Injured Control Group Research Articles

Comparison of Decontamination-Preservation Protocols for Delayed Surgical Re-implantation of Osteoarticular Fracture Fragments

Background: To avoid discarding contaminated, devascularized osteoarticular fragments required for joint reconstruction, fragments need to be decontaminated while preserving chondrocyte viability. We hypothesized that disinfection with povidone-iodine or chlorhexidine followed by preservation using the Missouri Osteochondral Preservation System (MOPS) would allow for effective decontamination while retaining essential chondrocyte viability in osteoarticular fracture fragments for up to 14 days of shelf-stable point-of-care storage. Methods: With IACUC approval, purpose-bred hounds (n=16) were humanely euthanized for unrelated purposes and subjected to captive bolt trauma to create open distal humeral fractures. For each elbow (n=32), humerus, radius and ulna tissues were recovered such that 96 contaminated, devascularized osteoarticular fragments were randomly allocated to one treatment: Betadine (n=42): saline irrigation (1L), immersion in 10% povidone-iodine (20 min), saline irrigation; Chlorhexidine (n=42): saline irrigation, immersion in 0.002% chlorhexidine gluconate (20 min), saline irrigation; Injured Control (n=12): no decontamination treatment. After 7 or 14 days in MOPS, tissues were assessed by quantitative microbial culture and Viable Chondrocyte Density (VCD) measures. Results: Captive bolt trauma consistently resulted in type 3 open articular fractures. Injured Control osteoarticular fragments produced high polymicrobial counts at days 7 and 14. Chlorhexidine treatment was effective for decontaminating fragments such that no CFUs for clinically relevant bacteria were produced, while Betadine treatment was not fully effective at decontamination. Chlorhexidine decontamination followed by MOPS preservation maintained VCD in osteoarticular tissues over the desired 70% mean for 14 days, whereas the Injured Control group was associated with significant loss of VCD (Day-7=59%, Day-14=13%), which was further exacerbated by Betadine treatment (Day-7=29%, Day-14=6%). Conclusion: Contaminated, devascularized osteoarticular fracture fragments can be effectively decontaminated while maintaining essential chondrocyte viability for 14 days after type 3 open articular fractures using a decontamination-preservation protocol that combines saline irrigation with 0.002% chlorhexidine immersion followed by shelf-stable point-of-care storage in MOPS.

Electrophysiological and histopathological evaluation of the effectiveness of melatonin and glatiramer acetate for traumatic facial nerve injuries

AimThis study aimed to evaluate the effect of systemic/local use of melatonin and glatiramer acetate on regeneration in traumatic nerve injury models. Materials and methodsA total of 42 male Wistar albino rats were randomly divided into 6 groups: healthy control (Group 1), injured control (Group 2), local melatonin (Group 3), systemic melatonin (Group 4), local glatiramer acetate (Group 5), and systemic glatiramer acetate (Group 6). In all groups, electromyography recordings of the facial nerve were obtained after surgery and before sacrifice, and the damaged nerve region was histopathologically examined after sacrifice. ResultsIn the electrophysiological evaluation, the control group had the greatest decrease in amplitude and extension in latency time following surgery than the treatment groups. Furthermore, a significant decrease in the degenerative axon count, edematous areas, and fibrotic areas as well as a significant increase in axonal surface areas was observed in all the treatment groups compared with the damage control group. ConclusionsAlthough both glatiramer acetate and melatonin are beneficial in regeneration in traumatic facial nerve injuries, it can be concluded that systemic use of melatonin can yield more positive results than glatiramer acetate and local use of both two drugs.

