Aetiology and pathogenesis of periodontal disease

Gingivitis is modified by several factors including smoking, ion channel blocking drugs and hormonal changes such as those seen in puberty or pregnancy. Periodontitis is also initiated by microbial plaque which follows on from gingivitis, but occurs in only 10 to 15% of the population and is influenced by the individual's immune and inflammatory response. Studies on the humoral and cellular immune response in periodontal disease indicate that: a) homing of relevant immune cells takes place within the periodontium; b) plasma cells are among the most active secretory cells in the gingiva; c) that immunoglobulin subclasses are similar between blood and the gingival pocket fluid for IgG but not for IgA; and that d) an individual's ability to mount a specific antibody response to periodontopathogenic organisms may indicate their susceptibility to the disease and their likely response to treatment. Recent reviews of the pathology of periodontal disease suggest that a histopathological established lesion with plasma cell predominance is likely to undergo periodontal bone loss. Furthermore, susceptibility to periodontitis may be related to whether plasma cells predominate in the tissues of an individual or a site as result of the microbial challenge of dental plaque. A tendency for an individual or site to form an extensive plasma cell infiltrate may indicate an inability to defend against periodontal bacteria and thus a predisposition to periodontitis. The various susceptibility factors such as smoking, medical condition, genetics, plaque control and local factors may all interact to influence the host response and specifically the immune response.