Abstract

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.

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