Table of contents:

1. What is Rheumatology? What is a Rheumatologist?
2. Osteoarthritis
3. Osteoarthritis of the Knee
4. PMR/TA

OSTEOARTHRITIS

Introduction Osteoarthritis (OA) is felt as pain. At its worst it can destroy a hip or a knee limiting or even eliminating the ability to ambulate. Its effects on the hand can prevent someone who uses their hands to work from earning a living. The constant pain, combined at times with severe stiffness, ruins quality of life.

OA does not kill. For years this fact has kept the government from supporting OA research. Age is a major risk factor for OA, and I believe (somewhat cynically) that with the graying of congress and politicians, those who control the research purse strings are now starting to understand “a longer life without quality of life is difficult to endure”. Moreover, OA is a major causal factor in conditions such as chronic low back, neck, hand, knee, hip and foot pain, which are major causes of time lost from work, decreased worker productivity, and chronic disability. Therefore, money has begun to appear for OA research. I intend to review the basics of diagnosis and treatment of OA. In a later paper I will go into osteoarthritis in greater detail. One caveat, however. Evidence based medicine is a new emphasis in clinical research. Evidence based medicine demands prospective randomized controlled trials of sufficient power (read this as statistical power or large enough numbers of participants to be able to support the hypothesis with sufficient probability) and reasonable duration. Contrast this with anecdotal reports that are simply case reports, and small, poorly controlled or unblended trials which are too susceptible to random events or sponsor/researcher prejudices. There is no problem with obtaining large numbers of study subjects in OA research. But since OA develops over decades, and very few studies ever extend past a year, the studies are limited to evaluating OA symptoms (pain, stiffness), their effects on function or short-term x-ray changes, but not the true progression of the disease. Lastly, with medical literature and scientists preference to report only positive results, we rarely have reports of drug failures, or evidence for what does not work. You must always try to separate treatment information which we know as “Evidence Based” versus that which is based on limited studies, anecdotal reports, or just personal opinion. Definitions OA may be defined radiologically by the findings of cartilage loss with joint space narrowing, osteophytes, subchondral sclerosis and bone cysts. Clinically it may be defined by pain, functional limitations, Heberden and Bouchard nodes, and bony swelling in the knees. The American College of Rheumatology classification criteria depends on site of involvement and includes clinical findings such as pain, crepitus, morning stiffness < 30 minutes and bone enlargement.

Epidemiology OA is the most common form of arthritis. Its prevalence increases with age starting at two percent at age 40, 30 percent by 50 years old and 65 percent at 70 years of age. Men have more OA of the hip while women have more hand (PIP and CMC) involve- ment. Weight is a major risk factor for knee involvement. Occupational factors may determine site of involvement, such as assembly line workers’ hands, knees and hips in miners, and elbows and wrists in pneumatic drill operators. Race, ethnicity or country of origin may have a genetic role, with OA hip more common in Caucasians and Japanese, and OA knee and DIP more common in Black women.

Etiopathogenesis Early in OA focal fibrillation of cartilage, followed by cleft formation then Ulcerations occur in load bearing parts of the joint cartilage. Osteophytes occur at joint margins, there is a loss of extracellular cartilage matrix, loss of chondrocytes in surface layers of cartilage, and reactive changes in deep chondrocytes as they attempt to repair injury. Early breakdown in cartilage may be genetically determined or trauma re- lated, but a variety of conditions affecting cartilage and underlying bone (see Table I) can also predispose to OA. Clinical Features Clinically OA may be asymptomatic for years, picked-up only on x-ray. Radiographic findings rarely correlate with clinical complaints. Distribution of joint involvement is largely determined by underlying pathogenesis (ex. prior trauma). Idio- pathic/genetically determined OA, also termed primary OA, involves the 1st MTP, 1st CMC, DIPs, PIPs, knee, hip, cervical and lumbar spine. Pain (aching), stiffness (gel phenomenon and morning stiffness) and loss of function are the most common symptoms. Bony enlargement with angulation deformities due to asymmetric cartilage destruction are the most common clinical findings. Treatment There is no cure for OA, just as there is no cure for at least 110 of the 120 known forms of arthritis. What exists is treatment that improves quality of life.