Short-term Complications of Open Latarjet Procedure for Recurrent Anterior Shoulder Dislocation.

Background: Anterior dislocation is the most common type of shoulder dislocation, and even after appropriate treatment, recurrence after a primary traumatic anterior dislocation is highly frequent. Surgical options for treating recurrent anterior dislocations mainly include Bankart arthroscopic and Latarjet open surgery. We aimed to evaluate the outcomes and complication rates of the open Latarjet procedure in a series of patients with recurrent anterior shoulder dislocation. Methods: A total of 55 patients with recurrent anterior shoulder dislocation who underwent an open Latarjet procedure were included in this retrospective cohort study. Shoulder range of motion and postoperative complications, including neurapraxia, re-dislocation, hematoma, infection, dehiscence, implant failure, and pain, were evaluated. Results: The mean age of the patients was 27.7 ± 6.5 years . The mean time interval after the first dislocation was 3.4 ± 2.7 years . The mean preoperative and postoperative forward flexion (P = 0.200), abduction (P = 0.200), external rotation (P = 0.066), and internal rotation (P = 0.310) were not significantly different. Postoperative complications included 1 case of postoperative musculocutaneous nerve neurapraxia, 1 case of re- dislocation, 1 case of wound dehiscence, and 2 cases of screw breakage. Postoperative pain was also recorded in 11 (20%) patients that were either in the form of occasional night pain (n = 6) or activity-dependent pain (n = 5). Conclusion: Open Latarjet procedure is an efficient procedure for the treatment of recurrent anterior shoulder dislocation. However, its rate of complications remains relatively high, and surgeons must consider this drawback in their decision-making and address patients' expectations.

Spinopelvic Parameters as Risk Factors of Nonspecific Low Back Pain: A Case-Control Study.

Background: The effect of spinopelvic alignment on low back pain (LBP) incidence has been studied in many investigations. However, the interrelation between spinopelvic parameters and LBP is poorly understood. In particular, it is unknown whether particular patterns of spinopelvic parameters render nonspecific LBP. In this study, we aimed to evaluate the role of spinopelvic parameters as risk factors of nonspecific LBP. Methods: In this case-control study, spinopelvic parameters, including lumbar lordosis (LL), sacral slope (SS), pelvic tilt (PT), and pelvic incidence (PI), were compared between 148 patients with nonspecific LBP and 148 healthy controls. Demographic characteristics of the patients, such as age, gender, occupation, smoking, diabetes mellitus, and body mass index (BMI), were recorded as confounders. Spinopelvic parameters were assessed using radiographic findings in 2 groups. The analysis was done once as univariate (Kolmogorov-Smirnov test) and once as multivariate (multivariate logistic regression) analysis. Results: Univariate analysis showed that female gender, higher BMI, smoking, and blue-collar jobs were associated with a higher risk of nonspecific LBP. LL, SS, and PI, but not PT, were all greater in LPB patients in the univariate analysis regarding the spinopelvic parameters. Multivariate analysis showed female gender (odds ratio adjusted (ORAdj) = 4.26 [95% CI, 2.11-9.58]; P = 0.001) and LL (ORAdj = 1.58; [95% CI, 1.18-3.22]; P = 0.026) were predictable risk factors for Nonspecific LBP. Conclusion: Spinopelvic parameters, particularly LL, could be considered as risk factors of nonspecific LBP so that a more significant LL might indicate a greater risk of LBP. However, the role of other parameters in this association could not be neglected.

A Study of Characteristic Features and Diagnostic Roles of X-ray and MRI in Calcifying Tendinitis of the Shoulder.

