Fascia Iliaca Pain Block Results in Lower Overall Opioid Usage and Shorter Hospital Stays than Epidural Anesthesia After Hip Reconstruction in Children With Cerebral Palsy.

INTRODUCTION AND OBJECTIVE: Epidural anesthesia (EA) is often used for pain control in children with cerebral palsy (CP) who undergo hip reconstructions. The purpose of this study is to determine if preoperative fascia iliaca (FI) pain blocks would improve pain scores, decrease opioid use, and result in shorter hospital stays in comparison to the use of EA. METHODS: This is a nonrandomized retrospective cohort study examining 60 consecutive patients with CP who underwent hip reconstruction utilizing either a fascia iliac compartment nerve block (FICNB) (N=37) or continuous lumbar epidural (N=22) from January 2017 to March 2019. Age at surgery was 8.5±4.6 years. We recorded age, weight, operating room (OR) time, FLACC (Face, Legs, Activity, Cry, Consolability scale) scores on postoperative days (PODs) 0, 1, 2, and 3, opioid doses, overall opioid (mg) used, and length of stay. We compared pain scores, opioid usage, OR time, and lengths of stay between our 2 patient groups. RESULTS: Pain scores were similar between groups on POD #0, 2, and 3 but were statistically improved on POD #1 (1.8±1.3 vs. 3.1±1.4, P<0.001). Total number of opiod doses (7.9±4.4 vs. 10.7±2.3, P=0.004), total milligram given (18.3±11.8 vs. 24.7±12.3, P<0.05), and milligram per kilogram given (0.77±0.42 vs. 1.11 mg/kg±0.36 mg/kg, P=0.001) were less for the FI group versus the epidural group. The OR time (which includes time for blocks/epidurals) was lower in the FI group (4.6±1.2 vs. 5.7±1.1 h, P=0.0002). Overall hospital stays were lower in the FI group (3.4±1.5 vs. 4.1±1.0 d, P<0.05). CONCLUSIONS: This study demonstrates that in the setting of hip reconstruction, patients that received preoperative FI blocks used a lower amount of opioids, required fewer rescue doses and ultimately had a shorter hospital length of stay than those undergoing EA.

Screw Anterior Distal Femoral Hemiepiphysiodesis in Children With Cerebral Palsy and Knee Flexion Contractures: A Retrospective Case-control Study.

BACKGROUND: In children with cerebral palsy who demonstrate hamstring tightness, increasing attention is being paid to less invasive methods of correcting knee flexion contractures. Guided growth principles represent one such approach, and in tandem with a serial extension casting protocol, may provide a less invasive method of addressing these contractures. To date, no evidence is available on this combination of procedures. The purpose of this study was to investigate the effectiveness of a combined lengthening/guided growth procedure (hamstring lengthening, percutaneous anterior screw hemiepiphysiodesis, and serial extension casting) in addressing knee flexion contracture, and to compare this approach to hamstring lengthening and serial extension casting alone. METHODS: Measures from preoperative and postoperative gait analyses were reviewed retrospectively for 10 patients with cerebral palsy who underwent anterior screw hemiepiphysiodesis and hamstring lengthening followed by serial extension casting [anterior epiphysiodesis (AE) group]. These findings were compared with measures from 19 patients with cerebral palsy who underwent hamstring lengthening followed by serial extension casting [no anterior epiphysiodesis (NAE) group]. Postoperative changes in clinical, functional, and kinematic parameters were assessed. Radiographic parameters were also assessed for the AE group. RESULTS: In the AE group, improvements were measured in knee contracture, popliteal angle, peak stance phase knee extension, knee range of motion, and Gait Deviation Index. Similar results were observed in the NAE group. In the AE group, the lateral distal femoral angle increased into extension by 20.9 degrees at an average of 26-month follow-up. Both groups showed an increase in pelvic tilt postoperatively. There were no surgical complications associated with the screw anterior hemiepiphysiodesis. Four patients did have complaints of knee pain, but the pain was attributable to the implants in only one patient. DISCUSSION: The AE group demonstrated statistically greater postoperative improvement in popliteal angle, knee flexion contracture, and peak knee extension during stance than the NAE group. Both procedures led to improvements in clinical and functional measures, indicating the validity of this approach as a means of correcting flexion contracture that is less invasive and allows immediate weight bearing. LEVEL OF EVIDENCE: Level III-therapeutic study.

Role of pulsed electromagnetic fields (PEMF) on tenocytes and myoblasts-potential application for treating rotator cuff tears.

