Capítulo 4 Carranza 11 Ed.

O
CHAPTER 4
Classfication of Diseases and Conditions
Affecting the Periodontium
James E. Hinrichs and M. John Novak

CHAPTER OUTLINE
PeriodontalEndodontic Lesions
Combined Lesions
DEVELOPMENTAL OR ACQUIRED DEFORMITIES AND
CONDITIONS
Localized Tooth-Related Factors That Modify or
Predispose to Plaque-Induced Gingival Diseases or
Periodontitis
Mucogingival Deformities and Conditions around
Teeth
Mucogingival Deformities and Conditions of
Edentulous Ridges
Occlusal Trauma

GINGIVAL DISEASES
Dental PlaqueInduced Gingival Diseases
Gingivitis that is associated with dental plaque formation is the
most common form of gingival disease (Figure 4-1). Box 4-2
outlines the classifications of gingival diseases. The epidemiology
of gingival disease is reviewed in Chapter 5, its etiology is
detailed in Chapters 21 through 28, and clinical characteristics are
discussed in Chapters 8 through 18 and elsewhere in this text-
book.9,13,14,24,25 Gingivitis has been previously characterized by the
presence of clinical signs of inflammation that are confined to the
gingiva and associated with teeth showing no attachment loss.
Gingivitis also has been observed to affect the gingiva of
periodontitis-affected teeth that have previously lost attachment
but have received periodontal therapy to stabilize any further
attachment loss. In these treated cases, plaque-induced gingival
GINGIVAL DISEASES
NonPlaque-Induced Gingival Lesions
PERIODONTITIS
Chronic Periodontitis
Aggressive Periodontitis
Periodontitis as a Manifestation of Systemic
Diseases
NECROTIZING PERIODONTAL DISEASES
Necrotizing Ulcerative Gingivitis
Necrotizing Ulcerative Periodontitis
ABSCESSES OF THE PERIODONTIUM
PERIODONTITIS ASSOCIATED WITH ENDODONTIC
LESIONS
EndodonticPeriodontal Lesions

ur understanding of the etiology and pathogenesis of oral
diseases and conditions is continually changing with
increased scientific knowledge.In light of this,a classifica-
tion can be most consistently defined by the differences in the
clinical manifestations of diseases and conditions because they are
clinically consistent and require little, if any, clarification by scien-
tific laboratory testing.The classification presented in this chapter
is based on the most recent, internationally accepted, consensus
opinion of the diseases and conditions affecting the tissues of the
periodontium and was presented and discussed at the 1999 Inter-
national Workshop for the Classification of the Periodontal Dis-
eases organized by the American Academy of Periodontology
(AAP).3 Box 4-1 presents the overall classification system,and each
of the diseases or conditions are discussed where clarification is
needed. In each case, the reader is referred to pertinent reviews on
the subject and specific chapters within this book that discuss the
topics in more detail.
34
35
Figure 4-1 A, Plaque-related gingivitis depicts marginal and papillary inflammation, with 1 to 4 mm probing depths and generalized zero clinical attach-
ment loss, except recession in tooth #28. B, Radiographic images of the patient.
A
*These diseases may occur on a periodontium with no attachment loss or on a periodontium with attachment loss that is stable and not progressing.
Chronic periodontitis can be further classified based on extent and severity. As a general guide, extent can be characterized as localized (<30% of sites involved) or general-
ized (>30% of sites involved). Severity can be characterized based on the amount of clinical attachment loss (CAL) as follows: slight = 1 or 2 mm CAL; moderate = 3 or 4 mm
CAL; and severe !5 mm CAL. Data from Armitage GC: Ann Periodontol 4:1, 1999.
CHAPTER 4 Classfication of Diseases and Conditions Affecting the Periodontium

BOX 4-1 Classification of Periodontal Diseases and Conditions
Gingival Diseases
Plaque-induced gingival diseases*
Nonplaque-induced gingival lesions

Localized
Generalized

Localized
Generalized

Periodontitis as a Manifestation of Systemic Diseases
Necrotizing Periodontal Diseases
Necrotizing ulcerative gingivitis (NUG)
Necrotizing ulcerative periodontitis (NUP)
Abscesses of the Periodontium
Gingival abscess
Periodontal abscess
Pericoronal abscess

Periodontitis Associated with Endodontic Lesions
Endodonticperiodontal lesion
Periodontalendodontic lesion
Combined lesion

Developmental or Acquired Deformities and Conditions
Localized tooth-related factors that predispose to plaque-induced
gingival diseases or periodontitis
Mucogingival deformities and conditions around teeth
Mucogingival deformities and conditions on edentulous ridges
Occlusal trauma
inflammation may recur but without any evidence of further
attachment loss.
From this evidence, it has been concluded that plaque-induced
gingivitis may occur on a periodontium with no attachment loss or
on a periodontium with previous attachment loss that is stable and
not progressing. This implies that gingivitis may be the diagnosis
for inflamed gingival tissues associated with a tooth with no previ-
ous attachment loss or with a tooth that has previously undergone
attachment and bone loss (reduced periodontal support) but is not
currently losing attachment or bone, even though gingival inflam-
mation is present (Figure 4-2). For this diagnosis to be made,
longitudinal records of periodontal status,including clinical attach-
ment levels, should be available.
Gingivitis Associated with Dental Plaque Only.
Plaque-induced gingival disease is the result of an interaction
between the microorganisms found in the dental plaque biofilm
and the tissues and inflammatory cells of the host.The plaque-host
PART 2 Classification and Epidemiology of Periodontal Diseases 36
BOX 4-2 Gingival Diseases
These diseases may occur on a periodontium with no attachment loss or
onaperiodontiumwithattachmentlossthatisstableandnotprogressing.
I.
Gingivitis associated with dental plaque only
A. Without local contributing factors
B. With local contributing factors (see Box 4-4)
II.
Gingival diseases modified by systemic factors
A. Associated with endocrine system
1. Puberty-associated gingivitis
2. Menstrual cycleassociated gingivitis
3. Pregnancy associated
a. Gingivitis
b. Pyogenic granuloma
4. Diabetes mellitusassociated gingivitis
B. Associated with blood dyscrasias
1. Leukemia-associated gingivitis
2. Other
III. Gingival diseases modified by medications
A. Drug-influenced gingival diseases
1. Drug-influenced gingival enlargements
2. Drug-influenced gingivitis
a. Oral contraceptiveassociated gingivitis
b. Other
IV. Gingival diseases modified by malnutrition
A. Ascorbic acid deficiency gingivitis
B. Other

I.

