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Purpose The purpose of this study was to identify if abnormal tibial alignment was a risk factor for lateral meniscus posterior root tears (LMPRT) in patients with acute anterior cruciate ligament (ACL) ruptures. Methods The medical charts of 200 patients treated for ACL ruptures between 2013 and 2016 were retrospectively reviewed and evaluated. MRI images and reports were assessed for concurrent meniscal tears. Radiographs were reviewed for tibia vara and tibial slope angles and MRI reports identifying lateral root tears were compared to intraoperative reports to determine accuracy. Multiple logistic regression models were constructed to identify potential risk factors for LMPRTs. Results Of the 200 patients reviewed, a total of 97 individuals with concurrent meniscal injuries were identified. In patients sustaining a concurrent meniscal injury, there was a 4% incidence of medial meniscus posterior root tears and a 10.3% incidence of LMPRTs. Patients sustaining an ACL injury with an LMPRT were found to have greater tibia vara angles (4.2 ± 1.0 vs. 2.9 ± 1.7; p = 0.024), increased tibial slopes (12.6 ± 1.5 vs. 10.7 ± 2.9; p = 0.034), and higher BMIs (27.3 ± 2.9 vs. 25.3 ± 5.9; p = 0.034) when compared to patients without meniscus tears. There was low agreement between MRI and arthroscopic findings (kappa rate = 0.54). Multiple logistic regression analysis demonstrated that a tibia vara angle > 3 was associated with a 5.2-fold increase (95% CI 0.99-27.01; p = 0.050), and a tibial slope > 12 with a 5.4-fold increase (95% CI 1.03-28.19; p = 0.046) in LMPRTs. Conclusions Patients with greater tibia varus angles, increased tibial slopes, and higher BMIs were found to have an increased risk of LMPRTs when sustaining an ACL rupture. There was a low rate of agreement between MRI and arthroscopy in identifying LMPRTs. In patients with ACL ruptures who have abnormal tibial alignment or increased BMI, physicians should be watchful for lateral meniscus posterior root tears. Level of evidence 3.

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Myocardial ischemia reperfusion injury is a negative pathophysiological event that may result in cardiac cell apoptosis and is a result of coronary revascularization and cardiac intervention procedures. The resulting loss of cardiomyocyte cells and the formation of scar tissue, leads to impaired heart function, a major prognostic determinant of long-term cardiac outcomes. Photobiomodulation is a novel cardiac intervention that has displayed therapeutic effects in reducing myocardial ischemia reperfusion related myocardial injury in animal models. A growing body of evidence supporting the use of photobiomodulation in myocardial infarct models has implicated multiple molecular interactions. A systematic review was conducted to identify the strength of the evidence for the therapeutic effect of photobiomodulation and to summarise the current evidence as to its mechanisms. Photobiomodulation in animal models showed consistently positive effects over a range of wavelengths and application parameters, with reductions in total infarct size (up to 76%), decreases in inflammation and scarring, and increases in tissue repair. Multiple molecular pathways were identified, including modulation of inflammatory cytokines, signalling molecules, transcription factors, enzymes and antioxidants. Current evidence regarding the use of photobiomodulation in acute and planned cardiac intervention is at an early stage but is sufficient to inform on clinical trials.

Deep space travel exposes astronauts to extended periods of space radiation and mechanical unloading, both of which may induce significant muscle and bone loss. Astronauts are exposed to space radiation from solar particle events (SPE) and background radiation referred to as galactic cosmic radiation (GCR). To explore interactions between skeletal muscle and bone under these conditions, we hypothesized that decreased mechanical load, as in the microgravity of space, would lead to increased susceptibility to space radiation-induced bone and muscle loss. We evaluated changes in bone and muscle of mice exposed to hind limb suspension (HLS) unloading alone or in addition to proton and high (H) atomic number (Z) and energy (E) (HZE) (16O) radiation. Adult male C57Bl/6J mice were randomly assigned to six groups: No radiation ± HLS, 50 cGy proton radiation ± HLS, and 50 cGy proton radiation + 10 cGy 16O radiation ± HLS. Radiation alone did not induce bone or muscle loss, whereas HLS alone resulted in both bone and muscle loss. Absolute trabecular and cortical bone volume fraction (BV/TV) was decreased 24% and 6% in HLS-no radiation vs the normally loaded no-radiation group. Trabecular thickness and mineral density also decreased with HLS. For some outcomes, such as BV/TV, trabecular number and tissue mineral density, additional bone loss was observed in the HLS+proton+HZE radiation group compared to HLS alone. In contrast, whereas HLS alone decreased muscle mass (19% gastrocnemius, 35% quadriceps), protein synthesis, and increased proteasome activity, radiation did not exacerbate these catabolic outcomes. Our results suggest that combining simulated space radiation with HLS results in additional bone loss that may not be experienced by muscle.

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Prolonged reduction in weightbearing causes bone loss. Disuse of bone is associated with recovery from common musculoskeletal injury and trauma, bed rest resulting from various medical conditions, and spaceflight. The hindlimb‐suspension rodent model is popular for simulating unloading and disuse. We hypothesized that controlled mechanical loading of the tibia would protect against bone loss occurring from concurrent disuse. Additionally, we hypothesized that areas of high mechanical peak strains (midshaft) would provide more protection than areas of lower strain (distal shaft). Adult C57BL6/J mice were suspended for 3 weeks, with one limb subjected to tibial compression four times per week. μCT imaging was completed at days 0, 11, and 21, in addition to serum analysis. Significant bone loss caused by hindlimb suspension was detected in trabecular bone by day 11 and worsened by day 21 (p < 0.05). Bone loss was also detected in cortical thickness and area fraction by day 21. However, four short bouts per week of compressive loading protected the loaded limb from much of this bone loss. At day 21, we observed a 50% loss in trabecular bone volume/total volume and a 6% loss in midshaft cortical thickness in unloaded limbs, but only 15% and 2% corresponding losses in contralateral loaded limbs (p = 0.001 and p = 0.02). Many bone geometry parameters of the loaded limbs of suspended animals did not significantly differ from non‐suspended control limbs. Conversely, this protective effect of loading was not detected in cortical bone at the lower‐strained distal shaft. Analysis of bone metabolism markers suggested that the benefits of loading occurred through increased formation instead of decreased resorption. This study uniquely isolates the role of externally applied mechanical loading of the mouse tibia, in the absence of muscle stimulation, in protecting bone from concurrent disuse‐related loss, and demonstrates that limited bouts of loading may be highly effective during prolonged disuse. © 2019 The Authors. JBMR Plus published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research.