Osteoarthritis (OA) was once thought to be an inevitable stage in the aging process, but there are significant unmet needs in the early diagnosis, monitoring and treatment of the disorder that could bring relief to suffering patients. Researchers are now taking a much closer look at OA and its underlying causes to find better ways to prevent and treat it.
To clarify why this topic has begun to draw more interest from the scientific and medical community, a few facts should be considered. In the United States, the importance of treating OA can be tied to the economic burden it has placed on society at an annual cost of $128 billion in disability. Today, OA affects 50 million Americans, or one in five adults. In 20 years, the number of people affected will be 67 million, or about 25% of the population. OA affects 300,000 children.
As a result of this disease, one in 20 Americans is forced to change jobs, stop working, or reduce the number of hours he or she can work. In addition, there are concomitant diseases associated with OA: 52% of adults with diabetes have OA, and 57% of adults with heart disease have OA.
Each year, arthritis results in 44 million clinician visits and almost 1,000,000 hospitalizations, with an estimated 1 million joint replacements being performed in an even younger population than in previous years.1 According to one report, “Obesity and OA of the knee are robbing millions of older Americans of an average…3.5 years of life in which they might otherwise be feeling healthy.”2 Moreover, as a result of the most recent wartime casualties, 32% of veterans have OA, compared to 22% of nonveterans. This is a result of the generally more than 100 lb of equipment the troops carry regularly. Thus, the gear used to protect troops may also injure them, and the tremendous impact of strenuous physical forces placed upon them in the performance of their duties increases their risk of injury, resulting in an unfortunate occupational hazard.3
OA has become a public health issue. All medical providers should be cognizant of this disease and become familiar with the newest evidenced-based research that could lead the way to treating the underlying cause(s) of OA, not just the symptoms. Clinical research helps to answer questions about the efficacy of biologic and pharmaceutical treatment.
At a 1994 workshop entitled “New Horizons in Osteoarthritis,” the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institute on Aging, National Arthritis Foundation and American Academy of Orthopaedic Surgeons (AAOS) developed a new definition of OA: “…[a] disease process that involves the entire joint-subchondral bone, ligaments, capsule, synovial membrane and periarticular muscles. Ultimately, the articular cartilage degenerates with fibrillation, fissures, ulceration and full thickness loss of the joint surface.”4
Eyre defined OA as the clinical and pathologic outcome of a range of disorders resulting in structural and functional failure of synovial joints. OA occurs when the dynamic equilibrium between the breakdown and repair of joint tissues is overwhelmed.5 The most commonly used criteria for diagnosis were published by the American College of Rheumatology (ACR).6-8
OA is widely believed to be the result of local mechanical factors acting within the context of systemic susceptibility. The systemic factors that increase the vulnerability of the joint to OA include age, gender, bone density, nutritional factors and genetic predisposition. In persons vulnerable to the development of OA, such local biomechanical factors as malalignment, muscle weakness, or alterations in the structural integrity of the joint environment (e.g., meniscal damage or bone marrow lesions), facilitate the progression of disease.9
The affect of genetics
Genetic predisposition to OA, which has been evident from anecdotal studies, was confirmed by Kellgren and coworkers, who reported that generalized nodal OA was twice as likely to occur in first-degree relatives as in control individuals.10
Because OA is so prevalent in the general population, the role of genetics has been difficult to analyze. Asking the patient about family history of OA is key during the patient assessment. In addition, additive factors that may contribute to the development of OA can be contained within specific genes.
Age is the single most strongly correlated risk factor associated with OA. Cohort studies have demonstrated a clear association between obesity and knee OA. Local mechanical factors, vulnerability of the knee joint, and joint loading are directly related to obesity and to occupation-related injury and physical trauma, whether from sports or accidents.
An increase in mechanical forces across weight-bearing joints is probably the primary factor leading to joint degeneration.11 “Obese adults with arthritis are 44% more likely to be physically inactive than obese people who do not suffer from this painful disease,” the CDC said in a recent statement.12
Joint malalignment and varus or valgus deformities are markers of disease severity associated with risk of OA progression. Patients with pes planus (flat feet) are more likely to experience knee OA. Female gender is a well-recognized risk factor, with a marked increase in OA prevalence after age 50 years, likely due to estrogen insufficiency.
Common sites of OA
The most common sites of OA involvement and prevalence are the hand (70%), knee (30%), hip (10%) and spine (60%).13 As previously noted, classification criteria of OA in specific joints (i.e., the hip, knee, and hand) have been published by the ACR.6-8
Signs and symptoms
A combination of typical symptoms, physical findings, and radiographic changes helps to differentiate OA from other rheumatic diseases.
Patients with early OA have localized joint pain that worsens with activity but is relieved with rest. Patients with OA often describe a sensation of “giving way” or “buckling” in the knee or subluxation in the hand joints. Gel phenomenon is a condition that occurs when a joint has been too long at rest and the synovial fluid becomes thickened, much like motor oil in a car that has been sitting at cold temperatures.
Physical findings of OA may include bony enlargement, crepitus, cool effusions and decreased range of motion. The presence of crepitus, whether it is heard or felt, indicates that the joint has minimal, if any, cartilage and is bone-on-bone. A sensation of warmth may indicate inflammation or even infection. This symptom requires evaluation to determine the proper therapy, ie, an anti-inflammatory agent or steroids versus antibiotics.
In some patients, there may be an inflammatory component to the OA. This can s,ometimes be misinterpreted as rheumatoid arthritis (RA). Joint swelling, deformity, or instability (laxity) of the joint may be seen. The distal phalanges of the hand may be affected with Heberden nodes (Figure 1), while the proximal phalanges may be affected with Bouchard nodes (Figure 2).
X-rays (Figure 3) may show osteophytes, joint space narrowing, subchondral sclerosis, and cysts. Joint space narrowing can occur as the cartilage breaks down.
Radiography is considered the gold standard for diagnosing OA, although other imaging modalities may be utilized, especially in the research arena.14
Laboratory or biologic markers for OA
Since OA is generally a noninflammatory disease, laboratory tests do not usually help with the diagnosis, although when there is readily apparent swelling of the joint, a lower erythrocyte sedimentation rate (ESR) may help differentiate OA from such other arthritides as RA.