December 19, 2011
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Expert Interview

Comprehensive Care With Martin Englund, MD, PhD

Why should OA be considered a chronic disease that affects multiple structures within a joint?

Dr. Englund: OA is an increasing problem as the population ages. The condition results in pain, reduced function and disability and is the most common cause of musculoskeletal pain in adults. Like many other chronic diseases of public health concern, such as ischemic heart disease or diabetes, OA is a disease of multifactorial origin—an often complex interplay between genes and environment. Further, in OA, all structures of the joint typically become affected, including cartilage, bone, ligaments, synovium, muscles and menisci, in the knee. OA has many different faces, and the degree of involvement of the different structures may vary. Still, with time the disease is usually progressive and may ultimately lead to the total failure of the joint and the need for total joint replacement surgery. The fact that multiple structures are involved is important to remember because the sources of patient symptoms can be manifold and often difficult to pinpoint.

How has our understanding of the epidemiology of OA changed over the last 10 years?

Dr. Englund: Some 10 to 15 years ago, OA was still very much considered a disease of the cartilage and its breakdown. In the last decade, thanks to large and ongoing prospective cohort studies, such as the Multicenter Osteoarthritis Study (MOST) and the Osteoarthritis Initiative (OAI), we have learned a lot about the complex chains of events and multiple structures involved in the disease. However, we have so far mostly studied relatively late-stage OA in middle-aged or older adults. We need to know more about the early physiologic, molecular, structural and functional changes occurring already at younger ages. These changes take place long before bony spurs and joint space narrowing are visible on x-rays.

What is the relative impact of biomechanics on OA?

Dr. Englund: Biomechanics influences most OA. For example, risk of OA is substantially increased after joint injury that has altered the biomechanical loading patterns on the cartilage, such as after a meniscal or anterior cruciate tear. Also, in patients with existing knee OA, once the protective function of the menisci is diminished, progression of disease is even more rapid as increased biomechanical loading on articular cartilage leads to further cartilage loss and subchondral bone changes.

The balance between exercise and overuse is delicate because the joint needs exercise to stay healthy. Lack of exercise in OA patients usually makes pain worse in the long run, and the risk for obesity and its related diseases increases. Finding the right level and the right type is key, and a good physiotherapist can help.

In some knee OA patients, surgical treatment by osteotomy, that is, realignment of the knee joint to unload the more diseased compartment, is an effective means of reducing pain and delaying disease progression and the need for total joint replacement—yet another proof of the great importance of biomechanics in OA.

What other abnormalities do you routinely encounter in patients with OA? Does surgical treatment of these other conditions help slow OA?

Dr. Englund: Meniscal lesions are extremely common in patients with knee OA, at least in the later stages of the disease, but are usually not reparable by surgery. The typical procedure performed at arthroscopy—surgical resection of damaged meniscal tissue—is usually not expected to improve the biomechanical load transfer to the joint cartilage. Currently, no evidence or strong rationale exists to suggest that surgical resection of meniscal tissue slows progression of OA or relieves symptoms. In the general population ages 50 to 90 years, we have seen that a meniscal tear is present in about every third knee, but most subjects with meniscal tears visible on MRI did not have knee pain. In other words, the meniscal tear in most knee OA patients may merely be an incidental finding and not directly responsible for knee pain.

On the other hand, large unstable meniscal tears may interfere with joint movements and contribute to synovitis. Although rare, the patients with these tears are likely to benefit from surgical resection at knee arthroscopy. That treatment decision should be based on the patient’s symptoms and findings from clinical examination rather than an MRI report of a meniscal tear.

If you could tell physicians to do one thing to help their OA patients, what would it be?

Dr. Englund: The major treatment guidelines such as those from the American College of Rheumatology or Osteoarthritis Research Society International are well thought through and should be considered in the daily management of OA patients. Then, I would recommend that practitioners think twice before sending knee OA patients for MRI to determine whether the patient is a candidate for surgery. Teasing out symptoms caused by OA from those possibly caused by meniscal tear is challenging. Damaged menisci will be found in most knee OA patients. While some meniscal tears can cause symptoms, the majority are silent. If unnecessary referrals for surgery can be avoided, that is a good thing.