Osteoarthritis (OA) is one of the commonest forms of arthritis. Any synovial joint can develop OA, but the spine, knees, hips and small joints of the hand are the most commonly affected. OA of the more common sites increases with age.1
OA in a joint causes pain, although the exact mechanism of this is not fully understood. It is known that locally active cartilage-damaging enzymes are released into the joint and the inflammatory process causes cartilage damage, similarly to a rheumatoid joint.
Risk factors for OA are outlined in the box below. Importantly, many environmental/lifestyle risk factors are reversible (for example, obesity).
First, take a detailed history. Which joints are painful and when are they painful? Is there morning stiffness, or 'gelling' (when joints become very stiff and difficult to mobilise after a period of rest)? Morning stiffness usually lasts less than half an hour and recurs after resting.
It can be easy to confuse OA with inflammatory arthritis such as rheumatoid arthritis (RA), particularly with hand OA in younger people.
In such cases, the duration of morning stiffness is important, as well as whether it affects other joints. RA will cause global morning stiffness of all joints.
RA also causes synovial swelling, typically of the metocarpophalangeal joints. It feels soft, boggy and warm, in contrast with the hard, bony swellings typical of OA.
Gouty tophi can also appear on fingers and may be confused with Heberden's nodes.
It can sometimes be difficult to differentiate gout, pseudo-gout and RA from OA, especially if the OA only affects some of the hand joints; referral to a rheumatologist is then advised.
Pain is the usual reason for patients to present to their GP. Ask about the impact the problem is having on the patient. Are they able to work or do their housework? Enquiring about sleep is also important.
How much exercise do they take and how far can they walk if they have OA in the knee or hip?
In general practice, a working diagnosis of OA is assumed in patients presenting with persistent joint pain that is worse with use, aged 45 years and over, and experiencing morning stiffness lasting no more than half an hour.
Look at each affected joint. Examine for joint effusions, which are uncommon in OA but can be present in gout, pseudo-gout and RA. Check for warmth around the joint.
Are there osteophytes and any muscle wasting around the joint? Muscle wasting leads to poor proprioception and loss of control of the joint movement and positioning. In postural joints such as the knee, this may contribute to falls in elderly patients.
What is the range of movement in the joint? Are there any fixed flexion deformities and what are the full excursions of the joint? A loss of range of movement indicates worse disease.
Check for any pain when the joint is moved passively. Pain on passive movement is likely to come from the joint itself. Pain only felt on active joint movement is more likely to be coming from muscles or ligaments.
In the knee, perform tests for ligament stability and meniscal pathology, such as McMurray and Thessaly tests. If the knee locks, there may be an osteochondral loose body or meniscal problem and further referral is indicated.
It is not always necessary to perform X-rays or blood tests to make the diagnosis. Clinical examination may reveal muscle wasting around the joint and osteophytes.
Blood tests for uric acid, FBC, ESR, anti-cyclic citrullinated peptide antibody (anti-CCP), CRP and rheumatoid factor will help differentiate OA and RA.
OA does not usually cause a rise in inflammatory markers, a positive rheumatoid factor or anti-CCP.
Gout may cause raised inflammatory markers, hence the need to check uric acid levels.
The X-ray appearances include loss of joint space, sub-chondral bony sclerosis and bony cysts. Radiographic features do not necessarily correlate with severity of patients' symptoms. Only half of adults aged 50 years and over with radiographic OA of the knee have any symptoms.2
Finally, discuss a treatment plan with each patient. Recent NICE guidance stress the importance of a holistic approach to the disease.3
Exercise should be a core treatment for patients with OA, irrespective of age, comorbidity, pain severity and disability. Exercise should include local muscle strengthening and general aerobic fitness.
Pain relief in the form of regular oral paracetamol and topical NSAIDs should also be offered.
A proton-pump inhibitor should be co-prescribed with NSAIDs and COX-2 inhibitors.
NICE found evidence that intra-articular steroid injections into the knee joint can give benefit for about a week. Injections into the hip and hand were not found as effective. However, many doctors use injections into the carpo-metacarpophalangeal joint and find these very effective, despite the lack of evidence for their efficacy.
Many patients find OTC glucosamine and chondroitin helpful for the symptoms of OA. Although NICE was unable to find enough evidence to recommend their prescription, they are not harmful.
Finally, referral for joint replacement surgery should be considered for patients with OA who experience joint symptoms (pain, stiffness and reduced function) that impact substantially on their quality of life and are refractory to non-surgical treatment. Referral should be made before there is prolonged and established functional limitation and severe pain.
In knee OA, once established, improvement in the structure of the joint is rare. However, improvement in pain and disability over time is common.
Hip OA has probably the poorest overall outcome. A significant number require hip replacement within one to five years. In contrast, some hips heal spontaneously, with improvement in the radiographic changes as well as symptoms.
Hand OA has a particularly good prognosis. Most cases of interphalangeal joint OA become asymptomatic after a few years, although patients are left with permanent swellings of the distal or proximal interphalangeal joints.
Involvement of the thumb base may have a worse prognosis, as in some cases this causes continuing pain on certain activities (such as pinch grip) and lasting disability.
OA is a common disease in an ageing population and every GP should be aware of the effects that OA can have on patients so that they can offer support and treatment. OA is rewarding to diagnose and treat if the principles described above are applied.
- Dr Warburton is a GPSI in rheumatology in Telford, Shropshire
Risk factors for OA
OA is defined not as a disease or a single condition but as a common complex disorder with multiple risk factors. These risk factors are broadly divisible into:
1. Arthritis and Musculoskeletal Alliance. Standards of care for people with osteoarthritis. London: ARMA, 2004.
2. Peat G, Thomas E, Duncan R, Wood L, Hay E, Croft P. Clinical classification criteria for knee osteoarthritis: performance in the general population and primary care. Ann Rheum Dis 2006; 65: 1,363-7.
3. NICE CG59. The care and management of osteoarthritis in adults. London: NICE, 2008.