Application of ultrasound in avoiding radial nerve injury during elbow arthroscopy: a retrospective follow-up study.

BACKGROUND: A safe and effective technique for anterolateral portal placement in elbow arthroscopy is significant. We compared the outcomes of patients who underwent elbow arthroscopy using different ultrasound-assisted techniques. METHODS: From May 2016 to June 2021 a retrospective analysis on all patients who underwent elbow arthroscopy in our department was performed. Patients were separated into three groups: non-ultrasound; preoperative ultrasound; and intraoperative ultrasound. The minimum follow-up period was 1 year. Nerve injuries, visual analog scale (VAS), Mayo elbow-performance score (MEPS), Disabilities of the Arm, Shoulder, and Hand Questionnaire (DASH), and range of motion (ROM) of the elbow were evaluated for comparison among the three groups pre- and post-operatively. RESULTS: All 55 patients completed a 1-year follow-up: non-ultrasound (n = 20); preoperative ultrasound (n = 17); and intraoperative ultrasound (n = 18). There were 3 cases (15.0%) of transient radial nerve palsy in the non-ultrasound group. No nerve complications occurred in preoperative ultrasound and intraoperative ultrasound groups. The probability of postoperative radial nerve injury in the three groups was statistically different (P < 0.05). There was no significant difference in the VAS score, MEPS, DASH score, and ROM among the three groups at the follow-up evaluation (P > 0.05). CONCLUSION: Performing anterolateral portal placement during elbow arthroscopy with ultrasound-assisted techniques successfully avoided radial nerve injury.

Endoscopic Ischial Tuberosity Osteophyte Resection for Treatment of Ischiofemoral Impingement: A Case Report.

ABSTRACT: Ischiofemoral impingement is a distinct pathologic finding with abnormal osseous contact between the ischium and the lesser trochanter of the femur. Lesser trochanter excision has been recommended for recalcitrant ischiofemoral impingement through an open or endoscopic approach; however, no study has included ischial tuberosity osteophyte resection and refixation of the hamstring tendon. We report an endoscopic procedure involving ischial tuberosity osteophyte resection with refixation of the partially detached hamstring insertion through a posterior approach in the prone position. Using this technique, it is easier to reach the lesion and less likely to injure the sciatic nerve. The postoperative pain score (visual analogy score) was significantly decreased, the modified Harris hip score increased from 39 preoperatively to 86 postoperatively, and there was no adverse effect on the hamstring tendon.

Arthroscopically assisted repair of the medial collateral ligament of the knee: A case report, description of a new technique.

Tears of the medial collateral ligament of the knee are common and often managed non-operatively [1]. Grade 3 tears that fail to heal are often treated with surgical repair through an open incision on the medial aspect of the knee. Many other ligament injuries of the knee are now managed with arthroscopic surgery. This has not yet been described for medial collateral ligament injuries of the knee. We describe a new arthroscopically assisted technique for MCL repair after grade III injury which avoids some of these complications.

Protective effects of naringin on glucocorticoid-induced osteoporosis through regulating the PI3K/Akt/mTOR signaling pathway.

