Diagnostic value of magnetic resonance imaging for patients with periprosthetic joint infection: a systematic review.

PURPOSE: The purpose of this study was to provide a critical systematic review of the role of magnetic resonance imaging (MRI) as a noninvasive method to assess periprosthetic joint infections (PJIs). METHODS: The electronic databases PubMed and EMBASE were searched, since their inception up to March 27, 2022. The included studies evaluated the reproducibility and accuracy of MRI features to diagnose PJIs. The article quality assessment was conducted by the COnsensus-based Standards for the selection of health Measurement INstruments (COSMIN) and Quality Assessment of Diagnostic Accuracy Studies-2 (QUADAS-2). RESULTS: Among 1909 studies identified in the initial search, 8 studies were eligible for final systematic review. The included studies evaluated the reproducibility and accuracy of MRI features to diagnose PJIs. Seven of 8 studies showed good to excellent reliability, but only one article among them in which accuracy was evaluated had a low risk of bias. The intraclass correlation coefficient (ICC) and Cohen coefficient (κ) varied between 0.44 and 1.00. The accuracy varied between 63.9% and 94.4%. Potential MRI features, such as lamellated hyperintense synovitis, edema, fluid collection, or lymphadenopathy, might be valuable for diagnosing PJIs. CONCLUSION: The quality of the evidence regarding the role of MRI for PJIs diagnosis was low. There is preliminary evidence that MRI has a noteworthy value of distinguishing suspected periprosthetic joint infection in patients with total knee arthroplasty or total hip arthroplasty, but the definition of specific MRI features related to PJIs diagnosis lacks consensus and standardization. Large-scale studies with robust quality were required to help make better clinical decisions in the future.

Surgical interventions for symptomatic knee osteoarthritis: a network meta-analysis of randomized control trials.

BACKGROUND: Multiple surgical interventions exist for the treatment of symptomatic knee osteoarthritis, but the surgeon and patient may often have difficulty deciding which interventions are the best option. METHODS: We conducted a systematic review to identify randomized clinical trials (RCTs) that compared complications, revisions, reoperations, and functional outcomes among TKA (total knee arthroplasty), UKA (unicompartmental knee arthroplasty), HTO (high tibial osteotomy), BCA (bicompartmental knee arthroplasty), BIU (bi-unicompartmental knee arthroplasty), and KJD (knee joint distraction). The PubMed, Embase, and Cochrane databases were reviewed for all studies comparing two or more surgical interventions. Direct-comparison meta-analysis and network meta-analysis (NMA) were performed to combine direct and indirect evidence. The risk of bias was assessed using the revised Cochrane risk of bias tool for RCTs. RESULTS: This NMA and systematic review included 21 studies (17 RCTs), with a total of 1749 patients. The overall risk-of-bias assessment of the RCTs revealed that 7 studies had low risk, 5 had some concerns, and 9 had high risk. SUCRA (the surface under the cumulative ranking curve) rankings revealed that KJD had the greatest risk of appearing postoperative complications, revisions, and reoperations, and UKA or TKA had the lowest risk. The majority of comparisons among various treatments showed no difference for functional outcomes. CONCLUSION: Each surgical intervention is noninferior to other treatments in functional outcomes, but UKA and TKA are better options to treat OA according to SUCRA rankings by comparing complications, revisions, and reoperations. KJD is an imperfect option for treating OA. Other treatments should be carefully considered for each patient in accordance with their actual conditions. However, this conclusion is limited by the selection of reviewed publications and individual variation of surgical indications for patients. TRIAL REGISTRATION: This study was registered with Research Registry (reviewregistry1395).

Prenatal diagnosis of anomalous origin of one pulmonary artery branch by two-dimensional echocardiography: summary of 12 cases.

OBJECTIVES: To improve the prenatal diagnosis for anomalous origin of pulmonary artery branches by comparing and analyzing different types of fetal echocardiography features. METHODS: Between June 2012 and December 2018, fetal echocardiographic features were analyzed retrospectively from fetuses with a prenatal diagnosis of anomalous origin of pulmonary artery branch. The main points of identification were summarized. RESULTS: A total of 12 fetuses were diagnosed, including anomalous origin of a pulmonary artery branch from the innominate artery and six cases with unilateral absence of pulmonary artery. The shared characteristic sonographic finding was the lack of confluence at the bifurcation of the main pulmonary artery. The differences between the two conditions are highlighted by the origin of the anomalous vessel. In fetuses with anomalous origin of one pulmonary artery branch, the affected pulmonary artery arose from the posterior wall of the ascending aorta as noted on three vessels and trachea view as well as the long axis of the left ventricular outflow tract. This is in contrast to fetuses with unilateral absence of pulmonary artery, where the origin of affected pulmonary artery arises from the base of the innominate artery via the ipsilateral patent arterial duct as evident on the three vessels and trachea view and the coronal view of innominate (brachiocephalic) artery. CONCLUSION: (1) The main similarity is an absence of a confluence at the bifurcation of the main pulmonary artery. (2) The main distinguishing feature is the origin of the anomalous vessel from either the subclavian or directly from the aorta.

Serum Fibrinogen Test Performs Well for the Diagnosis of Periprosthetic Joint Infection.

BACKGROUND: Serum fibrinogen (FIB) is an acute-phase glycoprotein in the infection response that may stop excessive bleeding. The purposes of this study are to determine the value of FIB that can be used to differentiate between periprosthetic joint infection (PJI) and aseptic loosening of the prosthesis, and to determine the clinical significance of FIB for analyzing infection outcomes after first-stage surgery. METHODS: This retrospective study included 90 patients undergoing total knee arthroplasty or total hip arthroplasty revision from January 2015 to August 2019. PJI was confirmed in 53 patients (group A), and the other 37 patients were diagnosed with aseptic loosening of the prosthesis (group B). Only 21 patients in group A documented the results for serum FIB, C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR) after spacer insertion, so the postoperative serological marker levels of the these patients were also assessed. RESULTS: The FIB, CRP, and ESR levels were significantly higher in group A than in group B (P < .001). The area under the receiver operating characteristic curve was highest for FIB at 0.928. Analyses of FIB levels revealed a sensitivity of 79.25% and a specificity of 94.59%. FIB levels were significantly lower in patients with PJI after spacer insertion (P < .001). CONCLUSION: FIB is an adequate test to aid in diagnosing PJI, and it is not inferior to CRP and ESR in distinguishing between PJI and aseptic loosening of the prosthesis. It is an especially useful tool in assessing infection outcomes after first-stage surgery.

Prenatal Diagnosis of Aortopulmonary Window by 2-Dimensional Echocardiography: Summary of 8 Cases.

Aortopulmonary window (APW) is a rare congenital heart anomaly. A total of 8 cases with APW confirmed by echocardiography and surgery were retrospectively reviewed and the echocardiographic features analyzed. Among the 8 APW cases, 5 were type II and 3 were type III, the latter of which includes 2 cases complicated with Berry syndrome. Prenatal echocardiography can provide accurate information for the diagnosis of fetal APW. The prognosis depends on the timing of surgery and the nature of the associated cardiac anomalies.

Fluid shear stress suppresses TNF-α-induced apoptosis in MC3T3-E1 cells: Involvement of ERK5-AKT-FoxO3a-Bim/FasL signaling pathways.

TNF-α is known to induce osteoblasts apoptosis, whereas mechanical stimulation has been shown to enhance osteoblast survival. In the present study, we found that mechanical stimulation in the form of fluid shear stress (FSS) suppresses TNF-α induced apoptosis in MC3T3-E1 cells. Extracellular signal-regulated kinase 5 (ERK5) is a member of the mitogen-activated protein kinase (MAPK) family that has been implicated in cell survival. We also demonstrated that FSS imposed by flow chamber in vitro leads to a markedly activation of ERK5, which was shown to be protective against TNF-α-induced apoptosis, whereas the transfection of siRNA against ERK5 (ERK5-siRNA) reversed the FSS-medicated anti-apoptotic effects. An initial FSS-mediated activation of ERK5 that phosphorylates AKT to increase its activity, and a following forkhead box O 3a (FoxO3a) was phosphorylated by activated AKT. Phosphorylated FoxO3a is sequestered in the cytoplasm, and prevents it from translocating to nucleus where it can increase the expression of FasL and Bim. The inhibition of AKT-FoxO3a signalings by a PI3K (PI3-kinase)/AKT inhibitor (LY294002) or the transfection of ERK5-siRNA led to the nuclear translocation of non-phosphorylated FoxO3a, and increased the protein expression of FasL and Bim. In addition, the activation of caspase-3 by TNF-α was significantly inhibited by aforementioned FSS-medicated mechanisms. In brief, the activation of ERK5-AKT-FoxO3a signaling pathways by FSS resulted in a decreased expression of FasL and Bim and an inhibition of caspase-3 activation, which exerts a protective effect that prevents osteoblasts from apoptosis.

