Periodontitis as an autoimmune disease
The microbial etiology is the primary etiology of periodontal diseases. However, Brandtzaeg and Kraus (1965) 1 were the first to postulate the autoimmune basis in the pathogenesis of the periodontal disease. Autoimmunity results when there is an imbalance between the effector and regulatory immune responses. Under normal conditions, the immune system exhibits tolerance (an inability to react) to molecules which are recognized as self-antigens. However, if the mechanism tolerance is hampered, the immune system starts to work against one or more of the body‘s own molecules, thereby leading to damage to self-tissues. Several studies have demonstrated the involvement of autoimmune responses in periodontal disease. The possible mechanisms involved in the autoimmune response in periodontitis include,
- Enhanced presentation of self-antigens.
- Altered T helper or T suppressor cell function.
- Polyclonal activation of cells, which produce autoantibodies.
- Idiosyncrasies of the antigen-idiotype network.
- Bacterial or viral cross-reactivity with self-antigen.
- Genetic predisposing factors.
- Cross-reactivity of human heat shock protein.
Enhanced presentation of self-antigens:
In many autoimmune disorders, it has been observed that there is an increase in antigen presentation, in particular on cells which do not normally express these molecules. Normally, antigen presenting cells, such as Langerhans cells, dendritic cells, etc. internalize and process the antigen. A portion of the antigen is then presented on the surface of the cell in association with major histocompatibility complex (MHC) which then activates the T-cells. In abnormal conditions, cells ……………..Contents available in the book………………….Contents available in the book………………..Contents available in the book………………..Contents available in the book………………..Contents available in the book………………..Contents available in the book………….
Altered T-helper or T-suppressor cell function:
It has been demonstrated that in periodontal disease, the T-helper or suppressor cell activity may be altered. The evidence for this proposal comes from investigations which demonstrate that in periodontitis, there is suppressed T-cell response along with an increased B-cell proliferation as a result of spontaneous lymphoblastic proliferation 2, 3. Thus, T-cell suppressor activity is increased in patients with periodontitis.
Polyclonal activation of cells, which produce autoantibodies:
The polyclonal expansion of the B-cell pool has also been found to be associated with autoimmune response. Here, we should know about natural antibody (Nab) producing cell pool. Normally, in the absence of disease, natural antibodies make the normal self-component. Such a pool of Nab may be expanded polyclonally by one of the polyclonal B-cell activators found in periodontal plaque (for example lipopolysaccharide) 4. Along with this, these antigens may also enhance the release of tissue components which expose the natural antigens to the immune system to a greater extent than usual.
Idiosyncrasies of the antigen-idiotype network:
The antigen-idiotype network theory was proposed by Jerne (1974) 5. According to this theory, an antigen stimulates the production of antibody exhibiting an idiotype. Later, anti-idiotype antibodies are formed which is followed by the production of anti-anti-idiotype antibodies. This results in the formation of an open network. These antibodies may ……….Contents available in the book………………….Contents available in the book………………..Contents available in the book………………..Contents available in the book………………..Contents available in the book………………..Contents available in the book………….
Bacterial or viral cross-reactivity with self-antigen:
The immune response generated against the bacteria or viruses may cross-react with the host antigens, thus causing damage to the host tissues. This type of damage has been described in the case of post-infective myocarditis. The bacteria and viruses present in the periodontal biofilm may initiate the production of auto-reactive antibodies that may be linked to the pathogenesis of periodontitis. The evidence for the presence of such antibodies has been provided by Watanabe (1987) 6 in an animal study. However, more research is required in this direction to authenticate this mechanism of autoimmune response in humans.
Genetic predisposing factors:
Genetic factors may also be associated with the development of autoimmune diseases. For example, higher incidences of selected histocompatibility complex antigens have been shown to be associated with systemic diseases like rheumatoid arthritis with HLA-DRw4 7 and systemic lupus erythematosus in association with HLA-DR3 and HLA-B8 8. These factors may also contribute to the pathogenesis of periodontal diseases. Studies have been done to find out the association of HLA antigens ……….Contents available in the book………………….Contents available in the book………………..Contents available in the book………………..Contents available in the book………………..Contents available in the book………………..Contents available in the book………….
Cross-reactivity of human heat shock protein:
The cross-reactivity of human heat shock protein (HSP) 60 and P. gingivalis GroEL has been demonstrated in periodontal diseases. HSP 60 specific as well as P. gingivalis cross-reactive T cells have also been demonstrated to accumulate in periodontitis lesions. It has been demonstrated in a study by Yamazaki et al. (2003) 10 that natural killer T-cells play a vital role in the generation of the immune response against autoantigens such as collagen Type I or HSP 60.
References:
References are available in the book.
Periobasics: A Textbook of Periodontics and Implantology
The book is usually delivered within one week anywhere in India and within three weeks anywhere throughout the world.
India Users:
International Users: