Garfinkel Rachel J, Dilisio Matthew F, Agrawal Devendra K
Department of Clinical and Translational Science, Creighton University School of Medicine, Omaha, Nebraska, USA.
CHI Health Alegent Creighton Clinic, Omaha, Nebraska, USA.
Orthop J Sports Med. 2017 Jun 20;5(6):2325967117711376. doi: 10.1177/2325967117711376. eCollection 2017 Jun.
Osteoarthritis (OA) currently affects 10% of the American population. There has been a recent push to determine exactly what causes OA and how it can be treated most effectively. Serum vitamin D levels have been associated with OA and may have an effect on articular cartilage remodeling.
To critically review the published research on the effect of vitamin D on articular cartilage and the development of OA as well as on the mechanism behind cartilage regeneration and degeneration.
Review.
A systematic search of PubMed and the Web of Science was performed for relevant studies published in the English language through April 30, 2016, using the terms , , and .
On a molecular level, 1α,25(OH)D, the activated form of vitamin D, plays a role in articular cartilage degeneration. Vitamin D binds to vitamin D receptors, triggering a signaling cascade that leads to chondrocyte hypertrophy. In clinical trials, vitamin D deficiency poses a risk factor for OA, and those with decreased cartilage thickness are more likely to be vitamin D-insufficient.
The role of vitamin D supplementation in the treatment or prevention of OA remains uncertain. More research is needed to reconcile these conflicting findings.
骨关节炎（OA）目前影响着10%的美国人口。最近人们一直在努力确切确定OA的病因以及如何最有效地治疗它。血清维生素D水平与OA有关，可能对关节软骨重塑有影响。
批判性地回顾已发表的关于维生素D对关节软骨、OA发展以及软骨再生和退变背后机制影响的研究。
综述。
使用相关术语对PubMed和科学网进行系统检索，以查找截至2016年4月30日以英文发表的相关研究。
在分子水平上，维生素D的活化形式1α,25(OH)D在关节软骨退变中起作用。维生素D与维生素D受体结合，触发信号级联反应，导致软骨细胞肥大。在临床试验中，维生素D缺乏是OA的一个危险因素，软骨厚度降低的人更有可能维生素D不足。
补充维生素D在治疗或预防OA中的作用仍不确定。需要更多研究来调和这些相互矛盾的发现。
