, de Slideshare Sitio web:
https://es.slideshare.net/abex07/parlisis-cerebral-46668076
- Teleton. (2010). Paralisis cerebral. 2017, de Teleton Sitio web:
http://www.teleton.cl/teleton/que-hacemos/rehabilitacion-integral/patologias/paralisis-
cerebral/

Esclerosis mltiple:

- Instituto Nacional de Trastornos Neurolgicos y Accidentes Cerebrovasculares. (2015).


Esclerosis multiple. 2017, de Medlineplus Sitio web:
https://medlineplus.gov/spanish/multiplesclerosis.html
- Esclerosis multiple espaa. (2014). Que es la esclerosis multiple. 2017, de M Sitio web:
http://www.esclerosismultiple.com/esclerosis-multiple/que-es
- Cuidate plus. (Diciembre, 2015). Esclerosis multiple. 2017, de Editorial revistas Sitio web:
http://www.cuidateplus.com/enfermedades/neurologicas/esclerosis-multiple.html
- Riverol, M. (2015). Esclerosis multiple: Sintomas. 2017, de Clinica universitaria de navarra
Sitio web: http://www.cun.es/enfermedades-tratamientos/enfermedades/esclerosis-
multiple
- Ministerio de salud. (2016). Esclerosis multiple, remitente recurrente. 2017, de Super
intendencia salud Sitio web: http://www.supersalud.gob.cl/difusion/665/w3-article-
5998.html
- Espaa, O. (Abril, 2013). Esclerosis multiple, efectos orales. 2017, de Blog dentista Sitio
web: http://dentistaentuciudad.com/blog/esclerosis-multiple-y-sus-efectos-orales/

~ 104 ~
- Melkonyan, R. (2005). Atencion dental para esclerosis multiple.. 2017, de Articles Phere
Sitio web: http://www.articlesphere.com/es/Article/Dental-Care-for-People-with-
Multiple-Sclerosis/168834

ELA:

- (ELA), E. Esclerosis lateral amiotrfica (ELA): MedlinePlus enciclopedia mdica. [online]


Medlineplus.gov. Available at: https://medlineplus.gov/spanish/ency/article/000688.htm
- Movil, e., Movil, e. and perfil, V. Esclerosis Lateral Amiotrfica (ELA). [online]
Esencialdent.blogspot.cl. Available at: http://esencialdent.blogspot.cl/2013/02/esclerosis-
lateral-amiotrofica-ela.html [Accessed 25 Mar
- Castro Correro, S. and Dez Andrs, M. Esclerosis lateral amiotrfica. Presentacin como
un hombro doloroso. [online] Available at: http://www.elsevier.es/es-revista-semergen-
medicina-familia-40-articulo-esclerosis-lateral-amiotrofica-presentacion-como-13071211

Alzherimer:

- Alzheimer, M. Mal de Alzheimer: MedlinePlus enciclopedia mdica. [online]


Medlineplus.gov. Available at: https://medlineplus.gov/spanish/ency/article/000760.htm.
- BrightFocus Foundation. Signos y Sntomas. [online] Available at:
http://www.brightfocus.org/espanol/la-enfermedad-de-alzheimer-y-la-
demencia/enfermedad-de-alzheimer-sintomas-y-etapas.
- Actaodontologica.com. (n.d.). ENFERMEDAD DE ALZHEIMER: CONSIDERACIONES
ODONTOLGICAS. [online] Available at:
http://www.actaodontologica.com/ediciones/2007/1/alzheimer.asp

Displacia:

- . (2015). informacin sobre la displaca ectodrmica. 24/03/2017, de asociacin de


afectados por la displaca ectodrmica Sitio web:
http://www.displasiaectodermica.org/displasia.php
- (ultima revisin 23/07/2015). Displaca ectodrmica. 24/03/2017, de Biblioteca Nacional
de Medicina de los EE. UU. Medline Sitio web:
https://medlineplus.gov/spanish/ency/article/001469.htm

Radio terapia:

- Dorshow, G. (2016). Radioterapia. 2017, de Medlineplus Sitio web:


https://medlineplus.gov/spanish/ency/article/001918.htm

Artritis reumatoide:

- (.). artritis reumatoides. 24/03/2017, de Universidad catlica de chile Sitio web:


http://publicacionesmedicina.uc.cl/ApuntesReumatologia/Pdf/ArtritisReumatoide.pdf
~ 105 ~
- (ltima revisin 16/01/2016). Artritis reumatoidea. 24/03/2017, de Biblioteca Nacional de
Medicina de los EE. UU., Medline Sitio web:
https://medlineplus.gov/spanish/ency/article/000431.htm

Hemofilia:

- Marimon Torres, M. (2008). Ciencias basicas. La habana: Ciencias medicas.


- GRIFFIN, R & BETHESDA. (2013). Manual de hematologa. Clinica 3edicion.
- Kummar, B.., Abbas,K & Fausto, R.., . (2005). Robbins and Cotran Pathologic Basis of
Disease. Wb Saunders: St Louis.

~ 106 ~