People who haven’t experienced arthritis can’t appreciate it. Its pain can get so bad almost nothing is worth incurring its wrath. Pants on fire? Let ‘em burn, if getting them off requires using your arthritic fingers. Screeching tires and blaring horn immediately behind you? Let it hit you; it would hurt less than turning your arthritic neck. You start living your whole life finding ways to do everyday things from the office to the bathroom without using any arthritic joints. You’d open your pill bottles with a hammer if you could pick up a hammer, those corny elastic beltless trousers are the only pants you can get on or off, and you get ‘em on and off with your teeth … if your jaw isn’t arthritic.
We may as well joke about our arthritis, because we can’t cure its most common form, osteoarthritis (OA), which is due to mechanical wear and tear rather than biological disease. Our joints, from jaw to toes, are intersections where bones slide over each other on a surface of cartilage. Cartilage starts out as slick and smooth and slippery as silicone on Teflon on wet ice, but when the Teflon – the cartilage – starts to wear thin, the friction increases as though someone threw sand in the joint. When the cartilage wears through in spots and bone starts grating on bone, the pain is so excruciating that almost no activity is worth provoking it.
You will probably get OA; 85% of us do before we reach 70, especially in our hips and knees. It is caused largely by such factors as general joint overuse (a decreasing suspect), certain kinds of overuse (high-impact, twisting games like football and soccer), a genetic predisposition (a major contributing factor, which may allow some people to make early lifestyle decisions), age, and previous joint injuries. Knee OA is very often self-inflicted the same way we cause our own adult-onset diabetes … by obesity.
People who usually work or play hard four hours a day are 7 times more likely (13 times, if obese) to develop knee OA than dedicated couch potatoes. Knees are our primary isolated weight-bearing joints, and obesity tears them up, often to the point of disability and artificial knees … a steep and lasting price to pay for too many calories and too little exercise. Hip OA can be severely crippling, to the point we can’t put on a pair of socks, let alone walk. Hand OA is very common and often runs in families. Spinal OA has driven even obsessed athletes away from their beloved sports; it cripples less driven people even more surely and quickly.
OA wakes you up, preventing sleep but hurting so much you don’t want to get out of bed. The only relief? Get out of bed. Once up, it hurts so much you don’t want to move. The only relief? Move. Even then you can’t possibly work or play. The only relief? Work or play. The most effective way to delay greater pain both short and long term involves pain.
The mantra “No pain, no gain” is appropriate in OA. Rest dries and hardens the damaged cartilage, leaving it more likely to break under impact. Movement lubricates, softens, and toughens it. The only proven way to slow cartilage degradation is motion.
But not just any motion. Running doesn’t cause OA like football can, but it beats up and can break already damaged cartilage. Low-impact exercise often significantly postpones the really crippling phase and may even let you resume normal activity almost pain-free. Swimming, cycling, dancing, and rowing are good for osteoarthritic joints, and strenuous weight-lifting is an excellent way to greatly reduce its symptoms and slow its progress. Stronger muscles help stabilize joints so they move as designed, reducing the damaging and painful bone-on-bone friction that can result from sloppy joint action. An OA joint is a classic and valid application of the Use It or Lose It mantra. Most varieties of exercise help, including strength building, aerobics, range of motion exercise such as stretching or yoga, specific agility exercises, and/or neck and back strength exercises. Of course, your physical therapist should advise, prescribe and train you in these.
If you overdo the exercise until the affected joints start hurting more rather than less, short layoffs, even a splint while you sleep, can help. You’ll have to find your own optimal balances between rest and exercise, cold packs and hot packs, and OTC and prescription drugs. Don’t jump into surgery until all other avenues have been exhausted. Knee and hip replacements usually get patients back on their feet adequately, but arthroscopic knee cleanup surgery for OA has shown to be often ineffective.
Are you developing OA? Maybe, if you’re experiencing joint pain without obvious sprain, joint stiffness or pain after a good rest, joint swelling or tenderness, or joint crunching you can feel or hear. X-rays may reveal it before any symptoms show, giving you time to lose excess weight, change your work or exercise, or start medicines which may slow its progression.
Oral estrogen lowers the risk of hip OA, and foods high in vitamins C, D and E and beta carotene may help slow the progression of knee OA. Another dietary consideration worth pursuing is your balance of omega 3 and omega 6 essential fatty acids, discussed here last August. Acupuncture seems to help some patients.
If rigorous, proper exercise and an occasional Tylenol don’t help enough, drug therapy may. It may also let the cartilage degrade faster if it masks abuse. Unlike exercise, drugs do just one or two things to help, but often have side effects, some serious, some even life-threatening (see our October 2002 issue). While exercise is a low-risk, straightforward, and clearly beneficial mitigator of OA, drugs can be almost the opposite. They include OTC and prescription pain killers and anti-inflammatories, various types of injections, and both valid and snake-oil supplements. Study the drug options, and if you didn’t go back and re-read the October ’02 column referenced above, do it now. Aspirin and similar OTC “pain candy” are most definitely not candy; both they and prescription drugs have strong potential for both benefit and harm. NSAIDS are the drug of choice, but their prolonged or intensive use should be monitored for the side effects discussed last October. Concern is rising from veterinary studies and some human indications that NSAIDS, commonly used for OA, may inhibit cartilage self-repair.
In addition to NSAIDS, your doctor may discuss topical analgesic lotions, mild narcotics, corticosteroids, and hyaluronic acid. If your doctor doesn’t explain those options at great length, ask for some reliable websites that do, and/or start with the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) search engine. They lead the nation in osteoarthritis research, and their reports include medical data for your doctor and plain-talk patient reports anyone reading this basic column can follow. Some readers may benefit in the future from NIAMS research in cartilage cell replacement, stem cell transplantation, and gene therapy.
Be wary of OTC supplements; many are useless or harmful. Two well worth considering, however, are the widely touted glucosamine/chondroitin tablets. They often relieve the pain as much as prescription meds, may slow the pathology progression, and may possibly even slightly heal cartilage damage. Very extensive testing is expected to address those issues by next year. The current bottom line is that they are safe and may help OA.
Research shows that self-care -- including education, participation, and informed treatment selection -- results in claims of decreased pain, fewer doctor visits, and better quality of life. You’ll find a lengthy patient-oriented tutorial at http://www.niams.nih.gov/hi/topics/arthritis/oahandout.htm, and many more highly informative links at http://www.nlm.nih.gov/medlineplus/osteoarthritis.html. When surfing the net for information on your OA, though, skip the countless web sites pitching supplements. Treat them as the unregulated paid commercials they are. You’ll quickly see that this column covers but a flea on a pinfeather on a penguin on the tip of the OA iceberg.