Conversion of a stable T-cell lesion to a progressive B-cell lesion in the pathogenesis of chronic inflammatory periodontal disease: an hypothesis.
Changes in the host's immunological response or, alternatively, changes in the oral microflora have been implicated as possible mechanisms by which a stable lesion of chronic inflammatory periodontal disease may become a progressive lesion leading to tissue destruction and tooth loss. It has recently been established that the progressive lesion in humans can be unequivocally considered as a B-cell response. Circumstantial evidence exists which suggests that the stable lesion is in fact a T-cell-mediated mechanism. An hypothesis is presented to explain the change from a stable to a progressive state in terms of a shift from a predominantly T-cell lesion to one involving large numbers of B-cells. Mechanisms of this shift in cell populations are considered together with a discussion of possible means of preventing such a shift.
D000818:Animals; D001402:B-Lymphocytes / Q000276:immunology*; D002908:Chronic Disease; D005891:Gingivitis / Q000139:chemically induced* / Q000209:etiology / Q000276:immunology; D006801:Humans; D007978:Levamisole / Q000009:adverse effects; D009055:Mouth / Q000382:microbiology; D010518:Periodontitis / Q000209:etiology* / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology*
D007978:Levamisole