Exploring the anti-inflammatory potential of topical hyaluronic acid for vocal fold injury in a rat model

PurposeVocal fold injuries are associated with fibrosis and dysphonia, which is a major obstacle to surgical treatment. The aim of this study is to evaluate the effect of topical hyaluronic acid with or without diclofenac on the inflammatory phase of vocal fold wound healing.MethodsForty-one male Sprague–Dawley rats were randomly assigned to four groups: an uninjured control group, an injured control group without any treatment, and two intervention groups in which hyaluronic acid with or without diclofenac was applied to the injured vocal fold. Gene expression of inflammatory markers and ECM-related molecules were examined.ResultsVocal fold injury resulted in a significant upregulation of inflammatory parameters [Ptgs2, Il1b and Il10] and Has1. Tgfb1, Has3 and Eln gene expression were significantly downregulated by the topical application of hyaluronic acid. The combination of hyaluronic acid and diclofenac did not result in any significant changes.ConclusionsVocal fold wound healing was significantly improved by a single post-operative topical application of hyaluronic acid. The addition of diclofenac may provide no additional benefit.

Transition between social protection systems for workers with long term health problems: A controlled retrospective cohort study

Many nations have established workers' compensation systems as a feature of their social protection system. These systems typically provide time-limited entitlements such as wage replacement benefits and funding for medical treatment. Entitlements may end for workers with long-term health conditions before they have returned to employment. We sought to determine the prevalence of transitions to alternative forms of social protection, specifically social security benefits, among injured workers with long-term disability, when workers' compensation benefits end. We linked Australian workers' compensation and social security data to examine receipt of social security payments one year before and after workers' compensation benefit cessation. Study groups included (1) injured workers whose workers' compensation benefits ceased due to reaching a 260-week limit introduced by legislative reform (N = 2761), (2) a control group of injured workers with at least 104 weeks workers compensation income support (N = 3890), and (3) a matched community control group (N = 10,114). Adjusted binary logistic regression examined the odds of transitions to social security in the injured worker groups relative to the community control group. Within 12 months of workers' compensation benefit cessation, 60% (N = 1669) of the exposed group received social security payments, of which 41% (N = 1120) received the unemployment allowance and 19% (N = 516) the disability pension. Among the work injured control group, 42% (N = 1676) received social security payments after workers compensation benefits ceased. Transitions to social security payments were significantly more common than community levels for both exposed (OR 25.0, 95%CI = 20.7, 30.1) and work injured control groups (OR 4.7, 95%CI = 4.2, 5.3). Many injured workers with long-term health problems transition to social security when their workers’ compensation benefits cease. Transitions were more common among workers whose claims ended due to legislative reform which time-limited benefits. Design and implementation of system level policy reform should consider the social and economic impacts of transitions between separate social protection systems.

A xenograft study of human adipose stromal cell-based vocal fold mucosal replacement in rabbits.

ObjectivesVocal fold (VF) scarring, manifested by increased collagen, decreased glycosaminoglycans (GAGs), and disrupted elastic fibers, remains a negative consequence of VF injury or resection. The objective of this study is to compare four reconstructive options after Vf mucosal resection in rabbits. A Cell‐Based Outer Vocal fold Replacement (COVR) using human adipose‐derived mesenchymal stromal cells (hASCs) in fibrin scaffold is directly compared with a decellularized scaffold implant, hASC injection, and resection alone without reconstruction. The primary hypothesis is that the cells‐in‐scaffold construct better reconstitutes the VF structure than either cells or scaffold alone, or than healing by secondary intention.MethodsA total of49 rabbits received bilateral VF cordectomy, followed by either COVR implant, decellularized scaffold implant, hASC injection, or no reconstruction (injured control group). Larynges were harvested after 6 weeks.ResultsHistology demonstrated greater lamina propria thickness, less collagen deposition, and more GAGs in COVR animals versus all other treatment groups. Evidence of persistent human cells was found in about half of the cell‐treated animals. RNA levels of fibrosis pathway and macrophage phenotype markers were statistically unchanged among treatment groups at 6 weeks.ConclusionThese data support the efficacy of COVR implantation in restoring VF microstructure in rabbits. The intact COVR was required; isolated components of decellularized scaffold or injected hASC still produced histologic scarring. We propose that the unique bilayered cell structure within fibrin enables controlled matrix remodeling to minimize wound contraction and fibrosis, and to promote GAG deposition.Level of EvidenceBasic science study

Comparing resting-state connectivity of working memory networks in U.S. Service members with mild traumatic brain injury and posttraumatic stress disorder

