No abstract

PurposeThe primary objective of this study is to evaluate the contact areas, contact pressures, and peak pressures in the medial compartment of the knee in six sequential testing conditions. The secondary objective is to establish how much the medial meniscus is able to extrude, secondary to soft tissue injury while keeping its roots intact. MethodsTen cadaveric knees were dissected and tested in six conditions: (1) intact meniscus, (2) 2 mm extrusion, (3) 3 mm extrusion, (4) 4 mm extrusion, (5) maximum extrusion, (6) capsular based meniscal repair. Knees were loaded with a 1000‐N axial compressive force at 0°, 30°, 60°, and 90° for each condition. Medial compartment contact area, average contact pressure, and peak contact pressure data were recorded. ResultsWhen compared to the intact state, there was no statistically significant difference in medial compartment contact area at 2 mm of extrusion or 3 mm of extrusion (n.s.). There was a statistically significant decrease in contact area compared to the intact state at 4 mm (p = 0.015) and maximum extrusion (p < 0.001). The repair state was able to improve medial compartment contact area, and there was no statistically significant difference between the repair and the intact states (n.s.). No significant differences were found in the average contact pressure between the repair, intact, or maximum extrusion conditions at any flexion angle (n.s.). No significant differences were found in the peak contact pressure between the repair, intact, or maximum extrusion conditions at any flexion angle (n.s.). ConclusionIn this in vitro model, medial meniscus extrusion greater than 4 mm reduced medial compartment contact area, but meniscal extrusion did not significantly increase pressure in the medial compartment. Additionally, meniscal centralization was effective in restoring the medial tibiofemoral contact area to intact state when the meniscal extrusion was secondary to meniscotibial ligament injury. The diagnosis of meniscal extrusion may not necessarily involve meniscal root injury. Since it is known that meniscal extrusion greater than 3 or 4 mm has a biomechanical impact on tibiofemoral compartment contact area and pressures, specific treatments can be established. Centralization restored medial compartment contact area to the intact state.

Purpose To evaluate the effect of magnesium on cellular adhesion and proliferation of human subacromial bursal tissue (SBT), osteoblasts, and tenocytes on nonabsorbable suture tape commonly used in rotator cuff surgery. Methods Human SBT cells, primary human osteoblasts (HOBs), and primary human tenocytes were isolated from tissue samples and cultured in growth media. Commercially available collagen-coated nonabsorbable suture tape was cut into one-inch pieces, placed into 48-well culture dishes, sterilized under ultraviolet light, and treated with (+) or without (–) magnesium. For the (+) magnesium group, a one-time dose of 5 mM sterile magnesium chloride was added. Subsequently, cells were plated at a density of 20,000 cells/cm 2 . For each cell source (SBT, HOBs, tenocytes) cellular proliferation and adhesion assays on suture tape treated (+) or (–) magnesium were performed. Results SBT, HOBs, and tenocytes each demonstrated the ability to adhere and proliferate on suture tape. Augmenting suture tape with magnesium resulted in a significantly increased cellular adhesion of SBT compared with nonaugmented sutures ( P = .001), whereas no significant differences were observed for HOBs ( P = .081) and tenocytes ( P = .907). Augmentation with magnesium demonstrated no significant difference in cellular proliferation of SBT ( P = .856), HOBs ( P = .672), and tenocytes ( P = .251) compared with nonaugmented sutures. Conclusions SBT, osteoblasts, and tenocytes each demonstrated the ability to adhere and proliferate on suture tape. In addition, augmenting the suture with magnesium resulted in a significantly increased cellular adhesion of SBT compared with nonaugmented sutures, whereas no significant differences were observed for osteoblasts and tenocytes. Further, magnesium did not impair the proliferative activity of SBT, osteoblasts, and tenocytes on suture tape used in rotator cuff surgery. Clinical Relevance Modifying the surface of the suture used for repair with application of magnesium may be an inexpensive and technically feasible option to improve the use of SBT for biologic augmentation of rotator cuff repair.

No abstract

Purpose To evaluate the effect of a one-time dose of insulin or insulin-like growth factor 1 (IGF-1) on cellular proliferation and migration of subacromial bursa tissue (SBT) over time. Methods SBT was harvested from over the rotator cuff tendon in 4 consecutive patients undergoing primary arthroscopic rotator cuff repair. SBT was cultured for 3 weeks in complete media until reaching confluence. The culture dishes were stored in a humidified, low oxygen tension (5% CO 2 ) incubator at 37°C. SBT of each patient underwent treatment with a one-time dose of insulin or IGF-1, whereas nontreated SBT served as a negative control. Cellular proliferation and migration were evaluated after 24, 48, 72, and 96 hours of incubation. SBT-derived cells migrated in the detection field were visualized using fluorescent microscopy. Results Cellular proliferation at 24, 48, 72, and 96 hours was 1.40 ± 0.27, 1.00 ± 0.20, 1.47 ± 0.31, and 1.68 ± 0.28 for IGF-1; 1.44 ± 0.24, 1.15 ± 0.27, 1.60 ± 0.36, and 1.61 ± 0.32 for insulin; and 1.51 ± 0.35, 1.29 ± 0.33, 1.53 ± 0.35, and 1.57 ± 0.38 for nontreated SBT. Untreated SBT demonstrated a significantly greater proliferation when compared with IGF-1 and insulin within the first 48 hours, although this effect was found to subside by 96 hours. Cellular migration at 24, 48, 72, and 96 hours was 575.7 ± 45.0, 641.6 ± 77.7, 728.3 ± 122.9, and 752.3 ± 114.5 for IGF-1; 528.4 ± 31.3, 592.5 ± 69.8, 664.2 ± 115.2, and 695.6 ± 148.2 for insulin; and 524.4 ± 41.9, 564.4 ± 49.8, 653.2 ± 81.5, and 685.7 ± 115.5 for nontreated SBT. Insulin showed no difference in migration at each timepoint compared to nontreated SBT ( P > .05, respectively). Conclusions Insulin and IGF-1 initially inhibit cellular proliferation of human SBT, although this effect was found to subside by 96 hours. Further, neither insulin nor IGF-1 changed the slope of cellular migration over time. However, each treatment group demonstrated a significant increase in cellular proliferation and migration. Clinical Relevance In the setting of biologic augmentation of rotator cuff repair, the compatibility and synergistic effect of insulin on human SBT is highly limited.