II.
Gingival diseases of specific bacterial origin
A. Neisseria gonorrhoeae
B. Treponema pallidum
C. Streptococcus species
D. Other
Gingival diseases of viral origin
A. Herpesvirus infections
III.
Gingival diseases of fungal origin
A. Candida species infections: generalized gingival candidiasis
B. Linear gingival erythema
C. Histoplasmosis
D. Other
IV. Gingival lesions of genetic origin
A. Hereditary gingival fibromatosis
B. Other
V.
Gingival manifestations of systemic conditions
A. Mucocutaneous lesions
1. Lichen planus
2. Pemphigoid
3. Pemphigus vulgaris
4. Erythema multiforme
5. Lupus erythematosus
6. Drug induced
7. Other
B. Allergic reactions
1. Dental restorative materials
a. Mercury
b. Nickel
c. Acrylic
d. Other
2. Reactions attributable to:
a. Toothpastes or dentifrices
b. Mouth rinses or mouthwashes
c. Chewing gum additives
d. Foods and additives
VI.

VII.
VIII.
3. Other
Traumatic lesions (factitious, iatrogenic, or accidental)
A. Chemical injury
B. Physical injury
C. Thermal injury
Foreign body reactions
Not otherwise specified
1. Primary herpetic gingivostomatitis
2. Recurrent oral herpes
3. Varicella zoster
B. Other
Data from Holmstrup P: Ann Periodontol 4:20, 1999; and Mariotti A: Ann Periodontol 4:7, 1999.

SCIENCE TRANSFER
and systemic diseases so that their diagnostic skills can give
significant benefit to their patients.
The most widely accepted classification of periodontal
diseases need to be routinely modified as new diagnostic
modalities are developed.In the future there will be an increased
utilization of genetic and biotech markets for more accurate
and objective diagnoses of periodontal pathology. One group
of diseases that are underrepresented in many classifications
are the benign and malignant tumors that affect periodontal
tissues.
Although plaque-induced gingivitis and periodontitis are the
most common diseases of the periodontium, there are many other
pathologic processes that are manifested in periodontal tissues.
Clinicians need to be cognizant that tissues of the oral cavity can
be subjected to a wide range of locally specific diseases and
deformities, as well as being an indicator of systemic pathologic
entities. Some diseases of the periodontium produce specific
diagnostic changes,and others modify the response to the dental
bacterial biofilms.These complexities require dentists to develop
a broad knowledge and understanding of a wide range of dental
37 CHAPTER 4 Classfication of Diseases and Conditions Affecting the Periodontium
Figure 4-4 A, Clinical image of pyogenic granuloma in 27-year-old pregnant female.B, Histologic image depicts dense inflammatory infiltrate and promi-
nent vessels.
B A
spongy gingival tissues caused by excessive infiltration of blood cells
(Figure 4-5).
Gingival Diseases Modified by Medications. Gingi-
val diseases modified by medications are increasingly prevalent
because of the increased use of drugs known to induce gingival
enlargement (e.g., anticonvulsant drugs such as phenytoin, immu-
nosuppressive drugs such as cyclosporine (Figure 4-6),and calcium
channel blockers such as nifedipine (Figure 4-7),verapamil,diltia-
zem, and sodium valproate.9,14,24 The development and severity of
gingival enlargement in response to medications are patient specific
and may be influenced by uncontrolled plaque accumulation,as well
as elevated hormonal levels.The increased use of oral contraceptives
by premenopausal women has been associated with a higher inci-
dence of gingival inflammation and development of gingival

A

B
Figure 4-3 Thirteen-year-old female with hormone exaggerated marginal
and papillary inflammation, with 1 to 4 mm probing depths yet minimal
clinical attachment loss. A, Facial view. B, Lingual view.
interaction can be altered by the effects of local factors, systemic
factors, medications, and malnutrition, all of which can influence
the severity and duration of the response. Local factors that may
contribute to gingivitis, in addition to plaque-retentive calculus
formation on crown and root surfaces (see Chapter 22). These
factors are contributory because of their ability to retain plaque
microorganisms and inhibit their removal by patient-initiated
plaque control techniques.
Gingival Diseases Modified by Systemic Factors.
Systemic factors contributing to gingivitis, such as the endocrine
changes associated with puberty (Figure 4-3), the menstrual cycle,
pregnancy (Figure 4-4, A), and diabetes, may be exacerbated
because of alterations in the gingival inflammatory response to
plaque.13,14,24This altered response appears to result from the effects
of systemic conditions on the hosts cellular and immunologic
functions. These changes are most apparent during pregnancy,
when the prevalence and severity of gingival inflammation may
increase, even in the presence of low levels of plaque. Blood dys-
crasias,such as leukemia,may alter immune function by disturbing
the normal balance of immunologically competent white blood
cells supplying the periodontium.Gingival enlargement and bleed-
ing are common findings and may be associated with swollen,

Figure 4-2 Maxillary second molar exhibits mild inflammation at mesial-
palatal surface.However,the clinical attachment loss has been stable for 15
years after apical positioned flap and periodontal maintenance. Diagnosis
is a history of moderate periodontitis, but the case is in remission.
Figure 4-6 Clinical images of 9-year-
old male with severe gingival overgrowth
secondary to heart transplant and cyclo-
sporine therapy.
C D
Figure 4-7 Clinical images of gingival over-
growth following use a of calcium channel
blocker to control hypertension.
A B
enlargement,which may be reversed by discontinuation of the oral
contraceptive.
Gingival Diseases Modified by Malnutrition. Gingi-
val diseases modified by malnutrition have received attention
because of clinical descriptions of bright red,swollen,and bleeding
gingiva associated with severe ascorbic acid (vitamin C) deficiency

Figure 4-5 Twelve-year-old female with a primary medical diagnosis of
leukemia that exhibits swollen/spongy gingiva.

