CHICAGO—Joint trauma is one of many potential drivers of osteoarthritis disease activity and structural progression. In Post-Traumatic OA: Pathogenesis, Clinical Evolution and Management, a session at the 2018 ACR/ARHP Annual Meeting, experts discussed the effects of sports and other injuries on even young patients’ joints.
Post-traumatic osteoarthritis (OA) may account for 12% of hip, knee and ankle OA cases, and in this form of knee OA, “biomechanics [are] important, as well as malalignment, gait abnormalities and tissue-specific effects,” said Tom Appleton, MD, PhD, assistant professor of medicine, Western University in London, Ontario, Canada.1
OA may develop following injury due to unresolved inflammation, hemarthrosis, chronic destabilization and biomechanical effects of the trauma on cartilage and other tissues. Catabolic responses, such as tissue necrosis and acute innate inflammation that never completely resolves, occur shortly after trauma, followed by anabolic responses, including bone remodeling and extracellular matrix (ECM) synthesis.2 Three weeks after anterior cruciate ligament (ACL) tears, patients have elevated cytokines in their synovial fluid.3 Lubricin, a glycoprotein secreted from synovial fibroblasts, may slowly resolve, and inflammatory markers, such as TNF-α or IL-6, may stay elevated.4
“Does severity of the joint injury matter in terms of pathophysiology and overall risk?” asked Dr. Appleton. Osteochondral fractures may lead to cytokine levels elevated in comparison with soft-tissue injury alone, suggesting more injury leads to more inflammation. More severe intra-articular fractures led to more severe synovitis in one study in mice, but “it didn’t translate to any worse damage in terms of the cartilage nor an increase in cell death.5 So it may depend, in a tissue-specific way, on how intense the injury to the cartilage in the joint is.”
‘Soft tissues are important sources of proteases that are known to damage cartilage & joint structures.’ —Tom Appleton, MD, PhD
Severe, repetitive loading may cause dose-dependent changes to cartilage and synovial lining.6 Hemarthrosis after a knee injury may lead to leukocyte activation and reactive oxygen species (ROS) production even in an otherwise healthy person, and this acute, substantial joint bleeding can damage knee cartilage, much more so than microbleeds.7,8
“What about effects on other joint tissues, such as the soft tissues?” asked Dr. Appleton. Gottingen minipigs showed elevated levels of matrix metalloproteinases (MMP) 1, 13 and the aggrecanase ADAMTS-4 in both their cartilage and ligament tissue after ACL injuries in one study.9 “These soft tissues are important sources of proteases that are known to damage cartilage and joint structures.”