Está en la página 1de 84

IMMUNOPATHOLOGY

OF ORAL DISEASES
BY
DR. FAMUREWA B.A.

OUTLINE
Introduction
Review of basic Immunology
Oral cavity and immune system
Immunopathology of common oral lesions
Conclusion
8/2/2012

FAMUREWA B.A. BChD

Introduction

Immunology is both the study of the


immune system and the field that treats
diseases of the immune system.
Immunity is the body's ability to resist a
disease, and the immune system is a body
wide network of interacting systems: bone
marrow, white blood cells, the entire
lymph system and even mucosal surfaces
8/2/2012

FAMUREWA B.A. BChD

NORMAL IMMUNE SYSTEM


The immune system function is to recognise

potentially infectious microbial agents (viruses,


bacteria, fungi, protozoa, and parasites as foreign
and to eliminate them from the body.
An immune response involves two functional

systems:
1. The innate system, or first line of defense.
2.

The acquired or adaptive system, the specific


response.
8/2/2012

FAMUREWA B.A. BChD

Innate versus acquired immunity


Innate immunity

Acquired immunity

Inborn

Adaptive

non-specific: Body

Derived during life

responds

Specific

the same way to all


antigens
Involves phagocytes

Involves prior sensitization


Depends on gene
rearrangements

Natural killer cells

Clonal expansion important

involved

Constantly evolves

Includes chemicals such

Basis of vaccination

as

May be active or passive

8/2/2012

B.A. BChDetc.
lysozyme, FAMUREWA
lactoferrin

IMMUNE SYSTEM

The major constituents of innate immunity are


o The cellular components, represented by
Phagocytes.
Natural killer (NK)cells.
o The molecular component includes the
complement cascade.
Cytokines.

8/2/2012

FAMUREWA B.A. BChD

Complement system
Complement system is a biochemical cascade
that attacks the surfaces of foreign cells.
It contains at least 20 different proteins and is

named for its ability to complement the


killing of pathogens by antibodies.
Complement is the major humoral component

of the innate immune response


8/2/2012

FAMUREWA B.A. BChD

Complement system
Pathway of complement activation:
Classical pathway

Alternate pathway

Mannan-binding lectin pathway


Classical pathway by antigen-antibody immune

complexes, apoptotic cells, C-reactive protein bound


to ligand and certain viruses and bacteria.

Alternative pathway by bacterial endotoxin, fungal cell

walls, viruses and tumour cells.


From Clinical immunology in Kumar & Clark

8/2/2012

FAMUREWA B.A. BChD

IMMUNE SYSTEM

8/2/2012

FAMUREWA B.A. BChD

IMMUNE SYSTEM
The adaptive immune system consists of:
Cellular immunity (lymphocytes and their products).
Humoral immunity (Antibodies).

8/2/2012

FAMUREWA B.A. BChD

10

8/2/2012

FAMUREWA B.A. BChD

11

Immune cells

These are cells involved in preventing or


combating invasion by foreign agents (biotic
and abiotic) as well as maintaining growth
cycle homeostasis by destruction of neoplastic
cells. They may be classified as:
antigen presenting cells (APCs) and
immune effector cells

8/2/2012

FAMUREWA B.A. BChD

12

Antigen presenting Cells


These degrade foreign bodies and microbes
into readily identifiable particles and present
them for recognition by immune effector
cells.
They include:
Dendritic cells
Langerhans cells
Macrophages
8/2/2012

FAMUREWA B.A. BChD

13

8/2/2012

FAMUREWA B.A. BChD

14

IMMUNE EFFECTOR
CELLS
B-lymphocytes

& plasma cells

T-lymphocytes
Natural

killer cells

It is noteworthy that immunity is a specific response to


foreign agents (biotic and abiotic) in contrast to inflammation
which is a non-specific response of vascularised tissue to
injury.
8/2/2012

FAMUREWA B.A. BChD

15

T-lymphocytes
Mediate cellular immunity.
60-70% of circulating peripheral lymphocytes.
Thymus-derived. Found in paracortex of lymph

node, periarteriolar sheath in spleen.

Recognize cell-bound antigen using T-cell receptors,

TCR.

