衰老和机械负荷对关节软骨代谢的影响。
The Effect of Aging and Mechanical Loading on the Metabolism of Articular Cartilage.
作者信息
Jørgensen Adam El Mongy, Kjær Michael, Heinemeier Katja Maria
机构信息
From the Institute of Sports Medicine, Department of Orthopedic Surgery M, Bispebjerg Hospital, and the Department of Biomedical Sciences, Center for Healthy Aging, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
A.E. Jørgensen, MD, Institute of Sports Medicine, Department of Orthopedic Surgery M, Bispebjerg Hospital, Center for Healthy Aging, Faculty of Health and Medical Sciences, University of Copenhagen; M. Kjær, MD, DMSc, Institute of Sports Medicine, Department of Orthopedic Surgery M, Bispebjerg Hospital, Center for Healthy Aging, Faculty of Health and Medical Sciences, University of Copenhagen; K.M. Heinemeier, MSc, PhD, Institute of Sports Medicine, Department of Orthopedic Surgery M, Bispebjerg Hospital, and Department of Biomedical Sciences, Center for Healthy Aging, Faculty of Health and Medical Sciences, University of Copenhagen.
出版信息
J Rheumatol. 2017 Apr;44(4):410-417. doi: 10.3899/jrheum.160226. Epub 2017 Mar 1.
OBJECTIVE
The morphology of articular cartilage (AC) enables painless movement. Aging and mechanical loading are believed to influence development of osteoarthritis (OA), yet the connection remains unclear.
METHODS
This narrative review describes the current knowledge regarding this area, with the literature search made on PubMed using appropriate keywords regarding AC, age, and mechanical loading.
RESULTS
Following skeletal maturation, chondrocyte numbers decline while increasing senescence occurs. Lower cartilage turnover causes diminished maintenance capacity, which produces accumulation of fibrillar crosslinks by advanced glycation end products, resulting in increased stiffness and thereby destruction susceptibility.
CONCLUSION
Mechanical loading changes proteoglycan content. Moderate mechanical loading causes hypertrophy and reduced mechanical loading causes atrophy. Overloading produces collagen network damage and proteoglycan loss, leading to irreversible cartilage destruction because of lack of regenerative capacity. Catabolic pathways involve inflammation and the transcription factor nuclear factor-κB. Thus, age seems to be a predisposing factor for OA, with mechanical overload being the likely triggering cause.
目的
关节软骨（AC）的形态结构使其能够实现无痛运动。衰老和机械负荷被认为会影响骨关节炎（OA）的发展，但其联系尚不清楚。
方法
本叙述性综述描述了该领域的现有知识，通过在PubMed上使用与AC、年龄和机械负荷相关的适当关键词进行文献检索。
结果
骨骼成熟后，软骨细胞数量减少，同时衰老增加。较低的软骨更新导致维持能力下降，进而导致晚期糖基化终产物引起的纤维状交联积累，导致硬度增加，从而易受破坏。
结论
机械负荷会改变蛋白聚糖含量。适度的机械负荷会导致肥大，而负荷降低会导致萎缩。过度负荷会导致胶原网络损伤和蛋白聚糖丢失，由于缺乏再生能力，导致不可逆的软骨破坏。分解代谢途径涉及炎症和转录因子核因子κB。因此，年龄似乎是OA的一个易感因素，而机械过载可能是触发原因。
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