Lessons from the Osteoarthritis (OA) Workshop: A Pre Congress Activity at APLAR 2014

Based on epidemiologic cohorts, osteoarthritis was diagnosed at a mean age of 69.4 years in the 1990s. This, however, shifted to 55.8 years in 2010. The younger age was driven by the problem of obesity which had become more prevalent in the latter years. 40% of the risk for developing OA is due to being overweight or obese followed by occupation and injury to the joints. Interventions directed at treating obesity may then significantly impact on the outcome of OA management.

It is projected that in 2050, targeting a weight loss of 10% body weight among the obese would save $700M in the care of arthritic patients. Not all anti-obesity interventions are the same – some are cost-saving in terms of preventing osteoarthritis and there are those that are cost-effective in treating osteoarthritis.

Treatment of osteoarthritis caries a substantial burden to society. In 2012, it was estimated that the overall economic costs was $8.5B in Australia. And this can be broken down to direct costs (mostly related to joint replacement related care, rehabilitation, medication, research and professional services), indirect costs (driven by lost of productivity resulting in early termination from work or early retirement) and intangible costs (reflected by the impact of pain, activity and role limitation, decreased quality of life and reduced participation at home, the community and society). If left uncheck, the economic burden could balloon to $27B in 2032 (that’s just a 20 year period).

There are differences observed in the OA epidemiology across countries. In Beijing for example, hip osteoarthritis is very lowly prevalent compared to western countries. Also, there are differences in knee compartment involvement and this was shown to be related to laterality of the patella in relation to the femoral sulcus. Among Chinese for example, there’s increased prevalence of lateral TF involvement. But overall, it remains that the medial TF compartment is more frequently involved (75%) followed by the lateral TF and the patellofemoral area.

Osteoarthritis is not the only condition that causes knee pain in elderly patients. Recent increases in knee pain but with no obvious inflammation may involve the anserine bursa (esp if localized to infero patellar area) or the popliteal fossa (i.e. Baker’s cyst if involving the posterior knee). Large osteophytes observed in relatively young patients with OA (age<60) should prompt for endocrine evaluation particularly hyperthyroidism. And if two knee compartments are simultaneously affected (i.e. bicompartmental involvement) consider infections, trauma and rheumatoid arthritis.

Likewise, osteoarthritis is not the only condition that causes hip pain. Femoro-acetabular impingement is one such condition. It is typically hip pain reproduced with hip flexion and internal rotation. It is difficult to document radiographically if only standard radiographs (AP-lateral) are used. A cross-table lateral XR of the hips is best at catching this condition.

Traditionally, it is believed that you either get osteoarthritis or osteoporosis in old age. Although there are risk factors common to both such as age, gender, inflammation and chronic diseases, the difference was attributed to risk factors related to weight (i.e. low body weight = osteoporosis; obesity = osteoarthritis). And this was further supported by studies on quartiles of bone density and prevalent osteoarthritis. Those is the highest quartile of BMD (those less likely to have osteoporosis) have the highest risk of developing osteoarthritis. This may no longer true if we review recent epidemiologic data.

Those with hip OA have been shown to have increased risks for osteoporotic fractures. While those with spine OA appear to be protected (i.e. having lower risks for fragility fractures). However, low vitamin D levels (<25) which predisposes to osteoporosis has been associated with increased knee pain but not hip pain. Furthermore, it has been observed that previous osteoporotic fracture (regardless of site) was associated with lower prevalence of knee osteophytosis. So, we must not be remiss in evaluating patients for osteoporosis just because they have OA.

Studies evaluating structure in OA and OP suggest similar pathophysiologic changes in both. For example, increased bone marrow lesions (BMLs) seen in OA are believed to be akin to increased microfractures seen in OP. Likewise, bone loss (in OP) has been observed to parallel cartilage loss (in OA). So trials evaluating anti-OP therapy in the treatment of OA have been on their way. Intervention trials on Vitamin D in OA failed to show reduction in joint pains. So far, only strontium appears to have a potential role in treating OA (with reduced pain and WOMAC scores in a single trial). But due to concerns over CV safety, strontium failed to get approval for this indication.

Due to differences in epidemiology and the way patients present, treatment of OA may never be successful if done only at a macro level. It should be individualized to our patients’ needs. For example, while obesity is a common factor, it’s absence in an OA patient should prompt evaluation for other risk factors such as occupation and injury instead of just advising patients to lose weight.

There is also poor correlation between radiographic OA and the patient’s pain experience. By age 60, 80% of all individuals would have radiographic changes consistent with knee OA but only 50% of them would be symptomatic and 10% would have very disabling pain. Likewise, those with non-painful hip OA are more likely to have radiographic progression. So, treat the patient, not the radiograph.

And by treating the patient, this does not only mean exclusively using medications. But more importantly, non-pharmacologic interventions should be made part of the treatment package/ plan. Guidelines for knee, hip and hand OA invariably recommend a combination of pharma and non-pharma interventions for optimal treatment. The problem, however, is that most trials evaluate the impact of single interventions which may not translate or be applicable in multi-modal and sequential treatment. Thus, most guidelines ascribe lower evidence to support non-pharma intervention or multimodal treatment.

So, patients should at least be educated, informed and empowered by allotting time to discuss their condition and addressing any other concerns they may have. Likewise, denying that they would need joint replacement is a disservice as this may be an eventuality for most. And a referral for evaluation for joint replacement should not be made as a last resort for “failed” medical treatment but an important component of holistic management.

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