Correlation of cartilage metabolic markers & antioxidants with the severity of knee osteoarthritis
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Osteoarthritis is characterized by the degeneration of articular cartilage. Cartilage metabolic markers have been explored as possible markers for osteoarthritis, and osteogenic protein -1 (OP-1) has emerged out to play a major role in cartilage repair. Oxidative stress has been implicated as a mediator of cartilage damage in patients with osteoarthritis. The aim of this study was to correlate the cartilage metabolic markers and antioxidants with the severity of knee osteoarthritis.Keywords:
Cartilage damage
Articular cartilage damage
Degeneration (medical)
Mediator
Abstract We examined the relationship between articular cartilage degeneration, as visualized arthroscopically, and joint space narrowing (JSN) in standing anteroposterior knee radiographs of 161 patients with chronic knee pain. The majority of these patients had radiographic findings of mild osteoarthritis. Twenty‐five (33%) of the 76 patients in the series whose radiographs showed tibiofemoral JSN had grossly normal articular cartilage in both tibiofemoral compartments at arthroscopy (false‐positive). The specificity of medial JSN for the presence of medial compartment articular cartilage degeneration was 0.61, i.e., only 61% of patients with normal (grade 0) medial compartment cartilage had a normal medial joint space. Of 22 patients with >50% medial JSN, 9 (41%) had normal articular cartilage in the medial compartment at arthroscopy. Of 6 patients with >50% lateral JSN, 3 (50%) had normal lateral compartment articular cartilage at arthroscopy. Among 36 patients with >25% JSN who had neither medial nor lateral compartemnt articular cartilage degeneration, JSN was associated with articular caartilage degeneration, JSN was associated with articular cartilage degeneration in the patellofemoral compartemnt in 8 (22%), with meniseus degeneration in 18 (50%), and with both in 8 (22%). Thus, in these patients with chronic knee pain, radiographic evidence of JSN in the tibiofemoral compartment did not permit confident prediction of the status of the articular cartilage.
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Degeneration (medical)
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Osteoarthritis is characterized by the degeneration of articular cartilage. Cartilage metabolic markers have been explored as possible markers for osteoarthritis, and osteogenic protein -1 (OP-1) has emerged out to play a major role in cartilage repair. Oxidative stress has been implicated as a mediator of cartilage damage in patients with osteoarthritis. The aim of this study was to correlate the cartilage metabolic markers and antioxidants with the severity of knee osteoarthritis.
Cartilage damage
Articular cartilage damage
Degeneration (medical)
Mediator
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Osteoarthritis or degenerative joint disease is a condition characterised by degeneration of articular cartilage often associated with the formation of new bone at joint surfaces or margins. Commonly encountered in dogs, osteoarthritis may have a gradual onset, but may also occur acutely. Osteoarthritis can be a primary disease of joint cartilage, but is more often secondary to abnormal stresses on joints. This article describes the pathogenesis and progression of cartilage degeneration as well as the dietary, lifestyle and pharmacological management of osteoarthritis. Recent pharmacological developments allow the clinician not only to control clinical signs of the disease, but also to slow the progression of cartilage degeneration.
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Osteoarthritis(OA) is a chronic joint disease that involves degeneration of articular cartilage,limited intraarticular inflammation manifested by synovitis and changes in the subchondral bone.It has been reported laterly that cytokines,such as mediator,regulate the functions of chondrocytes through various mechanisms and play important roles in joint cartilage degeneration.This review will focus on the correlative cytokines and their roles in the osteoarthritis cartilage degeneration.
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Abstract Osteoarthritis is a degenerative disease of synovial joints affecting all tissues, including the articular cartilage and underlying subchondral bone. Osteoarthritis animal models can recapitulate aspects of human disease progression and are commonly used to test the development of drugs, biomaterials, and cell therapies for treatment. The rat medial meniscus transection (MMT) model is a surgically induced post-traumatic osteoarthritis model and is one of the most commonly used models for therapeutic development; however, it is typically used to evaluate the efficacy of therapies to prevent disease development rather than testing the treatment of disease progression in already established disease. We describe herein, the qualitative and quantitative changes to articular cartilage, subchondral bone, and formation of osteophytes in rats at early-(3-weeks post-surgery), mid-(6-weeks post-surgery) and late-(12-weeks post-surgery) stages of osteoarthritis progression. Tibiae of MMT-operated animals showed loss of proteoglycan and fibrillation formation on articular cartilage surfaces as early as 3-weeks post-surgery. Using a contrast-enhanced μCT technique, quantitative, 3-dimensional analysis of the tibiae showed that the articular cartilage initially thickened at 3- and 6-weeks post-surgery and then decreased at 12-weeks post-surgery. This decrease in cartilage thickness corresponded with increased lesions in the articular cartilage, including fully degraded surfaces down to the subchondral bone layer. In this rat MMT model, subchondral bone thickening was significant at 6-weeks post-surgery and seem to follow cartilage damage. Osteophytes were found at 3-weeks post-surgery, which coincided with articular cartilage degradation. Cartilaginous osteophytes preceded mineralization suggesting that these marginal tissue growths most likely occurred through endochondral ossification. The use of the rat MMT model has predominantly been used out to 3-weeks, and most studies determine the effect of therapies to delay or prevent the onset of osteoarthritis. We provide evidence that an extension of the rat MMT model out to 6 and 12 weeks resembled more severe phenotypes of human osteoarthritis. The mid- to late-stages of rat MMT model can be used to evaluate the therapeutic efficacy of novel treatments to treat the progression of established disease — since patients typically present in the clinic when the disease is established and becomes symptomatic, thus evaluating the efficacy of new treatments at the late stage will be important for eventual clinical translation.
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Objective The objective of this study was to determine whether intra-articular injections of tenascin-C (TNC) could prevent cartilage damage in murine models of osteoarthritis (OA). Design Fluorescently labeled TNC was injected into knee joints and its distribution was examined at 1 day, 4 days, 1 week, 2 weeks, and 4 weeks postinjection. To investigate the effects of TNC on cartilage degeneration after surgery to knee joints, articular spaces were filled with 100 μg/mL (group I), 10 μg/mL (group II) of TNC solution, or control (group III). TNC solution of 10 μg/mL was additionally injected twice after 3 weeks (group IV) or weekly after 1 week, 2 weeks, and 3 weeks (group V). Joint tissues were histologically assessed using the Mankin score and the modified Chambers system at 2 to 8 weeks after surgery. Results Exogenous TNC was maintained in the cartilage and synovium for 1 week after administration. Histological scores in groups I and II were better than scores in group III at 4 and 6 weeks, but progressive cartilage damage was seen in all groups 8 weeks postoperatively. Sequential TNC injections (groups IV and V) showed significantly better Mankin score than single injection (group II) at 8 weeks. Conclusion TNC administered exogenously remained in the cartilage of knee joints for 1 week, and could decelerate articular cartilage degeneration in murine models of OA. We also showed that sequential administration of TNC was more effective than a single injection. TNC could be an important molecule for prevention of articular cartilage damage.
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