What is Osteoarthritis?

Osteoarthritis (OA) is the most prevalent type of arthritis affecting millions of individuals It differentially affects older individuals over the age of 65 years. OA is a chronic degenerative arthropathy that frequently leads to chronic pain and disability.

Osteoarthritis: Epidemiology & Risk Factors

Epidemiology

OA is the most common type of arthritis.

Reported incidence and prevalence rates of OA in specific joints vary widely, due to differences in the case definition of OA. OA may be defined by radiographic criteria alone (radiographic OA), typical symptoms (symptomatic OA), or by both. Using radiographic criteria, the distal and proximal interphalangeal joints of the hand have been identified as the joints most commonly affected by OA, but they are the least likely to be symptomatic. In contrast, the knee and hip, which constitute the second and third most common locations of radiographic OA, respectively, are nearly always symptomatic. The first metatarsal phalangeal and carpometacarpal joints are also frequent sites of radiographic OA, while the shoulder, elbow, wrist and metacarpophalangeal joints rarely develop idiopathic OA.

Risk Factors for Osteoarthritis

AGE: In demographic studies, age is the most consistently identified risk factor for OA, regardless of the joint being studied. Prevalence rates for both radiographic OA and, to a lesser extent, symptomatic OA rise steeply after age 50 in men and age 40 in women. OA is rarely present in individuals less than 35 years of age, and secondary causes of OA or other types of arthritis should strongly be considered in this population.

SEX: Female gender is also a well-recognized risk factor for OA. Hand OA is particularly prevalent among women.

OBESITY: Cohort studies have demonstrated a clear association of obesity with the development of radiographic knee OA in women and a weaker association with hip OA.

JOINT STRESS: Occupation-related repetitive injury and physical trauma contribute to the development of secondary (non-idiopathic) OA, sometimes occurring in joints that are not affected by primary (idiopathic) OA, such as the metacarpophalangeal joints, wrists and ankles.

GENETICS: Twin studies have demonstrated an important role for genetics in the development of OA.. Genome-wide studies continue to evaluate for particular chromosomes, particularly those involved in bone or articular cartilage structure and metabolism, and associations of familial OA.

Osteoarthritis: Differential Diagnosis

If a patient has the typical symptoms and radiographic features described above, the diagnosis of OA is relative straightforward and is unlikely to be confused with other entities. However, in less straightforward cases, other diagnoses should be considered:

Periarticular structure derrangement: Periarticular pain that is not reproduced by passive motion or palpation of the joint should suggest an alternate etiology such as bursitis, tendonitis or periostitis.

Inflammatory arthritis: If the distribution of painful joints includes MCP, wrist, elbow, ankle or shoulder, OA is unlikely, unless there are specific risk factors (such as occupational, sports-related, history of injury). Prolonged stiffness (greater than one hour) should raise suspicion for an inflammatory arthritis such as rheumatoid arthritis. Marked warmth and erythema in a joint suggests a crystalline etiology.

Other inflammatory / systemic condition: Weight loss, fatigue, fever and loss of appetite suggest a systemic illness such as polymyalgia rheumatica, rheumatoid arthritis, lupus or sepsis or malignancy. Current treatment for OA is limited to control of symptoms. At this time, there are no pharmacological agents capable of retarding the progression of OA or preventing OA.

Pharmacological Therapy

 Acetaminophin: Several studies have shown acetaminophen to be superior to placebo and equivalent to nonsteroidal anti-inflammatory agents (NSAIDs) for the short-term management of OA pain. At present, acetaminophen (up to 4,000 mg/daily) is the recommended initial analgesic of choice for symptomatic OA.

