A localized absence of interleukin-4 triggers periodontal disease activity: a novel hypothesis.

Pathogenic bacteria constitute the primary extrinsic agent in the etiology of Adult periodontitis. In addition to direct toxic effects, bacteria induce destructive immunologic and other inflammatory reactions in the host, leading to the observed pathologic alteration in the tissue. The risk to develop periodontal disease is not equal for all individuals, suggesting host factors are important in determining an individuals disease susceptibility. Regulation of immune response is important in maintaining the equilibrium between periodontal health and disease. We hypothesize that, in the case of Adult periodontitis, a localized lack of the regulatory cytokine interleukin-4 (IL-4) in the gingival tissues predisposes susceptible individuals to progress from gingivitis to periodontitis.