Divided into:

CD4- helper cells


8/2/2012

CD8- killer cells

FAMUREWA B.A. BChD

16

Natural killer cells

10-15% of peripheral lymphocytes

Bear neither TCR nor immunoglobulins


Large, with azurophilic granules
Innate ability to lyse:

Tumour cells
Virus-infected cells
Some normal cells
8/2/2012

NB

FAMUREWA B.A. BChD

without prior

17

8/2/2012

FAMUREWA B.A. BChD

18

B-lymphocytes & plasma


cells
10-20% of circulating peripheral
lymphocytes
Present in bone marrow, peripheral

lymphoid tissues and extralymphatic


organs
B-cell receptor IgM
Form plasma cells upon antigenic

stimulation (clonal expansion)


8/2/2012

FAMUREWA B.A. BChD

19

Immunological memory
When B cells and T cells are activated and begin to

replicate, some of their offspring will become longlived memory cells.

Throughout the lifetime of an individual, these

memory cells will remember each specific pathogen


encountered and can mount a strong response if the
pathogen is detected again.

This is "adaptive" because it occurs during the

lifetime of an individual as an adaptation to infection


with that pathogen and prepares the immune system
for future challenges.

Immunological memory can either be in the form of

passive
short-term
memory or active long-term
8/2/2012
FAMUREWA B.A. BChD

20

IMMUNOGLOBULINS
Immunoglobulins, or antibodies, are a
complex, heterogeneous mixture of
proteins that exhibit two fundamental
types of structural variation.
Subtle structural differences in their
antigen combining sites, or
variable regions, account for their
unique antigen binding specificities.
Structural differences outside their
antigen combining sites, in the socalled constant regions, correlate with
the different effector functions
mediated by antibodies.
8/2/2012

FAMUREWA B.A. BChD

21

Five major classes


:
IgG

IgA
IgD
IgE
IgM

unique heavy chain isotype:


(IgA), (IgD), (IgE), (IgG), or (IgM).

H chains associate with light chains

of two isotypes - and . Thus, the


basic H2L2 of an antibody can be
specified in terms of its H and L
8/2/2012

FAMUREWA B.A. BChD

22

FUNCTIONS OF
IMMUNOGLOBULINS

Antigen binding

Immunoglobulins bind specifically to one or a few


closely related antigens.
Binds to a specific antigenic determinant. The
valency of all antibodies is at least two and in some
instances more.

Effector Functions

Usually requires that the antibody bind to its


antigen.

1. Fixation of complement
2. Binding to various cell
types

8/2/2012

FAMUREWA B.A. BChD

23

Fab

Fc
8/2/2012

FAMUREWA B.A. BChD

24

IgG
Most versatile immunoglobulin because it is
capable of carrying out all of the functions of
immunoglobulin molecules.
IgG is the major Ig in serum - 75% of serum Ig
is IgG
IgG is the major Ig in extra vascular spaces
Placental transfer
Fixes complement
Binding to cells.
Opsonisation: The antibody has prepared the
antigen for eating by the phagocytic cells.
Binding of IgG to Fc receptors on other types of
8/2/2012

FAMUREWA B.A. BChD

25

IgM

Pentamer
Third most common serum Ig.
First Ig to be made by the fetus & by a

virgin B cell when stimulated by


antigen.
Complement fixing. Very efficient in

lysis of microorganisms.
As a consequence of its structure, IgM

is also a good agglutinating Ig.


8/2/2012

FAMUREWA B.A. BChD

26

IgA

2nd most common serum Ig.


Serum IgA is a monomer but IgA found in

secretions is a dimer with an associated J chain.

Secretory or T piece in secretory IgA; helps IgA to

be transported across mucosa and also protects it


from degradation.

Major class of Ig in secretions - tears, saliva,

colostrum, mucus. Important in local (mucosal)


immunity.

Normally IgA does not fix complement, unless


8/2/2012
aggregated.

FAMUREWA B.A. BChD

27

IgE
Very low concentration in serum
Membrane bound to mast cells & basophils
Antiparasitic in function
Important in type hypersensitivity(allergic or
atopic) diseases.

8/2/2012

FAMUREWA B.A. BChD

28

IgD
Low serum level
Function uncertain.
Present on B lymphocytes
Levels are high in B cell activation seen in SLE,
HIV infection and Hodgkins disease.

