Histomorphological studies on the effect of recombinant human superoxide dismutase in biochemically induced osteoarthritis.

Enzymatic scavenging of .O-2 radicals by injections of superoxide dismutase has been described to inhibit the free radical reactions resulting in tissue damage. Using a biochemically induced model of osteoarthritis (OA) in the knee joints of hens, we investigated the histomorphological alterations under therapy with recombinant human superoxide dismutase (rH-SOD) in various doses by histological-histochemical grading.

Prolonged effect of iodoacetate on articular cartilage and its modification by an anti-rheumatic drug.

The intra-articular injection of iodoacetate into the knee joint of rats produced changes in the articular cartilage which resembled those of osteoarthritis. It caused virtually total loss of many of the oxidative enzymes, indicating inhibition of the main oxidative pathways. Treatment with an anti-rheumatic drug had little early effect but ultimately led to partial restoration of these pathways.

Immunohistochemical localization of articular cartilage proteoglycan and link protein in situ using monoclonal antibodies and lectin-binding methods.

Lectins have specificity for certain carbohydrate structures in macromolecules. Lectins are, therefore, useful histochemical tools for demonstrating the composition and localization of components of connective tissue matrices, such as articular cartilage. In order to assess the significance of observed lectin-binding patterns, experiments were performed in which monoclonal antibodies against chondroitin sulphate- and keratan sulphate-containing proteoglycans and link proteins were applied to sections of bovine articular cartilage after enzymatic digestion with chondroitinase ABC and keratanase.

Structural and metabolic changes in articular cartilage induced by iodoacetate.

The chemically induced injury to articular cartilage, caused by two successive intra-articular injections of sodium iodoacetate, has been used in studies on the effects of anti-inflammatory and of potentially chondroprotective agents. It has been assumed that the injurious effects are caused by inhibition of the glycolytic pathway. In the present study this inhibition has been shown to be greater than expected from in vitro studies, and to influence equally other oxidative pathways.

Histomorphological and lectin-histochemical confirmation of the antidegenerative effect of diclofenac in experimental osteoarthrosis.

The integrity of cartilage matrix depends on the homeostasis of synthetic and degradative processes. Any disturbance of the rate of synthesis and catabolism may alter the amount of matrix components (e.g.

Lectin-binding histochemistry of normal and osteoarthritic cartilage tissue.

Fluorescein isothiocyanate (FITC) labelled lectins were applied to study the topographical localisation and distribution of cellular as well as extracellular glycoconjugates in histological sections of normal and degenerative cartilage tissue. Using a biochemically induced model of osteoarthrosis (OA) in the knee joints of rats, the binding pattern of several lectins (wheat germ agglutinin (WGA), concanavalin A (Con A), Ulex europeus agglutinin I (UEA I), soybean agglutinin (SBA), and peanut agglutinin (PNA] in degenerative cartilage was compared with results obtained from normal healthy tissue. In response to osteoarthritic metabolic lesions the binding pattern of WGA revealed an increased cellular staining throughout the whole depth of the tissue which represents the compensatory activity of chondrocytes.