Pregnancy Results in Lasting Changes in Knee Joint Laxity.

BACKGROUND: Altered joint laxity can contribute to joint dysfunction. Knee joint laxity has been shown to increase during pregnancy, but its long-term persistence is unknown. OBJECTIVE: To determine whether pregnancy leads to lasting increases in knee joint compliance and laxity that persist longer than 4 months postpartum. DESIGN: Prospective cohort study. SETTING: A motion analysis laboratory at an academic medical center. PARTICIPANTS: Fifty healthy women in their first trimester of pregnancy (mean ± SD 29.2 ± 4.3 years old and baseline body mass index 26.0 ± 5.4 kg/m2 ) were recruited. INTERVENTION: End-range knee laxity and midrange joint compliance were measured during the first trimester and 19 ± 4 weeks postpartum. Anterior-posterior and varus-valgus laxity were measured using 3-dimensional motion tracking while applying forces and moments in each respective plane using the Vermont Knee Laxity Device. Nonlinear models were constructed to assess relations between applied forces and joint translation, comparing early pregnancy with postpartum. OUTCOMES: Multiplanar knee laxity and compliance. RESULTS: Peak varus-valgus (20-22%; P = .001) and posterior translation (51%; P < .001) of the tibia relative to the femur decreased from baseline, with a concomitant decrease in laxity (P < .001) and compliance (P = .039) in the coronal plane and in the posterior direction in primiparous (P = .009) and multiparous (P = .014) women. For primiparous women, laxity (P < .001) and compliance (P = .009) increased in the anterior direction. CONCLUSIONS: Pregnancy resulted in a lasting decrease in multiplanar knee laxity and compliance in the varus and posterior directions with an increase in anterior compliance. The effects of these changes in laxity and compliance of the passive stabilizers on knee loading patterns, articular contact stresses, and risk for osteoarthritis and other musculoskeletal disorders will require additional research. LEVEL OF EVIDENCE: II.

The Effects of Topical Vancomycin on Mesenchymal Stem Cells: More May Not Be Better.

BACKGROUND: The use of topical vancomycin is increasingly popular in spine surgery. Large retrospective reviews suggest that topical vancomycin provides a cost-effective decrease in post-operative infection. Currently, there is little that is known about the maximum dose that can be applied locally. When 1 gram of vancomycin is mixed into the bone graft and another 1 gram applied freely in a spine wound, the local concentration of antibiotic ranges from 260-2900 µg/mL in the immediate post-op period and 50-730 µg/mL by the second post-operative day. We hypothesized that exuberant doses of vancomycin would be toxic to mesenchymal stem cells (MSCs). METHODS: Bone marrow was obtained from the femoral canal of patients undergoing routine elective total hip arthroplasty. Mesenchymal stem cells were isolated using plastic adhesion. Cells were exposed to a wide range of doses of vancomycin for 24 hours and then assessed for viability. Osteogenic potential was assessed with alizarin red staining. RESULTS: There was dose-dependent cell death with vancomycin use. MSC death was 9.43% at 400 µg/mL (p=0.047), 13.79% at 1600 µg/mL (p=0.0047), 19.35% at 3200 µg/mL (p<0.0001), 24.82% at 6400 µg/mL (p<0.0001) and 51.83% at 12800 µg/mL of vancomycin (p<0.0001) in comparison to the control group containing no vancomycin. CONCLUSIONS: Our in vitro study suggests that vancomycin has toxic effects on hMSCs, a cell population particularly important for bone formation. In the absence of any clinical evidence suggesting that "more vancomycin is better," and our data suggesting that more vancomycin is harmful in vitro, surgeons electing to use topical vancomycin in spine surgery should restrict their use to the doses currently reported in the available published studies unless specific reasons exist otherwise. This study does not establish a contraindication to the use of topical vancomycin, nor does it suggest that pseudarthroses are attributable to vancomycin use.

Joint instability and cartilage compression in a mouse model of posttraumatic osteoarthritis.

Joint instability and cartilage trauma have been previously studied and identified as key mediators in the development of posttraumatic osteoarthritis (PTOA). The purpose of this study was to use an in vivo model to compare the effect of joint instability, caused by the rupture of the anterior cruciate ligament (ACL), versus cartilage compression. In this study, mice were subjected to cyclical axial loads of twelve Newtons (N) for 240 cycles or until the ACL ruptured. One and eight weeks after this procedure, knees were sectioned coronally and evaluated for osteoarthritis by histology. Using a scoring scale established by [Pritzker K, Gay S, Jimenez S, et al. (2006): Osteoarthritis Cartilage 14:13-29], the articular cartilage across each surface was scored and combined to produce a total degeneration score. The ACL-ruptured group had a significantly greater total degeneration score than either control or compression treated joints at 1 and 8 weeks. Additionally, only sections from ACL-ruptured knees consistently showed synovitis after 1 week and osteophyte formation after 8 weeks. Thus, it appears using that ACL rupture consistently creates a severe osteoarthritis phenotype, while axial cartilage compression alone does not appear to be an appropriate method of inducing PTOA in vivo.