8/2/2012

FAMUREWA B.A. BChD

29

Host Defence In Oral Mucosa


A mechanical barrier to oral microorganisms.
The continuous shedding by exfoliation of epithelial

squames.
Membrane-coating granules discharged
extracellularly in the granular layer.
Transudation of antibody through the mucosa.
Intraepithelial dendritic Langerhans cells (APC)
process antigen.
Oral epithelial cells produce a range of cytokines
including IL-I , IL-6, TNF-alpha, GM-CSF, TGF-beta
and IL-8
8/2/2012

FAMUREWA B.A. BChD

30

Antimicrobial Properties of Saliva


Antimicrobial
agent

Activity

Secretory IgA (also s-IgG,


s-IgM)

Inhibits adherence. Agglutinates bacteria.


Virus neutralisation. IgA is the major
antibody in saliva

Lactoferrin

Iron-binding. Bacteriostatic.

Lysozyme

Effective against S. mutans

Agglutinins

Glycoproteins, mucins, fibronectin,


2-microglobulin, histatins, proline-rich
proteins

Myeloperoxidase system

Bactericidal in presence of
thiocyanate/halide-H202.

Salivary peroxidase
system

Enzyme-thioycyanate-H202

Complement (trace
amounts)

C3 probably largely derived from


gingival crevice fluid.

8/2/2012

Leukocytes

FAMUREWA B.A. BChD

>98% are neutrophils, but up to 50%

31

Host defence in Gingival Crevice


There is a continuous movement of neutrophils

from gingival capillaries into the gingival sulcus .


Circulating blood leukocytes accumulate in the

gingival tissues in response to dental plaque.

8/2/2012

FAMUREWA B.A. BChD

32

ORAL SOURCES OF Igs

Gingival crevicular fluid-

composition similar to that of blood serum


essentially IgG, no sIgA
Saliva-

Composition= crevicular transudate+ secretions of


gingival plasma cells
sIgA present. Most predominant Ig in whole saliva.
*IgE and IgM also present in whole saliva

8/2/2012

FAMUREWA B.A. BChD

33

Immunopathology
Branch of immunology that deals with
pathologies of the immune system.
Defect or malfunction in innate and or adaptive
immune response can initiate disease process.

8/2/2012

FAMUREWA B.A. BChD

34

Immunopathology
3 aspects:
Immonodeficiency
Hypersensitivity reactions
Autoimmunity
Hypersensitivity and autoimmune disorders are
hyperactive immune disorders.

8/2/2012

FAMUREWA B.A. BChD

35

Immunity- A two-edged
sword
Immune system

Immunodeficien
cy

Hyperactive immune
system

allergy
Infection
s

8/2/2012

Bacterial
Fungal
Viral

Neoplasia
Pemphigu
s
pemphigoi
FAMUREWA B.A. BChD

d
Erythema
multiforme
etc

autoimmunit
y

36

Immunodeficiency
Could be primary(congenital) or secondary.
1 immunodeficiency- intrinsic failure of
development of one/ more component of the
immune system. This can involve :
Phagocytes
Complements
B cells
T cells
Combined T & B cells
8/2/2012

FAMUREWA B.A. BChD

37

C) Phagocyte
disorders:

Clinical features: Affected individuals are prone to infections with low-grade


bacteria such as Staphylococcus aureus and gram-negative enteric bacteria.
Phagocyte Disorders in Children

Disorder

Inheritance

Clinical Features

Therapy

1) Chronic
granulomatous
disease

X-linked
(66%);
autosomal re
cessive (33%)

Infections with catalase-positive


bacteria and fungi affecting skin,
lungs, liver; granuloma formation;
NBT test is screening test

Antibiotics;
-interferon

2)Myeloperoxida Autosomal
se deficiency
Recessive

Fungal infections (candidiasis) in


Antibiotics
deep tissues, especially in presence of
diabetes

3)Leukocyte
adhesion
deficiency

Delayed separation of the umbilical


cord; skin infections; otitis media;
pneumonia; gingivitis; periodontitis

Antibiotics

Recurrent skin infections with


staphylococci. enteric bacteria,
Neuropathy, Occulo cultaneous
albinism in chediak higashi

