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Conversion of a stable T‐cell lesion to a progressive B‐cell lesion in the pathogenesis of chronic inflammatory periodontal disease: an hypothesis
Author(s) -
Seymour Gregory J.,
Powell R. N.,
Davies W. I. R.
Publication year - 1979
Publication title -
journal of clinical periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.456
H-Index - 151
eISSN - 1600-051X
pISSN - 0303-6979
DOI - 10.1111/j.1600-051x.1979.tb01930.x
Subject(s) - lesion , pathogenesis , cell , disease , mechanism (biology) , inflammation , pathology , medicine , biology , immunology , genetics , philosophy , epistemology
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.