The post-surgery integrity of the tendons and muscle quality are the two major factors in success of rotator cuff (RC) repair. Though surgical techniques for rotator cuff repair have significantly improved in the past two decades, there are no effective treatments to improve tendon-to-bone healing and muscle quality after repair at this point in time. Pulsed electromagnetic fields (PEMF) have previously been used for promoting fracture healing. Previous studies have shown that PEMF has a positive role in promoting osteoblast precursors proliferation and differentiation. However, PEMFs effect on tenocytes and muscle cells has not been determined fully yet. The purpose of this study is to define the role of a commercially available PEMF on tenocytes and myoblasts growth and differentiation in vitro. Human rotator cuff tenocytes and C2C12 murine myoblasts were cultured and treated with PEMF for 2 weeks under regular and inflammatory conditions. Our results showed that 2 weeks treatment of PEMF enhanced gene expressions of growth factors in human rotator cuff tenocytes under inflammatory conditions. PEMF significantly enhanced C2C12 myotube formation under normal and inflammatory conditions. Results from this study suggest that PEMF has a positive role in promoting tenocyte gene expression and myoblast differentiation. Therefore, PEMF may potentially serve as a non-operative treatment to improve clinical incomes rotator cuff tendon repairs. Results © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 35:956-964, 2017.

TGF-ß Small Molecule Inhibitor SB431542 Reduces Rotator Cuff Muscle Fibrosis and Fatty Infiltration By Promoting Fibro/Adipogenic Progenitor Apoptosis.

Rotator cuff tears represent a large burden of muscle-tendon injuries in our aging population. While small tears can be repaired surgically with good outcomes, critical size tears are marked by muscle atrophy, fibrosis, and fatty infiltration, which can lead to failed repair, frequent re-injury, and chronic disability. Previous animal studies have indicated that Transforming Growth Factor-ß (TGF-ß) signaling may play an important role in the development of these muscle pathologies after injury. Here, we demonstrated that inhibition of TGF-ß1 signaling with the small molecule inhibitor SB431542 in a mouse model of massive rotator cuff tear results in decreased fibrosis, fatty infiltration, and muscle weight loss. These observed phenotypic changes were accompanied by decreased fibrotic, adipogenic, and atrophy-related gene expression in the injured muscle of mice treated with SB431542. We further demonstrated that treatment with SB431542 reduces the number of fibro/adipogenic progenitor (FAP) cells-an important cellular origin of rotator cuff muscle fibrosis and fatty infiltration, in injured muscle by promoting apoptosis of FAPs. Together, these data indicate that the TGF-ß pathway is a critical regulator of the degenerative muscle changes seen after massive rotator cuff tears. TGF-ß promotes rotator cuff muscle fibrosis and fatty infiltration by preventing FAP apoptosis. TGF-ß regulated FAP apoptosis may serve as an important target pathway in the future development of novel therapeutics to improve muscle outcomes following rotator cuff tear.

Bone morphogenetic protein signaling in rotator cuff muscle atrophy and fatty infiltration.

BACKGROUND: reduced mass (atrophy) and increased fat content (fatty infiltration) of rotator cuff muscles are common complications of large or massive rotator cuff (RC) tears, and are believed to be irreversible even after tendon repairs. Clinically, both muscle atrophy and fatty infiltration are important factors contributing to poor functional outcomes after tendon repairs. The molecular mechanism of RC muscle atrophy and FI remains undefined. In this study, we investigated the role of bone morphogenetic proteins (BMP) signaling in RC muscle atrophy and fatty infiltration using a rat model. METHODS: unilateral massive RC tears was induced in adult rats. RC muscles were harvested at 2 and 6 weeks after injury for BMP signaling analysis. In a separate experiment, BMP inhibitor (LDN-193189) was injected to rats through daily intraperitoneal injection. RC muscles from rats in the treated and control groups were harvested at 6 weeks after injury for biochemistry and histology analysis. RESULTS: we found significantly increased BMP-14 and BMP-7 expression in rotator cuff muscles after RCT. Inhibiting BMP signaling resulted in increased muscle atrophy and reduced fatty infiltration in rotator cuff muscle after RC tears. CONCLUSION: this result suggests that BMP signaling inhibits RC muscle atrophy but promotes fatty infiltration.

Rat rotator cuff muscle responds differently from hindlimb muscle to a combined tendon-nerve injury.

