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Tunnel malposition is one of the most common technical reasons for anterior cruciate ligament reconstruction failure. Small changes in tunnel placement can result in significant differences in outcome. More anatomic placement of the tunnels can lead to greater knee stability and a more accurate reproduction of native knee kinematics. This Technical Note describes 2 tibial tunnel–independent methods to obtain anatomic femoral tunnel placement. The all-inside anteromedial portal technique requires only minimal surgical incisions but allows precise femoral tunnel placement. However, hyperflexion of the knee is required, adequate surgical assistance is necessary, and this technique may be susceptible to graft-tunnel mismatch. The outside-in technique may be more beneficial in obese patients, skeletally immature patients, or revision cases. On the downside, it does require an additional 2-cm surgical incision. This article also provides surgical pearls to fine-tune tibial tunnel placement.

Objectives: Regardless of surgical or conservative management, the majority of patients develop posttraumatic osteoarthritis (PTOA) within 15 years of anterior cruciate ligament (ACL) injury. In addition to MRI or radiographic evidence of cartilage degeneration, the onset of PTOA is associated with increased concentrations of chondrodegenerative and inflammatory biomarkers and reduced Knee Injury and Osteoarthritis Score Quality of Life (KOOS-QOL) scores. Postoperatively, biochemical biomarkers may offer the ability to detect the onset of PTOA earlier than traditional imaging methods; however, little is known about the ability of preoperatively collected biomarkers to predict postoperative symptoms often associated with early onset of PTOA. The purpose of this prospective study was to determine if patient demographics and biomarkers collected on the day of ACL reconstruction could accurately explain the variability in postoperative KOOS-QOL scores. We hypothesized that no combination of biomarkers collected on the day of ACL reconstruction would be associated with 2-year patient-reported outcomes. Methods: Participants included 18 patients (9 females, 9 males; age = 20.1 ± 5.2 years; height = 177.7 ± 11.9 cm; weight = 77.8 ± 18.0 kg) that had previously enrolled in a prospective randomized trial evaluating early anti-inflammatory treatment after ACL injury. As part of the initial trial, synovial, serum, and urinary biomarkers of chondrodegeneration and inflammation were collected on the day of ACL reconstruction. Patients were then contacted to complete patient-reported outcomes 2 years following surgery. A linear regression was performed to determine if a model generated from patient demographics and biomarkers on the day of surgery and could accurately explain the variability in KOOS-QOL scores at 2 years. Results: KOOS-QOL scores significantly improved from 39.9 ± 14.2 on the day of ACL reconstruction to 66.7 ± 19.7 at 2 years (p < 0.001). A model containing urinary CTX-II and sex explained 52% of the variability in 2-year KOOS-QOL scores (adjusted R2 = 0.52, p = 0.002), with higher urinary CTX-II values and female sex associated with poorer KOOS-QOL scores. Urinary CTX-II, which is a biomarker of type II collagen breakdown, individually explained 32% of the variability in 2-year KOOS-QOL scores (p = 0.01) with sex explaining 20% of the variability (p = 0.02). Conclusion: Previous studies have demonstrated that ACL injury triggers a biochemical cascade that worsens over the first 4-6 weeks after injury. The current results demonstrated that higher levels of collagen breakdown as measured via CTX-II levels at the time of surgery was associated with worse KOOS-QOL outcomes at 2 years. This data strongly suggests that initial biochemical changes after injury may have powerful consequences for the injured knee that are not mitigated by surgical stabilization alone. Early anti-catabolic intervention after ACL injury may need to be investigated as an adjunct treatment strategy, particularly in female patients with high CTX-II levels.

Objectives: We present the early results from the “Multicenter Orthopaedic Outcome Network Early Anti-inflammatory Treatment in Patients with Acute ACL Tear and Painful Effusions” (MOON-AAA) clinical trial (figure 1). This trial allows for a well controlled prospective cohort of patients with isolated ACL injury at risk for OA. We compared the effect of a single versus a repeated dosage of Kenalog within the first two weeks after ACL injury and its effect on chondral degradation in the first 4 weeks prior to surgical reconstruction of the ACL. Methods: 49 patients with isolated ACL tears were enrolled. Knee joints were aspirated and patients received an injection with 40 mg Kenalog either within 4 days, 10 days, both time points or not at all (saline injection control). Serum, synovial fluid and urine were collected at 3 time points. Permutated block randomization, triple blinding, independent monitoring and standardized x-ray was performed to comply with GCP standards. Patient reported outcomes were collected at 6 time points up to 6 months post-ACL reconstruction(IKDC, KOOS and Marx activity level). A standardized synovial fluid biomarker panel was analyzed according to OARSI guidelines. Statistical analysis were performed using SAS mixed models analysis. Results: Serum analysis shows significant change after injury. Chondrodegradatory markers such as CTX-II, MMP-1 and MMP-3 as well as COMP indicate a progressive destruction of chondral matrix and collagen breakdown . There is a dramatic (250%) increase of CTX-II in the first 4 weeks. Matrix proteins such as MMP-1 and 3 as well as COMP show an initial increase and then a steep decline (see figure 1). Inflammatory markers (IL-1 alpha, IL-1beta, IRAP) show a decline from the time of injury. IL-1 alpha, however shows a dramatic uptake after week 2. This longitudinal data confirms a dramatic onset of early osteoarthritic biomarker profiles immediately after ACL injury as measured in synovial fluid.The administration of 40 mg of Kenalog significantly changes this dynamic. CTX-II shows a dramatic reduction and stays close to baseline levels over the course of 4 weeks pre-operatively. COMP and MMP-1 show a significantly lesser decline.There is no significant difference in the effect of Kenalog if given within 4 days of injury or within 2 weeks. There is a statistical trend indicating that a repeated dose of Kenalog may be more efficient in normalizing the biomarker levels. No AE’s, infections were observed. Two of 49 patients suffered a retear at 6 months upon return to activities. Conclusion: Our data show that posttraumatic osteoarthritis begins at the time of injury and results early on in dramatic matrix changes in the knee joint. An early intervention with an antiinflammatory agent, such as Kenalog, maybe be able to prevent some of these changes observed.We do not currently know if the early intervention results in meaningful clinical differences in overall outcome. Further follow-up will answer this question. However, it is encouraging that a simple early intervention is able to affect early chondral degeneration. Should the early intervention with Kenalog lead to meaningful changes in outcome at 2 or 6 years the current treatment paradigm for ACL injured patients may have to be changed.

