Composites of chondrocytes and polymerised fibrin were supplemented with insulin-like growth factor-I (IGF-I) during the arthroscopic repair of full-thickness cartilage defects in a model of extensive loss of cartilage in horses. Repairs facilitated with IGF-I and chondrocyte-fibrin composites, or control defects treated with chondrocyte-fibrin composites alone, were compared before death by the clinical appearance and repeated analysis of synovial fluid, and at termination eight months after surgery by tissue morphology, collagen typing, and biochemical assays. The structure of cartilage was evaluated histologically by Toluidine Blue reaction and collagen type-I and type-II in situ hybridisation and immunohistochemistry. Repair tissue was biochemically evaluated by DNA assay, proteoglycan quantitation and characterisation, assessment of collagen by reverse-phase high-performance liquid chromatography, and collagen typing using cyanogen bromide digestion and peptide separation by polyacrylamide gel electrophoresis. The results at eight months showed that the addition of IGF-I to chondrocyte grafts enhanced chondrogenesis in cartilage defects, including incorporation into surrounding cartilage. Gross filling of defects was improved, and the tissue contained a higher proportion of cells producing type-II collagen. Measurements of collagen type II showed improved levels in IGF-I-treated defects, supporting in situ hybridisation and immunohistochemical assessments of the defects. IGF-I improves the repair capabilities of chondrocyte-fibrin grafts in large full-thickness repair models.

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Carbon fibre-polylactic acid composites and monofilament non-absorbable suture material were compared for the repair of surgically transected superficial digital flexor tendons in 10 horses. All surgical wounds healed by first intention. The repaired tendons were enlarged, the carbon implanted tendons being larger than those sutured. The horses were killed at six, eight, 12, 20 or 24 weeks. Greater fibrous thickening occurred in tendons repaired with carbon fibre, especially at 12 weeks postoperatively. Carbon fibre incited a greater histological response with macrophages, lymphocytes, plasma cells, eosinophils and fibroblasts. The fibrous tissue in the repair sites appeared to mature and the collagen to align at a similar rate irrespective of the method of repair. Only that tissue within and immediately surrounding the carbon bundles was immature at six months. There was minimal tendency for carbon filaments to separate and those that did were often surrounded by epithelioid macrophages forming a granuloma. Massive eosinophil concentrations were present between each granuloma. With each sequential test period the sutured tendons became increasingly stronger than the carbon implanted tendons. This may have been because of the immature core of tissue associated with the carbon bundles. No carbon particles were detected in draining lymph nodes.

Composites of chondrocytes and polymerised fibrin were supplemented with insulin-like growth factor-I (IGF-I) during the arthroscopic repair of full-thickness cartilage defects in a model of extensive loss of cartilage in horses. Repairs facilitated with IGF-I and chondrocyte-fibrin composites, or control defects treated with chondrocyte-fibrin composites alone, were compared before death by the clinical appearance and repeated analysis of synovial fluid, and at termination eight months after surgery by tissue morphology, collagen typing, and biochemical assays. The structure of cartilage was evaluated histologically by Toluidine Blue reaction and collagen type-I and type-II in situ hybridisation and immunohistochemistry. Repair tissue was biochemically evaluated by DNA assay, proteoglycan quantitation and characterisation, assessment of collagen by reverse-phase high-performance liquid chromatography, and collagen typing using cyanogen bromide digestion and peptide separation by polyacrylamide gel electrophoresis. The results at eight months showed that the addition of IGF-I to chondrocyte grafts enhanced chondrogenesis in cartilage defects, including incorporation into surrounding cartilage. Gross filling of defects was improved, and the tissue contained a higher proportion of cells producing type-II collagen. Measurements of collagen type II showed improved levels in IGF-I-treated defects, supporting in situ hybridisation and immunohistochemical assessments of the defects. IGF-I improves the repair capabilities of chondrocyte-fibrin grafts in large full-thickness repair models.

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SummaryThe ability of polysulphated glycosaminoglycans (PSGAGs, Adequan®) to modulate the transcription of major articular cartilage matrix proteins and enzymes was examined. Northern blot analyses were used to compare steady-state mRNA levels of type-II procollagen, aggrecan core protein, matrix metalloproteinase (MMP)-1, MMP-3, tissue inhibitor of metalloproteinase (TIMP)-1, and TIMP-3 in equine chondrocytes grown in monolayer culture. The groups included: control, low-dose (0.1mg/ml) Adequan®, high-dose (1.0mg/ml) Adequan®, IL-1 β (10ng/ml), IL-1 β with low-dose Adequan®, and IL-1 β with high-dose Adequan®. The responses (p<0.05) to treatment were compared with one-way analysis of variance and post hoc least significant difference test. Interleukin-1 β significantly decreased steady-state levels of type-II procollagen (0.5x) and aggrecan core protein (to undetectable levels) and significantly increased MMP-1 (11.7x), MMP-3 (1.8x), TIMP-1 (1.9x), and TIMP-3 (5.1 x). Adequan® alone significantly increased steady-state mRNA levels of type-II procollagen (1.6x) and decreased MMP-1 (0.3x at high-dose only), MMP-3 (0.5x), and TIMP-1 (0.3x at high-dose only). In IL-1 β-treated chondrocytes, Adequan® significantly increased steady-state mRNA levels of type-II procollagen (1.4x of IL-1 β-treated levels), aggrecan core protein (IL-1 β -treated had no detectable expression), and MMP-3 (3.6 x at high dose) and significantly decreased steady-state mRNA levels of MMP-1 (0.3 x), and TIMP-1 (0.2x). This study is the first to demonstrate that Adequan® alters steady-state mRNA levels of key matrix proteins and enzymes; that it counteracts some of the deleterious effects of IL-1 β; and that these effects are in part dose-dependent.