Polyclonal B-cell activation: Severe periodontal disease in young adults

Abstract

The proliferative response stimulated by the polyclonal B-cell activator staphylococcal protein A (Staph. A) was studied in cultures of peripheral blood lymphocytes obtained from young adults with severe periodontitis. The proliferative response stimulated by Staph. A was enhanced in this patient population in comparison to a control population of the same age. Differences were apparent by Day 3 in cultures stimulated by high doses of Staph. A, and were still apparent at Day 7 in cultures stimulated by low doses. Marked differences were apparent between the two groups at every Staph. A dose at Day 5 (peak response). In preliminary studies of proliferative responses in this select population, similar results were obtained using bacterial extracts from oral and nonoral organisms as the stimulators. To determine if these bacterial extracts contained polyclonal B-cell activators these same preparations were used in an assay for polyclonal antibody production. The extracts not only contained potent polyclonal B-cell activators, but in general the polyclonal antibody assays correlated with the previous proliferative assays. The most potent extracts were from Escherichia coli, followed by Bacteroides melaninogenicus, then Actinomyces viscosus, naeslundii, and israelii. These results support a hypothesis that severe periodontitis, in this select patient population, occurs as a consequence of B-cell hyperreactivity. The data further suggest the possibility that the polyclonal B-cell activators in dental plaque organisms may initiate this disease by nonspecifically stimulating B cells in the surrounding tissues. These stimulated B cells and the plasma cells derived from them could then release factors responsible for loss of periodontal support. This possible role for B cells and the potential for T cells and macrophages to regulate these responses are discussed.