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-alpha 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-kappa B 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. (C) 2012 Elsevier Inc. All rights reserved.