Neuromuscular aspects of osteoarthritis: a perspective

Osteoarthritis (OA) represents failure of the diarthrodial joint and may be due to a primary abnormality in any of the tissues of the joint, e.g. articular cartilage, subchondral bone, synovium, periarticular muscle, or sensory nerves whose termini lie within the joint. Neuropathic arthropathy, due to severe sensory neuropathy, causes severe and rapid breakdown of joints. We have shown that interruption of sensory input from the ipsilateral hind limb strikingly accelerates progression of OA after anterior cruciate ligament transection in the dog; a clinical correlate exists in humans with diabetic neuropathy who sustain even minor joint trauma. Knee OA in humans is accompanied by defects in proprioception, although it is not clear whether the neurological abnormality is primary or a consequence of intra-articular pathology. The magnitude of the load on a joint and, especially, the rate of impulsive loading, influence development of OA. It is relevant, therefore, that quadriceps weakness may precede development of knee OA in some people, insofar as this may diminish the effectiveness of protective muscular reflexes and thereby increase deleterious joint loading. Individuals vary with respect to how they load their joints, perhaps because of genetic differences in central program generators.