Fluid shear stress promotes osteoblast proliferation via the Gαq-ERK5 signaling pathway.

Fluid shear stress (FSS) is a ubiquitous mechanical stimulus that potently promotes osteoblast proliferation. Previously, we reported that extracellular signal-regulated kinase 5 (ERK5) is essential for FSS-induced osteoblast proliferation. However, the precise mechanism by which FSS promotes osteoblast proliferation via ERK5 activation is poorly understood. The aim of this study was to determine the critical role of Gαq in FSS-induced ERK5 phosphorylation and osteoblast proliferation, as well as the downstream targets of the Gαq-ERK5 pathway. MC3T3-E1 cells were transfected with 50 nM Gαq siRNA, treated with 5 mM XMD8-92 (a highly selective inhibitor of ERK5 activity), and/or exposed to FSS (12 dyn/cm(2)). Cell proliferation was evaluated using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The protein expression levels of Gαq, P-ERK5, ERK5, Cyclin B1, and CDK1 were analyzed by Western blot. Physiological FSS exposure for 60 min remarkably promoted MC3T3-E1 cell proliferation, however, this effect was suppressed by siRNA-mediated Gαq knockdown or inhibition of ERK5 activity by XMD8-92 treatment, suggesting that Gαq and ERK5 might modulate FSS-increased osteoblast proliferation. Furthermore, ERK5 phosphorylation was dramatically inhibited by Gαq siRNA. In addition, our study further revealed that FSS treatment of MC3T3-E1 cells for 60 min markedly upregulated the protein expression levels of Cyclin B1 and CDK1, and this increased expression was predominantly blocked by Gαq siRNA or XMD8-92 treatment. We propose that FSS acts on the Gαq-ERK5 signaling pathway to upregulate Cyclin B1 and CDK1 expression, thereby resulting in MC3T3-E1 cell proliferation. Thus, the Gαq-ERK5 signaling pathway may provide useful information regarding the treatment of bone metabolic disease.

Fluid shear stress inhibits TNF-α-induced osteoblast apoptosis via ERK5 signaling pathway.

Fluid shear stress (FSS) is a potent mechanical stimulus and prevents cells from TNF-a-induced apoptosis. Recently, Extracellular-signal-regulated kinase 5 (ERK5) has been found to be involved in regulation of cell survival. However, little is known about the role of ERK5 signaling pathway in FSS-mediated anti-apoptotic effects in osteoblast. In this study, we show that FSS blocks TNF-a-induced apoptosis of MC3T3-E1 cells via ERK5 signaling pathway. We found that physiological FSS for 1 h significantly decreased TNF-α-induced MC3T3-E1 cells apoptosis. After inhibition of ERK5 activity by XMD8-92, a highly-selective inhibitor of ERK5 activity, the ability of FSS to inhibit TNF-α induced apoptosis was significantly decreased. Analysis of anti-apoptotic mechanisms indicated that exposure of MC3T3-E1 cells to FSS for 1 h increased phosphorylation of Bad and inhibited caspase-3 activity. After treatment with XMD8-92, phosphorylation of Bad by FSS was significantly blocked, but caspase-3 activity was increased. In summary, these findings indicated that FSS inhibits TNF-α-mediated signaling events in osteoblast by a mechanism dependent on activation of ERK5, and Bad is a crucial downstream target for ERK5. Those results implied that ERK5 signaling pathway play a crucial role in FSS-mediated anti-apoptotic effect in osteoblast. Thus, ERK5 signaling pathway may be a new drug treatment target of osteoporosis and related bone-wasting diseases.

