Figure 1.

Osteoimmunology of periodontal disease. During periodontitis, the immune response induced by the dysbiotic microbiota enhances the production of local RANKL by different immune cells types such as Th1, Th17, B cells. Additionally, the increased gingival levels of IL-17 stimulate the membrane-bound expression of RANKL in osteoblasts and periodontal ligament fibroblasts; this provokes the activation of osteoclast and bone-loss. On the contrary, in health, different immune cells such as Tregs, Bregs, M2, and Th2 cells promote an anti-inflammatory and pro-anabolic state that sustain the alveolar-bone homeostasis. PMNs, polymorph nuclear neutrophil; B/P, B and plasma cell.