Osseous Pathway of Nutrition to Articular Cartilage of the Human Femoral Head

Mital, M.A.; Millington, P. F.

doi:10.1016/s0140-6736(70)92443-8

Cited by 24 publications

(12 citation statements)

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“…These changes would then lead to reactivation of the secondary ossification centre and a decrease in cartilage thickness [86], suggesting that the altered subchondral bone remodelling or turnover would initiate cartilage degradation. This is possible as clefts and channels in the tidemark were seen early on in OA as well as fatigue microcracks in articular cartilage [87][88][89][90][91].…”

Section: Interaction Between Subchondral Bone and Cartilagementioning

confidence: 99%

Targeting subchondral bone for treating osteoarthritis: what is the evidence?

Tat

Lajeunesse

Pelletier

et al. 2010

Best Practice & Research Clinical Rheumatology

153

121

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Over the past few decades, significant progress has been made with respect to new concepts about the pathogenesis of osteoarthritis (OA). This article summarises some of the knowledge we have today on the involvement of the subchondral bone in OA. It provides substantial evidence that changes in the metabolism of the subchondral bone are an integral part of the OA disease process and that these alterations are not merely secondary manifestations, but are part of a more active component of the disease. Thus, a strong rationale exists for therapeutic approaches that target subchondral bone resorption and/or formation, and data evaluating the drugs targeting bone remodelling raise the hope that new treatment options for OA may become available.

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Section: Interaction Between Subchondral Bone and Cartilagementioning

confidence: 99%

Targeting subchondral bone for treating osteoarthritis: what is the evidence?

Tat

Lajeunesse

Pelletier

et al. 2010

Best Practice & Research Clinical Rheumatology

153

121

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“…8,13,18,19,61,71,73 In OA, bone thickness is caused by a higher subchondral bone metabolism 84 characterized by an increased collagen Type I synthesis 56 and abnormal production of proinflammatory mediators 30,45,48,57 by stromal cells and osteoblasts. The presence of channels and fissures between cartilage and bone in a joint affected by OA provide a route for the delivery of biologic signals between these two compartments.…”

Section: Availability Of Chemokines To the Chondrocytes And The Role mentioning

confidence: 99%

Chemokines in Cartilage Degradation

Borzı̀¹,

Mazzetti²,

Marcu³

et al. 2004

Clinical Orthopaedics &Amp; Related Research

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Besides the well-known activities of the prototypical inflammatory cytokines (IL-1␤, TNF␣), a role for chemokines and their receptors in cartilage degradation in osteoarthritis has recently been reported. Human chondrocytes can produce CC and CXC chemokines and express chemokine receptors for both chemokine subfamilies. Engagement of these receptors can induce the release of matrix degrading enzymes such as matrix metalloproteinases 1, 3, and 13, and N-acetyl-␤-Dglucosaminidase. Furthermore GRO␣, a CXC chemokine acting on CXCR2, can activate an apoptotic pathway in chondrocytes that leads to chondrocyte cell death. These findings suggest that chemokines can act as an autocrine or paracrine loop on chondrocytes and can contribute to many pathophysiological patterns present in osteoarthritis. Chemokines and their downstream signaling pathways can be considered novel therapeutic targets in osteoarthritis.Cartilage degradation in osteoarthritis (OA) results from phenotypical instability of the chondrocytes that sets up different cellular reaction patterns (dedifferentiation, release of matrix degrading enzymes, hypertrophy and apoptosis) under the control of a number of soluble factors, mainly released by the chondrocytes themselves. 24,77 Recent reports would establish the concept that OA-affected chondrocytes behave as activated macrophages 28 and share the release of similar inflammatory mediators. 3 However, because cartilage is an avascular, alymphatic, and aneural tissue, OA does not fit to the classic definition of inflammatory disease.Osteoarthritis might be considered as the result of the loss of the differentiated phenotype of the chondrocytes, with an enhancement of both catabolism and anabolism. 77 In this perspective, the huge base of literature currently available concerning the protagonist role of interleukin-1 (IL-1) cannot also account for the pattern of frustrated anabolism seen in OA. Furthermore, enhanced catabolism and enhanced anabolism seem to be distinct or at least heterogeneous within the various layers of articular cartilage, with superficial layers more susceptible to the catabolic effects of IL-1␤. 27 Chondrocytes of the deeper layers exhibit higher rates of proliferation and higher collagen and proteoglycan synthesis. 36 This discloses a pathogenic role also for growth and/or anabolic factors besides that of classical-proinflammatory cytokines (IL-1␤ and tumor necrosis factor alpha [TNF␣]).Data obtained by means of gene-chip analysis of osteoarthritic chondrocytes versus normal chondrocytes indicate strong up-regulation of members of the chemokine family beyond that of classic proinflammatory cytokines. 3 On the protein side, available current data obtained in supernatants of normal and OA cartilage explants show that IL-8 and monocyte chemoattractant protein-1 (MCP-1) are present at concentrations that are one order of magnitude higher than those of IL-1 and TNF␣. 3 This strongly supports a role for chemokines in cartilage physiology and pathology.Chemoattractive cytokines (chemokines) ...

