Context: Although elite adolescent female soccer athletes have unique injury risk factors and management challenges, limited epidemiological data exist for this population. Objective: To describe lower-body injury patterns and to determine whether a screening hip physical examination is predictive of future injuries in elite adolescent female soccer athletes. Design: Prospective cohort study. Setting: One US premier soccer club. Participants: One hundred seventy-seven female soccer athletes aged 10–18 years (mean [SD] 14.6 [1.8] y) completed a demographic questionnaire and screening hip physical examination that included range of motion and provocative tests. Interventions: At least 5 years after baseline screening, athletes completed an electronic follow-up injury survey. Injury was defined as pain that interfered with sporting activity. Main Outcome Measures: In addition to descriptive analyses of athletes’ injury profiles, associations between players’ baseline demographics and subsequent injury profiles were evaluated using chi-square tests, and potential predictors of injury based on players’ baseline hip examinations were evaluated using multivariable logistic regression. Results: Ninety-four of 177 athletes (53%) were contacted for follow-up, and 88/94 (93.6%) completed the survey. With mean follow-up of 91.9 (9.3) months (range 66–108 mo), 42/88 (47.7%) reported sustaining a new lower-body injury. The low back was the most common injury region (16/42, 38.1%). Almost half of all injured athletes (20/42, 47.6%) sustained overuse injuries, and 16/42 (38.1%) had an incomplete recovery. Higher body mass index and reaching menarche were associated with sustaining an injury (P = .03 and .04, respectively). Athletes’ baseline hip examinations were not predictive of their subsequent rate of lower-body, lumbopelvic, overuse, or incomplete recovery injury (all P > .05). Conclusions: Lower-body injuries were common in elite adolescent female soccer athletes, with over one third of injured athletes reporting permanent negative impact of the injury on their playing ability. Baseline hip physical examinations were not associated with future injury rate.

Objectives: Adequate pain management is a critical component of facilitating same-day discharge for total knee arthroplasty (TKA). Adductor canal blocks (ACB) have been shown to be an effective technique for managing pain after TKA. The objective of this study was to investigate the impact of adding magnesium to local anesthetic in ACB on postoperative pain, opioid consumption, nausea, and overall patient satisfaction. Materials and Methods: A sample of 119 adults undergoing elective unilateral TKA were included. Patients were randomly assigned to receive ACB with magnesium and bupivacaine (n=56) or with bupivacaine only (n=63). Primary outcomes were total opioid consumption in the first 48 hours after surgery and pain scores. Secondary outcomes were the incidence of nausea in the first 48 hours after surgery and total overall satisfaction. Results: Opioid consumption decreased significantly in the Mg group compared with the no-Mg group over the first 24 hours (33.2±3.0 vs. 21.3±2.4, P=0.003), the second 24 hours (35.4±2.7 vs. 27.3±2.3, P=0.026), and the first 48 hours total after surgery (68.6±5.1 vs. 48.6±4.3, P=0.004). Pain scores were reduced in the Mg group (24 h: 5.1±2.3 vs. 3.5±2.0, P=0.000; 48 h: 5.1±1.6 vs. 3.9±1.6, P=0.000). Secondary outcomes showed no difference in the incidence of nausea over the first 48 hours and overall satisfaction. Conclusion: The addition of magnesium to local anesthetic in ACB decreases pain scores and opioid consumption, without increasing nausea, when compared with ACB with local anesthetic alone.

Low back pain (LBP) is a major medical issue and the primary cause for global disability. One common cause of LBP is osteoarthritis (OA) of the lumbar facet joints. OA involves numerous tissues that can induce pain. In particular, during facet joint OA in humans, the articular capsule thickens in response to mechanical and inflammatory stresses; this thickening is associated with LBP. We have previously reported a novel rat model using external spinal linkage to cause lumbar spinal hypomobility and induce OA the in lower lumbar facet joints (L4/5 and L5/6) that may model the progression of spinal OA in humans. This hypomobility results in significant macroscopic OA changes to the articular cartilage and subchondral bone bilaterally by 8‐weeks post linkage. The onset and progression of articular capsule changes and their relationship with pain behaviors is unexplored in this model. Here we examined if lumbar spinal segmental hypomobility in rats is associated with thickening of the ventral articular capsule (ligamentum flavum, LF) as evidenced by increases in morphometric measurements in the bilateral L5/6 facet joints. We hypothesized that 8 weeks of spinal linkage, a time point of significant facet joint OA, is associated with an increase in articular capsule thickness. We used a histological approach with morphometric analyses based upon previously reported methods to test our hypothesis in linked and time matched control rats. LF thickness measurements were performed on images obtained from a brightfield microscope (10X objective, Leica DMRB, optronics microfire camera) on formalin fixed, decalcified, paraffin embedded, Ehrlich's hematoxylin and light green stained 45 μm thick transverse sections of the bilateral L5/6 facet joints. Morphometric measurements were made (OsiriX Lite software) by drawing a line through the thickest region of the LF, perpendicular to the plane of the ventral LF surface. This morphometric approach demonstrated acceptable reliability (ICC= 0.8656). Statistical analysis was performed using an unpaired t‐test. Compared with control animals (n=4), 8 weeks of hypomobility (n=4) was associated with a significant increase in LF thickness (p<0.05). The articular capsule thickness increased at a time point previously shown to have significant OA changes, which is consistent with facet joint OA and LF thickening in human subjects. Increases in articular capsule thickness are hypothesized to contribute both to the induction or reflect the ongoing pathological processes of OA (e.g., prolonged inflammation and fibrosis). Further work is required to determine the onset, joint location, and mechanisms underlying these capsule changes. These findings suggest that lumbar spine hypomobility induces LF thickening.