Antibiotics

Autosomal
recessive

4)Abnormal
Variable
chemotaxis
-Hyper IgE
-chediak-Higashi
8/2/2012

FAMUREWA B.A. BChD

38

38

(D) Complement disorders


1. Deficiency of early complement components (C1, C4,
C2) results in a symptom complex resembling collagen
vascular disorders (e.g., systemic lupus erythematosus
(SLE)] and increased susceptibility to pyogenic infections.
2. C3 deficiency results in severe pyogenic infections.
Several patients have also had SLE and glomerulonephritis.
3. Deficiency of late complement components (C5, C6, C7,
C8) results in systemic Neisseria infections such as
meningococcal sepsis and meningitis, and disseminated
gonococcal infections.
4. Abnormalities of the control proteins of the alternative
pathway (factor H, factor I, properdin) may result in
recurrent infections.
5. Deficiency of complement inhibitors (C1 esterase
inhibitor, carboxypeptidase N) leads to recurrent
angioedema.
39
8/2/2012

FAMUREWA B.A. BChD

39

B-Cell Deficiency Disorders


Disorder

Clinical Features

Therapy

1- X-linked agammaglobu- Recurrent pyogenic infections;


linemia (Bruton disease)
infections of lungs, sinuses, middle
ear, skin, central nervous system

Immune serum
globulin; antibiotics

2-Transient hypogammaRecurrent pyogenic infections;


globulinemia of infancy (1st frequent in families with other
3 years of life)
immunodeficiencies

Antibiotics; immune
serum globulin
(selected patients)

3-Selective immunoglobulin deficiency


(IgA, IgM, IgG sub
classes)

Recurrent infections of lungs,


sinuses; gastrointestinal disease;
allergy; frequent in families with
common variable
immunodeficiencies

Antibiotics; immune
serum globulin (IgG
subclass deficiencies
only)

4-Immunoglobulin defi
ciency with increased IgM
(and IgD)

Infections of lungs, sinuses, middle


ear; increased frequency of
autoimmune disease Ectodermal
displasea

Immune serum
globulin; antibiotics

5-Common variable
immunodeficiency

Infections of lungs, sinuses, middle


ear; giardiasis; malabsorption;
autoimmune disease

Immune serum
globulin; antibiotics

8/2/2012

FAMUREWA B.A. BChD

40

40

T-Cell and Combined Deficiency


Disorder

Clinical Features

Therapy

*Severe combined immuno


deficiency
* Nezelof syndrome

Recurrent infections; wasting; chronic diarrhea; failure


to thrive: graft versus host disease, anemia, Alopecia

Bone marrow transplantation


Antibiotics and IV Ig

Defects of the purine sal


vage pathway
-Adenosine deaminase
deficiency
-Purine nucleoside
phosphorylase deficiency

Recurrent infections; dysostosis (adenosine deaminase


deficiency); anemia and mental retardation
(purinenucleoside phosphorylase deficiency)
Rib and Scapula abnormality in ADA

Bone marrow transplan


tation; enzyme
replacement therapy

*DiGeorge anomaly (third


and fourth pouch/arch
syndrome)

Hypoparathyroidism (hypocalcemia); facial


abnormalities; cardio vascular abnormalities; infections;
mental deficiency (some patients); gastrointestinal tract
malformation (some patients).

Thymus graft or thymosin


therapy)

*Chronic mucocutaneous
candidiasis

Chronic candidal infection of the skin, nails, scalp, and


mucous membranes; autoimmune endocrine disorders
Intestinal malabsorption recurrent infections

Topical and systemic


antifungal agents; transfer
factor; thymus transplantation

*Ataxia-telangiectasia

Oculocutaneous telangictasia; progressive cerebellar


ataxia; bronchiectasis, malignancy; defective
chromosomal repair; raised a-fetoprotein

Bone marrow transplantation

*Wiskott-Aldrich syndrome

Eczema; thrombocytopenia; susceptibility to


infections; malignancy; small, defective platelets

Bone marrow transplantation;


antibiotics; splenectomy

*Short-limbed dwarfism
Caltilage hair hypoplasia

Short-limbed dwarfism; lymphopenia

Immune serum globulin


IV Ig, Antibotics

8/2/2012

FAMUREWA B.A. BChD

41

41

Secondary
immunodeficiency
Modification or suppression of immune system
components by exogenous factors. These are:
Infection
Malignancy
Malnutrition
Drug
Trauma
Ageing -thymus deterioration no new T
cells also affects antibody production.
8/2/2012

FAMUREWA B.A. BChD

42

Secondary
immunodeficiency
Infections
Bacterial e.g. Mycobacterium leprae
Tuberculoid leprosy: antibody deficiency
Lepromatous leprosy: severe T-cell deficiency
Viral
Measles transient suppression of NK, T & B cells
Herpes (Epstein Barr, HSV,cytomegalovirus)
Influenza
HIV
8/2/2012

