The Biological Pathways of Vitamin D in Preventing Osteoclastogenesis of Alveolar Bone in Periodontitis: An Overview

Periodontitis is a chronic inflammatory disease of the periodontal tissue caused by an imbalance of bacteria and host responses. It is characterized by loss of periodontal adhesions, deepening of the periodontal pocket, and resorption of alveolar bone. Alveolar bone resorption in periodontitis occurs due to the osteoclastogenesis activated by proinflammatory cytokines via the activation of RANKL-OPG and TNF-α signaling pathways. Low serum vitamin D levels are often found in people with periodontitis. Vitamin D is a secosteroid hormone that plays a role in bone metabolism and suppressing cytokine production in the alveolar bone osteoclastogenesis process. Via VDR, vitamin D will affect RANKL and OPG expression regulation, resulting in a decrease in the RANKL/OPG ratio, which reduces osteoclast differentiation. In addition, vitamin D suppresses the c-Fos protein expression, a transcription factor for osteoclast differentiation. This review will highlight the interaction between vitamin D and osteoclastogenesis, especially in molecular pathways