Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8309418 | Clinica Chimica Acta | 2018 | 35 Pages |
Abstract
Osteoporosis is a systemic skeletal disorder characterized by a decrease in bone mass and microarchitectural deterioration of bone tissue. The World Health Organization has defined osteoporosis as a decrease in bone mass (50%) and bony quality (50%). Vitamin D, a steroid hormone, is crucial for skeletal health and in mineral metabolism. Its direct action on osteoblasts and osteoclasts and interaction with nonskeletal tissues help in maintaining a balance between bone turnover and bone growth. Vitamin D affects the activity of osteoblasts, osteoclasts, and osteocytes, suggesting that it affects bone formation, bone resorption, and bone quality. At physiological concentrations, active vitamin D maintains a normal rate of bone resorption and formation through the RANKL/OPG signal. However, active vitamin D at pharmacological concentration inhibits bone resorption at a higher rate than that of bone formation, which influences the bone quality and quantity. Nutritional vitamin D rather than active vitamin D activates osteoblasts and maintains serum 25(OH)D3 concentration. Despite many unanswered questions, much data support nutritional vitamin D use in osteoporosis patients. This article emphasizes the role of nutritional vitamin D replacement in different turnover status (high or low bone turnover disorders) of osteoporosis together with either anti-resorptive (Bisphosphonate, Denosumab et.) or anabolic (Teriparatide) agents when osteoporosis persists.
Keywords
PPAROPGDEXAVDRGFRpTHTregWntCaSRRAASQCTBMDrenin-angiotensin aldosterone systemNOSGIOECMTNFRUNX2RANKLROSRheumatoid arthritisOsteoblastOsteoprotegerinOsteoclastinterleukinChronic obstructive pulmonary diseaseCOPDchronic kidney diseaseBone mineral densityHigh-resolution peripheral quantitative computed tomographycomputed tomographydual-energy X-ray absorptiometryRegulatory T cellbody mass indexBMIRunt-related transcription factor 2Systemic lupus erythematosusSLEExtracellular matrixCKDGlomerular filtration ratenitric oxide synthaseparathyroid hormoneHypovitaminosisOsteoporosisGlucocorticoid-induced osteoporosisBone turnoverReactive oxygen speciesCalcium-sensing receptorPeroxisome proliferator-activated receptorsVitamin D receptor
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Authors
Yi-Chou Hou, Chia-Chao Wu, Min-Tser Liao, Jia-Fwu Shyu, Chi-Feng Hung, Tzung-Hai Yen, Chien-Lin Lu, Kuo-Cheng Lu,