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P086 Adipocytokines linking obesity and osteoarthritis

Introduction In the Western society, obesity and the resulting metabolic changes are an increasing field of medical research. Both conditions alter the expression of adipokines such as adiponectin, visfatin or leptin, which can modulate key pathways of the immune system or the progress of osteoarthritis (OA). Objectives To evaluate cross-linking influences of the abovementioned comorbidities, we combined a high-fat diet (HFD) with the DMM osteoarthritis mouse model (Destabilisation of the M edial M eniscus). The serologic as well as local tissue effects of HFD at different stages of OA development were correlated to the local and systemic adipokine expression. Methods ND (normal diet) and HFD were fed to C57Bl/6 mice over a period of 3 months followed by surgical OA induction (time point 0). Tissues and sera were collected 4, 6, and 8 weeks after surgery. Serum levels of adipokines were measured by ELISA. Liver fat was scored to evaluate metabolic changes. Arthritis progression was scored and quantified based on histologic stainings of the joints (H/E, safranin O, Pappenheim and Masson-Goldner’s trichrome). Immunohistochemical stainings of the joints were performed to evaluate local distribution of adipokine positive cells. Metabolic parameters were correlated to the progression of OA. Results At all time points, OA could be induced in all settings, especially when combined with HFD (e.g.: OA score at 6 weeks HFD 3.7 vs. ND 1.4). Systemically, leptin levels were significantly higher in HFD compared to ND, suggesting a leptin and established insulin resistance. However, DMM led to decreased leptin levels at all time points, independent from diet (e.g. 4 weeks: HFD healthy 18.4 ng/ml vs. HFD DMM 3.7 ng/ml). Systemic leptin levels and fatty-liver score were positively correlated. Interestingly, the systemic increase of adiponectin mediated by DMM was only visible at week 8 (HFD healthy 5176 ng/ml vs. HFD DMM 6149 ng/ml). HFD, DMM or the combination of both did not show significant effects on serum levels of adiponectin, visfatin or IL-6. The local adipokine distribution in the joints was independent from systemic parameters. Conclusions Our data show that similar to observations in humans, OA is deteriorated by HFD. This is reflected by increased numbers of adipokine positive cells in areas of destruction. This phenomenon appears to be based on local mechanisms as systemic adipokine levels did not reflect the intraarticular adipokine distribution. Disclosure of interest None declared