This 2012 narrative review by Loeser et al. synthesizes OA pathophysiology across all joint tissues: cartilage, subchondral bone, synovium, menisci, and ligaments. It argues that OA is not passive wear-and-tear but an active, inflammation-driven remodeling process affecting the entire joint as an organ. The review catalogs molecular targets and therapeutic rationale, establishing the 'joint failure' framework that now underpins OA research and clinical guidelines.
Two findings from this paper should change what you do before every TKA: nearly 1 in 4 symptomatic OA knees has a complete ACL rupture on MRI, and most patients have no recalled trauma history. Routine preoperative MRI before TKA can identify occult ACL deficiency and should shift implant selection toward a posterior-stabilized design. History alone is unreliable.
When a patient with knee pain has no radiographic OA, do not dismiss MRI synovitis or effusion as incidental. These findings predict cartilage erosion at 30 months, before any X-ray changes appear — they warrant closer follow-up and aggressive risk factor modification.
This framework also explains why isolated cartilage procedures often underperform in the OA milieu: if synovitis is sustaining catabolic enzyme production and subchondral bone lesions are generating pain, a chondral repair alone cannot address the full disease process. The 'joint failure' model introduced here has since been adopted in OARSI and EULAR guidelines mandating whole-joint structural assessment.
This 2012 narrative review by Loeser et al. synthesizes OA pathophysiology across all joint tissues: cartilage, subchondral bone, synovium, menisci, and ligaments. It argues that OA is not passive wear-and-tear but an active, inflammation-driven remodeling process affecting the entire joint as an organ. The review catalogs molecular targets and therapeutic rationale, establishing the 'joint failure' framework that now underpins OA research and clinical guidelines.
Two findings from this paper should change what you do before every TKA: nearly 1 in 4 symptomatic OA knees has a complete ACL rupture on MRI, and most patients have no recalled trauma history. Routine preoperative MRI before TKA can identify occult ACL deficiency and should shift implant selection toward a posterior-stabilized design. History alone is unreliable.
When a patient with knee pain has no radiographic OA, do not dismiss MRI synovitis or effusion as incidental. These findings predict cartilage erosion at 30 months, before any X-ray changes appear — they warrant closer follow-up and aggressive risk factor modification.
This framework also explains why isolated cartilage procedures often underperform in the OA milieu: if synovitis is sustaining catabolic enzyme production and subchondral bone lesions are generating pain, a chondral repair alone cannot address the full disease process. The 'joint failure' model introduced here has since been adopted in OARSI and EULAR guidelines mandating whole-joint structural assessment.