Boy M Bachtiar
Department of Oral Biology, Faculty of Dentistry, Universitas Indonesia
Periodontal disease is a pathological condition that involves inflammation process induced by mature subgingival plaque, which means un-controlled biofilm has occurred. This is a key point in clinical consideration when using antibiotic as adjunct in periodontal therapy as biofilm disruption is a necessary step. This is due to undisrupted biofilm may decrease the efficacy of antimicrobial therapy. Periodontopathogens that consistently associated with periodontal disease are the red complex (P. gingivalis, T. forsythia, and P. Intermedia). As Gram-negative bacteria, their cell wall consists of lipopolysaccharides that act as powerful stimulants for inflammatory reaction. Thus, the presence of these bacteria is a marker for destructive periodontal disease. The host defense system, including innate and adaptive immunity, is another determinant in the pathogenesis of periodontal disease. The initial inflammation in the periodontal tissues is a physiologic defense mechanism triggered by the microbial in biofilm. Thus, it is not pathology reaction. Failure to eradicate the biofilms, especially in sub-gingival pocket, the established lesion exist that reflects a pathology stage. This is also a period of transition from the innate to the acquired immune response. At this time, inflammatory cells such as macrophages, plasma cells, and T and B lymphocytes are dominant and will continue to produce inflammatory mediators in an effort to destroy the pathogens. Finally, researchers have found that genetic signaling pathways is the other determinant that affects individual response by influence the expression of inflammatory mediators in response to the presence of periodontopathogen.