Background: Calcifying tendinitis (CT) is an enigmatic lesion with several obscure aspects and it is a common disorder of the upper extremity characterized by the presence of calcifications in rotator cuff tendons and synovial tissues. In this study, we aimed to review the demographic and clinical characteristics, as well as radiologic and treatment history in CT patients who were referred with shoulder pain. Methods: In this cross-sectional study, a total of 146 patients who were referred with a shoulder CT were included. The definitive diagnosis was based on a combination of plain radiograph and magnetic resonance imaging (MRI). A predesigned independent t test was used to capture demographic and clinical data, as well as radiologic and treatment histories, and a chi-square test was utilized to assess the statistical correlation between qualitative variables. Results: The median age of the patients was 42.5 years. The female to male ratio was 2.3 to 1. The complaint of restricted shoulder movement was recorded in 107 (73.3%) patients and more frequently in women (p = 0.042). Night pain was present in 109 (74.7%) patients. The current and previous diagnoses matched in 36.1% (13 out of 36) of patients who only had MRI and in 63.6% (35 out of 55) patients who had both MRI and plain radiograph with them. Supraspinatus tendon was the main site of calcified deposition 65% (95 out of 146). Conclusion: CT is frequent at the age of around 40 and in the female gender. The diagnosis should be based on a combination of radiography and MRI and not based on MRI alone. The efficacy of different conservative treatments remains to be unwrapped.

Treatment of Symptomatic Flexible Flat Foot in Pediatrics with A Modified Mosca's Lateral Column Lengthening.

Background: The optimal treatment of flat foot is still controversial. In this study, we evaluated the outcome the Mosca's lateral column lengthening with the advancement of the tibialis posterior. Methods: In a retrospective study . fifty symptomatic pediatric flexible flat feet with or without hindfoot valgus were included in this study. Lateral column lengthening was done as described by Mosca. The tibialis posterior advancement was made on the navicular bone instead of the medial cuneiform. Radiographic measures of outcome were evaluated before the surgery and immediately after the surgery and included Calcaneal Inclination (Pitch) Angle, Talonavicular Coverage Angle, Talo-1st metatarsal Angle (Meary's Angle), Lateral Talocalcaneal Angle, Anteroposterior Talocalcaneal Angle (kite's angle), and Talar Declination Angle (Talo-Horizontal Angle). A paired t-test or its nonparametric counterpart (Wilcoxon T-test) was used to compare the mean value of preoperative and postoperative measures. A chi-square test was used to compare qualitative variables Results: The mean age of the patients was 9.2±2.2 years . The mean follow - up of the patients was 2.6±1.1 years . All radiographic measures were significantly improved after the surgery. According to the radiographic measures, under-correction was seen in seven feet. Overcorrection was seen in one of the patients. Union of the osteotomy site was observed in all feet. No patients had postoperative pain or limited ankle range of motion. One superficial infection occurred that was managed with oral antibiotics. Conclusion: Lateral column lengthening and advancement of tibials posterior on navicular bone is a safe and effective procedure in the treatment of the symptomatic pediatric flexible flat foot.

Mutations in the Reelin pathway are associated with abnormal expression of microglial IgG FC receptors in the cerebellar cortex.

Microglia are the immune cells of the central nervous system involved in a variety of developmental processes, such as regulation of cell death and survival, spatial patterning, and contribute to the development of Purkinje cells (PCs) during migration. Microglia express immunoglobulin G Fc receptors (FcgRs). In this report, we describe microglial FcgR expression and its relation to abnormal PC migration in the cerebellum during development. To detect microglial FcgR, the direct anti-IgG (secondary antisera) and high concentrations of Triton X-100 were applied as a method for labeling microglial cells without the use of any specific primary antiserum. By using Acp2-/- mice, which show an excessive PC migration into the molecular layer (ml), and 3 different types of mice with a null to alter the Reelin pathway (Reeler-, Dab1 (SCM)-, and Apoer mutant mice), we studied the location of PCs and the expression of FcgRs. Wild type littermates were used as controls in all studies. We show that the expression of microglial FcgRs was absent and PCs were ectopically located in the white matter in the cerebella of all mutant mice, except for the Acp2-/- mice (PCs were located in the ml). These results suggest a role for FcgRs in the Reelin signaling pathway, not in regulating PC migration, but rather in the adaptation to an environment with a relatively large number of ectopically located PCs. However, the exact correlation between the ectopic location of PCs and lack of FcgRs in Reeler, SCM, and Apoer-/- mice and the presence of FcgRs and directed PC location in the ml in Acp2-/- mice are yet to be determined.