Trans-interlamina percutaneous endoscopic cervical discectomy for symptomatic cervical spondylotic radiculopathy using the new Delta system.

To describe the rationale and surgical technique and compare the clinical effect of posterior percutaneous endoscopic cervical discectomy (PPECD) using the Delta system versus that of conventional PPECD (key-hole) surgery for the treatment of symptomatic cervical spondylotic radiculopathy (CSR). A retrospective analysis was performed on 106 single-segment CSR patients between February 2016 and February 2017, 50 of whom underwent conventional PPECD (key-hole), and 56 underwent PPECD using the Delta system. The operative time, intraoperative blood loss, intraoperative complications and postoperative hospital stay were recorded, and the clinical effect was evaluated by the indicators of the Neck Disability Index (NDI), arm-visual analog scale (arm-VAS), neck-VAS, EQ-5D and MacNab classification at the last follow-up. All patients underwent the operation successfully, and 106 patients were followed up. The operative time of the Delta group was 60.47 ± 0.71 min, while the operative time of the key-hole group was 75.46 ± 0.41 min. The difference between the two groups was statistically significant (P < 0.05). However, there was no significant difference between the two groups in terms of blood loss and hospital stay (P > 0.05). The VAS, NDI and EQ-5D scores of the neck and upper limbs in the two groups were significantly better than those before surgery at 1 week after surgery and at the last follow-up (P < 0.05). However, there was no significant difference between the two groups at the last follow-up (P > 0.05). At the last follow-up, there was no significant difference between the two surgical methods when evaluated using the modified MacNab criteria. The imaging results showed that the herniated disc was removed completely and the nerve root was decompressed. The complication rate in the Delta group (3/56, 5.35%) was significantly lower than that in the conventional key-hole group (5/50, 10.0%). PPECD using the Delta system for CSR may be a feasible and promising alternative surgical plan. Compared with the traditional key-hole method, this surgical system can not only provide the surgeon with a larger surgical field of vision but also reduces the operation time and complication rates.

Endogenous hydrogen sulfide regulates pulmonary artery collagen remodeling in rats with high pulmonary blood flow.

The mechanisms responsible for the structural remodeling of pulmonary vasculature induced by increased pulmonary blood flow are not fully understood. This study explores the effect of endogenous hydrogen sulfide (H2S), a novel gasotransmitter, on collagen remodeling of the pulmonary artery in rats with high pulmonary blood flow. Thirty-two Sprague-Dawley rats were randomly divided into sham, shunt, sham+PPG (D,L-propargylglycine, an inhibitor of cystathionine-gamma-lyase), and shunt+PPG groups. After 4 weeks of shunting, the relative medial thickness (RMT) of pulmonary arteries and H2S concentration in lung tissues were investigated. Collagen I and collagen III were evaluated by hydroxyproline assay, sirius-red staining, and immunohistochemistry. Pulmonary artery matrix metalloproteinase-13 (MMP-13), tissue inhibitor of metalloproteinase-1 (TIMP-1), and connective tissue growth factor (CTGF) were evaluated by immunohistochemistry. After 4 weeks of aortocaval shunting, resulting in an elevation of lung tissue H2S to 116.4%, rats exhibited collagen remodeling and increased CTGF expression in the pulmonary arteries. Compared with those of the shunt group, lung tissue H2S production was lowered by 23.4%, RMT of the pulmonary artery further increased by 39.5%, pulmonary artery collagen accumulation became obvious, and pulmonary artery CTGF expression elevated (P<0.01) in the shunted rats treated with PPG. However, pulmonary artery MMP-13 and TIMP-1 expressions decreased significantly in rats of shunt+PPG group (P<0.01). This study suggests that endogenous H2S exerts an important regulatory effect on pulmonary collagen remodeling induced by high pulmonary blood flow.

Dysfunction of myocardial sarcoplasmic reticulum in rats with myocardial calcification.

