Hand osteoarthritis (OA) is a common clinical problem associated with ageing, with 60-70% of the population over 55 having radiographic evidence of hand OA. 

Symptomatic hand OA is twice as common in women as men, affecting 26% of women and 13% of men over the age of 70. 

Our understanding of OA has developed from the old adage of a 'wear-and-tear' arthritis to a deeper underlying pathogenesis with genetic factors, biomechanical factors and varying degrees of synovial inflammation all playing a role. 

Large joint OA is readily identifiable clinically and has an effective treatment in joint replacement. 

Hand OA, however, presents a particular diagnostic and therapeutic difficulty. Proposed theories of clearly defined subsets of hand OA have not been substantiated by research. 

Variously termed nodal OA, inflammatory OA and erosive OA, its differentiation from other forms of arthritis, in particular rheumatoid arthritis (RA) and psoriatic arthritis (PsA), is crucial and often challenging.

Pathogenesis

Biomechanical factors are less important in hand OA than in large joint OA and the “wear-and-tear” hypothesis is particularly outdated in this form of OA. 

Genetic factors have a role to play and a number of genes have been identified, although all have a small part to play in the overall risk. The disease is a polygenic disorder with multiple genes with individually small effect sizes contributing and interacting. 

A noteworthy feature is the onset of a rapidly progressive form of nodal OA in females immediately after the menopause, suggesting a contributory role of hormonal factors. In addition, this form of nodal OA tends to recur within female members of the same family suggesting an interplay between genetic factors and hormonal changes. 

Modern imaging techniques have shed light on the pathogenesis of hand OA with evidence of previously unsuspected degrees of inflammation in the synovium of affected joints and the surrounding ligaments and soft tissues. Contrary to previous teachings this is not a purely mechanical non-inflammatory disease.

Clinical features

The end stage of nodal OA is familiar to all, with prominent bony outgrowths, most noticeably over the proximal and distal interphalangeal joints, termed Bouchard’s and Heberden’s nodes. 

The first carpometacarpal joint (base of the thumb) is also commonly affected and the metacarpophalangeal joints, especially the second and third, may be involved. 

Once the disease reaches this bony end stage it is often relatively painless but the deformities can be cosmetically undesirable and may interfere with function if severe. 

Greater difficulty is encountered in identifying the disease at an early stage. While the nodes are developing patients often experience significant pain. This tends to fluctuate and go through symptomatic periods interspersed with times of relative quiescence. 

Patients may report intermittent swelling and erythema that then resolve due to the inflammatory component of the disease. The classic severe early morning stiffness and marked diurnal variation in symptoms reported with RA is absent. Function may be affected, in particular patients may notice difficulty with fine motor movements, gripping and opening objects.

Laboratory and imaging findings

While most patients with hand OA will have normal levels of inflammatory markers, it is increasingly recognised that low levels of elevation of erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) may occur in keeping with the inflammatory component of the disease. 

Specific blood tests such as rheumatoid factor and anti-cyclic citrullinated peptide are no more commonly positive than in the normal population. Other blood tests are usually normal, although a watchful eye should be kept on the renal profile due to frequent self-medication with over-the-counter non-steroidal anti-inflammatory drugs (NSAIDs). 

Plain radiographs classically show osteophytes, joint space narrowing, subarticular sclerosis and subchondral cysts; the first two findings are very common, the others can be difficult to appreciate. 

In addition to these, however, two other findings occur reasonably commonly and may cause confusion: periarticular osteopenia and erosions. 

Periarticular osteopenia is classically a sign of RA but often occurs in nodal OA where it tends to be less marked and more in proportion to the damage at the adjacent joint. 

Erosions were long believed to be a good indicator of RA, however sensitive imaging techniques have shown them to be common in hand OA; they may also be seen on plain films, particularly at the distal interphalangeal joints.

Distinguishing from RA and PsA

Arguably the most important aspect of nodal OA in clinical practice is to distinguish it from RA and PsA. While in the late destructive stages of any of the three diseases this is relatively easy due to the presence of classical findings, in early disease (and in treated RA and PsA patients) this can be a difficult diagnosis. 