A
or scurvy.14 Nutritional deficiencies are known to affect immune
function and may alter the hosts ability to protect itself against
some of the detrimental effects of cellular products such as oxygen
radicals. Unfortunately, little scientific evidence is available to
support a role for specific nutritional deficiencies in the develop-
ment or severity of gingival inflammation or periodontitis in
humans.
Oral manifestations of systemic conditions that produce lesions in
the tissues of the periodontium are rare.These effects are observed
more frequently in lower socioeconomic groups, developing coun-
tries, and immunocompromised individuals.10 Benign mucous
membrane pemphigoid is an example of a nonplaque-induced
lesion without socioeconomic implications. Sloughing gingival
tissues leave painful ulcerations of the gingiva (Figure 4-8, A and
B). Autoimmune antibodies are targeted at the basement mem-
brane and cleave it from the underlying connective tissue. (Figure
4-8, C and D).
Gingival Diseases of Specific Bacterial Origin.
Gingival diseases of specific bacterial origin are increasing in
prevalence, especially as a result of sexually transmitted diseases,
such as gonorrhea (Neisseria gonorrhoeae), and to a lesser degree,
syphilis (Treponema pallidum).26,29 Oral lesions may be secondary
to systemic infection or may occur through direct infection. Strep-
tococcal gingivitis or gingivostomatitis is a rare entity that may

B
Gingival Diseases of Fungal Origin. Gingival diseases
of fungal origin are relatively uncommon in immunocompetent
individuals but occur more frequently in immunocompromised
individuals and those with normal oral flora disturbed by the long-
term use of broad-spectrum antibiotics.10,29,30 The most common
oral fungal infection is candidiasis, caused by infection with
Candida albicans, which also can be seen under prosthetic devices,
in individuals using topical steroids, and in individuals with
decreased salivary flow, increased salivary glucose, or decreased
salivary pH. A generalized candidal infection may manifest as
white patches on the gingiva, tongue, or oral mucous membrane
that can be removed with gauze, leaving a red, bleeding surface. In
individuals infected with human immunodeficiency virus (HIV),
candidal infection may present as erythema of the attached gingiva
and has been referred to as lineargingivalerythemaorHIV-associated
gingivitis (see Chapter 19).
present as an acute condition with fever, malaise, and pain associ-
ated with acutely inflamed, diffuse, red, and swollen gingiva
with increased bleeding and occasional gingival abscess formation.
The gingival infections usually are preceded by tonsillitis and
have been associated with group A "-hemolytic streptococcal
infections.
Gingival Diseases of Viral Origin. Gingival diseases of
viral origin may be caused by a variety of deoxyribonucleic acid
(DNA) and ribonucleic acid (RNA) viruses, the most common
being the herpesviruses (Figure 4-9, A and B). Lesions are fre-
quently related to reactivation of latent viruses,especially as a result
of reduced immune function.The oral manifestations of viral infec-
tion have been comprehensively reviewed.10,28 Viral gingival dis-
eases are treated with topical and/or systemic antiviral drugs
(Figure 4-9, C and D).
Figure 4-8 Sixty-two year-old female with
benign mucous membrane pemphigoid. A and
B, Clinical image with sloughing epithelial surface.
C, Hematoxylin and eosin (H&E) stain depicting
separation of epithelium from connective tissue.
D, Immunofluorescent-labeled antibodies to base-
ment membrane.
B

D
A

C
Figure 4-9 A and B,Twenty-nine year-
old male with primary herpetic infection
and severe gingival inflammation. C and
D, Six weeks postsystemic acyclovir.
B

D
A

C
Diagnosis of candidal infection can be made by culture, smear,
and biopsy. Less common fungal infections have also been
described.29,30
Gingival Diseases of Genetic Origin. Gingival diseases
of genetic origin may involve the tissues of the periodontium and
have been described in detail.1 One of the most clinically evident
conditions is hereditary gingival fibromatosis, which exhibits auto-
somal dominant or (rarely) autosomal recessive modes of inheri-
tance. The gingival enlargement may completely cover the teeth,
delay eruption,and present as an isolated finding or may be associ-
ated with several more generalized syndromes.
Gingival Manifestations of Systemic Conditions.
Gingival manifestations of systemic conditions may appear as des-

A
B
Figure 4-11 Generalized severe allergic response of gingiva as a result of
additive in chewing gum.
Figure 4-12 Self-inflicted gingival dehiscence induced via patients
fingernail.
Figure 4-10 A, Localized pronounced
gingival inflammation secondary to nickel
allergy. B and C, Biopsy depicts dense infil-
trate of plasma cells.
quamative lesions, ulceration of the gingiva, or both.10,23,29 Allergic
reactions that manifest with gingival changes are uncommon but
have been observed in association with several restorative materials
(Figure 4-10, A), toothpastes, mouthwashes, chewing gum (Figure
4-11), and foods (see Box 4-2). The diagnosis of these conditions
may prove difficult and may require an extensive history and selec-
tive elimination of potential causes. Histologic traits of biopsies
from gingival allergic reactions include dense infiltrate of eosino-
philic cells (Figure 4-10, B and C).
Traumatic Lesions. Traumatic lesions may be self-inflicted
and factitious in origin, produced by intentional or unintentional
artificial means (Figure 4-12).Other examples of traumatic lesions
include toothbrush trauma resulting in gingival ulceration, reces-
sion, or both. Iatrogenic trauma (induced by the dentist or health