OBJECTIVE: To investigate the protective effects of Naringin on glucocorticoid-induced osteoporosis (GIOP) through the PI3K/AKT/mTOR signaling pathway in vivo and in vitro. METHODS: Osteoblasts were cultured from the differentiated bone marrow mesenchymal stem cells (BM-MSCs) and were grouped as follows: the PBS group (the control group), the model group (Dexamethasone intervention), the LY294002 group (PI3K/AKT/mTOR pathway inhibitor intervention), the Naringin group (Naringin intervention), and the LY294002+ Naringin intervention group. Cell proliferation and differentiation were detected through cell counting kit-8 (CCK8) assay and alkaline phosphatase (ALP) staining, respectively. The formation of autophagosome was observed by Monodansylcadaverine (MDC) staining. Expressions of signaling pathway and autophagy related factors such as Beclin-1 and p62 were detected by qRT-PCR and western blot. Then, the rats were grouped as the PBS group (normal rats injected with PBS), the model group (GIOP rats injected with dexamethasone), the LY294002 group (GIOP rats injected with PI3K/AKT/mTOR pathway inhibitor LY294002), the Naringin group (GIOP rats injected with Naringin) and the LY294002+ Naringin group (GIOP rats injected with PI3K/AKT/mTOR pathway inhibitor LY294002 and Naringin). Bone mineral density and bone histomorphometry parameters of rats in each group were compared. In addition, the expressions of pathway and autophagy related factors in cartilage tissue of rats in each groups were also detected. RESULTS: The proliferation and differentiation abilities of osteoblasts were increased with an increasing concentration of Naringin in a dose-dependent manner. Compared with the model group, the expression of PI3K/AKT/mTOR pathway related phosphorylated proteins, the proliferation and differentiation abilities of osteoblasts, the expression of autophagosome and autophagy related factors were all increased in the Naringin group, but contrary results were found in the LY294002 group (all P<0.05). In vivo, GIOP rats had improved bone mineral density and bone morphology parameters , and elevated expressions of autophagy related factors in cartilage tissue compared to the model group through Naringin intervention, while LY294002 intervention showed the opposite effects (all P<0.05). What is more, LY294002 partially reversed the effects of Naringin on osteogenic differentiation and bone morphological parameters in GIOP. CONCLUSION: Naringin exerts protective effects in GIOP by the PI3K/AKT/mTOR pathway, which may be related to autophagy induction and enhanced proliferation of osteoblasts.

Impact of interleukin-6 gene polymorphisms and its interaction with obesity on osteoporosis risk in Chinese postmenopausal women.

AIMS: To investigate the association of four single-nucleotide polymorphisms (SNPs) of the IL-6 gene with osteoporosis (OST) susceptibility. METHODS: PCR restriction fragment length polymorphism (PCR-RFLP) was carried out for SNPs detection. Generalized multifactor dimensionality reduction (GMDR) model and logistic regression model were used to examine the interaction between SNP and obesity on OST. RESULTS: Logistic regression model revealed that G allele of rs1800796 and the T allele of rs2069849 were associated with increased OST risk, compared to those with wild genotype. However, no significant correlations were found when analyzing the association of rs1800795 and rs1554606 with OST risk. GMDR analysis suggested that the interaction model composed of the rs1800796 and obesity was the best model with statistical significance (P value from sign test [Psign] = 0.012), indicating a potential gene-environment interaction between rs1800796 and obesity. Overall, the two-locus models had a cross-validation consistency of 10/10 and had the testing accuracy of 0.641. We also conducted stratified analysis for rs1800796 genotype and obesity, and found that obese subjects with CG or GG genotype have the highest OST risk, compared to subjects with CC genotype, and normal BMI OR (95% CI) = 2.21 (1.52-3.49), after adjustment for age, smoke, and alcohol consumption status. CONCLUSIONS: Our results suggested that the C allele of rs1800796 and the C allele of rs2069849 of IL-6 gene interaction between rs1800796 and abdominal obesity were all associated with increased OST risk.

Colony-stimulating factor 1 receptor inhibition prevents against lipopolysaccharide -induced osteoporosis by inhibiting osteoclast formation.

Lipopolysaccharide (LPS) can induce bone loss by stimulating osteoclast formation. Colony-stimulating factor 1 receptor (CSF 1R) inhibitors have great potential for the treatment of rheumatoid arthritis and tumor-related bone erosion. However, its role in LPS-induced bone loss is still not clarified. In this study, we observed the effects of CSF 1R inhibitor, PLX3397, on LPS-induced bone damage in an animal model. The models were established by LPS administration in male Sprague-Dawley rats. PLX3397 (30 mg/kg body weight) was given by oral gavage. MicroCT analysis, biomechanical properties, biomarker assay, histological examination, and mRNA expression of osteoclast differentiation-related genes (Traf6, Fra1, c-fos and NFATc1) were performed on the 8th week. LPS induced bone loss was shown as the decrease in bone volume fraction and trabecular number and increase in trabecular separation (p < 0.05). LPS exposure also markedly decreased the bone biomechanical properties. PLX3397 significantly abolished the LPS-induced bone microstructure damage (p < 0.05) and loss of biomechanical properties. PLX3397 also inhibited the increases of serum tartrate-resistant acid phosphatase 5b level enhanced by LPS (p < 0.05). PLX3397 attenuated the high expression of Traf6, Fra1, c-fos and NFATc1 stimulated by LPS. Our data demonstrated that PLX3397, a type of CSF 1R inhibitor, can suppress LPS-induced bone loss via the inhibition osteoclast formation.