Minocycline attenuates depressive-like behaviors in mice treated with the low dose of intracerebroventricular streptozotocin; the role of mitochondrial function and neuroinflammation.

Neuroinflammation and mitochondrial dysfunction are suggested as mechanisms which are implicated in the pathophysiology of depression. Streptozotocin (STZ) is known to produce immune-inflammatory responses and mitochondrial dysfunction in different types of animal models of disease (e.g. type-1 diabetes and Alzheimer's disease). Therefore, a single low dose of Streptozotocin (STZ; intracerebroventricular, i.c.v, 0.2 mg/mouse) was used to induce an animal model of depression. The present study aims to investigate the effects of short (24 h) and long (14 days) exposure to minocycline on STZ-induced depressive-like behaviors (n = 6-8), hippocampal oxidative state biomarkers (n = 4), and the expression of hippocampal genes related to innate immunity (n = 3) in the hippocampus of male adult mice. In addition, the protective effects of different modes of minocycline (acute pretreatment (20 mg/kg, 1 h before STZ), acute post-treatment (20 mg/kg, 24 h after STZ), chronic pretreatment (5 mg/kg/day for 14 days before STZ), and chronic post-treatment (5 mg/kg/day for 14 days after STZ) were compared with the STZ effects. As the data showed, both short and long effects of STZ were associated with the depressive-like behaviors, abnormal mitochondrial function, and upregulation of neuroinflammatory genes in the hippocampus. Different modes of minocycline treatment could attenuate the negative impact of STZ on animals. The data suggested that minocycline at a human therapeutic dose (5 mg/kg) had protective effects against acute cellular damage induced by oxidation and the consequent inflammatory responses.

Pelargonidin exhibits restoring effects against amyloid ß-induced deficits in the hippocampus of male rats.

Background: Alzheimer's disease (AD) is characterized by amyloid-beta plaques, neuronal loss, and cognitive dysfunction. Oxidative stress plays a key role in the pathophysiology of AD, and it has been suggested that antioxidants may slow the progress of the disease. In this study, the possible protective effects of pelargonidin (a natural flavonoid) against amyloid ß (Aß)-induced behavioral deficits was investigated in rats. Methods: Adult Wistar male rats were treated with intrahippocampal injections of the Aß (aa 25-35) and intraperitoneal injection of pelargonidin. Learning and spatial memory were tested using the Morris water maze (MWM) task. The antioxidant activity was evaluated using the ferric reducing/antioxidant power assay (FRAP assay). Data were analyzed using SPSS 20, and value of p≤0.05 was considered significant. Results: The results of this study showed that Aß significantly increased escape latency and the distance traveled in the MWM, and pelargonidin attenuated these behavioral changes. Aß induced a significant decrease in the total thiol content of hippocampus, and pelargonidin restored the hippocampal antioxidant capacity. Conclusion: The results of this study suggest that pelargonidin can improve Aß-induced behavioral changes in rats.

Acute foot-shock stress decreased seizure susceptibility against pentylenetetrazole-induced seizures in mice: Interaction between endogenous opioids and cannabinoids.

