25-hydroxyvitamin D3 ameliorates periodontitis by modulating the expression of inflammation-associated factors in diabetic mice.

Periodontitis is a complication of diabetes mellitus, and the two diseases are highly associated with the dysfunction of inflammatory mediators. 25-hydroxyvitamin D(3) (25(OH)D(3)) plays a pivotal role in inflammatory modulation, but little is known about its effects on the progression of diabetic periodontitis and the underlying mechanism. In this paper, we showed that 25(OH)D(3) ameliorated experimental periodontitis in diabetic mice. The intraperitoneal administration of 25(OH)D(3) to streptozotocin-induced diabetic mice reduced fasting glucose and serum TNF-α levels, leading to decreased alveolar bone loss. Western blot analyses of gingival epithelia showed that vitamin D receptor (VDR) and protein tyrosine phosphatase N2 (PTPN2) were upregulated, while the expression of NF-κB and the phosphorylation of Janus family kinase 1 (JAK1) were attenuated upon 25(OH)D(3) treatment. These data may provide an explanation for the therapeutic benefits and anti-inflammatory effects of 25(OH)D(3). Our findings should have important implications for the clinical therapy of diabetic periodontitis.