Osteoarthritis (OA), the most common musculoskeletal condition to affect synovial joints, causes significant pain and disability because of numerous effects on the whole joint.
Approximately 1m primary care consultations for OA1 and about 135,000 hip and knee replacements take place in the UK every year.2
OA is a metabolically active process involving cartilage thinning and bone remodelling, the release of intra-articular cartilage debris, inflammatory cytokines and neuropeptides, and synovitis.
Pain, swelling and disuse lead to muscle weakness, which, with other changes to joint biomechanics, leads to further pain through soft tissue strains.
Hence inflammation, neuropeptides, bone remodelling, weakness and biomechanical changes are all targets for therapy.
The principle risk factors for primary OA are genetics, body weight, biomechanical abnormalities and associated diseases.
OA is closely linked to obesity. For every 5kg of weight gain, there is a commensurate 36% increased risk of developing OA.3
The link to obesity is not only mechanical, but also through systemic inflammatory effects on the joint, mediated by adipokines, and OA may simply be seen as a manifestation of metabolic disease.4 Metabolic factors, such as hypertension, hypercholesterolaemia and blood glucose level, are all also associated with OA, independent of obesity.5 The specific mechanisms involved are unclear.
Early osteoarthritis is often a clinical diagnosis. Patients typically present with activity-related joint pain, often localised. With time, swelling and limited early morning stiffness (<30 minutes="" can="" occur="" p="">
In the early stages of the disease, X-rays are frequently normal. As the disease progresses, loss of joint space, subchondral sclerosis and osteophyte formation are seen. But 'mild OA' radiologically represents relatively advanced disease.
Blood tests, including inflammatory markers, rheumatoid factor and uric acid, are normal, although some patients may have a slightly elevated CRP. Vitamin D levels should be checked; low levels can contribute to muscle weakness and pain.
MRI scans show cartilage thinning and underlying bone lesions and can demonstrate low-grade synovitis and soft tissue changes.
OA is an important diagnosis to make early, to allow for lifestyle changes that can help to influence prognosis. Subsequent follow-up is important to assess progress and reinforce lifestyle messages.
Patient education is paramount. Ensuring the patient understands risk factors for the condition, the importance of weight management, metabolic disease control, therapeutic exercise, biomechanical alterations and approaches to sound pain management are the foundations of good treatment.
Prognosis is strongly influenced by self-efficacy and the patient's locus of control.
Weight loss results in improvements in pain, function and progression of the arthritis. Every pound of weight lost will result in a fourfold reduction in the load exerted on the knee per step taken.6 Diet and exercise combined is the most effective behavioural method of weight loss; pain reduction in knee OA correlates with the amount of weight lost.7
Strengthening exercise is important to reduce pain and improve function. Aerobic activities and those promoting proprioception are also encouraged.
An initially supervised programme is more likely to be effective long-term and follow-up promotes adherence and better outcomes. Orthotics may help some with joint deformity.
Patients should be advised to eat a Mediterranean diet. Cod liver oil is rich in omega-3 and vitamin D; vitamin D deficiencies should be corrected if necessary.
NICE is reviewing its pharmacological recommendations for OA.8 Analgesics to allow therapeutic exercise should be selected on the lowest risk/benefit ratio. Topical NSAIDs for superficial focal pain may be effective, as may capsaicin cream.
Some patients respond to paracetamol but this should not be continued if ineffective. Those with more inflammatory symptoms should be prescribed an NSAID/COX-2 inhibitor at the lowest dose for the shortest time, with PPI cover. A trial of up to three agents may be necessary.
Low-dose colchicine may help those with inflammatory symptoms. Opiates should be used short-term and sparingly in recalcitrant pain.
Aspiration of swollen joints can improve pain and function. Injection therapies are used sparingly. Steroid injections are used only in severe inflammation and pain in the absence of sepsis. Viscosupplement injections, although not recommended by NICE, may offer longer duration of relief than steroids.
Hydroxychloroquine and/or low-dose colchicine may help some patients with hand OA. Agents under trial include biologics and those with effects on bone turnover. The latter may be particularly effective in those with bone lesions on MRI, which correlate with pain.
Surgical referral should be considered for patients who continue to have symptoms and for whom OA has a significant effect on quality of life.
- Professor Speed is consultant in rheumatology, sport and exercise medicine, Fortius Clinic London and Progress Clinic Cambridge
1. Arthritis Research UK, 2008.
2. National Joint Registry for England and Wales, 9th Annual Report - 2012.
3. Lementowski PW, Zelicof SB. Obesity and osteoarthritis. Am J Orthop 2008; 37(3): 148-51.
4. Sellam J, Berenbaum F. Is osteoarthritis a metabolic disease? J Bone Spine 2013; 80: 568-73.
5. Hart DJ, Doyle DV, Spector TD. Association between metabolic factors and knee osteoarthritis in women: the Chingford Study. J Rheumatol 1995; 22: 1118-23.
6. Messier SP, Gutekunst DJ, Davis C et al. Weight loss reduces knee-joint loads in overweight and obese older adults with knee osteoarthritis. Arthritis Rheum 2005; 52: 2026-32.
7. Messier SP, Loeser RF, Miller GD et al. Exercise and dietary weight loss in overweight and obese older adults with knee osteoarthritis: the Arthritis, Diet, and Activity Promotion Trial. Arthritis Rheum 2004; 50: 1501-10.
8. NICE. Osteoarthritis: care and management in adults. CG177. London, NICE, 2014.