Rotator cuff tears (RCTs) are among the most common musculoskeletal injuries seen by orthopaedic surgeons. Clinically, massive cuff tears lead to unique pathophysiological changes in rotator cuff muscle, including atrophy, and massive fatty infiltration, which are rarely seen in other skeletal muscles. Studies in a rodent model for RCT have demonstrated that these histologic findings are accompanied by activation of the Akt/mammalian target of rapamycin (mTOR) and transforming growth factor-ß (TGF-ß) pathways following combined tendon-nerve injury. The purpose of this study was to compare the histologic and molecular features of rotator cuff muscle and gastrocnemius muscle--a major hindlimb muscle, following combined tendon-nerve injury. Six weeks after injury, the rat gastrocnemius did not exhibit notable fatty infiltration compared to the rotator cuff. Likewise, the adipogenic markers SREBP-1 and PPARγ as well as the TGF-ß canonical pathway were upregulated in the rotator cuff, but not the gastrocnemius. Our study suggests that the rat rotator cuff and hindlimb muscles differ significantly in their response to a combined tendon-nerve injury. Clinically, these findings highlight the unique response of the rotator cuff to injury, and may begin to explain the poor outcomes of massive RCTs compared to other muscle-tendon injuries.

Upregulation of transforming growth factor-ß signaling in a rat model of rotator cuff tears.

BACKGROUND: Muscle atrophy, fatty infiltration, and fibrosis of the muscle have been described as important factors governing outcome after rotator cuff injury and repair. Muscle fibrosis is also thought to have a role in determining muscle compliance at the time of surgery. The transforming growth factor-ß (TGF-ß) pathways are highly conserved pathways that exert a potent level of control over muscle gene expression and are critical regulators of fibrosis in multiple organ systems. It has been shown that TGF-ß can regulate important pathways of muscle atrophy, including the Akt/mammalian target of rapamycin pathway. The purpose of this study was to evaluate the expression of TGF-ß and its downstream effectors of fibrosis after a massive rotator cuff tear (RCT) in a previously established rat model. METHODS: To simulate a massive RCT, infraspinatus and supraspinatus tenotomy and suprascapular nerve transection were performed on Sprague-Dawley rats with use of a validated model. Two and 6 weeks after surgery, supraspinatus muscles were harvested to study alterations in TGF-ß signaling by Western blotting, quantitative polymerase chain reaction, and histologic analysis. RESULTS: There was a significant increase in fibrosis in the rotator cuff muscle after RCT in our animal model. There was a concomitant increase in TGF-ß gene and protein expression at both 2 and 6 weeks after RCT. Evaluation of the TGF-ß signaling pathway revealed an increase in SMAD2 activation but not in SMAD3. There was an increase in profibrotic markers collagen I, collagen III, and α-smooth muscle actin. CONCLUSIONS: TGF-ß signaling is significantly upregulated in rat supraspinatus muscles after RCTs.

Advances in the orthopedic management of osteogenesis imperfecta.

The long-established study of osteogenesis imperfecta (OI) has opened a realm of scientific research surrounding connective tissue disorders. Over the past decade alone there have been vast advancements in the understanding of the underlying genetic variations of this disease, pharmacologic treatments, and the technological and surgical options for fracture deformity. It is important to appreciate the progressive nature of the advances concerning OI. This article aims to synthesize the expanding evolution of the field surrounding OI over the past decade.

Evaluation of cartilage degeneration in a rat model of rotator cuff tear arthropathy.

BACKGROUND AND HYPOTHESIS: Rotator cuff tears are the most common injury seen by shoulder surgeons. Glenohumeral osteoarthritis develops in many late-stage rotator cuff tear patients as a result of torn cuff tendons, termed "cuff tear arthropathy." However, the mechanisms of cuff tear arthropathy have not been fully established. It has been hypothesized that a combination of synovial and mechanical factors contribute equally to the development of cuff tear arthropathy. The goal of this study was to assess the utility of this model in investigating cuff tear arthropathy. MATERIALS AND METHODS: We used a rat model that accurately reflects rotator cuff muscle degradation after massive rotator cuff tears through either infraspinatus and supraspinatus tenotomy or suprascapular nerve transection. Using a modified Mankin scoring system, we found significant glenohumeral cartilage damage after both rotator cuff tenotomy and suprascapular nerve transection after only 12 weeks. RESULTS: Cartilage degeneration was similar between groups and was present on both the humeral head and the glenoid. Denervation of the supraspinatus and infraspinatus muscles without opening the joint capsule caused cartilage degeneration similar to that found in the tendon transection group. CONCLUSIONS: Our results suggest that altered mechanical loading after rotator cuff tears is the primary factor in cartilage degeneration after rotator cuff tears. Clinically, understanding the process of cartilage degeneration after rotator cuff injury will help guide treatment decisions in the setting of rotator cuff tears. LEVEL OF EVIDENCE: Basic science study, animal model.

MRI quantification of fatty infiltration and muscle atrophy in a mouse model of rotator cuff tears.