FAMUREWA B.A. BChD

43

Secondary
immunodeficiency
Malignancy
Immunodeficiency caused by lymphoid tumours
e.g
leukaemia, lymphoma, plasma cell dyscrasias
Hodgkins lymphoma: causes classic example
of
T-cell deficiency
Chronic lymphocytic leukaemia: causes classic
example of B-cell deficiency.
8/2/2012

FAMUREWA B.A. BChD

44

Secondary
immunodeficiency
Drugs

Cytotoxic drugs
e.g. azathioprine and cyclophosphamide kill
tumour cells but also lymphocytes
Corticosteroids
Down regulate lymphocytic genes
Mimic action of glucocorticoids

8/2/2012

FAMUREWA B.A. BChD

45

Secondary
immunodeficiency
Trauma
Glucocorticoids released naturally in response
to burns,surgery and any other stressor
induce
Immunodeficiency.
Systemic diseases like diabetis mellitus,

nephrotic syndrome

8/2/2012

FAMUREWA B.A. BChD

46

Secondary
immunodeficiency
Malnutrition
Most common cause of 2 immune deficiency
Protein-Calorie malnutrition can lead to
abnormalities of T cells, B cells & phagocytes
Atrophic and fibrotic thymus
Reduced lymphocyte proliferation in response
to antigens.

8/2/2012

FAMUREWA B.A. BChD

47

HYPERSENSITIVITY REACTION
A state of altered reactivity in which the body reacts
with an exaggerated immune response to what is
perceived as a foreign substance (exogenous
allergen) or an endogenous antigen.

8/2/2012

FAMUREWA B.A. BChD

48

REACTION
Type

Prototype Immune
Disorder
Mechanis
ms

Pathologi
c Lesions

Immediate (type
I)
hypersensitivity

Anaphylaxis;
allergies;
bronchial asthma
(atopic forms)

Production of IgE
antibody immediate
release of
vasoactive
amines and other
mediators from
mast cells;
recruitment of
inflammatory
cells (late-phase
reaction

Vascular dilation,
edema,
smooth muscle
contraction,
mucus
production,
inflammation

Antibodymediated (type II)


hypersensitivity

Autoimmune
hemolytic
anemia;
Goodpasture
FAMUREWA B.A. BChD
syndrome

Production of IgG,
IgM - binds to
antigen on target
cell or tissue phagocytosis or

Cell lysis;
inflammation

8/2/2012

49

HYPERSENSITIVITY REACTION
Type

Prototype Immune
Patholo
Disorder
Mechanisms gic
Lesions

Immune complexmediated
(type III)
hypersensitivity

Systemic lupus
erythematosus;
some forms of
glomerulonephriti
s; serum
sickness; Arthus
reaction

Deposition of antigenantibody complexes complement


activation
- recruitment of
leukocytes by
complement products
and Fc receptors release of enzymes
and other toxic
molecules

Necrotizing
vasculitis
(fibrinoid
necrosis);
inflammation

Cell-mediated
(type IV)
hypersensitivity

Contact
dermatitis;
multiple sclerosis;
type I, diabetes;
FAMUREWA B.A. BChD
transplant

Activated T
lymphocytes - release
of cytokines and
macrophage
activation; T cell-

Perivascular
cellular
infiltrates;
edema; cell
50
destruction;

8/2/2012

Autoimmune diseases
Involve the loss of normal immune homeostasis
such as that body produces an abnormal
response to its own tissues
Presence of self-reactive T cells, autoantibodies
and inflammation.
Examples Celiac disease, Graves disease,
Addisons disease.
Failure of tolerance or incomplete tolerance
results in autoimmune diseases
8/2/2012

FAMUREWA B.A. BChD

51

Autoimmune
diseases
Clinical features
1.Commoner in females
2.Onset is middle age(>45years)
3.Family history is frequently positive
4.Raised level of Ig autoantibodies
5.Circulating antibody is frequently detectable in
unaffected family members

8/2/2012

FAMUREWA B.A. BChD

52

Autoimmune diseases
Clinical features:
6.Presence of circulating autoantibodies to several
tissues
7.Increase risk of other autoimmune diseases
8.Immunoglobulin complement is often detectable
9.Immunosupressive treatment frequently limits
tissue damage

