1,25‐dihydroxyvitamin D deficiency accelerates alveolar bone loss independent of aging and extracellular calcium and phosphorus

• DOI: 10.1002/jper.17-0542
• Publication Date: 2018-05-04T07:51:15Z
• Authors: Aixiu Gong; Jie Chen; Jun Wu; Jing Li; Lin Wang; David Goltzman; Dengshun Miao
• Keywords: Mice; 03 medical and health sciences; 0302 clinical medicine; Alveolar Bone Loss; Animals; Calcium; Phosphorus; X-Ray Microtomography; Vitamin D

Vitamin D is critical for bone homeostasis and immunomodulation. We therefore assessed whether 1,25-dihydroxyvitamin (1,25(OH)2 D) deficiency in mice with targeted deletion of the gene encoding 25-hydroxyvitamin D-1α-hydroxylase (1α(OH)ase [1αOH)ase-/- mice]) results alveolar loss periodontal inflammation vivo.Ten-week-old 12-month-old 1α(OH)ase-/- wild-type littermates were fed a normal diet or rescue diet, phenotype periodontium was then analyzed using microcomputed tomography, histology, immunohistochemistry, real-time Reverse transcription-polymerase chain reaction (RT-PCR).Alveolar increased maxillary mineral density (BMD), osteoblast numbers, number osterix-positive cells decreased significantly compared mice. Although aging from 10 weeks to 12 months accentuated these changes, reduced them, alterations exceeded effects change. Nuclear factor kappa light-chain-enhancer activated B (NF-кB) p65 CD3 positive cells, expression levels interleukin (IL)-1β, tumor necrosis (TNF)-α, matrix metalloproteinase (MMP)-3 -8 all tissues Aging also however, change.1,25(OH)2 accelerated by inhibiting osteoblastic formation enhancing tissue degeneration calcium- phosphorus- as well an age-independent manner.