C
the periodontal ligament and alveolar bone with increased probing
depth formation, recession, or both.The clinical feature that dis-
tinguishes periodontitis from gingivitis is the presence of clinically
detectable attachment loss.This loss often is accompanied by peri-
odontal pocket formation and changes in the density and height
of subjacent alveolar bone.In some cases,recession of the marginal
gingiva may accompany attachment loss, thus masking ongoing
disease progression if only probing depth measurements are taken
without measurements of clinical attachment levels. Clinical signs
of inflammation,such as changes in color,contour,and consistency,
as well as bleeding on probing, may not always be positive indica-
tors of ongoing attachment loss. However, the presence of contin-
ued bleeding on probing at sequential visits has proved to be a
reliable indicator of the presence of inflammation and the potential
for subsequent attachment loss at the bleeding site.The attachment
loss associated with periodontitis has been shown to progress either
continuously or in episodic bursts of disease activity.
Although many classifications of the different clinical manifes-
tations of periodontitis have been presented over the past 20 years,
consensus workshops in North America in 19896 and Europe in
19934 identified that periodontitis may present in early-onset,
adult-onset, and necrotizing forms (Table 4-1). In addition, the
AAP consensus concluded that periodontitis may be associated
professional) to the gingiva can be caused by induction of orth-
odontic cement or preventive or restorative materials (Figure
4-13, A). Peripheral ossifying fibroma may develop in response to
embedment of a foreign body (Figure 4-13,B and C).Alternatively,
accidental damage to the gingiva may occur through minor burns
from hot foods and drinks.10
Foreign Body Reactions. Foreign body reactions lead to
localized inflammatory conditions of the gingiva and are caused by
the introduction of foreign material into the gingival connective
tissues through breaks in the epithelium.10 Common examples are
the introduction of amalgam into the gingiva during the placement
of a restoration, extraction of a tooth, or endodontic apicoectomy
with retrofill leaving an amalgam tattoo (Figure 4-14, A) with
resultant metal fragments observed in biopsies (Figure 4-14,B),or
the introduction of abrasives during polishing procedures.

PERIODONTITIS
Periodontitis is defined as an inflammatory disease of the support-
ing tissues of the teeth caused by specific microorganisms or groups
of specific microorganisms, resulting in progressive destruction of
Figure 4-13 A, Proliferative gingival over-
growth secondary to impaction of foreign body.
B, Histology of peripheral ossifying fibroma.
C, Higher magnification of image in B.D, Four
weeks postexcisional biopsy.
B

D
A

C
Figure 4-14 A, Gingival pigmentation associated with previous apicoectomy and amalgam retro-fill. B, Biopsy depicts metal fragments.
A
B
TABLE 4-1 Classification of the Various Forms of Periodontitis
Classification
AAP World Workshop in
Clinical Periodontics, 19895

European Workshop in
Periodontology, 19933

AAP International Workshop
for Classification of
Periodontal Diseases, 19992
Forms of Periodontitis
Adult periodontitis

Early-onset periodontitis (may be
prepubertal, juvenile, or rapidly
progressive)

Periodontitis associated with
systemic disease

Necrotizing ulcerative periodontitis

Refractory periodontitis
Adult periodontitis

Early-onset periodontitis

Necrotizing periodontitis
Chronic periodontitis
Aggressive periodontitis
Periodontitis as a manifestation of
Disease Characteristics
Age of onset >35 years
Slow rate of disease progression
No defects in host defenses
Age of onset <35 years
Rapid rate of disease progression
Defects in host defenses
Associated with specific microflora
Systemic diseases that predispose to rapid rates of
periodontitis
Diseases: diabetes, Down syndrome, HIV infection,
Papillon-Lefvre syndrome
Similar to acute necrotizing ulcerative gingivitis but with
associated clinical attachment loss
Recurrent periodontitis that does not respond to treatment
Age of onset: fourth decade of life
Slow rate of disease progression
No defects in host response
Age of onset: before fourth decade of life
Rapid rate of disease progression
Defects in host defense
Tissue necrosis with attachment and bone loss
See Box 4-3
systemic diseases
AAP, American Academy of Periodontology; HIV, human immunodeficiency virus.

with systemic conditions, such as diabetes and HIV infection, and
that some forms of periodontitis may be refractory to conventional
therapy. Early-onset disease was distinguished from adult-onset
disease by the age of onset (35 years of age was set as an arbitrary
separation of diseases), the rate of disease progression, and the
presence of alterations in host defenses. The early-onset diseases
were more aggressive,occurred in individuals younger than 35 years
of age, and were associated with defects in host defenses, whereas
adult forms of disease were slowly progressive, became clinically
more evident in the fourth decade of life, and were not associated
with defects in host defenses.In addition,early-onset periodontitis
was subclassified into prepubertal, juvenile, and rapidly progressive
forms with localized or generalized disease distributions.
Extensive clinical and basic scientific research of these disease
entities has been performed in many countries, and some disease
characteristics outlined 10 years ago no longer stand up to rigid
scientific scrutiny.7,13,31 In particular, supporting evidence was
lacking for the distinct classifications of adult periodontitis,refrac-
tory periodontitis, and the various different forms of early-onset
periodontitis as outlined by the AAP Workshop for the Interna-
tional Classification of Periodontal Diseases in 19993 (see
Table 4-1).
It has been observed that chronic periodontal destruction,
caused by the accumulation of local factors, such as plaque and
calculus, can occur before age 35 years and that the aggressive
disease seen in young patients may be independent of age but has
a familial (genetic) association. With respect to refractory peri-
odontitis, little evidence supports that this is indeed a distinct
clinical entity because the causes of continued loss of clinical
attachment and alveolar bone after periodontal therapy are cur-
rently poorly defined and apply to many disease entities. In
addition, the clinical and etiologic manifestations of the different
diseases outlined in North America in 1989 and in Europe in
1993 were not consistently observed in different countries around
the world and did not always fit the models presented. As a
result,the AAP held an International Workshop for the Classifica-
tion of Periodontal Diseases in 1999 to further refine the classifica-
tion system based on current clinical and scientific data.3 The
resulting classification of the different forms of periodontitis was
simplified to describe three general clinical manifestations of peri-
odontitis: chronic periodontitis, aggressive periodontitis, and peri-
odontitis as a manifestation of systemic diseases (see Table 4-1 and
Box 4-3).
Chronic periodontitis is the most common form of periodontitis7;
Box 4-3 includes the characteristics of this form of periodontitis.
Chronic periodontitis is most prevalent in adults but can be
observed in children; therefore the age range of older than 35 years
previously designated for the classification of this disease has been
discarded. Chronic periodontitis is associated with the accumula-
tion of plaque and calculus and generally has a slow-to-moderate
rate of disease progression, but periods of more rapid destruction
may be observed. Increases in the rate of disease progression may
be caused by the impact of local,systemic,or environmental factors
that may influence the normal host-bacteria interaction. Local
factors may influence plaque accumulation (Box 4-4); systemic
diseases,such as diabetes mellitus and HIV infection,may influence
BOX 4-3 Periodontitis
The disease periodontitis can be subclassified into the following three
major types based on clinical, radiographic, historical, and laboratory
characteristics.

