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1. DEFENCE MECHANISM OF ORAL CAVITY
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
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2. 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
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3. 2. Defradation of other intracellular organelles
3. Synthesis of cell membrane and extra cellular components associated
with cell adhesion and barrier function.
4. Basement membrane synthesis to provide attachment to the underlying
CT.
In the lamina propia adjacent to the basement membrane there are a
few lymphoid cells which may combat microorganisms that penetrate to
this depth. These intraoral lymphoid aggregations, function together with
the extra oral lymph nodes for the protection of the oral cavity as a whole.
There are in fact several intra oral lymphosis aggregations.
1. The palatine Tonsils comprise paired lymphoid masses, between the
glossopalatine and pharyngo palatine arches. The component lymphoid
tissue contains both B and T cells, IgG producing cells being the most
prominent.
2. The lingual Tonsils are much less prominent lying on each side of the
tongue just distal to the circum vallate papillae. They contain lymphoid
modules some of which have germinal centers in addition to
perifellicular diffuse lymphoid cells.
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4. 3. The pharyngeal tonsil comparison of simple mass of lymphoid tissue
under the nasopharangeal mucosa.
There are also scattered collections of lymphoid tissue in other
regions of the oral cavity. Lymphocytes and plasma cells are found in
small clusters in both major or minor SG. Most of the plasma cells secrete
Ig A.
ROLE OF GINGIVAL CREVICULAR FLUID
With continued plaque accumulation at the cervical surface of the
tooth, there is a corresponding increase in crevicular fluid formation. This
fluid contains immunoglobulins Ig G, A, M in adition to complement
components namely C3, C4 and C5 and C3 Pro activator. Thus the crevicular
fluid contains most of the humoral and cellular immune components found
in the blood, altering salivary Ig A is the predominant component. There
are abo, a number of other components of the crevicular fluids including:
a) Albumin 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.
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5. Crevicular fluid also contains macrophages and T and B cells which
migrate from the underlying blood vessels.
ROLE OF SALIVA
In addition to mechanical lavage the saliva function as a component
of the oral immune system saliva combines both specific and non specific
immune components.
A) NON SPECIFIC COMPONENTS
i) Lysozyme (Meramidase)
This is bactericidal enzyme that splits the bond between N acetyl
glucosomine and N acetyl inuramic acid in the micopeptide components of
bacterial cell wall. Apart from Str. Mutans, the oral flora is generally
resistant to lysozyme.
ii) Peroxidase
In the p/o thiocyanate ions and hydrogen peroxide, peroxidase kills
acidophilus by inhibiting lysin uptake and may inhibit some streptococci
by limiting the action of their glycolytic enzymes.
iii) Lactoferrin
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6. This has a bacteriostatic effect on a whole microbial spectrum,
possibly by depleting local environmental iron required for microbial
growth.
B) SPECIFIC COMPONENTS
SECRETORY Ig A
IgA is quantitatively the most important Ig present in saliva, mainly
derived locally from plasma cells. It is then trasported to the distal human
and exerted into the oral cavity S IG A is more resistant to microbial and
particularly suited for saliva, which then functions as an antisept paint for
various oral surfaces. SigA also appears to limit microbial adherence to the
mucosal surface.
PERIODONTAL DISEASE
The effect of dental plaque on the immune response are both
complex and varied. It results
1. In the activation of complement pathways.
2. Lymphocytic stimulation
3. Lymphokine release
4. Macrophages activation
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7. The potent reactions are probably modulated by effects of the dental
plaque components resulting primarily in a localized chronic inflammatory
response in the gingiva.
Unless meticulous oral hygiene is maintained chronic periodontic
diseases. For ease, it has been subdivided into four stages. Each stage in
associated with certain immune treatment.
1. In the initial lesion, there is a localized inflammatory reaction at the
fase of gingival sulcus. This correlates with a localized inflammatory
response of PMLs reflecting chemotactic action of plaque antigen and
complement activation.
2. The subsequent early lesion involves the local gingival tissue
infiltration of predominantly T cells and a few B- cells. In the
circulation, lymphocytes are sensitized as shown by their ability to
release lymphokines.
3. In the established lesion, there is a characteristic localized plasma cell
infiltration of the gingival tissues.
4. The advanced lesion marks the trasition to an advanced irreversible
destructive process readily and alveolar bone loss. This phase is
characterized by Types I, II, III, IV hypersensitivity treatment
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8. associated with the protective destructive mechanism of lyphocytic and
macnophagic function coupled with complement activation.
The role of specific G – ve microorganisms in the aetiology and
pathogenesis of destructive forms of PD diseases is well established.
a. B. gingivalis – severe aduct periodontitis
b. Actinobacillus actinomycetem comitans – LTP
c. B. intermidus – ANUG
d. B. Intermidus – Pregnancy gingivitis.
There are potective mechanisms operating to prevent the spread of
pathogenic microorganism extra oral sites in most individuals. These
protective mechanisms effectively localize the infection to the PD tissues.
