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doi: 10.1007/s11926-006-0019-1pmid: 16515759
Osteoarthritis is the most common form of arthritis and is a leading cause of disability in the elderly. Given the anticipated increase in osteoarthritis prevalence, the need to identify risk factors for incident osteoarthritis, osteoarthritis progression, osteoarthritis-associated physical function decline, and disability is an especially high priority. Findings have implicated several factors, including genetic factors, aging, joint deformity and injury, obesity, and hormonal deficiencies in the pathogenesis of osteoarthritis. Recent studies have identified risk factors associated with progression of the disease including varus-valgus alignment, bone marrow edema lesions, varus thrust, a reduced hip abduction moment, and obesity. Predictors of function decline in osteoarthritis include lower self-efficacy, knee laxity, less aerobic exercise, worse joint proprioception, and greater knee pain.
Peterfy, Charles; Kothari, Manish
doi: 10.1007/s11926-006-0020-8pmid: 16515760
Until recently, imaging evaluation of osteoarthritis has relied primarily on conventional radiography. Using radiography in clinical practice or clinical research, however, has been fraught with difficulty. Techniques for reproducibly acquiring serial radiographs of joints have improved considerably over the past several years. However, the greatest promise for advancing knowledge about osteoarthritis and its treatment lies in MRI and its unique ability to examine the joint as a whole organ. In contrast to conventional radiography, MRI can directly visualize the articular cartilage, synovium, menisci, and other intra-articular structures important to the functional integrity of joints. There have been considerable advances in MRI of articular cartilage in particular over the past several years. However, much of this has come from small cross-sectional studies. Larger, longitudinal studies are ongoing, and publications are just emerging. This paper reviews the current status of x-ray and MRI in osteoarthritis and points to where changes might be anticipated in the future.
McHughes, Mary; Lipman, Arthur
doi: 10.1007/s11926-006-0021-7pmid: 16515761
With no disease-modifying osteoarthritis drugs on the immediate horizon, the goal of osteoarthritis therapy remains management of pain and maintenance of function. Evidence supports use of nonpharmacologic measures including patient education, judicious exercise and weight loss, and assistive devices when appropriate to reduce pain and further loss of function. First line pharmacotherapy is acetaminophen or nonsteroidal anti-inflammatory drugs (NSAIDs). However, toxicities are associated with longterm use of these drugs. Evidence also supports the use of opioids in osteoarthritis pain management when other interventions are insufficient. NSAIDs and opioids are mutually dose sparing and combining relatively low doses of a drug from each class provides synergistic analgesia while limiting toxicity. Alternative therapies include tramadol and intra-articular injections of steroids and hyaluronic acid. There is evidence to support glucosamine as an adjunct in treating osteoarthritis. Evidence is lacking to support the use of chondroitin, S-adenosyl-methionine, or dimethyl sulfoxide in osteoarthritis pain management.
Martel-Pelletier, Johanne; Lajeunesse, Daniel; Fahmi, Hassan; Tardif, Ginette; Pelletier, Jean-Pierre
doi: 10.1007/s11926-006-0022-6pmid: 16515762
Osteoarthritis is considered an illness in which a complex interaction between the tissues of the joint plays a significant role in the initiation and/or progression of this pathophysiology. We do not yet completely understand all the factors that are responsible for initiating the degradation and loss of the articular tissues. This paper summarizes the novelties of three such mechanisms. The first one points to some factors involved in the regulation of one growth factor family, the bone morphogenetic proteins, the second, the regulation of prostaglandin E2 synthesis, and the third the factors involved in subchondral bone remodeling, all of which could be very significant events for osteoarthritis. This paper should help the reader better understand the most recent advances regarding the roles of these factors in this disease process, and how new therapeutic targets may be identified.
doi: 10.1007/s11926-006-0023-5pmid: 16515763
Osteoarthritis is characterized by progressive destruction of articular cartilage and subchondral bone and synovial reaction. Radiologic findings that form the basis of the diagnosis of osteoarthritis are poorly sensitive to detect early disease and for monitoring progression of joint damage. Blood-based proteomic analyses suggest that biochemical alterations can be observed well before radiologic damage is evidenced. New cartilage-specific markers, including assays for type II collagen synthesis and degradation, have been developed. Recent prospective studies indicate that blood and urine levels of these new markers are associated with progression of joint damage. Biological markers respond rapidly to treatment and therefore will certainly play an important role in the development and the monitoring of disease-modifying therapies. Because osteoarthritis involves different tissues and complex biologic processes, a combination of different biochemical markers appears to be the most promising diagnostic strategy.
doi: 10.1007/s11926-006-0026-2pmid: 16515766
The discovery and characterization of the RANKL/RANK/ OPG signaling pathway and the identification of its role in the pathogenesis of bone loss have provided the rationale for the development of drugs with the ability to modulate RANK-induced osteoclastogenesis. In vivo studies have identified interfering with the RANKL/RANK interaction as a potential therapeutic target in the management of osteoporosis. Two agents capable of blocking the binding of RANKL to RANK have been so far tested in clinical studies—osteoprotegerin (Fc-OPG fusion molecule) and the RANKL-antibody (AMG 162). Both have been found to have profound inhibitory effects on bone resorption, with AMG 162 appearing to be overall superior to OPG. Data are still very scarce, however, and much remains to be uncovered before novel strategies capable of modulating the RANKL/OPG signaling pathway could be safely and effectively used in the management of osteoporosis.
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