BACKGROUND: Stressful conditions affect the brain's neurotransmission and neural pathways that are involved in seizure susceptibility. Stress alters the intensity and/or frequency of seizures. Although evidence indicates that chronic stress exerts proconvulsant effects and acute stress has anticonvulsant properties, the underlying mechanisms which mediate these effects are not well understood. In the present study, we assessed the role of endogenous opioids, endocannabinoids, as well as functional interaction between opioid and cannabinoid systems in the anticonvulsant effects of acute foot-shock stress (FSS) against pentylenetetrazole (PTZ)-induced seizures in mice. METHODS: Prolonged intermittent FSS was chosen as an acute stress model. Seizure threshold was determined after 30 min of stress induction in male Naval Medical Research Institute (NMRI) mice (20-30 g). Opioid and cannabinoid receptor antagonists were administered before animal placement in the FSS apparatus. RESULTS: Acute FSS significantly decreased seizure susceptibility in animals. The administration of the cannabinoid receptor 1 (CB1) antagonist, AM251, completely blocked the anticonvulsant effect of acute FSS at the doses of 1 pg/kg-100 µg/kg but not at 1 fg/kg. Pretreatment with the nonspecific opioid receptor antagonist, naltrexone (NTX), significantly inhibited the anticonvulsant effects of acute FSS at 1 and 2 mg/kg but not at 0.3 mg/kg. However, coadministration of the subeffective doses of AM251 (1 fg/kg) and NTX (0.3 mg/kg) reversed the anticonvulsant effects of acute FSS. CONCLUSIONS: Opioid and cannabinoid systems are involved in the anticonvulsant effects of acute FSS, and these neurotransmission systems interact functionally in response to acute FSS.

Anticonvulsant effect of minocycline on pentylenetetrazole-induced seizure in mice: involvement of nitric oxide and N-methyl-d-aspartate receptor.

Anticonvulsant effects of minocycline have been explored recently. This study was designed to examine the anticonvulsant effect of acute administration of minocycline on pentylenetetrazole-induced seizures in mouse considering the possible role of the nitric oxide/N-methyl-d-aspartate (NMDA) pathway. We induced seizure using intravenous administration of pentylenetetrazole. Our results showed that acute administration of minocycline increased the seizure threshold. Furthermore, co-administration of subeffective doses of the nonselective nitric oxide synthase (NOS) inhibitor NG-l-arginine methyl ester (10 mg/kg) and the neuronal NOS inhibitor 7-nitroindazole (40 mg/kg) enhanced the anticonvulsant effect of subeffective doses of minocycline (40 mg/kg). We found that inducible NOS inhibitor aminoguanidine (100 mg/kg) had no effect on the antiseizure effect of minocycline. Moreover, l-arginine (60 mg/kg), as a NOS substrate, reduced the anticonvulsant effect of minocycline. We also demonstrated that pretreatment with the NMDA receptor antagonists ketamine (0.5 mg/kg) and MK-801 (0.05 mg/kg) increased the anticonvulsant effect of subeffective doses of minocycline. Results showed that minocycline significantly decreased the hippocampal nitrite level. Furthermore, co-administration of a neuronal NOS inhibitor like NMDA receptor antagonists augmented the effect of minocycline on the hippocampal nitrite level. In conclusion, we revealed that anticonvulsant effect of minocycline might be, at least in part, due to a decline in constitutive hippocampal nitric oxide activity as well as inhibition of NMDA receptors.

Tropisetron attenuated the anxiogenic effects of social isolation by modulating nitrergic system and mitochondrial function.

BACKGROUND: Early social isolation stress (SIS) is associated with the occurrence of anxiety behaviors. It seems interaction between the nitrergic system and mitochondrial function plays a role in mediating the anxiety-like behaviors. In this study, we aimed to investigate the anxiolytic effects of tropisetron in animal model of SIS and we try to illustrate the possible role of nitrergic system and mitochondrial function. METHODS: We applied early social isolation paradigm to male NMRI mice. Animals treated with various doses of tropisetron, nitric oxide agents or their combination and anxiety-like behaviors of animals were assessed using valid behavioral tests including elevated plus maze (EPM), open-field test (OFT) and hole-board test (HBT) in their adulthood. Effects of housing conditions and drug treatments on the mitochondrial function were investigated in the hippocampus by assessing the ATP, GSH, ROS and nitrite levels. RESULTS: Anxiogenic effects of early SIS were assessed in the EPM, OFT, and HBT. Also, SIS disrupted mitochondrial function and caused oxidative stress in the hippocampus of stressed animals. Tropisetron showed an anxiolytic effect in the stressed mice. Also, these effects were mediated by nitrergic system by affecting mitochondrial function and modulating the oxidative stress. L-arginine, a nitric oxide precursor, abolished the anxiolytic effects of tropisetron in the behavioral tasks and blocked the protective effects of it against mitochondrial and oxidative challenge. CONCLUSIONS AND GENERAL SIGNIFICANCE: Our results demonstrated tropisetron attenuated the anxiogenic effects of SIS by mitigation of the negative effects of nitric oxide on mitochondrial function.