Either secretory or scrum derived antibacillus may impede microbial
adherence and so colonization in the initial stages of dental plaque
accumulation. Also in the initial stages of microbial tissue invasion,
phagocytosis especially PMNLs acting in concert with opsonic antibodies
and complements, may play a role in limiting their pathological effects.
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9. HOST DEFENCE MECHANISM IN PERIODONTAL DISEASES
One of the major components of the host defence mechanisms in
periodontal diseases centres on the immune system. In fact the following
components of the immune system are implicted.
SECRETORY IMMUNE SYSTEM
The secretary immune system comprises mucosal associated
lymphoid tissues (eg. Local Ig A containing tissue, peyer’s patches) with
the Ig A antibodies comprising prominent antibodies in the secretion which
both the mucosal surface.
In the microbial colonization stage, antibody mediate inhibition of
adherence may play a role in influencing the microbial play a role in
influencing the microbial content of both dental plaque and the subgingival
microflora. Initially, such defence mechanisms may enter around SigA
antibodies from saliva, although serum derived and gingival crevicular
fluid antibodies may subsequently activity may include disruption of
colonization, microbial aggregation or enhancement of microbial
phagocytosis.
NEUTROPHIL – ANTIBODY – COMPLEMENT SYSTEM
The Neutrophil – antibody – complement system comprises
phagocytic blood and tissue PMNs Leucocytes whichare not only highly
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10. 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:
A) 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 H2O2 microbial lysis in the
p/o chloride.
B) 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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11. LYMPHOCYTE MACROPHAGE LYMPHOKINE SYSTEM
The lymphocyte macrophage lymphokine axis mainly comprises
effector T lymphocytes, whose function include the following:
a. T- helper and T- suppressor lymphocytes regulate T effector cell
activity and antibody production by B lymphocytes.
b. T lymphocyte modulations of macrophage activity.
c. Specific lymphocyte stimulation by antigens which results in
lymphokine production which includes
- Osteoblast activating factor (OAF)
- Lymphotoxin (LT)
- Macrophage activation factor (MAF)
- Migration inhibition factor (MIF)
- Lymphocyte inhibitory factor (LIF)
- Interference.
The lymphocyte macrophage lymphokenes axis has a potential to
exert marked pathological effects on the host tissues. It releases
lymphotoxin to kill fibroblasts and OAF to result in alveolar bone
resorption.
The healing stage of PD disease may be associated with
macrophagic phagocytosis of microorganisms and tissue debris whereas
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12. 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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13. INFLAMMATION AS A DEFENCE MECHANISM
It may be defined as the reaction of living tissues to the injury in
essence, it is a defence mechanism in itself. This reaction is a beneficial
one, for without inflammation, life would be impossible. It is evidently on
evolutionary adaptive response having several beneficial values or the
species.
The character and outcome of this reaction varies depending on the
nature of stimuli and the defence capacity of the host.
During inflammation, there is an increased dilatation of blood
vessels – healing in that area. The main cells of inflammatory exudates are
PMNs leucocytes, plasma cells and macrophages.
The inflammation reaction tends to present the dissemination of
infection. Speaking generally, the more intense the reaction, the more
likely the infection is localized.
7) A REFLEX MECHANISM AS A DEFENCE MECH.
A reflex is an involuntary, impremeidated unlearned “built in
response to a stimulus in general, most reflexes, no matter how basic they
may appear to be, are subject to alteration by learning , that is there is no
clear distinction between a basic reflex and a learned component.
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14. INTEGRATING CENTRE
AFFERENT PATHWAYS EFFERENT PATHWAYS
RECEPTOR EFFECTOR
STIMULUS RESPONSE
FEEDBACK
8) PAIN AS A PROTECIVE MECH
Pain is definitely regarded as a defence mechanism because
whenever there is an offending stimulus to the oral cavity, it is the pain
which is the primary sign and symptom of the patient. As soon as the
patient experience pain, the normal tendency is to withdraw the oral tissues
from the offending stimulus.
This procedure, in turn, helps to prevent further damage by the
offending stimulus to the oral cavity.
9) GAGGING AS A DEFENCE MECH
The gagging reaction ranges from mild choking when the palate is
inadvantantly touched by the mouth mirror, to violent, uncontroled
retching during impression taking.
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15. Gag reflex is a normal, healthy, defence mechanism. It function is to
prevent foreign bodies from entering the trachea by altering the shape of
thepharynx and its various openings to eject out foreign bodies.
Five regions in the oral cavity are identified as regions of maximum
sensitivity and are named “Triggen zones”. They are
1. The forces
2. Base of the tongue
3. Palate
4. Uvula
5. Post pharyngeal wall
8) MISC. FACTORS
Various other factors may also play a role in defence mechanisms of
the oral cavity these includes
a. Adaptive capacity of muscles to protect TMJ.
b. TMJ remodality
c. Protective (Cleansing) function of tongue
d. Prepodentinal factors like
- 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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