Dear Dr. Krant:
I am 35 years old and was just diagnosed with Osteoarthritis. I am 3 weeks out of Arthoscopic surgery to remove torn cartilage. When I went for my 2 week post op they told me I had OA and that there isn’t much I can do for it at this time, except avoid things like jumping, running and squatting. I believe this is hereditary as I have watched my mom fight tooth and nail to avoid knee replacement. She is getting gel injections right now. At this point I feel scared at what will be ahead of me in the future. I have seen her suffer so much. Is there anything that can be done to slow down this osteoarthritis?
People who lose cartilage are at significantly higher risk for arthritis of the knee decades later. Whether cartilage is torn in an accident or removed at surgery, its protective effect in cushioning the bony surfaces across the knee joint are lost with its removal. The canine model of knee osteoarthritis confirms this clinical impression. Surgical removal of articular cartilage in the knee will lead to rapid loss of joint space, fissuring and degradation of subchondral bone (bone lying beneath cartilage) and the elaboration of substances which serve as digestive enzymes (matrix metalloproteinase), accelerating the development of arthritis. To the best we can judge, the physiology of knee osteoarthritis in humans is identical to that of dogs, whose postoperative experience is remarkably similar to our own.
With respect to exercise following surgery, almost all treating physicians advocate quadriceps strengthening in patients with arthritis of the knee, in an effort to 'unload' the involved joint (in essence, decreasing the weight-bearing forces across the knee generated by impact loading). I have described in previous entries the ways in which patients can strengthen both quadriceps and hamstring muscle groups, utilizing both open and closed chain techniques. Repetitive sets of exercises with weight bench resistance (from 120 degrees of flexion to full extension) are strongly recommended in efforts to improve muscle strength and decrease the risk for subsequent arthritis.
Finally, there is almost complete agreement among treating rheumatologists that there is a genetic component to osteoarthritis risk. Although not completely understood, it is clear that children of first-degree relatives with osteoarthritis are at increased risk for developing the disease. Perhaps less compelling than the genetics of disease susceptibility observed in rheumatoid arthritis, osteoarthritis risk for first-degree relatives of patients with disease remains markedly elevated in family studies. The likelihood of osteoarthritis progression is increased by obesity, surgery or injury with loss of articular cartilage, and atrophy or disuse of large muscle groups surrounding the knee. Efforts to address these risks are reasonable, including weight reduction, muscle strengthening, acetaminophen or nonsteroidals in therapeutic doses and, following development of established disease, consideration of joint injection (including the viscoelastic gels) in efforts to forestall joint replacement surgery.