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