Involvement of ATP-sensitive potassium channels and the opioid system in the anticonvulsive effect of zolpidem in mice.

Zolpidem is a hypnotic medication that mainly exerts its function through activating γ-aminobutyric acid (GABA)A receptors. There is some evidence that zolpidem may have anticonvulsive effects. However, the mechanisms underlying this effect have not been elucidated yet. In the present study, we used the pentylentetrazole (PTZ)-induced generalized seizure model in mice to investigate whether zolpidem can affect seizure threshold. We also further evaluated the roles of ATP-sensitive potassium (KATP) channels as well as µ-opioid receptors in the effects of zolpidem on seizure threshold. Our data showed that zolpidem in a dose-dependent manner increased the PTZ-induced seizure threshold. The noneffective (i.e., did not significantly alter the PTZ-induced seizure threshold by itself) doses of KATP channel blocker (glibenclamide) and nonselective opioid receptor antagonist (naloxone) were able to inhibit the anticonvulsive effect of zolpidem. Additionally, noneffective doses of either KATP channel opener (cromakalim) or nonselective µ-opioid receptor agonist (morphine) in combination with a noneffective dose of zolpidem exerted a significant anticonvulsive effect on PTZ-induced seizures in mice. A combination of noneffective doses of naloxone and glibenclamide, which separately did not affect zolpidem effect on seizure threshold, inhibited the anticonvulsive effects of zolpidem. These results suggest a role for KATP channels and the opioid system, alone or in combination, in the anticonvulsive effects of zolpidem.

Lithium attenuates the proconvulsant effect of adolescent social isolation stress via involvement of the nitrergic system.

In this study, we tested whether acute administration of lithium mitigates the deleterious effect of adolescent social isolation stress (SIS) on seizure susceptibility. In comparison with socially conditioned (SC) mice, isolated conditioned (IC) mice exhibited an increase in seizure susceptibility to pentylenetetrazole. Acute administration of lithium (10mg/kg) reversed the proconvulsant effect of SIS in IC mice, but this effect was not observed in SC mice. Coadministration of subthreshold doses of lithium (3mg/kg) with nitric oxide synthase (NOS) inhibitors reversed the effect of SIS on seizure susceptibility and decreased hippocampal nitrite levels in IC animals. In addition, a subthreshold dose of a nitric oxide precursor reduced the protective effect of lithium on seizure susceptibility and increased nitrite levels in the hippocampus of IC mice. These results suggest that lithium exerts a protective influence against the proconvulsant effect of adolescent SIS via a nitrergic system that includes activation of neuronal NOS in the hippocampus.

Fluoxetine reverses the behavioral despair induced by neurogenic stress in mice: role of N-methyl-d-aspartate and opioid receptors.

