014.pathogenesis of periodontal diseases

1. Dr Jaffar Raza Syed Page 1
Pathogenesis of Periodontal Diseases
Bacteria  colonize the gingival crevice  attach to the tooth surface 
Gingivitis and PDD
Balance shifting from health to disease
Junctional epithelium:
Tissue most directly challenged by the pathogenic plaque bacteria.
The microbial mass releases toxic metabolites
----butyric acid
----propionic acids

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The keratinocytes respond by releasing
-Cytokines
-Proinflammatory mediators.  IL, PGE2 and MMP
-Neutrophils  presence as part of host defence.
-Activation of complement  earliest host response in the gingival crevice.

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Bacterial Invasion
Entry of bacteria  Produce virulence factor  Causes the disease
Bacterial Attachment is necessary
Bacterial enterance through ulceration in epithelium as wel.

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Exotoxins
A.a produces an exotoxin  leukotoxin  toxic effect on (PMNs).
The production of leucotoxin may enable A. a to evade the host defence.
Lipopolysaccharide (LPS)  toxic substances affecting the tissues directly and
through activation of the host responses.
Endotoxin produce substances that induce bone resorption and in stimulating
macrophages to produce prostaglandin and collagenases.

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Bacterial Enzymes
--collagenases,  P.g and A.a
--hyaluronidase, alters gingival permeability
--gelatinase,
--aminopeptidase,
--phospholipases,
--alkaline and acid phosphatases.
Are produced by bacterial enzymes that are capable of contributing to the
disease process.

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Evasion Of Host Responses
Bacterial factors can also indirectly compromise the host tissues.
These factors influence both the cellular and humoral immune responses.
1. Inhibition of PMNs by
-----leukotoxin chemotactic inhibitors
-----decreased phagocytosis.
2. Immunoglobulins are inactivated by proteases.
3. Lymphocyte alterations
4. Endotoxicity
5. Catalase reaction

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Mechanism which results in changes in epitheliumechanism which results in changes in epithelium
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echanism which results in changes in epithelium

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The Host Derived Bone Resorbing Agents
Cytokines
IL-1, TNF, TGF-B, L-6
Other Inflammatory Mediators
Prostaglandins, Leukotrienes
Role Of Cytokines
--Interleukins, growth factors, chemokines and interferon belong to the
family of cytokines.
--Transmit information or signals from one cell to another
--They act on fibroblasts, macrophages, keratinocytes and PMNLs to
release (MMPs) that degrade connective tissue matrix.
Various Cytokines are

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1. IL-1
--produced by macrophages and lymphocytes. Fibroblasts, platelets,
keratinocytes and endothelial cells.
--It activates T and B lymphocytes
--promotes antibody production.
--IL-1 αand IL-1 β are potent stimulators of connective tissue destructions.
--It triggers the release of large quantities of PGE2 from fibroblasts
and monocytes and stimulates secretion of MMP.

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2. IL-2:
--Produced by Monocytes and T lymphocytes.
--It stimulates T cells
3. IL-4, IL-5 & IL-10:
--produced by TH2 cells and help in the activation of beta cells into plasma cells
--down regulate monocytic response.

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4. IL-6:
--released by lymphocytes, fibroblasts and monocytes.
--LPS, IL-1 and TNF alpha upregulates the secretion of the IL-6.
--conversion of blood monocytes into osteoclasts.
5. IL-8:
--secreted by monocytes, keratinocytes and fibroblasts.
--strong chemoattractant of PMNLs at low concentrations.

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6. TNF:
--produced by macrophages and release lymphotoxins.
--stimulate the proliferation of osteoclast precursor cells
--activate the mature osteoclasts to resorb bone.
--It augments leukocyte chemotaxis, degranulation, adherence to
endothelial cells and its ability to kill bacteria.
7. Prostaglandin E2:
--Sources are macrophages and fibroblasts.
--IL-1 induces its production.
--It is a potent mediator of osteoclastic resorption.

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8. Matrix Metalloproteinases (MMPS):
--enzymes capable of degrading connective tissue matrix.
--These enzymes are secreted in the latent form by fibroblasts,
macrophages, keratinocytes and PMNLs,
e.g. collagenase, gelatinase, stromalysin, matrilysin.
--IL-1 play an important role in upregulation of MMPs.