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INTRODUCTION
The oral cavity is loaded with acrobes and anaerobes which are
normal commensals of the oral cavity. Any breach of the integrity of the
oral mucosa may lead to rapid attack by various other microorganisms
present in the environment. Hence, an effective defence mechanism is
necessary within the oral cavity to safeguard it from these attacks. These
defence mechanisms can be broadly divided into
a. Integrity of oral mucosa and role of lymphoid system.
b. Role of Gingival crevicular fluid
c. Role of saliva
d. Vascular component of most defence mechanism
1. Integrity of oral mucosa and role of lymphoid system
The health of oral cavity primarily depends on the integrity of the
oral mucosa. Provided this mucosa remains intact, few microorganisms can
penetrate the underlying tissues. This partly reflects the functions of the
Keratin barrier.
The oral mucosa can be broadly into
a. Masticatory mucosa : which covers the crest of the RR and the hard
palate.
b. Lining mucosa : which covers the lips and cheeks, the vestibular spaces,
the alveolingual sulcus, the soft palate the ventral surface of the tongue
and the unattached gingiva found of the slopes of RR.
c. The specialized mucosa: which covers the dorsum of the tongue.
The oral cavity is lined by a stratified squamous epithelium whose
functions include:
1. Forming a primary structure barrier between the internal and external
environment.
2. Protection against mechanical damage, entry of noxious substances or
organizing and loss of fluids.
Like the skin, the oral mucosa comprises a surface epithelium,
overlying the layer of basement membrane. This string sq epithelium
undergoes mitosis, synthetic activity and disintegration leaving the
underlying cells as a cohesive tissue.
The epithelial cells undertake a member of specialized synthetic
activities associated with the maintenance of a surface barrier including.
1. The synthesis of Keratin
f) lysosomal enzymes
b) Transferring
g) lysozyme
c) traptaglobulin
h) Tryaluronidase
d) Glycoproteins
I) Collagenase
e) Lipoproteins
Tube enzymes not only affect specific tissues e.g. collagen, but also
selective Ig A in activation results from specific protease activity.
B cells which
Lysozyme (Meramidase)
This is bactericidal enzyme that splits the bond between N acetyl
Peroxidase
In the p/o thiocyanate ions and hydrogen peroxide, peroxidase kills
Lactoferrin
motile but also migrate in large numbers from the gingival B v, through the
gingival CT and epithelium into the gingival crevice or the periodontal
pocket. They serve as a powerful host reference mechanism to combat the
colonization and invasion by oral microbial flora. The PMNs do met work
in isolation but in concert with Ig G and Ig M antibodies and complement.
The Ig G antibody coats the microorganism and the Ig G coated
microorganism then binds to PMNs surface receptors for the Fc portion of
the Ig G to enhance phagocytosis.
Once the microorganism has been phagocytosed by the PMN, it can
be killed by:
1. OXIDATIVE MECHANISMS
These involve reactive oxygen specie, is H2O2, superoxide ion and H
the catalase produced by either PMNs or micro effect inhibit peroxidase
effects whereas myeloperoxidase may enhance H 2O2 microbial lysis in the
p/o chloride.
2. NON OXIDATIVE MECHANISM
These important mechanisms result from PMN derived lysozyme,
lactoferrin and cathepsins which kill microorganisms directly in the
absence of O2 i.e. under anaerobic conditions which typify the gingival
crevice and particularly periodontal pocket.
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Lymphotoxin (LT)
Interference.
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there are also lymphokines e.g. Fibroblast activity factor that stimulate both
fibroblastic proliferation and collagen formation.
5) VASCULAR COMPONENTS
When the vessel is damaged or cut, there is an immediate transient
arteriolar vasoconstriction that serves to reduce the blood flow. Injuries to
the enodothelial cells exposes highly thrombogenic sub endothelial CT to
which the platelets adhere and undergo contact activation involving shape
change, a release treatment and further aggregation of more platelets.
Simultaneously, tissue factors released at the site of injury in combination
with platelet factors activate the plasma coagulation system.
Ulitmately, a permanent hemostatic plug is produced by the
combined activitis of endothelial cells, platelets and the coagulation
sequence, primarily as the result of the platelet serotinin release.
The initial platelet plug in therefore subsequently replacement by a
blood clot and fibrin plug formation. The coagulation sequence essentially
involves a cascade which begins as two separate pathways that ultimately
converge. One is the intrinsic to the blood and probably plays a major role
in hmostasis following an injury. The other is instrinsic and triggered by
the introduction into the blood of tissue factors containing thromboplastin.
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INTEGRATING CENTRE
AFFERENT PATHWAYS
EFFERENT PATHWAYS
RECEPTOR
EFFECTOR
STIMULUS
RESPONSE
FEEDBACK
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Dentinal pain
Tubular sclerosin
Smear layer
Irritation (reparetive) dentin
Information of subjacent CT
e. Cough reflex
f. Taste sensation, Temperature
g. Mutality protected occlusion?
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