Opioid and N-methyl-d-aspartate (NMDA) receptors mediate different effects of fluoxetine. We investigated whether opioid and NMDA receptors are involved in the protective effect of fluoxetine against the behavioral despair induced by acute physical stress in male mice. We used the forced swimming test (FST), tail suspension test (TST), and open-field test (OFT) for behavioral evaluation. We used fluoxetine, naltrexone (opioid receptor antagonist), MK-801 (NMDA receptor antagonist), morphine (opioid receptor agonist), and NMDA (NMDA receptor agonist). Acute foot-shock stress (FSS) significantly induced behavioral despair (depressive-like) and anxiety-like behaviors in tests. Fluoxetine (5 mg/kg) reversed the depressant-like effect of FSS, but it did not alter the locomotion and anxiety-like behavior in animals. Acute administration of subeffective doses of naltrexone (0.3 mg/kg) or MK-801 (0.01 mg/kg) potentiated the antidepressant-like effect of fluoxetine, while subeffective doses of morphine (1 mg/kg) and NMDA (75 mg/kg) abolished this effect of fluoxetine. Also, co-administration of subeffective doses of naltrexone (0.05 mg/kg) and MK-801 (0.003 mg/kg) with fluoxetine (1 mg/kg) induced a significant decrease in the immobility time in FST and TST. Our results showed that opioid and NMDA receptors (alone or in combination) are involved in the antidepressant-like effect of fluoxetine against physical stress.

Experiencing neonatal maternal separation increased the seizure threshold in adult male mice: Involvement of the opioid system.

Experiencing early-life stress has been considered as a potent risk factor for the development of many of brain disorders, including seizures. Intervening mechanisms through which neonatal maternal separation (MS) alters the seizure susceptibility in adulthood have not been well studied. In the current study, by applying 180 min of MS stress (PND 2-14), we determined the seizure susceptibility and considered the role of the opioid system. Maternal separation increased the seizure threshold, and administration of anticonvulsant/proconvulsant doses of morphine (1 and 30 mg/kg, respectively) reversed the impact of MS. Using tail flick and hot plate tests, we exposed animals to 30 min Restraint stress (RS) and found that MS decreased the pain threshold, suggesting the hyporesponsiveness of the opioid system. These results supported the abnormal seizure activity observed in the MS mice and suggested that abnormalities in the opioid system following MS alter seizure susceptibility in later life.

Involvement of the nitrergic system in the proconvulsant effect of social isolation stress in male mice.

Social isolation stress (SIS) in adolescence is accompanied by neurobehavioral disturbances and pathophysiological changes in certain regions of the CNS such as the hippocampus. In this study, we tested whether SIS impacts seizure susceptibility in postnatal male mice due to a role of hippocampal nitric oxide (NO). To do this, we used the pentylenetetrazole (PTZ) model of clonic seizures, open-field test, hole-board test, forced swimming test, and plasma corticosterone assay. We aimed to evaluate if 4 weeks of SIS is capable of decreasing seizure threshold along with altering affective and neuroendocrine responses in isolated conditioned (IC) animals in comparison with socially conditioned (SC) animals. In addition, we applied subeffective doses of NO precursor L-arginine (25, 50, and 100mg/kg) and NOS inhibitors 7-NI (15 and 40 mg/kg), aminoguanidine (50 and 100mg/kg), and L-NAME (10 and 15 mg/kg) to both IC and SC groups prior to the determination of seizure threshold. Injection of a single dose of all mentioned drugs did not induce changes in seizure threshold of SC mice. On the other hand, L-NAME and 7-NI, but not aminoguanidine, modulated the proconvulsant effect of SIS, while L-arginine augmented the latter effect. We also measured the hippocampal nitrite levels after the administration of the aforementioned drugs. Social isolation stress increased the nitrite levels in comparison with those in SC mice, whereas 7-NI and L-NAME, unlike aminoguanidine, mitigated the effect of SIS. Additionally, L-arginine boosted the effects of SIS on nitrite production. In summary, we showed that SIS enhanced seizure susceptibility in the PTZ model of clonic seizures through the activation of the nitrergic system in the hippocampus. Also, we proved that nNOS, but not iNOS, accounts for these changes following SIS.

Designing and synthesis of injectable hydrogel based on carboxymethyl cellulose/carboxymethyl chitosan containing QK peptide for femoral head osteonecrosis healing.