The following characteristics are common to patients with chronic
periodontitis:
Prevalent in adults but can occur in children.
Amount of destruction consistent with local factors.
Associated with a variable microbial pattern.
Subgingival calculus frequently found.
Slow-to-moderate rate of progression with possible periods of rapid
progression.
Possibly modified by or associated with the following:
Systemic diseases such as diabetes mellitus and human
immunodeficiency virus (HIV) infection.
Local factors predisposing to periodontitis.
Environmental factors such as cigarette smoking and emotional
stress.
Chronic periodontitis may be further subclassified into localized and
generalized forms and characterized as slight, moderate, or severe based
on the common features described above and the following specific
features:
Localized form: <30% of sites involved.
Generalized form: >30% of sites involved.
Slight: 1 to 2 mm clinical attachment loss (CAL).
Moderate: 3 to 4 mm CAL.
Severe: !5 mm CAL.

The following characteristics are common to patients with aggressive
periodontitis:
Otherwise clinically healthy patient.
Rapid attachment loss and bone destruction.
Amount of microbial deposits inconsistent with disease severity.
Familial aggregation of diseased individuals.
The following characteristics are common but not universal:
Diseased sites infected with Actinobacillus actinomycetemcomitans.
Abnormalities in phagocyte function.
Hyperresponsive macrophages, producing increased prostaglandin
E2 (PGE2) and interleukin-1" (IL-1").
In some cases, self-arresting disease progression.
Aggressive periodontitis may be further classified into localized and
generalized forms based on the common features described here and the
following specific features:

Localized form
Circumpubertal onset of disease.
Localized first molar or incisor disease with proximal attachment
loss on at least two permanent teeth, one of which is a first molar.
Robust serum antibody response to infecting agents.

Generalized form
Usually affecting persons under 30 years of age (however, may be
older).
Generalized proximal attachment loss affecting at least three teeth
other than first molars and incisors.
Pronounced episodic nature of periodontal destruction.
Poor serum antibody response to infecting agents.

Periodontitis as a Manifestation of Systemic Diseases
Periodontitis may be observed as a manifestation of the following
systemic diseases:
1. Hematologic disorders
a. Acquired neutropenia
b. Leukemias
c. Other
2. Genetic disorders
a. Familial and cyclic neutropenia
b. Down syndrome
c. Leukocyte adhesion deficiency syndromes
d. Papillon-Lefvre syndrome
e. Chdiak-Higashi syndrome
f. Histiocytosis syndromes
g. Glycogen storage disease
h. Infantile genetic agranulocytosis
i. Cohen syndrome
j. Ehlers-Danlos syndrome (types IV and VIII autosomal dominant
[AD])
k. Hypophosphatasia
l. Other
3. Not otherwise specified
Data from Flemmig TF: Ann Periodontol 4:32, 1999; Kinane DF: Ann Periodontol 4:54, 1999; and Tonetti MS, Mombelli A: Ann Periodontol 4:39, 1999.
the host defenses, and environmental factors, such as cigarette
smoking and stress, also may influence the response of the host to
plaque accumulation. Chronic periodontitis may occur as a local-
ized disease in which less than 30% of evaluated sites demonstrate
attachment and bone loss, or it may occur as a more generalized
disease in which greater than 30% of sites are affected.The disease
also may be described by the severity of disease as slight:1 to 2 mm
(Figure 4-15), moderate: 3 to 4 mm (Figure 4-16), or severe:
!5 mm (Figure 4-17) based on the amount of clinical attachment
loss (see Box 4-3).
Aggressive periodontitis differs from the chronic form primarily by
(1) the rapid rate of disease progression seen in an otherwise
healthy individual (Figures 4-18 and 4-19),(2) an absence of large
accumulations of plaque and calculus, and (3) a family history of
aggressive disease suggestive of a genetic trait20,31 (see Box 4-3).
This form of periodontitis was previously classified as early-onset
periodontitis (see Table 4-1) and therefore still includes many of
the characteristics previously identified with the localized and gen-
eralized forms of early-onset periodontitis. Although the clinical
presentation of aggressive disease appears to be universal, the etio-
logic factors involved are not always consistent. Box 4-3 outlines
additional clinical, microbiologic, and immunologic characteristics
of aggressive disease that may be present. As was previously
described for early-onset disease, aggressive forms of periodontitis
usually affect young individuals at or shortly after puberty and may
be observed during the second and third decades of life (i.e., 10 to
BOX 4-4 Developmental or Acquired Deformities and Conditions
Localized Tooth-Related Factors That Modify or Predispose to
Plaque-Induced Gingival Diseases or Periodontitis
1. Tooth anatomic factors
2. Dental restorations or appliances
3. Root fractures
4. Cervical root resorption and cemental tears

