PubMed · 1065966
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D Chatzephotiades. [Meniscectomy].. https://pubmed.ncbi.nlm.nih.gov/1065966/
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Osteoarthritis (OA), one of the most common age-related chronic disorders of articular cartilage, joints, and bone tissue, represents a major public health problem. Genetic studies have identified multiple gene variations associated with an increased risk of OA. These findings suggest that there is a large genetic component to OA and that the disorder belongs in the multigenetic, multifactorial class of genetic diseases. Studies of chondrodysplasias and associated hereditary OA have provided a better understanding of the role of structural genes in the maintenance and repair of articular cartilage, in the regulation of chondrocyte proliferation and gene expression, and in the pathogenesis of OA.
Biochemical and histologic data have validated the technique of delayed gadolinium-enhanced MRI, in which the T(1) values of cartilage after penetration of Gd(DTPA)2-allow assessment of the glycosaminoglycan (GAG) component of articular cartilage. This work describes the factors that have been found to be important for the practical implementation of the technique: 1) Exercise immediately after intravenous contrast administration was necessary for effective penetration of the contrast into the articular cartilage; 2) double-dose contrast was better than single-dose; 3) after contrast administration, a time window of 30-90 min for the hip, and 2-3 hr for all compartments of the knee proved to be appropriate for assessing articular cartilage; and 4) in some cases of hypointensities in the subchondral patellar bone, decreased penetration of the contrast agent into cartilage from bone was found. With the protocol described, ROIs on T(1) images were reproducible within 15% on two separate imaging sessions, and initial clinical studies demonstrated the possible applications of the technique. Magn Reson Med 45:36-41, 2001.
OBJECTIVE: To examine the expression of the chemokine RANTES and its receptors in normal and osteoarthritic (OA) human cartilage and to analyze its effects on chondrocyte function. METHODS: The expression of RANTES and its receptors were examined by reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry. The effect of RANTES on gene expression of other cytokines and on the release of mediators of cartilage degradation was also examined by PCR and enzyme-linked immunosorbent assay. RESULTS: The expression of RANTES was undetectable in normal chondrocytes until after stimulation with interleukin-1beta (IL-1beta) or IL-18. Cultures of normal cartilage also produced RANTES in response to IL-1beta, as demonstrated by immunohistochemistry. All OA cartilage samples analyzed expressed RANTES messenger RNA (mRNA); RANTES protein was detected by immunohistochemistry in the superficial and mid zones of the tissue. OA chondrocytes produced elevated levels of RANTES constitutively and after IL-1beta stimulation. Normal cartilage expressed the RANTES receptors CCR3 and CCR5, but not CCR1. CCR1 was expressed in OA cartilage, and CCR3 and CCR5 were increased. In normal chondrocytes, RANTES induced the expression of inducible nitric oxide synthase and IL-6. RANTES stimulated the release of matrix metalloproteinase 1 in normal and OA chondrocytes as effectively as IL-1beta. Treatment of normal articular cartilage with RANTES increased the release of glycosaminoglycans and profoundly reduced the intensity of Safranin O staining. CONCLUSION: Chondrocytes produce RANTES and express RANTES receptors. RANTES and CCR5 were markedly increased in OA and after in vitro treatment of normal chondrocytes with IL-1. Chondrocyte activation and cartilage degradation were identified as novel biologic and pathogenetic activities of this chemokine.