Mild traumatic brain injury (mTBI) and posttraumatic stress disorder (PTSD) are prevalent among military populations, and both have been associated with working memory (WM) impairments. Previous resting-state functional connectivity (rsFC) research conducted separately in PTSD and mTBI populations suggests that there may be similar and distinct abnormalities in WM-related networks. However, no studies have compared rsFC of WM brain regions in participants with mTBI versus PTSD. We used resting-state fMRI to investigate rsFC of WM networks in U.S. Service Members (n = 127; ages 18–59) with mTBI only (n = 46), PTSD only (n = 24), and an orthopedically injured (OI) control group (n = 57). We conducted voxelwise rsFC analyses with WM brain regions to test for differences in WM network connectivity in mTBI versus PTSD. Results revealed reduced rsFC between ventrolateral prefrontal cortex (vlPFC), lateral premotor cortex, and dorsolateral prefrontal cortex (dlPFC) WM regions and brain regions in the dorsal attention and somatomotor networks in both mTBI and PTSD groups versus controls. When compared to those with mTBI, individuals with PTSD had lower rsFC between both the lateral premotor WM seed region and middle occipital gyrus as well as between the dlPFC WM seed region and paracentral lobule. Interestingly, only vlPFC connectivity was significantly associated with WM performance across the samples. In conclusion, we found primarily overlapping patterns of reduced rsFC in WM brain regions in both mTBI and PTSD groups. Our finding of decreased vlPFC connectivity associated with WM is consistent with previous clinical and neuroimaging studies. Overall, these results provide support for shared neural substrates of WM in individuals with either mTBI or PTSD.

Impacts of past occupational injury and long-duration compensated work disability on future hospital admissions.

ObjectivesTo investigate changes in the prevalence and nature of hospital admissions towards the end of long-duration workers’ compensation claims (>2 years), and afterwards. To examine differences in hospitalisation when workers’ compensation claims end due to either a 260-week duration limit, or otherwise, and comparisons with hospitalisations of a community comparator. ApproachA retrospective cohort study examined 2475 workers, termed the s39 group, whose workers’ compensation ceased due to a 260-week limit in 2017/2018 under s39(1) of the Workers’ Compensation Act New South Wales 2012 legislative amendments (Australia). Comparator groups were injured workers with long-duration claims whose compensation ceased independently of s39 (termed the injured control group, N=3626) and a community group (N=8485). Workers’ compensation records were linked to national social security payments, and hospital admissions. Outcomes describe the prevalence and diagnostic categories of hospital admissions 12 months before, and after, the cessation of workers’ compensation stopped payments. ResultsMusculoskeletal health conditions were common diagnoses in overnight hospitalisations for injured workers. Single-day hospital care for mental health disorders were more common for injured workers (17% of same-day admissions) than for members of a community control (3% of same-day admissions) across two years. Exiting the workers’ compensation scheme is associated with significantly fewer annual hospital admissions for the injured control group (OR 0.76), but not for the s39 group (OR 1.01). Injured workers with long-duration compensated work disability were admitted to hospital more often than the community comparator group during the year after workers’ compensation stops (s39 group: OR 1.55, injured control group: OR 1.30). Across all study groups, hospital admission was more common for people receiving disability social security benefits and older age groups. ConclusionPolicy change in the New South Wales workers’ compensation system introduced a 260-week limit on compensation, leaving workers with an elevated need for hospital care after their compensation ended. Welfare policies that disrupt key determinants of health require dedicated inter-agency provisions to support the elevated health needs of those affected.

Changes in health and welfare after workers’ compensation benefits cease.

