Immunological aspect of Microbial-Host interaction

Immunological aspect of Microbial-Host interaction
Immunological aspect of microbial-Host interaction Involves following factors in response to bacterial infection:
Innate factors such as complement, resident leukocyte and especially mast cell play significant role in signaling endothelium thus initiating inflammation.
Acute inflammatory cells (neutrophils) protect local tissue by controlling the periodontal microbiota within the gingival crevice and junctional epithelium
Chronic inflammatory cells, macrophages and lymphocytes protect the entire host from within the subjacent connective tissue and do all that in necessary to prevent a local infection from becoming systemic and life threating.
Periodontal disease is a wall-regulated response to protracted bacterial infection directed by inflammatory cells of the host immune system.
Neutrophils primarily function as antimicrobial cells, and chronic inflammatory cells orchestra adaptive responses.
Neutrophils function to contain microbial challenge throw phagocytosis and killing and may contribute to local tissue changes by release of tissue-degrading enzymes.
The chronic inflammatory cells, the lymphocytes and monocytes orchestrate connective tissue changes associated with both periodontal infection and periodontal repair and healing.
Fig-1: Clinical example of established gingivitis with emphasis on the acute inflammatory reaction.
Innate factors and initiation of inflammation
Onset of inflammation there is edema and erythema leading to vascular changes
Complement activation in response to bacterial infection result in generation of C3a and C5a Degranulation of mast cell Mast cell constitutely transcribe TNF-alpha, TNF-B, IL-4, IL-6, IFN- gama.
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Controlling bacterial challenge primary role of neutrophils, neutrophils are the first leukocyte to arrive at site of inflammation and kill the bacteria by phagocytosis, N. can kill the bacteria by oxidative or non oxidative mechanisims.
The Phagocytic Process
Phagocytosis and destruction of engulfed bacteria involves the following sequence of events: 1. Delivery of phagocytic cells to the site of infection
2. Phagocytic adherence to the target
3. Ingestion or engulfment of the target particle
4. Phagolysosome formation
5. Intracellular killing
6. Intracellular digestion (and diegestion, in the case of macrophages)
These steps involved in the phagocytic process in macrophages are illustrated below.
Figure 2. Phagocytosis by a Macrophage. A bacterium, which may or may not be opsonized, is engulfed by the process of endocytosis. The bacterium is ingested in a membranous vesicle called the phagosome. Digestive granules (lysosomes) merge with phagosome, release their contents, and form a structure called the phagolysosome. The killing and digestion of the bacterial cell takes place in the phagolysosome. The macrophage egests debris while processing the antigenic components of the bacterium, which it returns to its surface in association with MHC II for antigen presentation to T cells.
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Defect in neutrophil function at any stage leads to aggressive periodontitis
Condition
Neutrophil Abnormality
Periodontal Manifestation
Neutropenia
Decreased no. of neutrophils
Severe aggressive periodontitis
Chediak Higashi syndrome
Decreased neutrophil chemotaxis and secretion
Neutrophils fuse to form characteristic giant granules called megabodies
Syndrome caused by mutation in the vesicle trafficking gene, lyst
Pappilon - lefevre syndrome
Multiple functional neutrophil defects, including myeloperoxide deficiency, defective chemotaxis and phagocytosis
Sever aggressive periodontal destruction at early age, involves primary and permanent dentition mutation in cathepsin C gene
Leukocyte adhesion deficiency
Defect in leukocyte function
Aggressive periodontitis at young stage
Fig-3: The clinical photo and the X-Ray of this 28 year -old man show the advanced alveolar bone loss in the absence of significant gingival inflammation, typical of the localized aggressive periodontitis.
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Fig-4: The patient has advanced generalized aggressive periodontitis with deep pockets through out the mouth.
Fig-5: Papillon –Lefevre syndrome
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1.GAP (generalized aggressive periodontitis) patients have a decreased ability to mount high titers of specific IgG2 antibodies to A.a (A. actinomycetemcomitans). These subjects exhibit a tendency towards progressive periodontal destruction leading to tooth loss over a relatively short period of time.
HIV infection attacks the T-helper cells of the body, causing a drastic change in the T- helper(CD4+)/T- suppressor(CD8+) ratio with severe impairment of the host s resistance to infection. Depleted peripheral helper T-lymphocyte counts correlate closely with the occurrence of NG (Necrotizing gingivitis as demonstrated in a study of 390 US HIV- seropositive soldiers (Thompson et al. 1992). Furthermore, a complete absence of T-cells in gingival tissue of HIV-infected patients with periodontitis has been reported (Steidley et al. 1992). The lack of local immune effector and regulatory cells in HIV-seropositive (AIDS patients). NP has been revealed as a marker for immune deterioration, with a 95% predictive value that CD4+ cell counts were below 200 cells/mm3, and, if untreated, a cumulative probability of death within 24 months (Glick et al. 1994). As a consequence of this finding, if possible all NPD (necrotizing periodontal disease (NPD), patients may be recommended to be given a test for HIV infection.
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Fig. 10-10. (a) Necrotizing stomatitis affecting the mandible of an HIV-seropositive patient. Two years after treatment (b) the result of treatment is satisfactory, and there has been no recurrence.
Fig. 10-17. Necrotizing periodontitis with severe pain. The entire gingival margin is the seat of a necrotic ulcer. ( a) Facial aspect. (b) Palatal aspect. The patient was treated with scaling supplemented with metronidazole and the next day the patient was free of symptoms and the clinical features were significantly improved (c & d).
Prof. Dr. Raad Ali
A. Prof. Dr. Zainab Al-Mahdi
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