Rotator cuff pathology is the most common shoulder problem seen by orthopedic surgeons. Rotator cuff muscle fatty infiltration and muscle atrophy are common in larger tears and are considered predicting factors for the prognosis of cuff repair. Clinically, MRI is the gold standard in determining fatty infiltration and muscle atrophy; however, analysis for MRI imaging is primarily qualitative in nature with the results lacking further validation. We have recently developed a mouse model of rotator cuff tears. The goal of this study is to quantify and verify rotator cuff muscle atrophy and fatty infiltration using high-resolution MRI in our mouse model. The rotator cuff muscles were analyzed for fat using a triglyceride quantification assay (TQA), muscle volume was measured through water displacement (WD), and histology. The study revealed that MRI had a high correlation with fat as measured with histology and TQA (R(2) =098). MRI also correlated well with atrophy measured with WD and wet weight. This suggests that MRI is a reliable modality in evaluating the progression of fatty infiltration and muscle atrophy following rotator cuff tears in a small animal model.

A mouse model of massive rotator cuff tears.

BACKGROUND: Rotator cuff tears are the most common tendon injury seen in orthopaedic patients. Muscle atrophy and fatty infiltration in rotator cuff muscles are considered among the key factors responsible for the failure of attempted repair of a massive rotator cuff tear. However, the pathophysiology of rotator cuff muscle atrophy and fatty infiltration remains largely unknown, partly because of the lack of appropriate small animal models. The goal of this study was to develop a mouse model of muscle atrophy and fatty infiltration after a rotator cuff tear. We also sought to study the role of denervation on muscle atrophy and fatty infiltration after a rotator cuff tear. METHODS: Adult wild-type FVB/N mice were randomly divided into three groups. Mice in different groups received unilateral complete supraspinatus and infraspinatus tendon transection, suprascapular nerve transection, or both procedures. Sham surgery was performed on the contralateral shoulder to serve as a control. Mice were killed twelve weeks after surgery. Histological analysis and high-resolution magnetic resonance imaging were used to evaluate muscle atrophy and fat infiltration after a rotator cuff tear. RESULTS: Significant and consistent muscle atrophy and fatty infiltration were observed in the rotator cuff muscles after rotator cuff tendon transection. We further found that denervation significantly increases the amount of muscle atrophy and fatty infiltration after a rotator cuff tear. CONCLUSIONS: We successfully developed a novel mouse model of a massive rotator cuff tear, which simulates major pathological changes, including muscle atrophy and fatty infiltration after massive rotator cuff tears seen in patients.

Evaluation of Akt/mTOR activity in muscle atrophy after rotator cuff tears in a rat model.

Atrophy of the rotator cuff muscles is a factor that complicates the treatment of a massive rotator cuff tear (RCT). However, the molecular mechanisms that govern the development of muscle atrophy after RCTs have not been well defined. The Akt/mammalian target of rapamycin (mTOR) signaling pathway plays a central role in maintaining muscle mass in response to mechanical loading. The role of this pathway in the development of muscle atrophy after a massive RCT remains unknown. The purpose of this study was to investigate the regulation of the Akt/mTOR pathway in the development of muscle atrophy after a RCT and suprascapular nerve (SSN) injury. We evaluated the activity of the Akt/mTOR signaling pathway and how this pathway interacts with two atrophy-related genes, MuRF-1 and MAFbx, in supraspinatus muscles of rats that underwent unilateral complete rotator cuff tendon transection or SSN transection. Akt/mTOR activity was significantly reduced after tendon rupture, but increased after nerve injury. MuRF-1 and MAFbx were only up-regulated following denervation. These results suggest that tendon transection leads to a decrease in protein synthesis with down-regulation of the Akt/mTOR signaling pathway, whereas denervation leads to an increase in protein degradation via up-regulation of expression of MuRF-1 and MAFbx.

Muscle degeneration in rotator cuff tears.

Rotator cuff tears are among the most common injuries seen by orthopedic surgeons. Although small- and medium-sized tears do well after arthroscopic and open repair, large and massive tears have been shown to develop marked muscle atrophy and fatty infiltration within the rotator cuff muscles. These pathologic changes have been found to be independent predictors of failed surgical repair with poor functional outcomes. To understand the pathophysiology of rotator cuff disease, we must first develop an understanding of the changes that occur within the cuff muscles themselves. The purpose of this review is to summarize the molecular pathways behind muscular degeneration and emphasize new findings related to the clinical relevance of muscle atrophy and fatty infiltration seen with rotator cuff tears. Understanding these molecular pathways will help guide further research and treatment options that can aim to alter expression of these pathways and improve outcomes after surgical repair of massive rotator cuff tears.