Osteoarthritis: An Overview of the Disease and Its Treatment Strategies

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Osteoarthritis (OA) is currently defined by the American College of Rheumatology as a “heterogeneous group of conditions that leads to joint symptoms and signs which are associated with defective integrity of articular cartilage, in addition to related changes in the underlying bone at the joint margins.” Its prevalence after the age of 65 years is about 60% in men and 70% in women. The etiology of OA is multifactorial, with inflammatory, metabolic, and mechanical causes. A number of environmental risk factors, such as obesity, occupation, and trauma, may initiate various pathological pathways. OA indicates the degeneration of articular cartilage together with changes in subchondral bone and mild intraarticular inflammation. The principal treatment objectives are to control pain adequately, improve function, and reduce disability. Acetaminophen is frequently used for symptomatic OA with mild to moderate pain. Nonsteroidal antiinflammatory drugs (NSAIDs) are more effective in the case of moderate–severe pain, but they have an increased risk of serious upper gastrointestinal adverse events. The newer cyclooxygenase COX-2 specific inhibitors (Coxibs) are as efficacious as traditional NSAIDs and have a better gastrointestinal safety profile. Other compounds (eg, chondroitin sulfate, diacerein, glucosamine sulfate) have a symptomatic effect that is slower and less than that of NSAIDs. The structure-modifying effects of drugs are currently being evaluated, and both glucosamine sulfate and diacerein have been shown in some trials to have a beneficial structural effect. Nonpharmacological interventions are frequently and widely used in the management of OA patients, but there is little evidence that they are effective: the best studied and most successful nonpharmacological interventions are patient education, self-management, and exercise. There is some evidence for the pain-relieving efficacy of thermotherapy and transcutaneous electrical nerve stimulation (TENS) but not of electrotherapy, acupuncture, homeopathy, or manual therapy. The value of interventions aimed at improving function and maximizing independence (occupational therapy, walking aids, workplace adaptation) is also unclear. The disease course and patient's requirements often change over time, thus requiring a periodic review and readjustment of therapy rather than the rigid continuation of a single treatment.

Section snippets

Etiopathogenesis of OA

The pathological characteristics of OA are loss of cartilage with associated underlying bony changes consisting of sclerosis, subchondral bone collapse, bone cysts, and osteophyte formation (10). The loss of articular cartilage in OA may start as a focal lesion and progressively extend to involve specific joint compartments, thus inducing alterations in articulating surfaces (11) and leading to progressive loss of cartilage (12). Superficial fibrillation is associated with the loss of the small

Symptoms and Signs

The cardinal symptom of OA is pain, which occurs with joint use and is relieved by rest. It is usually aching in character and poorly located (33). There is no strict correlation between joint symptoms and the extent or degree of pathological or radiographic changes (34). Only 30% of the patients with radiographic evidence of OA complain of pain at relevant sites (35). In advanced cases, pain may awaken the patient from sleep because of the loss of protective muscular joint splinting, which

General Aspects of Management

The principal objectives of treatment are to control pain adequately, improve function, and reduce disability. The status and requirements of patients often change over time, thus making it necessary to review and adjust treatment regularly rather than rigidly continuing a single intervention. Education is one of the most important issues for patients with OA.

Analgesics

Mild to moderate pain in OA patients can be relieved using simple analgesics such as acetaminophen. Bradley and coworkers demonstrated that acetaminophen 1000 mg 4 times a day had the same effect as ibuprofen 1200 or 2400 mg/day in patients with knee and hip OA (79), and it was also better tolerated. However, the results of a number of studies suggest that nonsteroidal antiinflammatory drugs (NSAIDs) are more efficacious (80). Acetaminophen-induced toxicity includes hepatotoxicity and potential

Conclusions

The overall burden of OA is increasing because of the prevalence of symptomatic OA in an aging world population, and the inadequacy of symptom-relieving and disease-modifying treatments. New insights into the pathophysiology of OA are clarifying the mechanisms underlying its different clinical aspects, the treatment of which requires a multidisciplinary approach. Education and preventive measures must accompany symptomatic treatment. In the near future, drugs capable of modifying the natural

Acknowledgments

The authors would like to thank all of the specialists and general practitioners who participated in the study, the scientific societies (SIR-Società Italiana di Reumatologia and CRO-Collegio dei Reumatologi Ospedalieri) and social and patient associations (LIMAR-Lega Italiana Malattie Reumatiche and ANMAR-Associazione Nazionale Malati Reumatici) who endorsed and supported the project, and OPIS Data srl for helping in data management and analysis. The authors are very grateful to all of the

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