gms | German Medical Science

45. Kongress der Deutschen Gesellschaft für Rheumatologie, 31. Jahrestagung der Deutschen Gesellschaft für Orthopädische Rheumatologie, 27. Jahrestagung der Gesellschaft für Kinder- und Jugendrheumatologie

06.09. - 09.09.2017, Stuttgart

Interaction of Osteoarthritis and Metabolism

Meeting Abstract

  • Marie-Lisa Hülser - Justus-Liebig-Universität Gießen, Kerckhoff-Klinik GmbH, Rheumatologie u. klinische Immunologie, Osteologie, Physikalische Therapie, Bad Nauheim
  • Carina Schreiyaeck - Justus-Liebig-Universität Gießen, Kerckhoff-Klinik GmbH, Rheumatologie u. klinische Immunologie, Osteologie, Physikalische Therapie, Bad Nauheim
  • Yubin Luo - University of Erlangen-Nürnberg, Department Clinic of Medicine 3 - Immunology and Rheumatology, Erlangen, Germany, Erlangen
  • Aline Bozec - University of Erlangen-Nürnberg, Department Clinic of Medicine 3 - Immunology and Rheumatology, Erlangen, Germany, Erlangen
  • Georg Schett - Universitätsklinikum Erlangen, Medizinische Klinik 3, Rheumatologie und Immunologie, Erlangen
  • Elena Neumann - Justus-Liebig-Universität Gießen, Kerckhoff-Klinik GmbH, Rheumatologie u. klinische Immunologie, Osteologie, Physikalische Therapie, Bad Nauheim
  • Ulf Müller-Ladner - Justus-Liebig-Universität Gießen, Kerckhoff-Klinik GmbH, Rheumatologie u. klinische Immunologie, Osteologie, Physikalische Therapie, Bad Nauheim

Deutsche Gesellschaft für Rheumatologie. Deutsche Gesellschaft für Orthopädische Rheumatologie. Gesellschaft für Kinder- und Jugendrheumatologie. 45. Kongress der Deutschen Gesellschaft für Rheumatologie (DGRh), 31. Jahrestagung der Deutschen Gesellschaft für Orthopädische Rheumatologie (DGORh), 27. Jahrestagung der Gesellschaft für Kinder- und Jugendrheumatologie (GKJR). Stuttgart, 06.-09.09.2017. Düsseldorf: German Medical Science GMS Publishing House; 2017. DocER.21

doi: 10.3205/17dgrh098, urn:nbn:de:0183-17dgrh0981

Veröffentlicht: 4. September 2017

© 2017 Hülser et al.
Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung). Lizenz-Angaben siehe http://creativecommons.org/licenses/by/4.0/.


Gliederung

Text

Background: Obesity and metabolic syndrome are of increasing importance in the Western society. Both lead to changes in expression of adipokines such as adiponectin, visfatin or leptin, which can work as modulatory factors also in osteoarthritis (OA).

Since OA is often accompanied by obesity, we combined the DMM mouse model (destabilization of the medial meniscus) with a high-fat diet (HFD). The systemic and local effects of HFD at different states of OA development was evaluated and correlated to local/systemic adipokine expression.

Methods: HFD and ND (normal diet) as control were fed to C57Bl/6 mice for 3 months followed by surgical OA induction (time point 0). Tissues and sera were collected at 4, 6, 8 weeks after surgery. Adipocytokine (leptin, visfatin, adiponectin and IL-6) serum levels were measured by ELISA. Arthritis was scored using histologic stainings of the joints (H/E, safranin O, Pappenheim and Masson-Goldner’s trichrome). Immunohistochemical stainings of the joints were performed to evaluate the local distribution of adipokines. Adipokine levels were correlated to e.g. arthritis scores and weight.

Results: At all time points, OA induction was visible, especially with HFD compared to ND (e.g.: OA score: 6 weeks ND 1.4, HFD 3.7). Systemically, leptin levels were significantly induced by HFD, but DMM decreased leptin levels at all time points (e.g. 4 weeks: HFD healthy 18.4 ng/ml vs. HFD DMM 3.7ng/ml). Interestingly, the systemic increase of adiponectin by DMM was time dependent (maximum at week 8: HFD healthy 5176ng/ml vs. HFD DMM 6149ng/ml). The combination of HFD and DMM did not show significant effects on serum levels of adiponectin, visfatin or IL-6. Interestingly, local adipokine expression in the joints was not directly correlated with systemic adipokine levels.

Conclusion: OA in the DMM model is deteriorated by HFD. Systemic leptin levels were elevated by HFD but reduced by DMM which could not be observed for the proinflammatory adipokine visfatin. Systemic adiponectin expression was dependent on the stage of OA development. Therefore, local and systemic adipokine expression appears not directly linked and systemic alterations seem to affect OA by indirect mechanisms.