As the leading cause of disability in the United States, arthritis is a chronic disease with a significant impact on the population. Based on 2003–2005 data from the National Health Interview Survey (NHIS), an estimated one in five or 46.4 million of U.S. adults have self-reported doctor-diagnosed arthritis. Almost 41% (19 million) of these 46 million adults report limitations in their usual activities due to their arthritis. In addition to activity limitations, 31% (8.2 million) of working age adults with doctor-diagnosed arthritis report being limited in work activities. As the U.S. population ages, these numbers are likely to increase considerably. Each year, arthritis results in 750,000 hospitalizations and 36 million outpatient visits. In 2003, direct medical costs for arthritis were $81 billion while indirect costs were another $47 billion. This economic burden explains the increasing attention that is being directed to arthritis and to finding pharmacological agents to help control the disease.
Arthritis refers to damage to the joints that can be caused by a variety of pathological processes, including osteoarthritis and rheumatoid arthritis. It manifests clinically as abnormal and degraded cartilage, inflamed and thickened synovial tissue, and altered bone structure resulting in pain, decreased mobility, impairment, and disability.1–3
The diagnosis of arthritis is made based on the patient’s history, physical exam, and radiographs. However, plain radiographs only provide indirect information on cartilage, unlike the direct information it gives on bone. This is because damage to bone can be easily visualized in its actuality on a x-ray while injury to cartilage may only be gleaned from indirect cues such as joint space narrowing, bone erosions or osteophytes, osteopenia or sclerosis, and soft-tissue swelling.4,5
Serial examinations over several years may be used for assessments of prognosis, treatment, and clinical outcomes. But, sensitivity to change is limited, and clinical manifestations of arthritis do not develop until late in the disease process. By then, the disease process of cartilage degeneration has progressed too far for the chondrocytes to be able to stop or reverse the joint disease, making it too late for early diagnosis and treatment.6–11
Arthroscopy provides a direct and magnified view of the cartilage surface, but this is an invasive technique that cannot be routinely applied to all patients. Laboratory markers such as erythrocyte sedimentation rate (ESR) and levels of C-reactive protein (CRP) provide useful information about the general inflammation process in some patients, but these markers are not specific to inflammation in joints and correlate poorly with cartilage damage at the individual level.12–15
Serum IgM rheumatoid factor (RF) and anti-cyclic citrullinated peptide antibodies (anti-CCP) have some diagnostic and prognostic value in the evaluation of rheumatoid arthritis, but positive results can occur with other diseases such as systemic lupus erythematosus, Sjogren’s syndrome, cryoglobulinemia, polymyositis/dermatomyositis, psoriatic arthritis, scleroderma, polymyalgia rheumatica, viral infections, active tuberculosis, tumor, Lyme disease, autoimmune thyroid disease, and palindromic rheumatism.16–28
By the late stages of arthritis, treatment options are mainly palliative including medications, intra-articular injections, weight loss, ambulatory aids, orthotics, and physical therapy with surgical intervention being the last and most effective option for treatment.