Department of Anatomy, Paracelsus Medical University, Prof. Ernst Nathan Str. 1, 90419, Nuremberg, Germany.
Institute of Anatomy, Paracelsus Medical University, Salzburg, Austria.
Inflamm Res. 2018 Apr;67(4):285-300. doi: 10.1007/s00011-017-1121-8. Epub 2017 Dec 1.
Today, not only the existence of an interrelation between obesity/adipositas and osteoarthritis (OA) but also the association of OA and diabetes mellitus (DM) are widely recognized. Nevertheless, shared influence factors facilitating OA development in DM patients still remain speculative up until now. To supplement the analysis of clinical data, appropriate in vitro models could help to identify shared pathogenetic pathways. Informative in vitro studies could later be complemented by in vivo data obtained from suitable animal models.
Therefore, this detailed review of available literature was undertaken to discuss and compare the results of currently published in vitro studies focusing on the interrelation between OA, the metabolic syndrome and DM and to propose models to further study the molecular pathways.
The survey of literature presented here supports the hypothesis that the pathogenesis of OA in DM is based on imbalanced molecular pathways with a putative crucial role of antiinflammatory cytokines such as IL-10.
Future development of versatile micro-scaled in vitro models such as combining DM and OA on chip could allow the identification of common pathogenetic pathways and might help to develop novel therapeutic strategies.
如今，肥胖/脂肪过多症与骨关节炎（OA）之间存在相互关系，OA 与糖尿病（DM）之间存在关联，这已得到广泛认可。然而，目前仍有推测认为，在 DM 患者中促进 OA 发展的共同影响因素仍然存在。为了补充对临床数据的分析，适当的体外模型有助于确定共同的发病机制途径。随后，可通过从合适的动物模型中获得的体内数据对有意义的体外研究进行补充。
因此，进行了这项详细的文献综述，以讨论和比较目前发表的重点关注 OA、代谢综合征和 DM 之间相互关系的体外研究结果，并提出进一步研究分子途径的模型。
本文对文献的综述支持了这样一种假设，即 DM 中 OA 的发病机制基于失衡的分子途径，具有抗炎细胞因子（如 IL-10）的潜在关键作用。
未来开发多功能微尺度的体外模型，例如将 DM 和 OA 结合在芯片上，可能有助于识别共同的发病机制途径，并可能有助于开发新的治疗策略。