Low back pain (LBP) is a leading cause of worldwide disability and socioeconomic burden. Degeneration of the lumbar facet joints (FJ) or spinal osteoarthritis (OA) is one clinically relevant source of LBP. Recent studies suggest that the increased prevalence of OA may be a result of not only overuse of a synovial joint but also less joint movement. A better understanding of how FJ degeneration is induced and progresses may provide the foundation to reveal the underlying mechanisms of spinal OA and LBP.OA is a whole joint disease involving several tissues. The avascular articular cartilage relies upon adjacent tissues to maintain its homeostasis. Of particular importance is the synovial fluid from the synovium that is largely responsible for nutrient supply and waste removal for the cartilage; this requires appropriate joint movement. When cartilage loses access to synovial fluid, vascular channel ingrowth into cartilage and neovascularization from the subchondral bone can occur to promote degeneration. Less joint movement (hypomobility) could contribute to OA through a similar process. Although previous studies implicated neovascularization in OA induction and progression in other joints, less is known in the FJ. It was reported that during spinal OA there were increased subchondral channels invading the FJ articular cartilage. Here, we used a preclinical rat model of spinal OA to examine lumbar FJ degeneration after hypomobility. Previously, we found that hypomobility in lumbar FJs leads to cartilage degeneration that mimics the location and progression of spinal OA. We also observed that the synovial fold (SF) regressed from the FJ cavity by 2 weeks after hypomobility in the same location as early cartilage degeneration. As synovium pathology can induce subchondral processes to promote degeneration, we examined the onset, location, and progression of subchondral vascular channels after hypomobility. We hypothesized that channels would increase in the cephalad regions of the FJ superior articular process (SAP) by 2 weeks after hypomobility adjacent to cartilage degeneration and SF regression. We performed histological analyses on brightfield microscopic images of sections from the cephalad and cephalad‐middle regions of bilateral L4/5 and L5/6 FJ in hypomobile and control rats at 1, 2, and 4 weeks. The tissues were formalin fixed, decalcified, paraffin embedded, transversely sectioned (45 μm), and stained with Ehrlich's hematoxylin and light green. Intra‐ and inter‐rater reliability was acceptable for channel counts (K = 0.88 & 0.76) and a severity scale of vascular channel ingrowth (Kw = 0.81 & 0.89). Spinal hypomobility was associated with significant increases in vascular channel counts and severity of cartilage invasion in the FJ SAP margins by 2 weeks. In hypomobile rats, we also observed changes to the appearance of blood vessels in the adjacent SF (increased numbers of enlarged & disorganized vessels). These changes correlate with the onset and locations of SAP cartilage degeneration after hypomobility. Our findings mimic spinal OA and suggest a role for the subchondral bone and SF in FJ degeneration.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Low back pain (LBP) is a primary cause of global disability. The lumbar facet joint is recognized as a clinically relevant pain generator. Pain can occur through the onset and progression of facet joint degeneration consistent with spinal osteoarthritis (OA). OA is now defined as a whole joint disease involving many tissues in addition to the articular cartilage, including the joint capsule. Capsular thickening due to mechanical and inflammatory stress can present clinically as a source of LBP. We have previously examined capsular thickening that occurs during OA, by using a rat model of external spinal linkage to cause lumbar spinal hypomobility and induce degeneration in the lower lumbar facet joints (L4/5 and L5/6). We have shown that this model mimics the location, progression, and histopathological changes of the articular cartilage typically reported in human spinal OA. Additionally, we found that by 8 weeks post linkage this degeneration is associated with significant thickening of the ventral articular capsule (ligamentum flavum, LF) in the cephalad portion of the joint. These articular capsule changes are unexplored at later stages of this model when degeneration is more advanced. Here we used a morphometric approach to examine if spinal hypomobility of the bilateral L4/5 and L5/6 facet joints in rats is associated with LF thickening. We hypothesized that 12 weeks of spinal linkage would be associated with an increase in articular capsule thickness in joint regions undergoing cartilage degeneration. We tested our hypothesis by comparing LF thickness in linked and time matched control rats at 12 weeks post linkage. LF thickness measurements were performed on images obtained from a brightfield microscope (10× objective, Leica DMRB, optronics microfire camera) on formalin fixed, decalcified, paraffin embedded, Ehrlich's hematoxylin and light green stained 45 μm thick sections. Morphometric measurements were made by drawing a line through the thickest region of the LF, perpendicular to the plane of the ventral LF surface. This approach demonstrated acceptable inter‐ and intra‐rater reliability (ICC= 0.94 and 0.99). Twelve weeks of hypomobility was associated with a significant increase in LF thickness (p<0.05) compared with control animals in the cephalad and caudal regions. This agrees with our recent findings that significant degeneration is present in the superior articular process (predominantly cephalad region) and inferior articular process (predominantly caudal region) by week 12. Our findings suggest that advanced cartilage degeneration is associated with LF thickening. These findings require additional study to examine the causes of LF thickening (e.g., prolonged inflammation and fibrosis) to better understand the role of the LF in the pathophysiology of OA and OA induced LBP.Support or Funding InformationNCMIC