We investigated the relationship between cardiac dysfunction and Ca2+ transport in the myocardial sarcoplasmic reticulum (SR) during the pathogenesis of cardiovascular calcification in rats. The possible mechanism of SR dysfunction was explored by detecting the alteration of the nitric oxide/nitric oxide synthase (NO/NOS) pathway in the SR. Using the vitamin D plus nicotine (VDN treatment for 2 week and 6 week) experimental model of cardiac calcification, cardiac function and sarcoplasmic reticulum function were measured. Inhibition of cardiac functions in vivo (peak rate of contraction and peak rate of relaxation, P < 0.05 or P < 0.01) were observed in all calcification groups, simultaneously, Ca2+ release and uptake in the SR as well as the Ca2+ release channel and Ca2+ pump activity were inhibited. Myocardial Ca2+ concentration and cardiac and SR dysfunction were inversely related (P < 0.05). The specific NO/NOS pathway (NO production, NOS activity and nNOS expression in the SR) was upregulated in the SR and associated with calcification (both 2- and 6 week VDN groups). These results indicate that cardiac dysfunction associated with myocardial calcification might be mediated by SR dysfunction, which may result from an impaired SR-specific NO/NOS pathway.

Changes in arterial hydrogen sulfide (H(2)S) content during septic shock and endotoxin shock in rats.

OBJECTIVES: To explore the changes of hydrogen sulfide (H(2)S) in vascular tissues of rats with septic shock and endotoxin shock and its possible pathophysiological implication. METHODS: Rat models of septic shock induced by cecal ligation and puncture and of endotoxic shock induced by injection of endotoxin were used in this study. The authors measured hymodynamic variations, metabolic data, H(2)S and nitric oxide (NO) contents of different arteries in rats with septic shock and endotoxic shock. RESULTS: The results showed that hemodynamic parameters including the heart rate (HR), the mean arterial pressure (BP), and the +dP/dt max decreased markedly, while the left ventricular end-diastolic pressure (LVEDP) increased significantly and the rats developed hypoglycemia and lactic acidosis. Arterial H(2)S contents were significantly increased (P<0.01) in both septic and endotoxic shock (P<0.01). Endogenous H(2)S and NO contents all negatively correlated with BP, cardiac function and the degree of hypoglycemia (P<0.01). CONCLUSIONS: The results of our study demonstrated that endogenous vascular H(2)S increased in rats with septic shock and endotoxic shock. It was suggested that endogenous H(2)S was involved in physiological and pathophysiological process during shock.

The possible role of hydrogen sulfide as a smooth muscle cell proliferation inhibitor in rat cultured cells.

Hydrogen sulfide (H(2)S) was recently suggested to be a possible endogenous gasotransmitter in physiological concentration. For the purpose of understanding its possible role in the regulation of the cardiovascular system, we explored the potential effect of H(2)S on the proliferation of cultured aortic vascular smooth muscle cells (VSMCs) of rats and mitrogen-activated protein kinase (MAPK) as a signaling transduction pathway. Vascular smooth muscle cells were cultured in vitro and the cells were divided into six groups: (1). control group, (2). serum group, (3). endothelin group, (4). NaHS group, (5). serum + NaHS group, and (6). endothelin + NaHS group. VSMC proliferation was measured by [(3)H]thymidine ([(3)H]TdR) incorporation and MAPK activity in the VSMCs was determined by radioactivity assay. The results showed that endothelin-1 increased VSMC [(3)H]TdR incorporation 2.39-fold ( P << 0.01) and MAPK activity 1.62-fold ( P << 0.01), as compared with controls. Hydrogen sulfide at 5 x 10(-5) mol/l, 1 x 10(-4) mol/l, and 5 x 10(-4) mol/l decreased VSMC [(3)H]TdR incorporation by 16.8%, 26.60%, and 37.40%, respectively, and reduced MAPK activity by 7.37% ( P >> 0.05), 23.39%, and 33.57%, respectively ( P << 0.01). The results demonstrated that H(2)S could dose-dependently suppress the proliferation of VSMCs through the MAPK pathway.