Abstract
Post-traumatic osteoarthritis (PTOA) is a degenerative joint disease, leading to articular cartilage breakdown, osteophyte formation, and synovitis, caused by an initial joint trauma. Pro-inflammatory cytokines increase catabolic activity and may perpetuate inflammation following joint trauma. Interleukin-15 (IL-15), a pro-inflammatory cytokine, is increased in OA patients, although its roles in PTOA pathophysiology are not well characterized. Here, we utilized Il15 deficient rats to examine the role of IL-15 in PTOA pathogenesis in an injury-induced model. OA was surgically induced in Il15 deficient Holtzman Sprague-Dawley rats and control wild-type rats to compare PTOA progression. Semi-quantitative scoring of the articular cartilage, subchondral bone, osteophyte size, and synovium was performed by two blinded observers. There was no significant difference between Il15 deficient rats and wild-type rats following PTOA-induction across articular cartilage damage, subchondral bone damage, and osteophyte scoring. Similarly, synovitis scoring across six parameters found no significant difference between genetic variants. Overall, IL-15 does not appear to play a key role in the development of structural changes in this surgically-induced rat model of PTOA.
Highlights
Osteoarthritis (OA) is a musculoskeletal disorder that presents a significant global burden, with over 303 million cases of hip and knee OA, which is expected to increase [1]
Post-traumatic osteoarthritis (PTOA) is a subtype of OA that develops after joint trauma, such as meniscal or ligament injury, and occurs most often in the lower extremities [3]
We investigated the role of IL-15 in the development of structural joint changes related to knee PTOA using a well-established rat model of surgically-induced PTOA in Il15−/− rats and control Il15+/+ rats
Summary
Osteoarthritis (OA) is a musculoskeletal disorder that presents a significant global burden, with over 303 million cases of hip and knee OA, which is expected to increase [1]. OA is a disorder of the entire joint, initially categorized by abnormal joint tissue metabolism and later by structural joint tissue changes. Each tissue reacts to the disease both independently and in response to changes in neighbouring tissue, resulting in joint pathologies including cartilage degeneration, subchondral bone remodeling, osteophyte formation, and synovial inflammation [2]. Post-traumatic osteoarthritis (PTOA) is a subtype of OA that develops after joint trauma, such as meniscal or ligament injury, and occurs most often in the lower extremities [3]. PTOA is estimated to account for 12% of all lower extremity OA cases, with costs of about USD 3 billion annually [4]. PTOA may affect any joint, knees and ankles are the most commonly affected [3]
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