ObjectivesTo investigate welfare and health service use among workers with long-duration workers’ compensation claims after workers’ compensation stopped. To identify changes in health and welfare of workers whose compensation benefits ended due to a 260-week limit under s39(1) of the Workers’ Compensation Act New South Wales 2012 legislative amendments, Australia. ApproachWorkers’ compensation claims from the New South Wales State Insurance Regulatory Authority were linked to records for social security payments, hospital and emergency department admissions, and health professional services. A cohort of 15,258 workers with long-duration workers’ compensation claims (>2 years) were classified based on whether compensation ended due to a 260-week limit (s39 group), or in circumstances where compensation benefits stopped independently of a 260-week limit (injured control group), and are contextualised with a community comparator (N=10,703). Changes in welfare and health service use were examined 12 months preceding, and 12 months following, a final workers’ compensation benefit payment. ResultsAfter workers’ compensation benefits ceased under a 260-week limit there was a 53% increase in the uptake of social security benefits such as unemployment or disability payments by the s39 group, and levels of hospitalisation remained elevated compared to a community comparator. In contrast, workers whose compensation ended for other reasons, such as returning to work, saw a 28% increase in receipt of social security payments, and coincided with decreased hospitalisation incidence after exiting the workers’ compensation scheme. Overall, receipt of welfare and use of hospital health services after workers’ compensation ended was more common for people aged 65 or older, non-homeowners, single parents, and people living outside major cities. Social security payments were underrepresented for people with compensable psychological injuries, whilst hospitalisation was overrepresented. ConclusionThe introduction of a 260-week limit on workers’ compensation benefits resulted in a cohort of workers transitioning to the social security system, and did not coincide with a characteristic reduction in hospital service use. Policy changes must recognise interconnected consequences of changes to welfare and health. Transitional supports are encouraged.

Antioxidant and gastroprotective effects of the ethyl acetate extract from Stemodia maritima L. in ethanol-induced gastric ulcer model

Stemodia maritima L., is a shrub of the Plantaginaceae family, with some biological activities already described, such as: larvicide, antimicrobial, and anti-inflammatory. Thus, the objective of this work was to evaluate the antioxidant, and gastroprotective activities of the ethyl acetate extract from S. maritima. The phytochemical profile was investigated through the quantification of total phenolic compounds, flavonoids, and CCD analysis. The toxicity of the extract was performed through cell viability using L929 line cell, and acute toxicity by the OECD Guide 423. The antioxidant activity was analyzed by the methods of reduction of the ferric ion (FRAP), total antioxidant activity (TAA), and the gastroprotective activity by the absolute ethanol-induced gastric ulcer model, with analysis of NO, MDA, GSH and MPO levels in the stomach tissues. In the phytochemical profile it was possible to identify the presence of flavonoids, triterpenes, steroids, mono, and sesquiterpenes. The extract was not cytotoxic against L929 lineage, maintaining cell viability above 70% at the doses tested, and in acute toxicity it did not show physiological changes indicative of toxicity compared to the control group. The extract presented antioxidant activity of 157.3 ± 9.7 mg equivalent of Trolox/g of extract in the FRAP method, and 50.0 ± 1.1 % by TAA. The ethyl acetate extract of S. maritima, at the doses tested, reduced the ulcerative lesion index compared to the injured control group, increased the levels of NO and GSH, and was able to decrease the concentrations of MDA and MPO, enhancing their gastroprotective activity.

Sleep disturbances following traumatic brain injury are associated with poor neurobehavioral outcomes in US military service members and veterans.

This study examined whether sleep disturbances were associated with neurobehavioral outcome following a traumatic brain injury (TBI) in a well characterized group of service members and veterans. Six hundred and six participants were enrolled into the Defense and Veterans Brain Injury Center, 15-Year Longitudinal TBI study. All participants completed a battery of tests measuring self-reported sleep disturbances, neurobehavioral symptoms, and posttraumatic stress disorder symptoms. Data were analyzed using analysis of variance with post hoc comparisons. Four groups were analyzed separately: uncomplicated mild TBI; complicated mild, moderate, severe, or penetrating combined TBI; injured controls (ie, orthopedic or soft-tissue injury without TBI); and noninjured controls. A higher proportion of the mild TBI group reported moderate-severe sleep disturbances (66.5%) compared to the injured control group (54.9%), combined TBI (47.5%), and noninjured control groups (34.3%). Participants classified as having Poor Sleep had significantly worse scores on the majority of TBI-Quality of Life scales compared to those classified as having Good Sleep, regardless of TBI severity or the presence of TBI. There was a significant interaction between sleep disturbances and posttraumatic stress disorder. While sleep disturbances and posttraumatic stress disorder by themselves were significant factors associated with worse outcome, both factors combined resulted in worse outcome than either singularly. Regardless of group (injured or noninjured control), sleep disturbances were common and were associated with significantly worse neurobehavioral functioning. When experienced concurrently with posttraumatic stress disorder, sleep disturbances pose significant burden to service members and veterans. Pattinson CL, Brickell TA, Bailie J, etal. Sleep disturbances following traumatic brain injury are associated with poor neurobehavioral outcomes in US military service members and veterans. J Clin Sleep Med. 2021;17(12):2425-2438.