Mucogingival Deformities and Conditions around Teeth
1. Gingival or soft tissue recession
a. Facial or lingual surfaces
b. Interproximal (papillary)
2. Lack of keratinized gingiva
3. Decreased vestibular depth
4. Aberrant frenum or muscle position
5. Gingival excess
a. Pseudopocket
b. Inconsistent gingival margin
Data from Blieden TM: Ann Periodontol 4:91, 1999; Halmon WW: Ann Periodontol 4:102, 1999; and Pini Prato GP: Ann Periodontol 4:98, 1999.
c. Excessive gingival display
d. Gingival enlargement (see Box 4-2)
e. Abnormal color

Mucogingival Deformities and Conditions on Edentulous Edges
1. Vertical and/or horizontal ridge deficiency
2. Lack of gingiva or keratinized tissue
3. Gingival or soft tissue enlargements
4. Aberrant frenum or muscle position
5. Decreased vestibular depth
6. Abnormal color

Occlusal Trauma
1. Primary occlusal trauma
2. Secondary occlusal trauma
A
B
Figure 4-15 A, Clinical image of plaque-related slight/early chronic periodontitis with 1 to 2 mm clinical attachment loss in 40-year-old female.
B, Radiographic images of the patient.
30yearsofage).Thediseasemaybelocalizedaspreviouslydescribed
for localized juvenile periodontitis (LJP) or generalized as previ-
ously described for generalized juvenile periodontitis (GJP) and
rapidly progressive periodontitis (RPP) (see Table 4-1). Box 4-3
provides the common features of the localized and generalized
forms of aggressive periodontitis.
Periodontitis as a Manifestation
of Systemic Diseases
Several hematologic and genetic disorders have been associated
with the development of periodontitis in affected individuals12,13
(see Box 4-3).The majority of these observations of effects on the
periodontium are the result of case reports,and few research studies
have been performed to investigate the exact nature of the effect
of the specific condition on the tissues of the periodontium. It is
speculated that the major effect of these disorders is through altera-
tions in host defense mechanisms that have been clearly described
for disorders,such as neutropenia and leukocyte adhesion deficien-
cies, but are less well understood for multifaceted syndromes. The
clinical manifestation of many of these disorders appears at an early
age and may be confused with aggressive forms of periodontitis
with rapid attachment loss and the potential for early tooth loss.
With the introduction of this form of periodontitis in this and
previous classification systems (see Table 4-1), the potential exists
B
Figure 4-16 A, Clinical image of plaque-related moderate chronic periodontitis with 3 to 4 mm clinical attachment loss in 53-year-old male smoker.
A
B
Figure 4-17 A, Clinical image of plaque-related severe/advanced chronic periodontitis with !5 mm clinical attachment loss in 47-year-old female.
A
for overlap and confusion between periodontitis as a manifestation
of systemic disease and both the aggressive and the chronic form
of disease when a systemic component is suspected. At present,
periodontitis as a manifestation of systemic disease is the diagnosis to
be used when the systemic condition is the major predisposing
factor and local factors, such as large quantities of plaque and
calculus, are not clearly evident. In the case in which periodontal
destruction is clearly the result of local factors but has been exac-
erbatedbytheonsetofsuchconditionsasdiabetesmellitus(Figures
4-20 and 4-21) or HIV infection, the diagnosis should be chronic
periodontitis modified by the systemic condition.
Sarcoidosis is a chronic disease expressed as a cell-mediated
delayed-type hypersensitivity that primarily affects the lungs,
lymph nodes, skin, eyes, liver, spleen, and small bones of the hands
and feet, etc.21 Sarcoidosis rarely affects the oral cavity, with inci-
dence of occurrence in descending order noted in the lymph nodes,
A
B
Figure 4-18 A, Clinical image of plaque-related aggressive moderate periodontitis with 1 to 7 mm PD and 3 to 4 mm clinical attachment loss in 31-year-
old male. B, Radiographic images of the patient.
A
B
Figure 4-19 A, Clinical image of plaque-related aggressive severe periodontitis with 3 to 13 mm PD and 7 to 15 mm clinical attachment loss in 32-year-
old male. B, Radiographic images of the patient.
NECROTIZING PERIODONTAL DISEASES
The clinical characteristics of necrotizing periodontal diseases may
include but are not limited to ulcerated and necrotic papillary and
marginal gingiva covered by a yellowish white or grayish slough or
pseudomembrane, blunting and cratering of papillae, bleeding on
provocation or spontaneous bleeding, pain, and fetid breath.These
diseases may be accompanied by fever,malaise,and lymphadenopa-
thy,although these characteristics are not consistent.Two forms of
necrotizing periodontal disease have been described: necrotizing
B
Figure 4-20 A, Clinical image of plaque-related severe aggressive periodontitis in 53-year-old male, smoker, with diabetes and hemoglobin A1c (HbA1c) =
10.7. B, Radiographic images of the patient.
A
Figure 4-21 Selective probing depths of same 53-year-old diabetic patient shown in Figure 4-20 with severe aggressive periodontitis.
B
C
D
A
lips,soft palate,buccal mucosa,gingiva,tongue,and bone.21 Figure
4-22 depicts the pretreatment pattern of bone loss and recession
associated with sarcoidosis, as well as pulmonary parenchymal
fibrous infiltrate noted in the lungs as depicted by a white lacy
pattern on the chest x-ray (Figure 4-22, C). Histologic features of
sarcoidosis include the presence of an intense chronic inflammatory
infiltrate with focal areas of noncaseating granulomas and a positive
Kveim test2 (Figure 4-23, C). Remineralization of alveolar bone is
noted on radiographs obtained 1-year after systemic administration
of steroids (Prednisone)18 (Figure 4-23, A).
Figure 4-22 Sarcoidosis pretreatment. A, Intraoral x-rays depict more extensive bone loss for anterior teeth than clinical attachment loss. B, Extensive
recession plus clinical attachment loss. C, Pulmonary parenchymal fibrous infiltrate.
A
B C
Figure 4-23 Sarcoidosis after treatment with prednisone. A, Intraoral x-rays depict remineralization of bone. B, Reduction in gingival inflammation while
extensive recession and clinical attachment loss persist. C, Pretreatment biopsy.
C
B
A
ulcerative gingivitis (NUG) (Figure 4-24) and necrotizing ulcerative
periodontitis (NUP) (Figure 4-25). NUG has been previously clas-
sified under gingival diseases or gingivitis because clinical
attachment loss is not a consistent feature, whereas NUP has been
classified as a form of periodontitis because attachment loss is
present. Recent reviews of the etiologic and clinical characteristics
of NUG and NUP have suggested that the two diseases represent
clinical manifestations of the same disease, except that distinct
features of NUP are clinical attachment and bone loss. As a result,
both NUG and NUP have been determined as a separate group of
diseases that have tissue necrosis as a primary clinical feature (see
Box 4-1).
Necrotizing Ulcerative Gingivitis
The clinical and etiologic characteristics of NUG27 are described in
detail in Chapter 10. The defining characteristics of NUG are its
bacterial etiology, its necrotic lesion, and predisposing factors such
as psychologic stress, smoking, and immunosuppression. In addi-
tion,malnutrition may be a contributing factor in developing coun-
tries. NUG is usually seen as an acute lesion that responds well to
A

