More recently, Boutry and colleagues reported magnetic resonance imaging (MRI) findings of this form of osteoarthritis. Because of the rapidity of the process, the radiographic presentation of this condition is marked by very little, if any, reparative changes, mimicking infectious or neuropathic arthritis (Charcot joint) ( Fig. Others have proposed subchondral insufficiency fracture of the femoral head as a cause of this arthritis. Some investigators have suggested that intraarticular deposition of hydroxyapatite crystals might lead to joint destruction. The precise pathogenesis of this condition remains unclear, although direct drug toxicity and the analgesic effects of nonsteroidal antiinflammatory drugs have been implicated. Occasionally, one can observe foci of fibrosis, interstitial edema and hemorrhage in the marrow spaces, focal marrow fat fibrosis, and focal areas of bone resorption. The bone trabeculae are either abnormally thickened or abnormally thinned. Hypervascularity in the subchondral bone is a common finding. However, osteophyte formation is absent or minimal. The histologic findings are those of conventional osteoarthritis with severe degenerative changes in the articular cartilage. In all cases, a rapid clinical course of hip pain is the consistent common symptom. Originally described by Lequesne, and also by Postel and Kerboull in 1970, this unique hip disorder occurs predominantly in women, with age of onset at 60 to 70 years. This destructive arthrosis of the hip joint is known as Postel coxarthropathy, a condition characterized by rapid chondrolysis that may quickly lead to complete destruction of the hip joint. Occasionally, the degenerative process in the hip may run a more rapid course. Obesity is associated with a higher incidence of osteoarthritis in the knees, which may be related to an excessive weight-bearing load on these joints. In the population older than 65 years, osteoarthritis affects Caucasians more commonly than African Americans. It has been shown that osteoarthritis tends to affect women more commonly than men, particularly in the proximal and distal interphalangeal joints and the first carpometacarpal joints. This form may be related to genetic factors, as well as to gender, race, and obesity. Marked by progressive destruction of the articular cartilage and reparative processes such as osteophyte formation and subchondral sclerosis, true osteoarthritis progresses rapidly, leading to significant joint deformity. Some investigators suggested that osteoarthritis in some families may be caused by the mutations in the type II collagen gene COL2A1, which encodes a protein expressed almost exclusively in cartilage. Most recent studies also suggested that mutations in the gene GDF5, also known as cartilage-derived morphogenetic protein 1, can be linked with etiology of osteoarthritis of the hip and knee. Implicated genes include VDR AGC1 IGF-1 ER alpha TGF beta cartilage matrix protein (CRTM) cartilage link protein (CRTL) and collagen II, IX, and XI. Several studies have implicated linkages to osteoarthritis on chromosomes 2q, 9q, 11q, and 16p, among others. The nature of the genetic influence, however, is partially speculative and may involve either a structural defect (i.e., collagen), alterations in cartilage or bone metabolism, or alternatively a genetic influence on a known environmental risk factors such as obesity, sports, and trauma. Genetic factors have been found to be strong determination of this form of osteoarthritis. The second type, a true osteoarthritis, is unrelated to the aging process, although it shows an increased prevalence with age. This process is not affected by gender or race. It characteristically shows limited destruction of the cartilage, slow progression, lack of significant joint deformity, and no restriction of joint function. The first form is apparently closely related to the aging process (“wear and tear”) and represents not a true arthritis but a senescent process of the joint. Some authorities postulate that there are two types of primary degenerative joint disease.
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