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Diagnosing and Managing Hand Osteoarthritis

Pain and decreased function are the cornerstone of osteoarthritis of the hand (HOA). An individualized stepped-up approach may have broadest appeal in pain management of HOA.
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Osteoarthritis (OA) is the most significant cause of musculoskeletal morbidity in the elderly, and the hand is the most frequently affected area of the body.1 A study in the United States found that among people older than 26 years, the prevalence of radiographic-confirmed osteoarthritis of the hand (HOA) and symptomatic HOA were 27.2% and 6.8%, respectively.2

The disability of HOA is primarily due to the combined impact of pain and decreased functionality, which significantly decreases quality of life for those who suffer from it.3 The small size of the bones and joints in the hand also make it a unique site for treatment. Current guidelines on the management of HOA are centered primarily on pain management, as there is a dearth of disease-modifying medical treatments, and surgical interventions are not as well developed as for OA of the knee, hip, and shoulder.

This paper aims to review the suspected causes and risk factors of HOA, to outline the appropriate diagnostic approach for a patient who presents with possible HOA, and to describe the appropriate management of a patient with HOA.

Evolving Etiology and Risk Factors

Once regarded as simply a “wear and tear” phenomenon, the etiology of OA has become remarkably complex. No longer thought of as solely a disease of cartilage, the model for OA development involves the entire joint and includes such pathological changes as loss of articular cartilage, osteophyte formation at the joint margins, subchondral bone remodeling with cysts and sclerosis, ligamentous dysfunction, muscle dysfunction, and synovial inflammation.4 Still, the basic biomechanical premise remains the same—accelerated damage to cartilage leads to bone-on-bone contact, pain, stiffness, and dysfunction. On the biochemical nature of the disease, some data posit that inflammatory cytokines play a role in altering the balance between cartilage buildup and breakdown,5 suggesting that a systemic understanding of OA is also necessary.

The pathogenesis of OA is dependent on the age at presentation. In the under-40 age group, for example, OA is almost always associated with some injury to the affected joint,2 suggesting that in this minority of patients, trauma is a key factor in disease development. In patients older than 40, the pathogenesis appears not to rely on trauma, although it may be contributory. The most significant risk factor for HOA, or for OA of any joint, is age. The incidence of OA is greatly increased between the ages of 40 and 70, after which it seems to return to under-40 levels. The significance of the 30-year window of increased OA development is unknown, but it is useful in making a differential diagnosis. Any patient within the 40- to 70-year-old range or any patient with a history of joint trauma should be regarded as at risk.6

Although not necessary for the development of HOA, some kind of occupational or recreational history involving repeated hand motions is often present. This supposed link to the “wear and tear” hypothesis is simply that increased usage causes a thinning of the cartilage and when that damaged cartilage cannot be replaced, OA results. The effect of activity on HOA is dose dependent and shows differential distributions of joints involved depending on the particular repetitive task.7 Patients with a history of repetitive use damage should receive counseling on how to best care for their joints, and an immobilizing splint should be considered.

Whereas the connection between OA and obesity seems somewhat common sense in the context of the hip joint or the knee joint, obesity is also a known risk factor for the development of HOA,8 a finding that supports the systemic, biochemical nature of the disease. Proposed mechanisms focus on the endocrine function of adipose tissue possibly increasing the systemic levels of adipokines, such as leptin, and thereby impacting cartilage throughout the body.5 Published evidence from knee OA suggests that body fat percentage, not increased weight or body mass index (BMI), is the important feature in this relationship.9 Weight loss, when indicated, may be therapeutic in overweight patients with HOA and perhaps is preventative in those who have not yet developed the disease.

Female sex is a risk factor that is particularly predictive of OA of the hand.10 Unfortunately, another major cause of hand pain, rheumatoid arthritis (RA), also has higher prevalence in women. These two entities can be differentiated by a combination of age of onset, clinical presentation, joints presenting with pain, and laboratory testing. Family history is a pertinent risk factor,11 although a specific genetic component has not been identified (see Table 1).

Table 1. Risk Factors for HOA

Table 2. Diagnosis of HOA


Diagnosis of HOA requires a multifaceted approach, as there is no single test or finding that holds adequate sensitivity and specificity to make the diagnosis on its own (see Table 2). The European League Against Rheumatism (EULAR) published a set of recommendations for the diagnosis of HOA that were developed using a combined evidence-based and expert consensus methodology.12 Prior to the EULAR task force, the best resource for the diagnostic criteria of HOA was the American College of Rheumatology (ACR) Criteria for the Classification and Reporting of Osteoarthritis of the Hand (1990).

The first step in diagnosis is comparing a patient’s complaints with the typical presenting symptomatology. HOA most often presents as hand pain on usage, with or without mild morning stiffness, affecting one or more joints of the hand. The distal interphalangeal joint (DIP) is most often involved, followed in order by the thumb base and proximal interphalangeal joint (PIP). This distribution of joints involved can be somewhat helpful in differentiating OA from other hand arthroses (Figure 1), but the specificity of this diagnostic approach is low.

Similarly, the presence of Heberden’s or Bouchard’s nodes may aid in the diagnosis but are not specific enough to be considered as a sole diagnostic marker. Some degree of functional impairment is to be expected but may be very similar to impairment seen in RA. An important subset of HOA is that of erosive OA. Patients with this condition may present with abrupt onset of marked pain, functional impairment, inflammatory signs and symptoms, and mildly elevated C-reactive protein (CRP). In general, these patients have a worse outcome and more rapidly developing symptoms than those with nonerosive OA.

Radiologic evaluation of HOA includes a posterior-anterior x-ray of both hands. Magnetic resonance imaging (MRI), scintography, and ultrasound have been evaluated as imaging modalities, but studies have yet to illustrate a true, reproducible benefit. X-ray indicators of HOA include joint space narrowing, osteophyte formation, subchondral bone sclerosis, and subchondral cysts. The correlation between x-ray findings and clinical OA is very weak in the hand, worse than in the hip or knee. There currently are no recommended interventions for asymptomatic HOA found incidentally on hand radiography.

Last updated on: October 21, 2015
First published on: May 1, 2011
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