The disappearance of articular cartilage will be the impetus for serious disability. Several nice researchers have studied the issue in depth. One fascinating study is named, “Imaging of acute injuries of the articular surfaces (chondral, osteochondral and subchondral fractures)” by Klaus Bohndorf - Skeletal Radiology Volume 28, Number 10 - October, 1999.
Here is an excerpt: “Abstract - Fractures involving the articulating surfaces of bone are a standard explanation for chronic incapacity once joint injury. Acute fractures of the articular surface typically run parallel to the surface and are confined to the cartilage and/or the immediate subchondral cancellous bone. They ought to be distinguished from vertical or oblique bone fractures with intra-articular extension. This article reviews the mechanism of acute articular surface injuries, and their incidence, clinical presentation, radiologic appearance and treatment. A classification is presented based mostly on direct inspection (arthroscopy) and imaging (particularly MRI), emphasizing the excellence between lesions with intact (subchondral impaction and subchondral bone bruises) and disrupted (chondral, osteochondral lesions) cartilage. Hyaline cartilage, subchondral bone plate and subchondral cancellous bone are to be thought-about an anatomic unit. Subchondral articular surface lesions, osteochondral fractures and solely chondral fractures are different manifestations of impaction injuries that have an effect on the articulating surface. Of the noninvasive imaging modalities, typical radiography and MRI offer the most relevant information. The acceptable use of short tau inversion recovery, T1-weighted and T2-weighted (turbo) spin-echo furthermore gradient-echo sequences, permits MRI to classify the numerous acute articular surface lesions with great accuracy and provides therapeutic guidance.”
Another fascinating study is named, “Fibronectin fragments cause chondrolysis of bovine articular cartilage slices in culture.” By G A Homandberg, R Meyers and D L Xie -
February 25, 1992 The Journal of Biological Chemistry, 267, 3597-3604. Here is an excerpt: “Abstract - Elevated fibronectin (Fn) and Fn fragment concentrations are found within the synovial fluid of osteoarthritic and rheumatoid arthritic patients. Fn has been shown to affect expression of chondrocytic matrix proteins, and Fn fragments are shown to elevate gene expression of neutral proteinases in synoviocytes. For these reasons, we tested the effects of Fn fragments on protease release and resultant proteoglycan unharness from cartilage in serum-free bovine articular cartilage explant cultures. We tend to have found that one microM amino-terminal twenty nine- and fifty-kDa gelatin-binding Fn fragments caused over a 50-fold enhancement of gelatinolytic and collagenolytic proteinase release with a 23-fold enhancement of proteoglycan (PG) release. Release was important at fragment concentrations as low as twenty nM. An integrin-binding 140-kDa fragment mixture was the smallest amount active fragment, whereas native Fn had very little activity. The relative activities of the fragments correlated with their relative talents to bind to cartilage. The RGDS integrin-recognition peptide additionally caused release, though sequence mutants did not. PG unleash was blocked by actinomycin D, cycloheximide, and deoxyglucose. Fn fragment-mediated PG unharness was decreased in ten% serum by over ten-fold but was still a pair of-fold larger than in controls. In the presence of insulin-like growth issue-1, PG release was as nice as without serum. We recommend that Fn fragments, as found in diseased synovial fluid, might contribute to protease-mediated injury to cartilage.”
If you found either of those excerpts attention-grabbing, please browse the studies in their entirety.
Author Resource:
William Evan has been writing articles online for nearly 2 years now. Not only does this author specialize in Disability, you can also check out his latest website about:
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