Use of Virtual Reality Cognitive Training to Improve Executive and Complex Attentional Functions: Can Virtual Reality Performance PredictNeurorehabilitation Outcomes?

Background: VR has proven successful in simulating activities and settings that prove inaccessible or unsafe to rehabilitate patients in. Current VR rehabilitation studies largely focus on assessing cognitive skills, not on training cognitive deficits. The current study focused on repeated exposure with a VR-based cognitive intervention to improve deficits known to impact the ability to resume complex activities. Associations between the VR Stroop and neuropsychological, speech therapy, and global rehabilitation measures were examined. We included a brain injured control group to address this frequently cited methodological concern. Design: This was a mixed design study with quasi-experimental Intervention group (N = 12) and retrospective Control group (N = 12). Both groups comprised individuals with brain injury admitted to an outpatient day neurorehabilitation program. Results: Patients with higher level of education and shorter acute medical course deliberated longer before responding on specific Virtual Stroop indices. The brain injury group receiving Virtual Stroop intervention demonstrated a significant increase in level of independence in the home and in community participation by discharge from day neurorehabilitation, compared with the Control group. Increased independence of the virtual reality group was associated with improved attention and self-monitoring, and less disinhibition on the Virtual Stroop. Conclusion: Patients with brain injury demonstrated improvements in various executive functioning and attention indices on the Virtual Stroop, compared with patients who received standard neurorehabilitation. Neurocognitive training within an immersive real-world setting was associated with improved global and specific neurorehabilitation outcomes. Performance on the Virtual Stroop also demonstrated a relationship with cognitive flexibility on traditional neuropsychological testing.

Upregulated protein O-GlcNAcylation promoted functional and structural recovery of the contused spinal cord injury in rats by Thiamet-G treatment

ABSTRACTObjectives-Elevated protein O-GlcNAcylation could benefit cell survival and promote organ functional recovery. Thiamet-G (O-GlcNAcase inhibitor) could upregulate protein O-GlcNAcylation level to improve dyskinesia in models of neurodegenerative diseases without any obvious detrimental side-effects. Therefore, we conducted this study to investigate the effects of protein O-GlcNAcylation upregulation by Thiamet-G on the spinal cord injury (SCI) in rats. Methods-We randomly assigned 74 rats to three groups: sham-operated group (Sham) with no lesion (n = 22), injured control group (SCI+SS) with saline solution (n = 26), and Thiamet-G treated group (SCI+Thiamet-G) (n = 26). We assessed Locomotor behavior using the Basso, Beattice, and Bresnahan (BBB) scale and evaluated histopathological alterations by morphometry and histochemistry. We also assessed potential inflammatory effects by microglia/macrophages immunohistochemistry, and potential apoptosis effects by caspase-3 western blot. Results-Thiamet-G treatment improved hindlimb motor functional recovery by inducing elevated protein O-GlcNAcylation, and mitigated the severity, reduced the lesion size and promoted the structural recovery of the injured spinal cord. Thiamet-G treatment also inhibited microglia/macrophages infiltration at the injury sites and the caspase-3 mediated apoptosis pathway. Discussion-We conclude that Thiamet-G induced elevated protein O-GlcNAcylation to ameliorate acute SCI, which could provide a potential novel therapeutic approach for SCI treatment.

Signatures of altered long noncoding RNAs and messenger RNAs expression in the early acute phase of spinal cord injury.

