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Our research focus in brief

Osteoarthritis (OA) is the most prevalent joint disease worldwide and is associated with excessive degeneration of the intraarticular cartilage, a tissue with very poor intrinsic regeneration. Besides age, accidental injuries of the articular cartilage represent a crucial risk factor in OA, resulting in a so-called posttraumatic osteoarthritis – a special form of OA, which can already be developed in early lifetime. As OA is hitherto considered as uncurable, our research focuses on the clarification of trauma-associated pathomechanisms in cartilage tissue with the objective of finding new therapeutic targets. Potential treatment options not only include acute harm reduction but also tissue regenerative approaches.

Today we know that cartilage cells (chondrocytes) themselves contribute decisively to ongoing degeneration of the extracellular matrix. Therefore, we aim on the characterization of dysfunctional chondrocytes and identification of mediators as well as cellular mechanisms driving the pathogenesis of OA. For the investigation of early posttraumatic processes, we use a well-established ex vivo cartilage trauma model (see below). By means of this model, we have gained valuable insights into the behavior and fate of surviving chondrocytes [1,2,3], identified potential therapeutic targets [4] and tested ne treatment strategies [5,6]. Moreover, we are interested in the role and regenerative potential of chondrogenic stem-/ progenitor cells (CSPC) within the cartilage, which respond to tissue injury by migration, proliferation and immunomodulation [7].

References: [1] Riegger J and Brenner RE. Pathomechanisms of Posttraumatic Osteoarthritis: Chondrocyte Behavior and Fate in a Precarious Environment. Int J Mol Sci. 2020, 21:1560. [2] Riegger J and Brenner R. Evidence of necroptosis in osteoarthritic disease: Investigation of blunt mechanical impact as possible trigger in regulated necrosis. Cell Death Dis. 2019, 10:683. [3] Kirsch V, Ramge J-M, Schoppa A, Ignatius A, Riegger J. In Vitro Characterization of Doxorubicin-Mediated Stress-Induced Premature Senescence in Human Chondrocytes. Cells. 2022, 11(7): 1106. [4] Riegger J, Huber-Lang M and Brenner RE. Crucial role of the terminal complement complex in chondrocyte death and hypertrophy after cartilage trauma. Osteoarthritis Cartilage. 2020; 28(5):685-697. doi:10.1016/j.joca.2020.01.004. [5] Riegger J, Joos H, Palm HG, Friemert B, Reichel H, Ignatius A, Brenner RE. Striking a new path in reducing cartilage breakdown: combination of antioxidative therapy and chondroanabolic stimulation after blunt cartilage trauma. J Cell Mol Med. 2018, 22(1):77-88. [6] Riegger J, Joos H, Palm HG, Friemert B, Reichel H, Ignatius A, Brenner RE. Antioxidative therapy in an ex vivo human cartilage trauma-model: attenuation of trauma-induced cell loss and ECM-destructive enzymes by N-acetyl cysteine. Osteoarthritis Cartilage. 2016, 24(12):2171-80. [7] Riegger J, Palm HG, Brenner RE. The functional role of chondrogenic stem/ progenitor cells: Novel evidence for immunomodulatory properties and regenerative potentials after cartilage injury. Eur Cell Mater. 2018, 36:110-127.

Drop Tower_Scheme 1 Kopie.tiff

Our ex vivo cartilage trauma model

After pulling out the "trigger", the weight falls down and gains energy due to gravity. By reaching the end of the guide rail, the kinetic energy is transmitted in the sample, which is placed in the sample slot under the "indenter". The support frame stabilizes the guide rail and thus guarantees a perfect vertical fall of the weight without loss of energy.

Our cooperations

Our lab has various national and internation collaboration partners. Internal collaborators: - Prof. Markus Huber-Lang (Institut für Klinische und Experimentelle Trauma-Immunologie) - Prof. Anita Ignatius (Institut für Unfallchirurgische Forschung und Biomechanik) - PD Christoph Schmidt (Institut für Naturheilkunde und Klinische Pharmakologie) - Prof. Jan Münch (Institut für Molekulare Virologie) External collaborators: - Prof. Frank Zaucke (Dr. Rolf M. Schwiete Forschungsbereich für Arthrose, Orthopädische Universitätsklinik Friedrichsheim/ Frankfurt) - Prof. Tonia Vincent (Kennedy Institute of Rheumatology, University of Oxford)

Our funding

Our research is currently funded by - European Social Fund and the Ministry of Science, Research and Arts Baden-Württemberg - German Research foundation (DFG) - Professorinnenprogramm III (University of Ulm) - Collaborative Research Centre (CRC) 1149 Ulm - German Ministry of Defence - German Society of Orthopedics and Orthopedic Surgery (DGOOC)

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