The Enigma of Posttraumatic Osteoarthritis

Abstract

Although methods to prevent the progression of posttraumatic osteoarthritis (PTOA) remain elusive, understanding its underlying mechanisms is an important first step toward this goal. In tackling the challenging issue of instability-related PTOA of the shoulder, Aleem and colleagues present novel data on differential chondrocyte gene expression in acute versus chronic shoulder instability while also comparing these conditions with the advanced shoulder osteoarthritis state. Their results are consistent with similar analyses of chondrocyte gene expression after anterior cruciate ligament (ACL) injury 1,2 but also highlight the extreme complexity of how articular cartilage interacts with and responds to external factors. Momentary mechanical trauma on the articular surface during shoulder dislocation results in focal injury to the cartilage matrix and chondrocyte apoptosis. However, the trauma alone is insufficient to explain why global cartilage degeneration in the shoulder joint occurs over time.To understand the mechanisms responsible for PTOA, the joint must be thought of as an organ, with multiple tissues including the synovium, tendon, and subchondral bone contributing to the disease process 3,4 . Additionally, both biologic and mechanical changes must be studied together, as it is the interaction between these factors that determines the risk and rate of progression of PTOA 5 . Native articular cartilage exists in a state of relative cellular quiescence and homeostasis. Traumatic insults tip that state out of equilibrium, and the biologic processes that follow remain unclear. The inherent reparative capabilities of chondrocytes are typically insufficient, and the production of a complex milieu of inflammatory cytokines and catabolic enzymes evolves over time. The disease processes not only differ between acute and chronic instability conditions but also vary depending on the tissue type. Whereas this study found a greater pro-inflammatory transcriptional response within chondrocytes in the acute instability versus chronic instability conditions, Jacobs et al. reported higher concentrations of pro-inflammatory cytokines within the synovium of multiple dislocators compared with first-time dislocators 4 . The contribution of paracrine effects of other tissues, particularly the synovium, to the progressive degradation of cartilage remain ill-defined.Furthermore, one cannot discount the effects of shoulder instability on joint kinematics and mechanical loading of the cartilage surface. Damage to the static stabilizers such as the labrum, ligaments, and capsule, as well as the apprehension and fear that likely result in alterations of the muscle activation patterns and dynamic stability of the shoulder, ultimately may result in higher loads transmitted across certain areas of the joint. Chondrocytes are highly sensitive to their mechanical microenvironment, and in response to mechanical stresses, they can drive changes in the structure and composition of the local extracellular matrix. Surgical stabilization has g...