When David Pisetsky, MD, PhD, physician editor of The Rheumatologist, asked me to contribute an article on osteoarthritis, I said yes without hesitation, looking forward to communicating all the exciting new advances taking place regarding osteoarthritis (OA). (Accepting the invitation had its risks. In addition to needing to meet the deadline—which always comes sooner than expected—my wife, Peta, keeps telling me to say no to new academic requests or to stop complaining about being busy!)
There were a number of alternatives—this could be a highly scientific article on everything we know about osteoarthritis (obviously this would be much too long) or a New Yorker–type article with interesting vignettes, a quasi-scientific rendition, or something in between.
After thinking about the content of the article, I decided to write about some of the prevailing quandaries and controversies in the field of osteoarthritis, with respect to etiopathology, guidelines for symptomatic therapy, and our quest for disease modification, the Holy Grail of our search.
I have been an investigator in the osteoarthritis field for almost four decades. I began at a time when the disease was ignored and the victim of a number of myths: it never cripples, it’s an inevitable disease of aging, you can live with the pain without difficulty, and there’s nothing in the way of treatment that really works anyway. Perhaps Sir William Osler was right when he said, “osteoarthritis is an easy disease to take care of—when the patient walks in the front door, I walk out the back door.”
There was a time when, if I gave a lecture on osteoarthritis, five people would show up—three would be technicians in my lab and two would be family members. Now, I have seen 1,500 people attending a lecture on Gene Mutations in Osteoarthritis with a standing room–only audience. The fourth edition of our textbook Osteoarthritis—Medical and Surgical Management, is 750 pages long. We could have added another 750 pages, but the publisher thought that would make the book too costly to sell. Forty years ago, an osteoarthritis textbook would have done well to take up 100 pages. So, with this background, I would like to reflect on OA—what is and what might be.
Table 1: Sources of Pain in OA
- Medullary hypertension
- Subchondral fracture
- Periosteal reaction
- Nerve compression
Pathophysiology and Etiopathology
For many years, osteoarthritis was looked at purely as a degenerative disease. (See Figure 1, p. 15.) The analogy was a correlation to erosions that occur over the years as water falls on a rock. It has become obvious over the past decade that osteoarthritis is not only a disease of cartilage and is not only degenerative. Many tissues are involved in the process—subchondral bone characterized by eburnation; synovial involvement characterized by inflammation; bone marrow edema (uncertain pathology but has a relationship to pain); new bone and cartilage formation at the periphery of the joint in the form of osteophytes; inflammatory effusions; and ligamentous and muscle changes.1