Osteoarthritis (OA) is the most common form of arthritis. It has been regarded as a disease of articular cartilage, with evidence of articular cartilage degeneration followed by erosion, the main identifying characteristic. The etiology is multifactorial, but common features can be observed. The end point of OA is cartilage destruction that impairs joint movement and causes pain. In knee joints, the cartilage destruction is associated with or preceded by subchondral bone sclerosis. Joint destruction is also associated with joint inflammation, with the synovial membrane playing a key role. The chronologic events of these phenomena are still debated in the literature. However, because of the complexity of the disease, it maybe initiated via each of these tissues, although inflammation of the synovial membrane is less likely to be a primary cause.
The widely held belief that OA is a disease of cartilage has been a subject of debate, particularly in recent years. Several investigations, including our own, have led to the hypothesis that bone changes may account for joint deterioration and development of OA. Indeed, individuals with OA exhibit striking increases in bone mass at affected sites, such as the knee and hip, as well as at nonsynovial sites like the lumbar spine. Individuals with OA also have a high body mass index (BMI) and exhibit an increase in bone mineral density (BMD).
The latter may be the result of an abnormally high rate of metabolism of osteoblasts, observable in vivo and in vitro, and most particularly in subchondral bone. However, stiffness and BMD are not uniform in OA bone, as assessed by quantitative backscattered electron imaging, Fourier transform infrared spectroscopy, and fractal analysis [70,142,228]. Actually, only bone closest to the articular cartilage influences the integrity of cartilage and variations in stiffness and BMD in OA bone tissue may cause more damage to cartilage integrity than to normal bone [43,66]. Moreover, the apparent elevations in BMD in OA may be due to an increase in material density resulting from a more abundant, yet undermineralized osteoid collagen matrix [8, 144,145]. Indeed, the increase in osteoid matrix in OA bone tissue [125,246] is an indication of abnormal mineralization and of general bone metabolic disease [80-82,188]. The altered metabolism of osteoblasts from subchondral bone tissue is not due to changed serum levels of humoral factors or hormones , but to an alteration in local signals. Even in the early stages of osteoarthritis, pheno-typic differences in subchondral osteoblasts become manifest as a result of a higher rate of metabolism. Indeed, a large number of factors, including inflammatory and growth factors and proteases, are produced in excessive amounts in the diseased tissue [101,135,136,208,241]. These factors may act locally, via autocrine/paracrine signaling, but increasing evidence indicates that these factors interact with the overlying articular cartilage [92,124,207]. Alterations in the crosstalk between bone and articular tissues may contribute to the pathogenesis of OA.
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