This issue has become more pertinent due to the availability of highly effective, but potentially toxic or expensive, treatments for both RA and PsA that are best instituted in early disease to prevent joint destruction. 

The first point to make on this count is that this is a tricky area which may need experienced input; in addition, two diseases may coexist, and if there is any uncertainty then referral to a rheumatologist is warranted. A number of clinical clues may aid in the diagnosis. 

The first is the pattern of joint involvement. RA virtually never affects the distal interphalangeal joints whereas nodal OA very frequently does. 

PsA does affect the distal interphalangeal joints but tends to be more patchy and asymmetrical than nodal OA, the characteristic nail and skin changes may also help but may be absent. 

Significantly raised inflammatory markers point away from OA, however the converse is not necessarily true and in RA they may be slightly raised or even normal. 

A high titre of rheumatoid factor or anti-cyclic citrullinated peptide may suggest RA, but an elevated rheumatoid factor not infrequently occurs in the normal population.

Management

Existing pharmaceutical treatments for hand OA have modest effect sizes. First-line treatment is with simple analgesics, eg. paracetamol or tramadol (Zydol). NSAIDs may be slightly more effective but, given their side-effect profile, must be used cautiously if at all. 

Topical agents, associated with less adverse events, are attractive in view of the small size and superficial nature of the affected joints: topical NSAIDs and topical capsaicin are both effective. 

Given the inflammatory component of the disease it was logical to assess disease-modifying anti-rheumatic drugs (DMARDs) in this setting. Hydroxychloroquine, methotrexate, sulfasalazine and anti-tumour necrosis factor alpha (anti-TNF) drugs have all been used with little evidence of success to date. 

A large clinical trial has commenced evaluating hydroxychloroquine in this setting. There is reasonably good evidence that several commonly used treatments are no better than placebo, for example the nutraceuticals chondroitin and glucosamine sulphate (Dona). 

Steroid injections to the hand joints are of unproven efficacy, technically difficult and often extremely painful, and so rarely used. 

Given the absence of highly effective pharmaceutical therapy it is important to involve other modalities of therapy including physiotherapy for an exercise programme and occupational therapy for joint protection advice, functional assistance, splinting and symptomatic treatments such as thermal therapy with wax. 

The natural history of nodal OA is one of short-to-medium-term intermittently painful development of nodes followed by permanent fixed bony nodes with a significant reduction or disappearance of the pain. A careful explanation of the condition and a reassurance that it is not RA and will not lead to the historical deformities associated with this is often remarkably therapeutic for patients. 

A careful discussion of the limited benefits of pharmaceutical treatments can empower patients to be more involved in their treatment decisions and use symptomatic treatments as they feel appropriate. 

Efforts are ongoing to investigate novel treatment options and we may eventually have an effective and safe treatment that can arrest the development of the disease, but until then we can at least ensure a correct diagnosis and that we do no harm.

Reading list

1. Zhang W, Doherty M, Leeb BF et al. EULAR evidence based recommendations for the management of hand osteoarthritis: report of a Task Force of the EULAR Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT). Ann Rheum Dis 2007; 66: 377-388
2. Hochberg MC, Altman RD et al. American College of Rheumatology 2012 recommendations for the use of nonpharmacologic and pharmacologic therapies in osteoarthritis of the hand, hip and knee. Arthritis Care Res (Hoboken) 2012; 64: 465-474
3. National Institute for Health and Care Excellence. Osteoarthritis: the care and management of osteoarthritis in adults. CG59. London: National Institute for Health and Care Excellence, 2008. Available from: http://www.nice.org.uk/nicemedia/pdf/cg59niceguideline.pdf. Accessed 08/11/2013
4. Kingsbury SR, Tharmanathan P, Adamson J et al. Hydroxychloroquine effectiveness in reducing symptoms of hand osteoarthritis (HERO): study protocol for a randomized controlled trial. Trials 2013; 14: 64