Femoral head necrosis is a debilitating disorder that typically caused by impaired blood supply to the hip joint. In this study, a novel injectable hydrogel based on Oxidized Carboxymethyl Cellulose (OCMC)-Carboxymethyl Chitosan (CMCS) polymers containing an angiogenesis stimulator peptide (QK) with a non-toxic crosslinking interaction (Schiff based reaction) was synthesized to enhance angiogenesis following femoral head necrosis in an animal model. The physicochemical features of fabricated injectable hydrogel were analyzed by FTIR, swelling and degradation rate, rheometry, and peptide release. Also, the safety and efficacy were evaluated following an in vitro hydrogel injection study and an avascular necrosis (AVN) animal model. According to the results, the hydrogel exhibited an appropriate swelling ratio and water uptake (>90 %, 24 h) as well as a suitable degradation rate over 21 days accompanied by a continuous peptide release. Also, data showed that hydrogels containing QK peptide boosted the proliferation, differentiation, angiogenesis, and osteogenic potential of both Bone Marrow mesenchymal Stem Cells (BM-MSCs) and human umbilical vein endothelial cells (HUVECs) (****p < 0.0001 and ***p < 0.001, respectively). Furthermore, molecular and histological evaluations significantly demonstrated the overexpression of Runx2, Osteocalcin, Collagen I, VEGF and CD34 genes (**p < 0.01 and ***p < 0.001, respectively), and also femoral head necrosis was effectively prohibited, and more blood vessels were detected in defect area by OCMC-CMCS hydrogel containing QK peptide (bone trabeculae >9000, ***p < 0.001). In conclusion, the findings demonstrate that OCMC-CMCS-QK injectable hydrogel could be considered as an impressive therapeutic construct for femoral head AVN healing.

Management of Iatrogenic Medial Collateral Ligament Injury in Primary Total Knee Arthroplasty: A Systematic Review.

Objectives: The medial collateral ligament (MCL) injury is one of the possible complications of primary total knee arthroplasty (TKA), which can lead to coronal-plane instability that requires surgical revision. Injured MCL can result in joint instability and polyethylene wear. Different strategies have been proposed for MCL reconstruction based on the location of the injury. However, there is a lack of clarity regarding the optimal method for handling an iatrogenic MCL injury throughout a TKA. Methods: A PRISMA flow diagram was used to guide the systematic literature review. An extensive search was conducted in PubMed, Embase, Scopus, Web of Science, and Google Scholar. Newcastle Ottawa scale checklist was used to assess the methodological quality of the articles. Results: A total of 19 qualitative studies, including non-cadaveric patients with MCL injury during TKA, were identified after analyzing the full text of the articles. All included studies were either retrospective, observational cohort or case series. A total of 486 patients were studied to gather information on the methods used to repair the MCL and their results. Most injuries arose in the tibial attachment, which surgeons mostly realized during the final stages of surgery. Used techniques can be categorized into three main groups: Primary repair, Repair with augmentation, and changing prosthesis characteristics. Conclusion: This systematic review demonstrated that the most popular management of iatrogenic MCL injury was using suture anchors, staples, screws and washers, and more constrained prostheses. The proper method should be decided considering the site of the MCL injury.

A narrative review on adverse drug reactions of COVID-19 treatments on the kidney.

