Skip to main content

From joint injury to joint replacement – Untangling the pathomechanisms of posttraumatic osteoarthritis

Edited by:

Dr. Jana Riegger-Koch, University of Ulm, Germany
Dr. Zsuzsa Jenei-Lanzl, PD, Goethe University Frankfurt, University Hospital, Germany

Submission Status: Open   |   Submission Deadline: 28 February 2025

Arthritis Research & Therapy is calling for submissions to our Collection on From joint injury to joint replacement – Untangling the pathomechanisms of posttraumatic osteoarthritis. Osteoarthritis (OA) is a chronic degenerative disease of the entire joint, affecting not only articular cartilage, but also other joint-related tissues such as synovium, subchondral bone, ligaments, tendons or even menisci and fat pad. The degenerative and inflammatory processes in these tissues lead to chronic pain and an enormous limitation of mobility and thus quality of life. OA pathogenesis is multifactorial and thus associated with various risk factors, including aging, genetics, sex, joint misalignment or injuries among others. Thus, OA is a heterogeneous disease with different clinical phenotypes. This might be the primary reason for the fact that therapeutic options are rare and OA still represents an incurable disease. Upon joint injuries, pathophysiologic mediators including cytokines or reactive oxygen species (ROS), accumulate in the damaged tissue and induce various molecular pathomechanisms, such as regulated cell death and phenotypical alteration of chondrocytes, pro-inflammatory activation of synovial cells, infiltration of immune cells, or changes in subchondral osteoblast and osteoclast activities. At the same time, various catabolic and inflammatory molecules also activate sensory nerve fibers resulting in pain. Altogether, processes like enhanced inflammation and oxidative stress affect the behavior and fate of joint-related cells, which are thought to substantially contribute to cartilage degeneration. These processes may proceed over many years and even decades, eventually leading to the onset of an early form of OA, so-called posttraumatic OA (PTOA). Despite many reports about cartilage-resident chondrogenic stem/progenitor cells and certain intrinsic regenerative attempts (e.g., increased expression of matrix components at early stages, proliferation of cartilage cells), cartilage is widely considered as non-healing tissue. 
Although great progress has been made in uncovering the underlying pathomechanisms of PTOA, our understanding of the disease is still incomplete.
This collection aims to present recent advances in untangling the underlying pathomechanisms involved in PTOA progression and deducing novel approaches in PTOA therapy. We welcome the submission of original research articles describing basic research findings, translational and/or clinical studies, as well as systematic or narrative reviews.

Articles should be focused on, but not limited to, the following topics:

• new in vitro/ in vivo or clinical models to study PTOA (e.g. co-cultures, organ-on-chip models, animal models, novel imaging techniques etc.) and disease-related genesis of joint pain (peripheral-/central sensitization)

• cell fate decision as a consequence of cellular damage/ stress, including regulated cell death and phenotypical alteration (senescence, hypertrophy, dedifferentiation, pro-inflammatory activation etc.), after trauma

• catabolic or inflammatory cellular processes in joint tissues/cells in particular in the early stage of OA

• novel biomarkers or clinical characteristics, e.g., to differentiate OA pheno-/endotypes or describe risk groups (systemic effects of joint trauma / PTOA)

• identification of novel therapeutic targets and modulators in cartilage degeneration and regeneration (e.g., redox-/ mechano-responsive pathways)

• therapeutic approaches and strategies focusing on specific pathomechanisms/ disease drivers involved in OA, for example, complement activation products, ROS, cytokines, catabolic mediators, …

Image credit: Zsuzsa Jenei-Lanzl

New Content ItemThis Collection supports and amplifies research related to SDG 3: Good health and well-being.

Meet the Guest Editors

Back to top

Dr. Jana Riegger-Koch, University of Ulm, Germany

Dr. Jana Riegger-Koch is a junior research group leader and Fellow of the Margarete von Wrangell Habilitation Program at the Division for Biochemistry of Joint and Connective Tissue Diseases, Ulm University, Germany. Since 2019, she holds a Dr. biol. hum. in experimental orthopedics (summa cum laude). Her research mainly focuses on the molecular pathomechanisms of posttraumatic osteoarthritis, including regulated cell death, cellular senescence, and complement activation. Further, Jana is interested in intrinsic cartilage repair by chondrogenic progenitor cells and tissue engineering and regeneration in general. In 2022 Jana performed a 6-months research stay at the Kennedy Institute of Rheumatology (Oxford, UK), which was supported by a DAAD fellowship. Her work has been (inter-)nationally recognized with scientific awards including the Basic Research Award of the German Society for Orthopedics and Trauma Surgery 2017 (Riegger et al., Osteoarthritis Cartilage, 2016), Young Investigator Award of the German Society for Matrix Biology 2019 (Riegger et al., eCell Mater, 2018), GRAMMER/European Spine Journal Award 2021 (Teixeira et al., Eur Spine J, 2021). Lately, she received the ExzellenziaUlm research prize 2024 of the Ulm University for outstanding research work and reconciling family and academic career, thus being a role model for other female researchers and students.


Dr. Zsuzsa Jenei-Lanzl, PD, Goethe University Frankfurt, University Hospital, Germany

PD Dr. Zsuzsa Jenei-Lanzl is a group leader in the Dr. Rolf M. Schwiete Research Unit for Osteoarthritis at the Department of Trauma Surgery and Orthopedics, Goethe University Frankfurt, Germany. After earning her PhD in experimental trauma surgery with a focus on stem cell-dependent regeneration of articular cartilage at the University Hospital Regensburg, she worked as a Postdoc in the Laboratory of Experimental Rheumatology and Neuroendocrine Immunology at the Department of Internal Medicine I, also at the University Hospital Regensburg. Here, she built up expertise in the areas of cellular neuroendocrine immunology as well as murine arthritis models. In 2016, Zsuzsa moved from Regensburg to Frankfurt am Main to set up an orthopedic basic research group together with Prof. Dr. Frank Zaucke. Here, she established her own working group and research area focusing on the involvement of the autonomic nervous system in the pathogenesis of degenerative joint diseases such as osteoarthritis or disc degeneration. In 2023, she received the Venia legendi in experimental orthopedics.


There are currently no articles in this collection.

Submission Guidelines

Back to top

This Collection welcomes submission of original research articles describing basic research findings, translational and/or clinical studies, as well as systematic or narrative reviews. Should you wish to submit a different article type, please read our submission guidelines to confirm that type is accepted by the journal. 

Articles for this Collection should be submitted via our submission system, Snapp. Please, select the appropriate Collection title “From joint injury to joint replacement – Untangling the pathomechanisms of posttraumatic osteoarthritis" under the “Details” tab during the submission stage.

Articles will undergo the journal’s standard peer-review process and are subject to all the journal’s standard policies. Articles will be added to the Collection as they are published.

The Editors have no competing interests with the submissions which they handle through the peer-review process. The peer-review of any submissions for which the Editors have competing interests is handled by another Editorial Board Member who has no competing interests.