B
Figure 4-24 A, Ulcerative gingivitis illustrating sloughing of marginal
gingiva. B, Phase-contrast microscopy reveals spirochetes in subgingival
plaque sample.

A

B
Figure 4-25 A, Necrotizing ulcerative periodontitis with severe clinical
attachment loss in 28-year-old male infected with human immunodefi-
ciency virus (HIV). B, Spirochetes noted on surface of sloughed epithelial
cells.

antimicrobial therapy combined with professional plaque and cal-
culus removal and improved oral hygiene.
Necrotizing Ulcerative Periodontitis
NUP differs from NUG in that loss of clinical attachment and
alveolar bone is a consistent feature.19 All other characteristics
appear to be the same between the two forms of necrotizing disease.
The characteristics of NUP are described in detail in Chapter 17.
NUP may be observed among patients with HIV infection and
manifests as local ulceration and necrosis of gingival tissue with
exposure and rapid destruction of underlying bone, spontaneous
bleeding, and severe pain. HIV-infected patients with NUP are
20.8 times more likely to have CD4+ cell counts below 200 cells/
mm3 of peripheral blood than HIV-infected patients without NUP,
suggesting that immunosuppression is a major contributing factor.
In addition,the predictive value of NUP for HIV-infected patients
with CD4+ cell counts below 200 cells/mm3 was 95.1%, and the
cumulative probability of death within 24 months of a NUP diag-
nosis in HIV-infected individuals was 72.9%. In developing coun-
tries,NUP also has been associated with severe malnutrition,which
may lead to immunosuppression in some patients.

ABSCESSES OF THE PERIODONTIUM
A periodontal abscess is a localized purulent infection of periodon-
tal tissues and is classified by its tissue of origin.16 The clinical,
microbiologic, immunologic, and predisposing characteristics are
discussed in Chapters 5 and 23.

