Flexor tendon healing within the tendon sheath using bioabsorbable poly-L/D-lactide 96/4 suture. A histological in vivo study with rabbits.

The bioabsorbable poly-L/D-lactide (PLDLA) 96/4 suture has good biomechanical and knot properties, and sufficient tensile strength half-life for flexor tendon repair. In the present study, the biocompatibility of PLDLA suture was compared with that of coated braided polyester suture in the rabbit flexor digitorum profundus tendon repaired within the tendon sheath. Postoperative unrestricted active mobilization was allowed. The tendons were studied histologically after 1-, 3-, 6-, 12-, 26-, and 52-week follow-ups. No differences were found in the biocompatibility between the suture materials, with only scattered multinuclear giant cells near the sutures in both groups from 6 weeks onwards. At 52 weeks, most of the PLDLA material was absorbed and the histological structure of the tendon appeared normal, whereas in the polyester repairs the suture knots filled the repair site, causing bulking of the tendon surface, and the collagen alignment appeared disoriented. The results suggest that the PLDLA 96/4 is a suitable suture material for flexor tendon repair.

Bioabsorbable poly-L/D-lactide (PLDLA) 96/4 triple-stranded bound suture in the modified Kessler repair: an ex vivo static and cyclic tensile testing study in a porcine extensor tendon model.

Previously the biomechanical properties of the bioabsorbable poly-L: /D: -lactide (PLDLA) 96/4 suture were found suitable for flexor tendon repair. In this study, three PLDLA suture strands were bound together parallel to each other side-by-side to form a triple-stranded bound suture and the modified Kessler tendon repair was performed. The biomechanical properties of the PLDLA repair in porcine extensor tendons ex vivo were investigated with static and cyclic tensile testing. In both biomechanical tests, the strength of the PLDLA repair achieved the estimated forces needed to withstand active mobilization.

The strength of the 6-strand modified Kessler repair performed with triple-stranded or triple-stranded bound suture in a porcine extensor tendon model: an ex vivo study.

PURPOSE: To investigate the biomechanic influence of triple-stranded sutures and the spatial arrangement of the strands on the strength of the 6-strand Pennington modified Kessler repair. METHODS: In the present ex vivo study of pig extensor tendons 2 techniques were used: (1) triple-stranded suture (3 suture strands in the same needle) and (2) triple-stranded bound suture (3 suture strands in the same needle that were bound together, parallel to each other, side by side). The repairs were subjected to static tensile testing. RESULTS: The 6-strand modified Kessler repair performed with triple-stranded bound suture reached significantly higher yield force, ultimate force, and both partial and total 1-, 2-, and 3-mm gap forces compared with the repairs performed with triple-stranded suture. The stiffness and strain values at the yield point and at the ultimate point did not differ significantly. CONCLUSIONS: This experimental study introduces a way to improve the strength of the tendon repair. The triple-stranded bound suture significantly increased both the gap resistance and ultimate force of the 6-strand modified Kessler repair. We assume the improvements are due to increased holding capacity of the locking loops. The triple-stranded bound suture is easy to use and avoids several problems associated with traditional multistrand repairs. Further studies are needed before clinical use can be considered.

Downregulation of angiotensin converting enzyme by TNF-alpha in differentiating human macrophages.

OBJECTIVE: To investigate regulation of angiotensin converting enzyme (ACE) by tumour necrosis factor alpha (TNF-alpha) in differentiating human peripheral blood monocytes (PBM). METHODS: Human PBM were allowed to differentiate to macrophages for 0-7 days and ACE amount was measured during differentiation. Experiments with TNF-alpha were performed after 2 days of differentiation. Cell cultures were incubated with TNF-alpha (0.5-10ng/ml) without or with SB 202190 (5microM), or PD 98059 (40microM). ACE amounts were measured by an inhibitor binding assay (IBA) and ACE mRNA levels by RNase protection assay (RPA). Activated p44/42 and p38 MAP kinases were measured by Western Blot analysis using phospho-p44/42 and -p38 MAPK antibodies. RESULTS: ACE amount increased by 40-fold along with macrophage differentiation. TNF-alpha caused dose dependent suppression of the amount of ACE and decreased levels of ACE mRNA. TNF-alpha activated p44/42 and p38 MAP kinases, which was inhibited by the specific inhibitors of these kinases, PD98059 or SB202190, respectively. Pretreatment of the cells with SB 202190, or PD 98059 both partly reversed TNF-alpha induced ACE suppression. CONCLUSIONS: TNF-alpha downregulated ACE, which effect was probably mediated by both p44/42 and p38 MAPK pathways. Local downregulation of ACE by TNF-alpha may be a counterbalancing mechanism in inflammatory processes.