Spinal cord injury (SCI) is a highly severe disease and it can lead to the destruction of the motor and sensory function resulting in temporary or permanent disability. Long noncoding RNAs (lncRNAs) are transcripts longer than 200 nt that play a critical role in central nervous system (CNS) injury. However, the exact roles of lncRNAs and messenger RNAs (mRNAs) in the early acute phase of SCI remain to be elucidated. We examined the expression of mRNAs and lncRNAs in a rat model at 2 days after SCI and identified the differentially expressed lncRNAs (DE lncRNAs) and differentially expressed mRNAs (DE mRNAs) using microarray analysis. Subsequently, a comprehensive bioinformatics analysis was also performed to clarify the interaction between DE mRNAs. A total of 3,193 DE lncRNAs and 4,308 DE mRNAs were identified between the injured group and control group. Classification, length distribution, and chromosomal distribution of the dysregulated lncRNAs were also performed. The gene ontology analysis and Kyoto Encyclopedia of Genes and Genomes enrichment analysis were performed to identify the critical biological processes and pathways. A protein-protein interaction (PPI) network indicated that IL6, TOP2A, CDK1, POLE, CCNB1, TNF, CCNA2, CDC20, ITGAM, and MYC were the top 10 core genes. The subnetworks from the PPI network were identified to further elucidate the most significant functional modules of the DE mRNAs. These data may provide novel insights into the molecular mechanism of the early acute phase of SCI. The identification of lncRNAs and mRNAs may offer potential diagnostic and therapeutic targets for SCI.

The alcohol-intoxicated trauma patient: impact on imaging and radiation exposure.

The purpose of this study was to investigate the effects of alcohol intoxication in trauma patients in regard to its impact on application of computed tomography (CT) and associated radiation exposure. We conducted a retrospective study from a continuous patient cohort. admission to the emergency room of an urban Level 1 trauma center with trauma team activation during a 12-month period (Jan 1st-Dec 31st 2012). Patients with incomplete data, age ≤12years and with neurological diseases were excluded. Demographics, mechanisms, severity and patterns of injury (Abbreviated Injury Scale, Injury Severity Score, Glasgow Coma Scale), blood alcohol concentration (BAC, in permille, ‰), imaging studies (head/whole body CT), radiation exposure, and hospital length of stay, surgical procedures and mortality were evaluated with SPSS statistics (Version 25, IBM Inc., Armonk, New York). A positive BAC (mean 1.80 ± 0.767) was reported in 19.2% (n = 41/214) of the cohort. Alcohol intoxication was associated with higher utilization of head CT (65.9 vs. 46.8%, p = 0.017) and radiation exposure (231.75 vs. 151.25mAS, p = 0.045; dose-length product, 583.03 vs. 391.04, p = 0.006). In general, the presence of alcohol was associated with over-triage (p = 0.001), despite minor injury severity (ISS < 9) and a comparable rate of head injuries (p = 0.275). Head injury (AIS ≥ 3) and positive BAC (OR 2.34, 95% CI 1.096-5.001) were identified as strongest independent predictors for head CT. Alcohol intoxication is a common finding in trauma patients, and the rate of moderate and serious head injuries seems to be comparable to a more severely injured control group. Furthermore, head CT utilization in intoxicated patients is associated with significant radiation exposure, despite poor image quality, due to motion artifacts (27%). Future strategies are required to exclude head injuries safely, while reducing the rate of head CT and associated radiation exposure in intoxicated patients.

333 Intervertebral Disc Repair Following Microdiscectomy Mediated by Pentosan Polysulfate Primed Mesenchymal Progenitor Cells in an Ovine Model

