Silke Schwarz1,2, Ingo Mrosewski3, Sandeep Silawal1,2, Gundula Schulze-Tanzil4,5. 1. Department of Anatomy, Paracelsus Medical University, Prof. Ernst Nathan Str. 1, 90419, Nuremberg, Germany. 2. Institute of Anatomy, Paracelsus Medical University, Salzburg, Austria. 3. MVZ Limbach Laboratories, Aroser Allee 84, 13407, Berlin, Germany. 4. Department of Anatomy, Paracelsus Medical University, Prof. Ernst Nathan Str. 1, 90419, Nuremberg, Germany. gundula.schulze@pmu.ac.at. 5. Institute of Anatomy, Paracelsus Medical University, Salzburg, Austria. gundula.schulze@pmu.ac.at.
Abstract
INTRODUCTION: 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. MATERIALS AND METHODS: 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. RESULTS: 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. CONCLUSION: 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.
INTRODUCTION: 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 DMpatients 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. MATERIALS AND METHODS: 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. RESULTS: 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. CONCLUSION: 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.
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