 Non-steroidal Anti-inflammatory Agents (NSAIDs): NSAIDs have been an important treatment for the symptoms of OA for a very long time. The mechanism by which NSAIDs exert their anti-inflammatory and analgesic effects is via inhibition of the prostaglandin-generating enzyme, cyclooxygenase (COX) . In addition to their inflammatory potential, prostaglandins also contribute to important homeostatic functions, such as maintenance of the gastric lining, renal blood flow, and platelet aggregation. Reduction of prostaglandin levels in these organs can result in the well-recognized side effects of traditional non-selective NSAIDs (ibuprofen, naprosyn, indomethacin) – that is, gastric ulceration, renal insufficiency, and prolonged bleeding time. The elderly are at higher risk for these side effects. Other risk factors for NSAID-induced GI bleed include prior peptic ulcer disease and concomitant steroid use. Potential renal toxicities of NSAIDs include azotemia, proteinura, and renal failure requiring hospitalization. Hematologic and cognitive abnormalities have also been reported with several NSAIDs. Therefore, in elderly patients, and those with a documented history of NSAID-induced ulcers, traditional non-selective NSAIDs should be used with caution, usually in lower dose and in conjunction with a proton pump inhibitor. Renal function should be monitored in the elderly. In addition, prophylactic treatment to reduce risk of gastrointestinal ulceration, perforation and bleeding is recommended in patients > 60 years of age with: prior history of peptic ulcer disease; anticipated duration of therapy of > 3 months; moderate to high dose of NSAIDs; and, concurrent corticosteroids. The development of selective cyclooxygenase-2 (COX-2) inhibitors offers a strategy for the management of pain and inflammation that is likely to be less toxic to the GI tract.

COX-2 Inhibitors: Cyclooxygenase-2 (COX-2) inhibitors are a class of NSAIDs) that recently received Food and Drug Administration (FDA) approval. These specific COX-2 inhibitors are effective for the pain and inflammation of OA. Their theoretical advantage, however, is that they will cause significantly less toxicity than conventional NSAIDs, particularly in the GI tract. NSAIDs exert their anti-inflammatory effect primarily by inhibiting an enzyme called cyclooxygenase (COX), also known as prostaglandin (PG) synthase. COX catalyzes the conversion of the substrate molecule, arachidonic acid, to prostanoids.

Other Oral Analgesic Agents: For patients who cannot tolerate NSAIDs or COX-2 inhibitors other analgesics alone or in combination may be apporrpriate. Tramadol, a non-NSAID/COX2 non-opioid pain medication, can be effective to manage pain symptoms alone or in combination with acetaminophen. Opioids should be a last resort for pain management, often in late-stage disease, given their many side effects including constipation, somnolence, and potential for abuse.

Topical Agents: Topical analgesic therapies include topical capsaicin and methyl salicylate creams. There is an FDA approved topical NSAID for the treatment of OA, diclofenac gel, which can be particularly useful for patients who are intolerant to the gastrointestinal side effects of NSAIDs.

Intraarticular Therapies: The judicious use of intra-articular glucocorticoid injections is appropriate for OA patients who cannot tolerate, or whose pain is not well controlled by, oral analgesic and anti-inflammatory agents. Periarticular injections may effectively treat bursitis or tendonitis that can accompany OA. The need for four or more intra-articular injections suggests the need for orthopedic intervention. Intraarticular injection of hyaluronate preparations has been demonstrated in several small clinical trials to reduce pain in OA of the knee. These injections are given in a series of 3 or 5 weekly injections (depending on the specific preparation) and may reduce pain for up to 6 months in some patients.

Non-pharmacological Management

Weight reduction in obese patients has been shown to significantly relieve pain, presumably by reducing biomechanical stress on weight bearing joints. Exercise has also been shown to be safe and beneficial in the management of OA. It has been suggested that joint loading and mobilization are essential for articular integrity. In addition, quadricep weakness, which develops early in OA, may contribute independently to progressive articular damage. Several studies in older adults with symptomatic knee OA have shown consistent improvements in physical performance, pain and self-reported disability after 3 months of aerobic or resistance exercise. Other studies have shown that resistive strengthening improves gait, strength and overall function. Low-impact activities, including water-resistive exercises or bicycle training, may enhance peripheral muscle tone and strength and cardiovascular endurance, without causing excessive force across, or injury, to joints. Studies of nursing home and community-dwelling elderly clearly demonstrate that one additional important benefit of exercise is a reduction in the number of falls.

Surgical Management

Patients in whom function and mobility remain compromised despite maximal medical therapy, and those in whom the joint is structurally unstable, should be considered for surgical intervention. Patients in whom pain has progressed to unacceptable levels-that is, pain at rest and/or nighttime pain-should also be considered as surgical candidates