Abstract INTRODUCTION Lumbar microdiscectomy treats neural compression but fails to halt disc degeneration. Consequently, 10 20% of patients develop debilitating back pain and approximately 15% undergo further surgical intervention. In-vitro pre-incubation of mesenchymal precursor cells (MPCs) with pentosan polysulfate (PPS), enhances viability and chondrogenic differentiation, but inhibits osteogenesis. This study investigated the potential of PPS primed mesenchymal precursor cells (pMPCs) in a gelatin scaffold to facilitate disc repair in an ovine model. METHODS Eighteen adult ewes underwent pre-operative 3T MRI followed by lumbar microdiscectomy at two levels. Sheep were randomized into three groups. The injured control (IC) group received no further treatment; the MPC group were implanted with non-primed MPC + scaffold; the pMPC group received the pMPC + scaffold. Necropsies were performed at six months. Analysis consisted of 3T and 9.4T MRI, gross morphological, histological and biochemical analysis for proteoglycans, collagen and DNA content. RESULTS &gt;MPC and pMPC discs demonstrated significantly reduced disc height loss (P &lt; 0.05) and reduced Pfirrmann grades (P &lt; 0.001) relative to IC discs. pMPC disc segments were significantly less degenerate than IC discs on gross morphology. Proteoglycan content of pMPC discs was significantly greater than IC discs and not significantly different to controls for the injured annulus fibrosus (AF) region and nucleus pulposus (NP) region contralateral to the injury. DNA content for pMPC discs was significantly less than IC discs for the NP &amp; AF injury and adjacent regions. Histological analysis demonstrated increased organization and decreased degeneration in pMPC discs while MPC discs displayed increased vascular infiltration. CONCLUSION pMPCs post microdiscectomy reduced disc degeneration, improved disc height and matrix organization, NP proteoglycan content and histological degeneration relative to microdiscectomy alone. This suggests a potential therapeutic application of pMPCs in promoting disc repair and reducing the incidence of low back pain and further surgery following microdiscectomy.

Effect of electrical stimulation and stem cells on experimentally induced peripheral nerve injury in rats

Objective This work aimed to study the effect of low intensity electrical stimulation and Mesenchymal stem cells transplantation on repair of sciatic nerve crush injury. Background Injury of peripheral nerves results in temporary or life-long neuronal dysfunction that can subsequently lead to economic or social disability. Despite early diagnosis and use of modern surgical techniques, functional recovery can never reach the pre-injury level. Several alternate approaches have been proposed to get beneficial effects on peripheral nerve regeneration, including application of electric field, transplantation of stem cells, and administration of neurotrophic factors. Materials and Methods 48 albino rats weighing 180:250 gm were used in this study. Rats were divided into four equal groups (12 rats each): Sham surgery group: sciatic nerve was exposed but not crushed. Injured sciatic nerve control group: sciatic nerve was exposed and crushed. Mesenchymal stem cells (MSCs) transplantation group: Sciatic nerve injury was done, followed by Transplantation of (3 ΄ 10 5 cells/rat) mesenchymal stem cells intra-lesion immediately after injury. Electrical stimulation (ES) group: sciatic nerve injury was followed by electrical stimulation for 30 minutes. All procedures were followed by wound closure and post-surgical care. Serum malondialdehyde and total antioxidant capacity were estimated 48 hours after injury then electrophysiological studies were measured 8 weeks after injury. Results Treatment with either ES or MSCs transplantation could accelerate and promote sciatic nerve functional regeneration over 8 weeks. Conclusion We concluded that both ES and MSCs transplantation improve peripheral nerve functional regeneration following crush nerve injury. Such effect makes those treatments beneficial for accelerating and giving better outcome of peripheral nerve functional regeneration.

Low-level laser therapy prevents degenerative morphological changes in an experimental model of anterior cruciate ligament transection in rats.

The aim of this study was to analyze the effects of low-level laser therapy (LLLT) on the prevention of cartilage damage after the anterior cruciate ligament transection (ACLT) in knees of rats. Thirty male rats (Wistar) were distributed into three groups (n = 10 each): injured control group (CG); injured laser-treated group at 10 J/cm(2) (L10), and injured laser-treated group at 50 J/cm(2) (L50). Laser treatment started immediately after the surgery and it was performed for 15 sessions. An 808 nm laser, at 10 and 50 J/cm(2), was used. To evaluate the effects of LLLT, the qualitative and semi-quantitative histological, morphometric, and immunohistochemistry analysis were performed. Initial signs of tissue degradation were observed in CG. Interestingly, laser-treated animals presented a better tissue organization, especially at the fluence of 10 J/cm(2). Furthermore, laser phototherapy was able of modulating some of the aspects related to the degenerative process, such as the prevention of proteoglycans loss and the increase in cartilage area. However, LLLT was not able of modulating chondrocytes proliferation and the immunoexpression of markers related to inflammatory process (IL-1 and MMP-13). This study showed that 808 nm laser, at both fluences, prevented features related to the articular degenerative process in the knees of rats after ACLT.

