Osteoarthritis OA is a disorder that confines itself to affected joints; however, impairment, functional limitation, and disability related to OA can reach far beyond the perimeters of articular cartilage and subchondral bone. OA often is compared to other arthritides and defined by what it is not: OA is not a systemic disease; OA is not a disease of primary inflammation; OA is not life threatening. Too often OA also has been considered not interesting, not important, and not responsive to conservative treatment. However, reports documenting the personal and socioeconomic impact of OA are increasing recognition of its importance [1] and recent advances in understanding its pathogenesis are stimulating research [2]. OA is characterized by specific changes in articular cartilage and subchondral bone. Cartilage shows fibrillations, increased water content, and loss of integrity. Underlying bone is less compliant and may exhibit microfractures, sclerosis, and osteophytes at joint margins [3]. These changes result in increased friction, decreased shock absorption, and greater impact loading of the joint. The traditional view of OA is that the disease process starts with an unrepaired injury to articular cartilage. There is also evidence, however, that reduced compliance in bone and periarticular structures may initiate degenerative processes [4,5]. Although radiographic evidence of joint space narrowing and osteophytes may help confirm a diagnosis of OA, the clinical criteria for classification and reporting of hip and knee OA are described in terms of pain and limitation of motion [6,7] Table 1. Radiographic and laboratory data add little to the accuracy of these criteria [6]. Moreover, there is no clear association between radiographic findings and function or pain [8].(ABSTRACT TRUNCATED AT 250 WORDS)