PERIODONTITIS ASSOCIATED WITH
ENDODONTIC LESIONS
Classification of lesions affecting the periodontium and pulp is
based on the sequence of the disease process.
EndodonticPeriodontal Lesions
In endodonticperiodontal lesions, pulpal necrosis precedes peri-
odontal changes.A periapical lesion originating in pulpal infection
and necrosis may drain to the oral cavity through the periodontal
ligament, resulting in destruction of the periodontal ligament and
adjacent alveolar bone. This may present clinically as a localized,
deep,periodontal probing depth extending to the apex of the tooth
(Figure 4-26,A).A resultant extensive alveolar ridge defect (Figure
4-26,B and C) may necessitate reconstructive surgery (Figure 4-26,
D) before placement of implants and prosthesis (Figure 4-27) to
reestablish a functional and esthetic outcome.Pulpal infection also
may drain through accessory canals, especially in the area of the
furcation,and may lead to furcal involvement through loss of clini-
cal attachment and alveolar bone.
PeriodontalEndodontic Lesions
In periodontalendodontic lesions, bacterial infection from a
periodontal pocket associated with loss of attachment and root
exposure may spread through accessory canals to the pulp,resulting
in pulpal necrosis. In the case of advanced periodontal disease,
the infection may reach the pulp through the apical foramen.
Scaling and root planing removes cementum and underlying dentin
and may lead to chronic pulpitis through bacterial penetration of
dentinal tubules. However, many periodontitis-affected teeth that
have been scaled and root planed show no evidence of pulpal
involvement.
Combined Lesions
Combined lesions occur when pulpal necrosis and a periapical
lesion occur on a tooth that is also periodontally involved. An
angular intrabony defect that communicates with a periapical
lesionofpulpaloriginresultsinacombinedperiodontal-endodontic
lesion.
In all cases of periodontitis associated with endodontic lesions,
the endodontic infection should be controlled before beginning
definitive management of the periodontal lesion, especially when
regenerative or bone-grafting techniques are planned.
Figure 4-27 Same patient depicted in Figure 4-26. A and B, CT scan of regenerated ridge with implants placed in area 7, 9, and 10. C and D, Clinical
image of implant-supported bridge.
B
C D
A
Figure 4-26 A and C, Clinical image of extensive loss of alveolar ridge secondary to periapical endodontic lesion. B, CT scan depicts alveolar bone loss.
D, CT image of regenerated ridge via allogenic bone graft, tenting screw and membrane.
C
B
D
A
DEVELOPMENTAL OR ACQUIRED
DEFORMITIES AND CONDITIONS
Localized Tooth-Related Factors That Modify
or Predispose to Plaque-Induced Gingival
Diseases or Periodontitis
In general, these localized tooth-related factors contribute to the
initiation and progression of periodontal disease through an
enhancement of plaque accumulation or the prevention of effective
plaque removal by normal oral hygiene measures.5These factors fall
into four subgroups as outlined in Box 4-4.
Tooth Anatomic Factors. Tooth anatomic factors are asso-
ciated with malformations of tooth development or tooth location.
Anatomic factors, such as cervical enamel projections and enamel
pearls,have been associated with clinical attachment loss,especially
in furcation areas. Cervical enamel projections are found on 15%
to 24% of mandibular molars and 9% to 25% of maxillary molars,
and strong associations have been observed with furcation involve-
ment.15 Palatogingival grooves, found primarily on maxillary inci-
sors, are observed in 8.5% of individuals and are associated with
increased plaque accumulation, clinical attachment, and bone loss.
Proximal root grooves on incisors and maxillary premolars also
Figure 4-28 A and B, Clinical image of fistula tract. C, Root fracture. D, Resultant alveolar ridge defect.
D C
predispose to plaque accumulation,inflammation,and loss of clini-
cal attachment and bone.
Tooth location is considered important in the initiation and
development of disease.Malaligned teeth predispose individuals to
plaque accumulation with resultant inflammation in children and
may predispose to clinical attachment loss in adults, especially
when associated with poor oral hygiene habits. In addition, open
contacts have been associated with increased loss of alveolar bone,
most probably through food impaction.11
Dental Restorations or Appliances. Dental restorations
or appliances are frequently associated with the development of
gingival inflammation, especially when they are located subgingi-
vally.This may apply to subgingivally placed onlays,crowns,fillings,
and orthodontic bands. Restorations may impinge on the biologic
width by being placed deep in the sulcus or within the junctional
epithelium. This may promote inflammation and loss of clinical
attachment and bone, with apical migration of the junctional epi-
thelium and reestablishment of the attachment apparatus at a more
apical level.
Root Fractures. Root fractures caused by traumatic forces,
restorative or endodontic procedures (Figure 4-28, A to C) may
lead to periodontal involvement through an apical migration of
plaque along the fracture when the fracture originates coronal to
the clinical attachment and is exposed to the oral environment with
resultant alveolar ridge defect (Figure 4-28, D).
Cervical Root Resorption and Cemental Tears.
Cervical root resorption, as noted on the computed tomography
(CT) scans in Figure 4-29, A and B, and cemental tears may lead
to periodontal destruction when the lesion communicates with the
oral cavity and allows bacteria to migrate subgingivally. Avulsed

A
teeth that are re-implants frequently develop ankylosis and cervical
resorption many years after re-implantation. Atraumatic removal
of such ankylosed teeth and reconstruction of resultant ridge
defects with bone grafts, dental implants, and prostheses are viable
solutions for such defects (Figure 4-30).
Mucogingival Deformities and Conditions
around Teeth
Mucogingivaldeformity is a generic term used to describe the muco-
gingival junction and its relationship to the gingiva (Figure 4-31),
alveolar mucosa, and frenula muscle attachments. A mucogingival
deformity is a significant departure from the normal shape of
gingiva and alveolar mucosa and may involve the underlying alveo-
lar bone. Mucogingival surgery corrects defects in the morphology,
position, and/or amount of gingiva and is described in detail in
Chapter 63. The surgical correction of mucogingival deformities
may be performed for esthetic reasons, to enhance function, or to
facilitate oral hygiene.22
Mucogingival Deformities and Conditions
of Edentulous Ridges
Mucogingival deformities such as lack of stable keratinized gingiva
between the vestibular fornices and the floor of the mouth (Figure
4-32, A) may require soft tissue grafting and vestibular deepening
before prosthodontic reconstruction (Figure 4-32,B to D).Alveolar
bone defects in edentulous ridges (Figure 4-33, A and B) usually
require corrective surgery (Figure 4-33, C and D) to restore form
and function before placement of implants and prosthesis to replace
missing teeth (Figure 4-34).22
Occlusal Trauma
The etiology of trauma from occlusion and its effects on the peri-
odontium8 is discussed in detail in Chapters 20 and 49.

B
Figure 4-30 A, Posttreatment clinical image of same patient depicted in Figure 4-29 with implant-supported crowns and veneers on laterals. B and C, CT
scan of bone grafts and implants replacing central incisors lost as the result of severe cervical root resorption.
A
B C
B A
C

D
Figure 4-29 A and B, CT scan reveals severe cervical root resorption of maxillary central incisors and periapical abscess. C, Crowns fractured because of
resorption. D, Biopsy of soft tissue from resorption.
B
Figure 4-31 A, Mucogingival defect depicted by recession. B, Defects
extend into alveolar mucosa and lacks keratinized gingiva.
A
Figure 4-32 A, Mucogingival ridge defect from floor of mouth to vestibular fornix. B, Partial thickness flap with vestibular deepening. C, Placement of
free gingival graft. D, Reestablishment of vestibular depth and keratinized attached gingiva.
C
B
D
A
C B A
Figure 4-34 A, Clinical image of ridge 6 months after grafting. B, Placement of implants in area of teeth #23 and 25. C, Porcelain fused to metal (PFM)
crowns for maxillary incisors and implant-supported bridge from teeth #23 to #25.

References can be found on the companion
website at www.expertconsult.com.
B

D
A

C

Figure 4-33 A, Clinical image of edentulous
ridge defect. B, Pretreatment CT image of
defect. C, Reconstructed ridge using ramus
block graft. D, CT scan of grafted site.

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