Influence of prolonged immersion on the resistance of arthroscopy knots in biological media.

INTRODUCTION: Biomechanical studies of arthroscopic knots have been performed on sutures that were tied manually and tested immediately after tying. We performed this study to evaluate the knot and the suture during the healing phase, which was not evaluated in these previous studies. Our hypothesis was that the biomechanics features of arthroscopic knots may change in relation to the duration of incubation in biological media simulating synovial fluid. Thus our goal was to study the influence of incubation for 30 days in biological media simulating body fluid using a device to standardize knot tying and allow comparison of arthroscopic sutures. MATERIALS AND METHODS: Three Ultra-High Molecular Weight PolyEthylene (UHMPWE) sutures (Fiberwire, Orthocord and Maxbraid) were tested with a self-locking slip knot (SMC knot). Sixty identical knots were tied using a standardized device, and divided into two groups: the control group « D0 ¼ and the group « D30 ¼ where the knots were soaked in biological media simulating body fluid for 30 days. Cyclic loading tests were then performed on the knots in each group using a machine to define four variables: clinical failure, ultimate failure, knot slippage and the characteristics of failure. RESULTS: There was no significant difference between the two groups for knot resistance at clinical failure or ultimate failure, without regard to the suture, (P<0.05). After cyclic loading, the most slippage occurred in the Orthocord (≈5.6mm) then the Maxbraid (≈3.55mm) and the Fiberwire (≈2.51mm). The only suture whose slippage was influenced by the duration of incubation was Orthocord. At clinical failure, the loop that slipped the most was the Orthocord suture (≈5.45mm) then the Fiberwire (≈4.8mm) and the Maxbraid (≈4.1mm). In the Orthocord and Maxbraid sutures, knot slippage after clinical failure significantly increased with the duration of suture incubation (P<0.05). The reason for failure was breakage from tearing of suture fibers in all cases. CONCLUSION: Prolonged incubation of arthroscopic suture knots influences slippage, which could result in unsuccessful primary attachment of the tendon during the healing phase. LEVEL OF EVIDENCE: Level IV. Biomechanical study.

A potential role of chondroitin sulfate on bone in osteoarthritis: inhibition of prostaglandin E2 and matrix metalloproteinases synthesis in interleukin-1ß-stimulated osteoblasts.

OBJECTIVES: To determine the effect of chondroitin sulfate (CS) on inflammatory mediators and proteolytic enzymes induced by interleukin-1ß (IL-1ß) and related to cartilage catabolism in murine osteoblasts. DESIGN: Osteoblasts were obtained by enzymatic digestion of calvaria from Swiss mice and cultured for 3 weeks as a primary culture. Cells were then stimulated with IL-1ß (1 or 10 ng/ml). CS-treated osteoblasts were incubated with 100 µg/ml of CS during the last week of culture w/o IL-1ß for the last 24 h. Expressions of cyclooxygenase-2 (COX-2), microsomal prostaglandin E synthase-1 (mPGES-1), 15-PG dehydrogenase (15-PGDH), matrix metalloproteinases-3 and -13 (MMP-3 and -13), osteoprotegerin (OPG) and receptor activator of nuclear factor-kappa B ligand (RANKL) were determined by real-time polymerase chain reaction (PCR). PGE2, MMP-3 and MMP-13 release were assessed in the medium by enzyme-linked immunosorbent assay or western-blotting. RESULTS: IL-1ß increased COX-2, mPGES-1, MMP-3, MMP-13, RANKL expressions, decreased 15-PGDH expression, and increased PGE2, MMP-3 and MMP-13 release. Interestingly, 7 days of CS treatment significantly counteracted IL-1ß-induced expression of COX-2 (-62%, P<0.001), mPGES-1 (-63%, P<0.001), MMP-3 (-39%, P=0.08), MMP-13 (-60%, P<0.001) and RANKL (-84%, P<0.001). Accordingly, IL-1ß-induced PGE2, MMP-3 and MMP-13 releases were inhibited by 86% (P<0.001), 58%(P<0.001) and 38% (P<0.01) respectively. CONCLUSIONS: In conclusion, our data demonstrate that, in an inflammatory context, CS inhibits the production of PGE2 and MMPs. Since CS has previously been shown to counteract the production of these mediators in chondrocytes, we speculate that the beneficial effect of CS in Osteoarthritis (OA) could not only be due to its action on cartilage but also on subchondral bone.