The effects of dihydroartemisinin on inflammatory bowel disease-related bone loss in a rat model.

Bone loss is one of the important extra-intestinal manifestations in patients with inflammatory bowel diseases (IBDs). Compounds derived from natural products have been used to treat IBDs. However, the role of natural products on IBD-induced bone loss is not completely clarified. In the present study, we observed the effects of dihydroartemisinin (DHA), an antimalaria drug, on IBD and IBD-induced bone loss in a rat model. Chronic IBD model was established in Sprague-Dawley rats by giving them 2.5% dextran sodium sulfate in drinking water. DHA was given by intraperitoneal injection. Blood, colon, and bone samples were collected for biomarker assay and histological analysis. There was an obvious increase in tumor necrotic factor (TNF) α and receptor activator of nuclear factor (NF)-kB ligand (RANKL), and decrease in procollagen type 1 N-terminal propeptide (P1NP) level in IBD groups compared with the normal control (p < 0.05). The disease activity score of IBD rats was significantly higher than the control (p < 0.01). Obvious decrease in disease activity score, TNFα, and RANKL level and increase in P1NP were observed in DHA-treated IBD rats. Bone loss, shown as the decrease in bone mineral density, bone volume fraction, and trabecular number and increase in trabecular separation were observed in IBD rats compared with control (p < 0.01). DHA treatment obviously abolished the bone loss, in particular in the high-dose group (p < 0.05). DHA treatment also inhibited the excessive osteoclast formation; RANKL protein expression; and RANK, TRAF6, Fra-1, NFATc1 mRNA expression induced by IBD. Our data indicated that DHA may be a potential therapeutic agent for IBD and IBD-induced bone loss. Impact statement Bone loss is one of the important extra-intestinal manifestations in patients with inflammatory bowel diseases (IBDs). Studies have shown that compounds derived from natural products are useful in the treatment of IBDs. However, few studies have investigated the role of compounds derived from natural products in treatment of osteoporosis in IBDs. The current study aimed to show the effects of dihydroartemisinin (DHA), antimalaria drug, on bone loss in a rat model of IBD. The findings showed that DHA intervention dose dependently protected against bone loss in IBD rats by inhibiting tumor necrotic factor α production and osteoclast formation. These findings highlights that DHA may be beneficial for bone health in those patients with IBD.

The use of red wristbands for allergy documentation in day case surgery.

In England over six million day case surgical procedures are performed each year. Many of these patients have an allergy and are given a red armband to notify staff of this. This audit compared the use of red armbands to indicate allergy at two institutions undertaking day case surgery. The presence of wristbands, the allergies recorded on them and the correlation to allergies documented in the patient notes were analysed.

Naringin protects against bone loss in steroid-treated inflammatory bowel disease in a rat model.

We observed the effects of naringin on bone loss in glucocorticoid-treated inflammatory bowel disease (IBD) in a rat model. The IBD model was established in Sprague-Dawley rats by administering 5.0% dextran sodium sulfate. Dexamethasone (DEX) and naringin were given at the second week. Blood, colon and bone samples were collected for biomarker assay, histological analysis or microCT analysis. Superoxide dismutase, catalase and malonaldehyde were measured in bone. A significant decrease of procollagen type 1 N-terminal propeptide (P1NP) level was observed in DEX-treated IBD groups compared with the control (p < 0.05). P1NP levels were dose-dependently increased in the presence of naringin intervention. Bone loss and decreased bone biomechanical properties were observed in DEX-treated IBD rats compared with control rats (p < 0.01). Naringin intervention protected against bone loss and decreased bone biomechanical properties. Bone formation related gene mRNA expressions were significantly decreased in DEX-treated IBD rats compared with control rats. Naringin administration reversed the down-regulation of the expressions of those genes. Naringin treatment reduced the oxidative stress in bone from DEX-treated IBD rats. Our data indicated that naringin may have great potential for the treatment of bone loss in glucocorticoid-treated IBD patients via blocking oxidative stress and promoting bone formation.