The role of muscles in joint degeneration and osteoarthritis. J Biomech. (2007)

Abstract
The purpose of this work was to establish a controlled and reversible muscle weakness model for studying the effects of weakness on joint degeneration leading to osteoarthritis (OA). The knee extensor muscles of rabbits were injected with single or repeat doses of Botulinum type-A toxin (BTX-A) to partially inhibit acetylcholine (ACh) release at the neuromuscular junction. BTX-A-injected muscles atrophied, they became weaker and push-off forces during hopping were reduced compared to control. BTX-A injections had the greatest effect at short-muscle length and low-stimulation frequencies. Superimposing BTX-A injections on anterior cruciate ligament transection did not cause greater muscle atrophy or weakness than BTX-A injections alone. Monthly repeat injections could be used to keep muscles weak for half a year without any obvious adverse effects to the animals. Gross morphology of the knees and histology of articular cartilage suggested that, in some animals, 4 weeks of muscle weakness resulted in initial signs of joint degeneration, indicating that weakness may be an independent risk factor for joint degeneration leading to OA.

My comments
This study was very interesting because it is part of a few papers taken together which are starting to indicate that muscle weakness leads to arthritic changes in the joints. Hitherto, the primary assumption has been that arthritis caused pain, which then caused less activity, which was followed by muscle atrophy.  This one shows that the effect can go the other way as well. The paper showed this by injecting small amounts of botox into the muscles in one limb of rabbits, enough to cause weakness but not paralysis. The rabbits were tested 4 weeks later and researchers found the start of arthritic changes in that limb.

The findings I think are of particular importance in treatment of knee or hip injuries, after joint arthroscopies, and ACL reconstructions for which studies show that leg range of motion returns but strength levels often are not fully restored.  This and a few other studies would indicate that the increased number of joint replacements could be avoided with adequate strengthening either in physical therapy or continuing with an independent exercise program. The problem with the latter is that if fitness isn’t a lifestyle for the patient, then most likely they will stop exercising when they are done with physical therapy.  The other problem is insurance companies using self-evaluated surveys of function to their advantage to force the discharge of patients before they have fully recovered, because they don’t have any remaining “functional limitations”. Apparently muscle weakness isn’t a “functional limitation.”