8/2/2012

FAMUREWA B.A. BChD

53

Immunopathology of oral diseases


Immunodeficiency:
Chronic oral candidiasis
Herpes simplex infection
Recurrent oral ulceration(aphthous-like)
Gingivitis
Periodontitis
Periodontal abscess
Hereditary angioedema

8/2/2012

FAMUREWA B.A. BChD

54

Immunopathology of oral diseases


Autoimmune oral diseases:
Pemphigus vulgaris
Paraneoplastic pemphigus
Bullous pemphigoid
Mucous membrane pemphigod
Epidermolysis bullosa acquisita
Lupus erythematosus
Sjogren syndrome

8/2/2012

FAMUREWA B.A. BChD

55

Autoimmune oral
diseases
Pemphigus vulgaris
mediated by autoantibodies that target the extracellular

skin +/ oral mucosal components that link one epidermal


cell to another (intraepidermal )blistering diseases.
IgG autoantibodies binds with desmoglein 1 and 3 present

on desmosomes, on the cell surface of the keratinocyte.


The immune reaction against these glycoproteins causes a

loss of cell-to-cell adhesion (acantholysis), resulting in the


formation of intraepithelial bullae.
Ig A & Ig M may be involved

8/2/2012

FAMUREWA B.A. BChD

56

Fish net pattern of


binding site

8/2/2012

FAMUREWA B.A. BChD

57

Autoimmune oral diseases


Mucous Membrane Pemphigoid
Mediated by autoantibodies that target the
extracellular skin components that link the skin
basement membrane components either to the
lowermost layer of epidermal cells or to the dermal
components(subepidermal) blistering disease.
Autoantibodies directed against proteins (antigen)

in the lamina lucida or densa basement membrane


zone, acting with complement (C3) and neutrophils,
cause a subepithelial split and subsequent vesicle
formation.
8/2/2012

FAMUREWA B.A. BChD

58

Mucous Membrane Pemphigoid

8/2/2012

FAMUREWA B.A. BChD

59

Mucous Membrane Pemphigoid

8/2/2012

FAMUREWA B.A. BChD

60

Mucous Membrane
Pemphigoid

8/2/2012

FAMUREWA B.A. BChD

61

Autoimmune oral
diseases
Epidermolysis bullosa acquisita
Autoimmune form of EB.
Ig G directed against basement membrane

type V collagen & upper dermis or lamina


propria.

8/2/2012

FAMUREWA B.A. BChD

62

Autoimmune oral
diseases
Lupus erythematosus
Circulating serum antibodies against cell nucleus
components- antinuclear antibody(ANA).
ANA includes- antihistones, anti-DNA,

antiribonuclear and antinucleolar antibodies.


Lupus band test-demonstrable autoantibodies

towards basement membrane using direct


immunofluorescent stain.
SLE-if autoIg is deposited in glomerular BM of kidney.
8/2/2012

FAMUREWA B.A. BChD

63

DIF- Lupus band test

8/2/2012

FAMUREWA B.A. BChD

64

Autoimmune oral diseases


Sjogrens Syndrome
Sjogrens syndrome is an inflammatory

autoimmune disease that manifests as a chronic,


slowly progressive disease.
They arise as result of immune system activation

with the production of various auto antibodies with


lymphocyte invasion of the salivary and lacrimal
glands and other affected organs.

8/2/2012

FAMUREWA B.A. BChD

65

Oral hypersensitivity
disorders
Erythema multiforme
Acquired angioedema
Contact stomatitis
Allergic drug reaction(stomatitis

medicamentosa).
Urticaria (anaphylactic shock)
8/2/2012

FAMUREWA B.A. BChD

66

Oral hypersensitivity
disorders
Erythema multiforme
Type hypersensitivity reaction
Antigenic peptides form complex with Ig(IgG & IgM).
The immune complex fixes complements(C3)
This initiates leukocytic infiltrates(PMN & Macrophages)
Necrosis of epithelium(skin and or oral mucosa) by

PMNs & macrophages.


