Relationship Between Posterior-Inferior Tibial Slope and Bilateral Noncontact ACL Injury.

Is there a correlation between increased posterior-inferior tibial slope angle and noncontact anterior cruciate ligament (ACL) injury? Does increasing the posterior-inferior tibial slope angle increase the risk of bilateral ACL injury? A computerized relational database (Access 2007; Microsoft Inc, Redmond, Washington) was used to conduct a retrospective review of patients undergoing bilateral or unilateral ACL reconstruction surgery or treatment by a single surgeon between 1995 and 2013. Included in the study were patients with bilateral and unilateral ACL injuries and patellofemoral pain syndrome with no associated ACL deficiency. Exclusion criteria included concomitant ligament injury, previous ACL reconstruction, and previous knee surgery. Also excluded were patients who did not have plain lateral radiographs. Fifty patients were randomly selected from each group. After controlling for age and Tegner activity level, the authors found that the posterior-inferior tibial slope angle was a significant predictor (P=.002) of noncontact ACL injury. Mean posterior-inferior tibial slope angle for the bilateral, unilateral, and control groups was 11.8°±2.3°, 9.3°±2.4°, and 7.5°±2.3°, respectively. In the group with unilateral ACL injury vs the group without ACL deficiency, a 1° increase in posterior-inferior tibial slope angle (P=.03) was associated with a 20% increase in unilateral ACL injury. In those with bilateral ACL injury vs those without ACL deficiency, a 1° increase in posterior-inferior tibial slope angle (P=.001) increased bilateral knee injury by 34%. The difference between the mean angles of the control group without ACL deficiency and both the bilateral injury and unilateral injury cohorts was statistically significant (P=.003). Increased posterior-inferior tibial slope angle is associated with an increased risk of noncontact bilateral and unilateral ACL injury. [Orthopedics. 2017; 40(1):e136-e140.].

Insulin resistance and obesity in a mouse model of systemic lupus erythematosus.

Accumulating data indicate that metabolic syndrome is an inflammatory condition. Systemic lupus erythematosus (SLE) is an autoimmune disorder associated with nephritis and cardiovascular disease. Evidence suggests that individuals with SLE are at risk for developing insulin resistance; however, this has not been directly examined. Using an established mouse strain with SLE (NZBWF1), we examined whether SLE is associated with increased body weight and fat deposition. Mean arterial pressure was significantly increased (140+/-4 versus 114+/-2 mm Hg; n > or = 5) in SLE mice by 36 weeks of age compared with control mice (NZW/LacJ). Body weight in SLE mice was higher at each age compared with controls by 12%, 22%, and 34% (n > 30). Visceral adipose tissue weight was increased in SLE by 44%, 74%, and 117% at 8, 20, and 36 weeks, respectively (n > or = 12). Plasma leptin was increased in SLE mice (8.6+/-1.0 versus 24.7+/-2.2 ng/mL; n = 5), and renal and adipose tissue exhibited macrophage infiltration. Fasted insulin was higher in SLE mice (0.6+/-0.1 versus 1.4+/-0.3 ng/mL; n > or = 10), but fasted glucose was not different (94+/-5 versus 80+/-9; n > or = 9). A glucose tolerance test caused a significantly greater and longer increase in blood glucose from mice with SLE compared with control mice. Food intake was not different between control and SLE mice. However, mice with SLE demonstrated lower levels of nighttime activity than controls. These data show that the NZBWF1 strain may be an important model to study the effects of obesity and insulin resistance on SLE-associated hypertension.