Background: Rate of torque development (RTD) measures the ability of a muscle to produce torque quickly. Decreased quadriceps RTD may impair performance of sporting tasks after surgery. Currently, little is known about variations in quadriceps RTD between anterior cruciate ligament (ACL)–reconstructed and noninjured limbs. Purpose: To determine the differences in RTD of the quadriceps, the rate and timing of knee extensor moment (KEM) development, and knee flexion excursion during running after ACL reconstruction with patellar tendon autograft. Study Design: Cross-sectional study; Level of evidence, 3. Methods: This study involved 21 patients (11 female) 6 months after ACL reconstruction with patellar tendon autograft (median [IQR]: age, 18 [16-20] years; mass, 68.18 [61.34-75] kg; height, 1.74 [1.66-1.78] m). Patients performed four 5-second maximal voluntary isometric strength trials of both limbs on an isokinetic dynamometer. RTD was calculated as the mean slope of the torque-time curve between 20% and 80% of total time to peak torque. Then, patients underwent 3-dimensional motion analysis while running on an instrumented treadmill at a self-selected running speed (mean ± SD, 2.68 ± 0.28 m/s). The rate of knee extensor moment (RKEM) was calculated as the mean slope of the moment curve between 10% and 30% of stance phase. Between-limb comparisons were determined with a paired t test for peak KEM, RKEM, knee flexion excursion during 10% to 30% of stance, and time to generate KEM. Results: In the reconstructed limb, deficits in the peak rate of quadriceps torque development compared with the noninjured limb existed both isometrically (RTD, 257.56 vs 569.11 Nm/s; P < .001) and dynamically (RKEM, 16.47 vs 22.38 Nm/kg·m·s; P < .001). The reconstructed limb also generated a KEM later in the stance phase compared with the noninjured limb (11.37% vs 9.61% stance; P < .001) and underwent less knee flexion excursion (15.5° vs 19.8°; P < .001). Conclusion: After ACL reconstruction with patellar tendon autograft, patients have lower RTD and RKEM in the reconstructed limb. Deviations in RTD and the timing of the KEM can change the way the knee is loaded and can potentially increase injury risk and future development of posttraumatic osteoarthritis. Rehabilitation should consider exercises designed to improve RTD and prepare the limb for the demands of sport performance.

This retrospective study assessed 5 male and 5 female patients, age 35.1+/-16 years, height 171.8+/-12 cm, and weight 75.5+/-18 kg (mean+/-SD) who were more than 1 year post isolated tibial fracture (18+/-6 months) and had been treated with an intramedullary tibial nail. Subjects completed a 12-question visual analog scale, a physical symptom and activity of daily living survey, and were also tested for bilateral isokinetic (60 degrees/s) quadriceps femoris and hamstring strength. Knee pain during activity, stiffness, swelling, and buckling were the primary symptomatic complaints. Perceived functional task deficits were greatest for climbing or descending stairs, pivoting, squatting, and walking on uneven surfaces. Involved lower extremity knee extensor and flexor torque production deficits were 25% and 17%, respectively. Early rehabilitation focuses on maintaining adequate operative site bony fixation while providing controlled, progressive, and regular biomechanical loading to restore functionally competent tissue. Following adequate fracture healing, greater emphasis should be placed on lower extremity functional recovery including commonly performed activities of daily living and other functional tasks that are relevant to the patient's disability level. A cyclic rehabilitation program that progresses the weight-bearing environment to facilitate bone and soft tissue healing and neuromuscular re-education is proposed.

Lysophosphatidic acid (LPA) enhances cell migration and promotes wound healing in vivo, but the intracellular signaling pathways regulating these processes remain incompletely understood. Here we investigated the involvement of agonist-induced Ca(2+) entry and STIM1 and Orai1 proteins in regulating nuclear factor of activated T cell (NFAT) signaling and LPA-induced keratinocyte cell motility. As monitored by Fluo-4 imaging, stimulation with 10 μM LPA in 60 μM Ca(2+)(o) evoked Ca(2+)(i) transients owing to store release, whereas addition of LPA in physiological 1.2 mM Ca(2+)(o) triggered store release coupled to extracellular Ca(2+) entry. Store-operated Ca(2+) entry (SOCE) was blocked by the SOCE inhibitor diethylstilbestrol (DES), STIM1 silencing using RNA interference (RNAi), and expression of dominant/negative Orai1(R91W). LPA induced significant NFAT activation as monitored by nuclear translocation of green fluorescent protein-tagged NFAT2 and a luciferase reporter assay, which was impaired by DES, expression of Orai1(R91W), and inhibition of calcineurin using cyclosporin A (CsA). By using chemotactic migration assays, LPA-induced cell motility was significantly impaired by STIM1, CsA, and NFAT2 knockdown using RNAi. These data indicate that in conditions relevant to epidermal wound healing, LPA induces SOCE and NFAT activation through Orai1 channels and promotes cell migration through a calcineurin/NFAT2-dependent pathway.