Studies showed that the respiratory is not the only system affected by coronavirus 2, while cardiovascular, digestive, and nervous systems, as well as essential organs such as the kidneys, can be affected by this virus. In this review, we have studied the epidemiology, clinical, and laboratory findings on COVID-19 infection renal involvement, mortality, physiopathology, remaining renal sequels after recovery, underlying renal disease, and renal injury due to its treatment. Also, protective measures for kidney injury are explained in three levels. Evidence of viral particles and genome in the urine and renal tubular cells and signs of damage such as microangiopathy, hypercoagulopathy, and fibrosis are found in COVID-19 patients. The result of this study showed, in hospitalized COVID-19 patients, that the rate of acute kidney injury (AKI) was up to 46%, with a mortality ranging from 11 to 96%. A considerable proportion of patients with AKI would remain on renal replacement therapy. Proteinuria and hematuria are observed in 87 and 75% patients, and increased Cr and glomerular filtration rate (GFR) <60 ml/min per 1.73 m2 are observed in 29.6 and 35.3% of the patients, respectively. Remedsivir is considered to have adverse effects on GFR. COVID-19 patients need special attention to prevent AKI. Those with underlying chronic kidney disease or AKI need proper and explicit evaluation and treatment to improve their prognosis and decrease mortality, which should not be limited to the hospitalization period.

Excellent accuracy of magnetic resonance imaging for diagnosis of discoid meniscus tears: A systematic review and meta-analysis.

Purpose: The discoid meniscus (DM) is distinguished by its thickened, disc-shaped formation, which extends over the tibial plateau. The likelihood of developing osteoarthritis escalates if a DM tear remains undiagnosed and untreated. While DM tears can be diagnosed through arthroscopy, the high cost, invasive nature and limited availability of this procedure highlight the need for a better diagnostic modality. This study aims to determine the accuracy of magnetic resonance imaging (MRI) in diagnosing DM tears. Methods: A systematic review was conducted to gather articles with at least 10 cases on the comparison of MRI and arthroscopy as the gold standard for DM tear diagnosis. Stata and MetaDisc were used to conduct the statistical analysis. The quality of the included studies was evaluated using the Quality Assessment of Diagnostic Accuracy Studies-2 tool. Results: Five diagnostic performance studies, derived from four original research papers involving 305 patients, were evaluated. Based on the pooled data, the sensitivity, specificity, diagnostic odds ratio, positive limit of detection and negative limit of detection were found to be 0.87 (95% confidence interval [CI], 0.82-0.91) and 0.84 (95% CI, 0.75-0.90), 32.88 (95% CI, 5.81-186.02), 5.22 (95% CI, 1.71-15.92) and 0.18 (95% CI, 0.09-0.38), respectively. A hierarchical summary receiver operating characteristic curve with an area under the curve of 0.92 was generated. Conclusion: This meta-analysis demonstrates that MRI has excellent sensitivity and specificity for diagnosing DM tears. Despite its lower accuracy compared to arthroscopy, MRI can be used in symptomatic patients as a viable alternative to arthroscopy due to its inherent advantages. Level of Evidence: Level IV.

Unraveling the molecular and immunological landscape: Exploring signaling pathways in osteoporosis.

Osteoporosis, characterized by compromised bone density and microarchitecture, represents a significant global health challenge, particularly in aging populations. This comprehensive review delves into the intricate signaling pathways implicated in the pathogenesis of osteoporosis, providing valuable insights into the pivotal role of signal transduction in maintaining bone homeostasis. The exploration encompasses cellular signaling pathways such as Wnt, Notch, JAK/STAT, NF-κB, and TGF-ß, all of which play crucial roles in bone remodeling. The dysregulation of these pathways is a contributing factor to osteoporosis, necessitating a profound understanding of their complexities to unveil the molecular mechanisms underlying bone loss. The review highlights the pathological significance of disrupted signaling in osteoporosis, emphasizing how these deviations impact the functionality of osteoblasts and osteoclasts, ultimately resulting in heightened bone resorption and compromised bone formation. A nuanced analysis of the intricate crosstalk between these pathways is provided to underscore their relevance in the pathophysiology of osteoporosis. Furthermore, the study addresses some of the most crucial long non-coding RNAs (lncRNAs) associated with osteoporosis, adding an additional layer of academic depth to the exploration of immune system involvement in various types of osteoporosis. Finally, we propose that SKP1 can serve as a potential biomarker in osteoporosis.