Osteoarthritis and allied disorders are the primary diagnosis for approximately 48,000 patients who receive home health care in the United States. When it comes to nursing home care, over 11 percent of nursing home residents have osteoarthritis and allied disorders. With these statistics in mind, our expert panelists address common misperceptions about the disease and offer key diagnostic insights as well.

Q: Isn’t osteoarthritis (OA) just the normal aging of joints that everyone gets?
A: While aging is a very important component of cartilage loss, Rick Pope, PA-C, says it is certainly not the only one. Pope and Brian Peck, MD, agree that OA is a multifactorial disease and the symptoms can vary with each patient.

Pope notes that each patient has an inherited genetic predisposition to the building blocks of cartilage, including collagen Type 1 and 2 as well as other matrix proteins such as proteoglycans. The primary lesion of OA is in the articular cartilage (AC) that covers the ends of the long bones at the joints, according to Dr. Peck.

Dr. Peck says the main function of AC is to act as a shock absorber. He notes the weight of each activity compresses the cartilage and squeezes its water out into the joint space where it obtains oxygen and nutrients, and protects the bone from the shock of normal activities. When there is a loss of these protective, shock-absorbing functions, Dr. Peck says normal traumas of life can transmit forces to the bones, which suffer numerous, undetectable microfractures. With these microfractures, the bones hypertrophy around the edges of the joints and in the subchondral areas under the AC, according to Dr. Peck.

“This proliferative new bone ultimately grows into the osteophytes we see on X-rays,” notes Dr. Peck.

Dr. Peck says joint spaces gradually become smaller on weightbearing X-rays as osteophytes interfere with range of motion. These changes cause symptoms such as pain, tenderness, decreased range of motion, crepitation, bony enlargement and weakness of supportive musculature, according to Dr. Peck.

As both panelists noted, there is a variety of different risk factors for OA. For example, Dr. Peck notes the full surgical removal of a meniscus from a knee alters the anatomical relationships and results in increased stress on the AC, and the relatively rapid development of OA.

Pope adds that other contributing factors to OA may include weight, muscle tone, leg length discrepancy and genetic factors. Some families have genetically poor collagen and their AC wears out prematurely, points out Dr. Peck.

Isolated trauma in any particular joint may also lead to rapid AC deterioration. Dr. Peck says examples include a twisting knee injury that occurs early in one’s life or chronic repetitive trauma in the workplace to the small joints of the hands.

“OA is not a normal part of aging but is the result of a confluence of various risk factors,” explains Dr. Peck.

Pope says there are preventive measures people can take to minimize the risk and possible severity of the condition.

“If we keep our weight down, exercise daily within reason and keep up our overall muscle tone, we can all delay at least the symptoms of OA if not the entire process,” maintains Pope.

Q: How can I tell the difference between OA and RA?
A: RA is a systemic immune response to synovial lining proteins that can lead to joint erosion and deformity over years, according to Pope. Dr. Peck says the cartilage damage with RA is mediated by enzymes and other materials that result from the extensive activity of immune cells that are distributed more or less uniformly through the synovium and the synovial fluid.

“Therefore, the resulting damage is more likely to be spread out somewhat evenly, yielding more uniform and extensive areas of damage or ‘stripping away’ of cartilage,” notes Dr. Peck.

Accordingly, Dr. Peck says the joint space loss with RA is much more likely to be uniform and symmetrical within each affected joint, and is also much more likely to affect both sides of the body. In a full-blown presentation of RA, Pope says the disease will involve multiple peripheral joints including the metacarpophalangeal joints, the proximal interphalangeal joints in the hands and similar locations in the feet. He says the disease process can affect almost any joint in the body but avoids the distal interphalangeal joint, which is primarily affected by OA.

On the other hand, Pope and Dr. Peck say OA primarily involves cartilage degradation, which is usually caused by mechanical forces. Pope notes that OA usually affects one to three joints and is asymmetrical in presentation. As Dr. Peck points out, one side of a joint is more likely to be affected than the other side (i.e. the medial versus the lateral compartments of the knee). The patient history will often reveal pain in weightbearing joints such as the knees and hips, according to Pope. When OA strikes the hands in the DIPJS (Heberden’s Nodes) and the PIPJS (Bouchard’s Nodes), Pope says the OA commonly runs in the family.

Dr. Peck says OA is a disease of proliferative new bone, which grows in response to the irritating effects of losing the shock-absorbing function of the AC. RA is a disease of bone loss, according to Dr. Peck, who says the condition is marked by erosions eating away bone near the joint surfaces and the development of osteoporosis in the periarticular regions.

The differences between OA and RA “can be striking” on radiographs, emphasizes Dr. Peck. Pope says radiographs of OA will show bony overgrowth and an asymmetrical loss of cartilage. When one aspirates fluid from these patients, Pope says clinicians will notice a low white blood cell (WBC) count (generally less than 1,000 cells per cu. mm.) and differential that does not favor granulocytes. However, with RA, one will note an elevated WBC count, a cloudy appearance and a preponderance of granulocytes on differential. Dr. Peck concurs. While OA exhibits no specific laboratory abnormalities, Dr. Peck says RA may be associated with numerous laboratory abnormalities, such as ESR and CRP elevations, positive rheumatoid factor (RF), positive anti-nuclear antibody (ANA) and anemia.

Clinically, Dr. Peck says the OA joint is usually not inflamed and most swelling is due to bone enlargement. He notes that joints affected by RA may be quite warm, and exhibit swelling of the synovium and other nearby soft tissues.

Q: Isn’t it true that the only treatment for OA is pain control or antiinflammatory medications until the joint needs to be replaced?
A: This is a common misperception, according to Dr. Peck. He emphasizes that, regardless of any underlying propensities, the primary mechanism of joint damage in OA is wear and tear so one should gear treatment toward reducing damaging stressors.

Dr. Peck says clinicians should encourage patients to “unload” the joints by strengthening supportive musculature. For example, he suggests that patients with OA of the knees should frequently do isometric quadriceps exercises. Dr. Peck also points out that at the first sign of OA symptoms, affected individuals will adopt protective postures and movements. This leads to normal daily activities requiring less work than before and can subsequently lead to muscle atrophy, which Dr. Peck says is a “very early finding in OA of any joint, especially the knees.”

While there have been anecdotal claims of the ability of the nutriceutical glucosamine to relieve pain, Pope says recent findings from a large meta-analysis show the agent actually prevents cartilage loss when it was compared to a placebo. He says he is looking forward to the final analysis of a three-year study on the use of glucosamine hydrochloride in preventing cartilage degradation. Supplements like glucosamine and chondroitin show promise but Dr. Peck notes they are not yet proven.

Pope says there is some evidence that hyaluronan, in particular, may prevent cartilage degradation. He adds that some small trials have shown that diacerin may prevent cartilage degradation as well.

Dr. Peck emphasizes that clinicians should never employ medications, such as NSAIDs or analgesics, as sole therapies for OA. The purpose of these medications should be to help patients more easily tolerate appropriate exercise techniques or physical therapy, according to Dr. Peck. “The real treatment of OA is physical,” offers Dr. Peck.

Brian Peck, MD, is an Assistant Clinical Professor of Medicine at the Yale University School of Medicine, and is an Adjunct Clinical Professor of Medicine within the Physician Assistant Program at Quinnipiac University in New Haven, Ct. He is the Medical Director of the Arthritis Center of Connecticut in Waterbury, Ct.

Rick Pope, PA-C, is the founder and President of the Society of Physician Assistants in Rheumatology. He is the senior PA at the Arthritis Center of Connecticut in Waterbury, Ct.