Bone and Musculoskeletal Research Program, Division of Applied Medicine, University of Aberdeen, Institute of Medical Sciences, Foresterhill, Aberdeen AB25 2ZD, UK.
Nat Rev Rheumatol. 2011 Jan;7(1):65-8. doi: 10.1038/nrrheum.2010.123. Epub 2010 Aug 17.
Arthritis Research UK published a report in 2009 entitled "Osteoarthritis and obesity" in which they highlight the severe consequences of obesity for musculoskeletal health. Throughout the report, however, the mechanical effect of excess body weight is assumed to be the direct cause of osteoarthritis (OA). Although this assumption is common, is it supported by the evidence? A survey of the studies associating OA with obesity is inconclusive on whether body weight is the causative factor. The increase in direct-loading on joints due to weight-gain is not as great as is often believed, and compensatory gait patterns ameliorate much of the kinematic effects. One manifestation of obesity, however, is increased adipose tissue--a rich source of proinflammatory endocrine factors. I propose that body weight might not be the main problem in OA pathogenesis, but that increased adipose tissue itself might be both an indicator and a driver of widespread disease.
关节炎研究英国在 2009 年发表了一份题为“骨关节炎和肥胖”的报告，其中强调了肥胖对肌肉骨骼健康的严重后果。然而，在整个报告中，超重的机械效应被假设为骨关节炎（OA）的直接原因。尽管这种假设很常见，但它是否有证据支持呢？一项对肥胖与 OA 相关的研究的调查表明，体重是否是致病因素尚无定论。由于体重增加而导致关节的直接负荷增加并不像人们通常认为的那么大，而且代偿性步态模式减轻了大部分运动学效应。然而，肥胖的一个表现是脂肪组织增加——这是促炎内分泌因素的丰富来源。我提出，体重可能不是 OA 发病机制中的主要问题，而是增加的脂肪组织本身可能既是广泛疾病的一个指标，也是其驱动因素。