Effects of low-level laser therapy on cartilage repair in an experimental model of osteoarthritis

AbstractObjective:The aim of this study was to evaluate the effects of low level laser therapy (LLLT) on the degenerative process in the articular cartilage after an anterior cruciate ligament transection (ACLT) model in rats.Methods:Eighty male rats (Wistar) were divided into four groups: 1.) intact control group (CG), 2.) injured control group (ICG), 3.) injured laser-treated group at 10 J/cmResults:Initial signs of tissue degradation could be observed 5 weeks post-ACLT, evidenced by the decrease of proteoglycan concentration and increase in cartilage thickness of the ICG. After 8 weeks post-surgery, analysis showed a progression of the degenerative processes in the ICG revealed by the increased cellularity and higher TNF-α, IL1-β and MMP-13 immunoexpression. LLLT was able to modulate some of the aspects relating to the degradative process, such as biomodulation of the number of chondrocyte proliferation, prevention of proteoglycan loss, and decrease of MMP-13 immunoexpression.Conclusion:This study showed that the 685-nm laser irradiation, especially at 10 J/cm

Laser photobiomodulation influences the expression of genes related to the inflammatory process and muscle cell differentiation during the process of muscle healing

AbstractThe aim of this study was to evaluate the effects of 780-nm laser therapy on the expression of genes related to muscle healing.Sixty-three rats were distributed into three groups: 1) injured control group (CG), 2) injured treatment group at 10 J/cmAt day 7, G10 presented a smaller necrosis area compared to CG and G50. Fourteen days post-surgery, G10 and G50 presented a smaller amount of inflammatory cells and a better tissue organization compared to CG. On day 21, G10 and G50 showed better muscle structure than the control. A significantly decreased COX-2 expression was observed in groups G10 and G50 at day 7 compared to the control animals. No difference was found among the experimental groups after 14 days, but G50 presented statistically higher COX-2 down-regulation at day 21. VEGF expression decreased in the first period analyzed in both treatment groups, increased after 14 days in G10, and increased after 21 days in G50. Both irradiated groups had a higher MyoD expression in all the evaluated periods and myogenin levels increased after 14 days in both treatment groups and in G10 after 21 days.780-nm laser therapy had positive effects during muscle regeneration through the gene expression modulation related to the inflammatory process and the new muscle fibers formation, in both fluencies used in the present study, but the fluence of 10 J/cm

Effects of phototherapy on cartilage structure and inflammatory markers in an experimental model of osteoarthritis

The aim of this study was to evaluate the effects of laser phototherapy on the degenerative modifications on the articular cartilage after the anterior cruciate ligament transection (ACLT) in the knee of rats. Eighty male rats (Wistar) were distributed into four groups: intact control group (IG), injured control group (CG), injured laser treated group at 10 J/cm(2) (L10), and injured laser treated group at 50 J/cm(2) (L50). Animals were distributed into two subgroups, sacrificed in 5 and 8 weeks postsurgery. The ACLT was used to induce knee osteoarthritis in rats. After 2 weeks postsurgery, laser phototherapy initiated and it was performed for 15 and 30 sessions. The histological findings revealed that laser irradiation, especially at 10 J/cm(2), modulated the progression of the degenerative process, showing a better cartilage structure and lower number of condrocytes compared to the other groups. Laser phototherapy was not able to decrease the degenerative process measured by Mankin score and prevent the increase of cartilage thickness related to the degenerative process. Moreover, it did not have any effect in the biomodulation of the expression of markers IL1β, tumor necrosis factor-α, and metalloprotein-13. Furthermore, laser irradiated animals, at 50 J/cm(2) showed a lower amount of collagen type 1.