Department of Orthopaedic Surgery, Washington University, Couch Biomedical Research Bldg., Room 3121, Campus Box 8233, Saint Louis, Missouri 63110.
Shriners Hospitals for Children - St. Louis, Saint Louis, Missouri 63110.
J Orthop Res. 2019 Mar;37(3):779-788. doi: 10.1002/jor.24219. Epub 2019 Feb 12.
Obesity is a primary risk factor for osteoarthritis (OA), and previous studies have shown that dietary content may play an important role in the pathogenesis of cartilage and bone in knee OA. Several previous studies have shown that the ratio of ω-3 polyunsaturated fatty acids (PUFAs), ω-6 PUFAs, and saturated fatty acids can significantly influence bone structure and OA progression. However, the influence of obesity or dietary fatty acid content on shoulder OA is not well understood. The goal of this study was to investigate the role of dietary fatty acid content on bone and cartilage structure in the mouse shoulder in a model of diet-induced obesity. For 24 weeks, mice were fed control or high-fat diets supplemented with ω-3 PUFAs, ω-6 PUFAs, or saturated fatty acids. The humeral heads were analyzed for bone morphometry and mineral density by microCT. Cartilage structure and joint synovitis were determined by histological grading, and microscale mechanical properties of the cartilage extracellular and pericellular matrices were quantified using atomic force microscopy. Diet-induced obesity significantly altered bone morphology and mineral density in a manner that was dependent on dietary free fatty acid content. In general, high-fat diet groups showed decreased bone quality, with the ω-3 diet being partially protective. Cartilage mechanical properties and OA scores showed no changes with obesity or diet. These findings are consistent with clinical literature showing little if any relationship between obesity and shoulder OA (unlike knee OA), but suggest that diet-induced obesity may influence other joint tissues. © 2019 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res.
肥胖是骨关节炎（OA）的一个主要危险因素，先前的研究表明，饮食内容可能在膝 OA 中软骨和骨骼的发病机制中发挥重要作用。几项先前的研究表明，ω-3 多不饱和脂肪酸（PUFAs）、ω-6 PUFAs 和饱和脂肪酸的比例可以显著影响骨骼结构和 OA 的进展。然而，肥胖或饮食脂肪酸含量对肩 OA 的影响尚不清楚。本研究的目的是研究饮食脂肪酸含量对肥胖诱导模型中小鼠肩部骨和软骨结构的作用。在 24 周的时间里，用对照或高脂肪饮食喂养小鼠，这些饮食补充了 ω-3 PUFAs、ω-6 PUFAs 或饱和脂肪酸。通过 microCT 分析肱骨头的骨形态计量学和矿物质密度。通过组织学分级确定软骨结构和关节滑膜炎，使用原子力显微镜定量测量软骨细胞外和细胞周基质的微尺度力学特性。饮食诱导的肥胖以依赖于饮食游离脂肪酸含量的方式显著改变了骨骼形态和矿物质密度。一般来说，高脂肪饮食组的骨质量下降，而 ω-3 饮食具有部分保护作用。软骨力学性能和 OA 评分与肥胖或饮食无关。这些发现与临床文献一致，即肥胖与肩 OA（与膝 OA 不同）之间几乎没有关系，但表明饮食诱导的肥胖可能会影响其他关节组织。版权所有©2019 矫形研究学会。由 Wiley Periodicals, Inc. 出版。J 矫形研究。