8/2/2012

FAMUREWA B.A. BChD

67

EM

8/2/2012

FAMUREWA B.A. BChD

68

Oral hypersensitivity
disorders
Acquired angioedema
Ig E mediated hypersensitivity reaction
There is normal functioning C1 esterase

inhibitor.
Precipitated by :
Drugs- ACE inhibitors, NSAIDS.
Stress(emotional), food,dust,plant,heat/cold
8/2/2012

FAMUREWA B.A. BChD

69

Oral hypersensitivity
disorders
Contact stomatitis
Synonyms- allergic contact reaction,contact mucositis, stomatitis
venenata
Analogous reation on the skin is contact dermatitis
It is an allergic reaction of the oral mucosa to the exposed allergen. This

could be:
Foods nuts, cinnamon, shellfish, fruits, some vegetables
Metals- amalgam,
Chemicals- acrylic, denture cleansers, ingredients in toothpastes,

mouthwash, chewing gum latex gloves, rubber dam


Cosmetics- lipsticks

8/2/2012

FAMUREWA B.A. BChD

70

Oral hypersensitivity
disorders
Allergic drug reaction
(stomatitis medicamentosa)
o Allergic oral mucosa reaction to administration
of systemic drugs.
o Drugs- penicilline, sulfa containing drugs
o Mimics lichen planus , Lupus Erythematosus &

Pempigus
8/2/2012

FAMUREWA B.A. BChD

71

Other immune-mediated oral


diseases
Oral lichen planus
Recurrent aphthous stomatitis
Behcets syndrome
Orofacial granulomatosis

8/2/2012

FAMUREWA B.A. BChD

72

Oral lichen planus


Mediated by a T lymphocyte reaction to antigenic

stimuli residing in the epithelial layer.


It is characterized by an intense T-cell infiltrate

(CD4 and especially CD8 cells) localized to the


epitheliumconnective tissue interface.
Excessive amounts of fibrinogen are deposited
Other basement membrane molecules, such as

fibronectin, laminin, and types IV and VII collagens


are
upregulated
8/2/2012
FAMUREWA B.A. BChD
73

Oral lichen planus

8/2/2012

FAMUREWA B.A. BChD

74

Oral lichen planus

8/2/2012

FAMUREWA B.A. BChD

75

Oral lichen planus

8/2/2012

FAMUREWA B.A. BChD

76

Other immune-mediated oral diseases


Recurrent Aphthous Stomatitis
Influx of Cytotoxic T lymphocyte cells directed

against antigenic determinant located on or within


keratinocytes.
The release of various immunoreactive cytokines

and chemokines induces a cell mediated response


that is believed to result in keratinocyte lysis.

8/2/2012

FAMUREWA B.A. BChD

77

Other immune-mediated oral diseases


Behets Syndrome
Deposition of immunocomplexes that lead to

vasculitis of small and medium-sized blood vessels.


Inflammation of epithelium caused by

immunocompetent T lymphocytes and plasma cells.

8/2/2012

FAMUREWA B.A. BChD

78

Behets Syndrome
Genetic aspects of Behcets disease
The strongest association of BD is with HLA-

B51.
Factor V Leiden mutation and the thrombotic

tendency in BD.

8/2/2012

FAMUREWA B.A. BChD

79

Oral malignancies
Tumour Specific Transplantation Antigen (TSTA)-

expressed on tumour cell surface.


Antibody/cell mediated immune response directed

against TSTA
Immune surveillances: minute tumours arise

constantly in nature but are destroyed by the immune


surveillance
Tumour escape : tumours escape immune

surveillance; immune system becomes tolerant to


8/2/2012
FAMUREWA B.A. BChD
tumours.

80

ORAL CANCERS
Abnormalities in cell mediated
immune responses in patients with
head and neck carcinoma
1

Delayed skin hypersensitivity reaction


impaired
T lymphocyte numbers reduced.

Changes in T lymphocyte subpopulations.

T lymphocyte lymphoproliferative response to


some mitogens and antigens impaired.
Lymphokine production reduced.

8/2/2012

FAMUREWA B.A. BChD

81

Conclusion
A sound knowledge of the

immunopathogenesis of oral lesions will aid in


instituting appropriate management.
This will make for patients satisfaction and

fulfillment of the attending clinicians.

8/2/2012

FAMUREWA B.A. BChD

82

Reference

Contemporary Oral and Maxillofacial Pathology


Burkets Oral Medicine: Diagnosis and Treatment
Clinical Atlas of Clinical Oral Pathology
Tyldesleys Oral Medicine
Essentials of Oral Medicine
Warrington R et al. An introduction to immunology and

immunopathology. Allergy, Asthma & Clinical Immunology


2011.
8/2/2012

FAMUREWA B.A. BChD

83

Thanks for the


attention!!!

8/2/2012

FAMUREWA B.A. BChD

84

También podría gustarte