A preliminary study of the effects of glucosamine sulphate and chondroitin sulphate on surgically treated and untreated focal cartilage damage

Abstract

The effects of Glucosamine Sulphate (GS) and Chondroitin Sulphate (CS) on the healing of damaged and repaired articular cartilage were investigated. This study was conducted using 18 New Zealand white rabbits as experimental models. Focal cartilage defects, surgically created in the medial femoral condyle, were either treated by means of autologous chondrocyte implantation (ACI) or left untreated as controls. Rabbits were then divided into groups which received either GS+/-CS or no pharmacotherapy. Three rabbits from each group were sacrificed at 12 and 24 weeks post-surgery. Knees dissected from rabbits were then evaluated using gross quantification of repair tissue, glycosaminoglycan (GAG) assays, immunoassays and histological assessments. It was observed that, in contrast to untreated sites, surfaces of the ACI-repaired sites appeared smooth and continuous with the surrounding native cartilage. Histological examination demonstrated a typical hyaline cartilage structure; with proteoglycans, type II collagen and GAGs being highly expressed in repair areas. The improved regeneration of these repair sites was also noted to be significant over time (6 months vs. 3 months) and in GS and GS+CS groups compared to the untreated (without pharmacotherapy) group. Combination of ACI and pharmacotherapy (with glucosamine sulphate alone/ or with chondroitin sulphate) may prove beneficial for healing of damaged cartilage, particularly in relation to focal cartilage defects.

Osteochondral Repair Using Porous Three-dimensional Nanocomposite Scaffolds in a Rabbit Model

“…Similar conclusions were reached by authors studying the fixation of similar biomaterials in osteochondral defects in rats and rabbits when compared to control groups without implantation (4,27). In another study of osteochondral defects in rabbits, in groups where defects were left to heal spontaneously, the histopathological and macroscopic assessment of the formed tissue was also unsatisfactory, despite additional oral supplementation with glucosamine sulphate and chondroitin preparations (50). Gradual changes in BAP concentrations observed in the conducted study are consistent with the results reported by Kim et al who studied the behaviour of osteoblasts on porous bases of PLGA copolymer modified with nanohydroxyapatite.…”

The effects of staged intra-articular injection of cultured autologous mesenchymal stromal cells on the repair of damaged cartilage: a pilot study in caprine model

“…Bioactive factors secreted by MSCs have been shown to inhibit tissue scarring; suppress apoptosis, inflammatory and fibrotic; stimulate angiogenesis where MSCs secrete a growth factor, VEGF (Vascular Endothelium Growth Factor), which stimulates vascularization; and enhance mitosis of tissue-intrinsic stem or progenitor cells. Other studies have shown that MSCs attach to the defect sites while others have shown that in the transplanted site MSCs regress dramatically to a point that they are no longer viable [26,27]. Regardless of the mechanisms involved, the present study clearly demonstrated a correlation between the use of MSCs with superior tissue repair, which will require further investigations if we wish to elicit the mechanisms involved.…”

Treatment of Articular Cartilage Defects: Focus on Tissue Engineering

“…In the course of long-term research and observations of patients undergoing reparative treatment conducted by Steadman, among others, the clinical effectiveness of this approach has been generally assessed as satisfactory (8). Analyses of the makeup of the reconstructed tissue revealed that it primarily consists of fibrocartilaginous tissue.…”

“…They revealed that glucosamine sulphate is an efficient analgesic, whose pain-relieving effects last far longer than those of non-steroidal drugs. Furthermore, it helps to inhibit the development of degenerative disease, as measured radiologically with regard to its effect of slowing-down the narrowing of the articular space in human knee joints (8,18).…”

“…Mankind has struggled with cartilage trauma and its treatment for centuries. As famously observed by the Scottish anatomist and surgeon William Hunter in 1743, cartilage trauma had been recognized as particularly troublesome since the days of Hippocrates because once damaged, it will not regenerate (6)(7)(8)(9). A hundred years later, another scholar named Leid made a nearly identical comment, saying that "damaged cartilage fragments never form union, cartilage tissue has no regenerative capacity".…”