Purpose of review: In addition to the actions of the endocrine hormone, 1alpha,25-dihydroxyvitamin D (1,25(OH)2D) in stimulating intestinal calcium absorption, the regulation of bone mineral metabolism by 1,25(OH)2D is also considered an important contributor to calcium homeostasis. However, recent evidence suggest that 1,25(OH)2D acting either via endocrine or autocrine pathways plays varied roles in bone, which suggests that vitamin D contributes to the maintenance of bone mineral in addition to its catabolic roles. This review highlights the contrasting evidence for the direct action for vitamin D metabolism and activity in bone.
Recent findings: Numerous cells within bone express vitamin D receptor (VDR), synthesise and catabolise 1,25(OH)2D via 25-hydroxyvitamin D 1alpha-hydroxylase (CYP27B1), and 25-hydroxyvitamin D 24-hydroxylase (CYP24A1) enzymes, respectively. Recent evidence suggests that all three genes are required to regulate processes of bone resorption, mineralization and fracture repair. The actions of vitamin D in bone appear to negatively or positively regulate bone mineral depending on the physiological and pathological circumstances, suggesting that vitamin D plays pleiotropic roles in bone.
Keywords: CYP24A1; CYP27B1; Mineralisation; Osteoblasts; Vitamin D; Vitamin D receptor.