Update on B Cell Response in Periodontitis.

Abstract

B cells have a central and dual role in the physio-pathological mechanisms of periodontitis. They take part in the elimination of the periodontal germs, the induction of tissue destructions and the regulation of the immune response. B cells play an essential role in the destruction of alveolar bone in periodontitis by immunomodulation, rather than by production of antibodies. In the periodontal cell network, B cells are in constant interaction with other immune cells and mesenchymal cells. Periodontitis is characterized by a cellular conversion from a dominant T-cell lesion to a dominant B-cell lesion, particularly enriched in plasma cells. This evolution results from abnormal interactions between B and T cells in periodontitis. Moreover, B cells are at the crossroads of the immune and the bone systems and are involved in the autoimmune mechanisms described in periodontitis. Different subsets of B cells are involved in periodontal destruction, in particular memory B cells, plasma cells and B1 cells. Effector memory B cells strongly express mRANKL in periodontitis and constitute the precursors of plasma cells. B1 cells are also involved in tissue destruction but also in the mechanisms of regulation, in particular via the natural secretion of IL-10 by CD11b+ B1 cells which form a part of the B10 cells that regulate the inflammatory response. As such, periodontitis seems to be associated with a deficit in regulation. In peripheral blood, B cells can also be systemic markers of infection and periodontal inflammation: circulating memory B cells are increased in periodontitis while circulating CD11b+ B1 cells are decreased. The study of B cells in periodontitis is constantly evolving for a better knowledge of the periodontitis setting, the evaluation and the follow-up of periodontitis, but also for the design of new therapeutic targets that may be promising in the management of severe periodontitis.