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“…Since most patients with noncollapsed osteonecrosis are asymptomatic, it has been hypothesized that the femoral head articular cartilage in such patients is in normal condition and that as long as their articular cartilage remains in normal condition, their hip joint eventually will completely recover by a spontaneous repair process in which the osteonecrotic lesion is gradually replaced by viable bone tissue (6). On the other hand, because articular cartilage is thought to be nourished mainly by articular fluid and partly by subchondral bone (10,11), it has been further hypothesized that circulatory disturbance due to subchondral bone necrosis is responsible for cartilage degeneration. However, to our knowledge, few studies have been published that have actually examined the articular cartilage in SLE patients with noncollapsed osteonecrosis of the femoral head.…”

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confidence: 99%

Quantitative T2 mapping of femoral head cartilage in systemic lupus erythematosus patients with noncollapsed osteonecrosis of the femoral head associated with corticosteroid therapy

Yamamoto

Watanabe

Nakamura

et al. 2011

Magnetic Resonance Imaging

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Purpose:To evaluate articular cartilage degeneration with transverse relaxation time (T2) mapping in systemic lupus erythematosus (SLE) patients with noncollapsed and asymptomatic osteonecrosis of the femoral head associated with corticosteroids.Materials and Methods:T2 mapping with a 1.5‐T magnetic resonance imaging system was prospectively performed for 28 normal hips from 14 healthy volunteers (control group) and 15 hips from 10 SLE patients that met the inclusion criteria of noncollapsed and asymptomatic osteonecrosis of the femoral head (osteonecrosis group). Exclusion criteria were past experience of pain, trauma, infection, or prior hip joint surgery. Distribution of T2 values of the femoral head cartilage were compared between the control group and the osteonecrosis group with respect to acetabular dysplasia by center‐edge angle (CEA).Results:T2 values of the femoral head cartilage were significantly higher in the osteonecrosis group than in the control group (34.4 msec vs. 30.8 msec, P = 0.001). Multiple regression analysis revealed that the osteonecrosis group and decreased CEA was significantly associated with high T2 values (T2 value = 34.6 + 3.6 × [osteonecrosis] − 0.14 × CEA, R2 = 0.52, P = 0.003).Conclusion:Degeneration of articular cartilage was associated with osteonecrosis of the femoral head in SLE patients and acetabular dysplasia. J. Magn. Reson. Imaging 2011;. © 2011 Wiley Periodicals, Inc.

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Osseous Pathway of Nutrition to Articular Cartilage of the Human Femoral Head

Cited by 24 publications

References 1 publication

Targeting subchondral bone for treating osteoarthritis: what is the evidence?

Targeting subchondral bone for treating osteoarthritis: what is the evidence?

Chemokines in Cartilage Degradation

Quantitative T2 mapping of femoral head cartilage in systemic lupus erythematosus patients with noncollapsed osteonecrosis of the femoral head associated with corticosteroid therapy

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