Low back pain (LBP) is a leading cause of labour loss and disability worldwide, and it also imposes a severe economic burden on patients and society. Among symptomatic LBP, approximately 40% is caused by intervertebral disc degeneration (IDD). IDD is the pathological basis of many spinal degenerative diseases such as disc herniation and spinal stenosis. Currently, the therapeutic approaches for IDD mainly include conservative treatment and surgical treatment, neither of which can solve the problem from the root by terminating the degenerative process of the intervertebral disc (IVD). Therefore, further exploring the pathogenic mechanisms of IDD and adopting targeted therapeutic strategies is one of the current research hotspots. Among the complex pathophysiological processes and pathogenic mechanisms of IDD, oxidative stress is considered as the main pathogenic factor. The delicate balance between reactive oxygen species (ROS) and antioxidants is essential for maintaining the normal function and survival of IVD cells. Excessive ROS levels can cause damage to macromolecules such as nucleic acids, lipids, and proteins of cells, affect normal cellular activities and functions, and ultimately lead to cell senescence or death. This review discusses the potential role of oxidative stress in IDD to further understand the pathophysiological processes and pathogenic mechanisms of IDD and provides potential therapeutic strategies for the treatment of IDD.

Intervertebral disc degeneration (IDD) is the primary cause of intervertebral disc (IVD) disease. With the increased ageing of society, an increasing number of patients are plagued by intervertebral disc disease. Ageing not only accelerates the decreased vitality and functional loss of intervertebral disc cells but also increases intracellular oxidative stress. Moreover, the speed of intervertebral disc ageing is also linked to high levels of reactive oxygen species (ROS) production. Not only is the production of ROS increased in ageing intervertebral disc cells, but antioxidant levels in degenerative intervertebral discs also decrease. In addition to the intervertebral disc, the structural components of the intervertebral disc matrix are vulnerable to oxidative damage. After chronic mitochondrial dysfunction, ROS can be produced in large quantities, while autophagy can eliminate these impaired mitochondria to reduce the production of ROS. Oxidative stress has a marked impact on the occurrence of IDD. In the future, IDD treatment is aiming to improve oxidative stress by regulating the redox balance in intervertebral disc cells. In summary, ageing and oxidative stress promote the degeneration of IVD, but further basic and clinical trials are needed to determine how to treat oxidative stress. At present, although there are many in-depth studies on the relationship between oxidative stress and degeneration of intervertebral disc cells, the specific mechanism has not been elucidated. In this paper, the main causes of intervertebral disc diseases are studied and summarized, and the impact of oxidative stress on intervertebral disc degeneration is studied.

Background: The incidence and prevalence of gout have been steadily increasing globally, which has resulted in gout research attracting consistently increased attention. This study aimed to visualize the knowledge structure and research trends in gout research through bibliometrics to help understand the future development of basic and clinical research.Methods: Articles and reviews on gout from 2001 to 2021 were extracted from the Web of Science Core Collection database. CiteSpace and VOSviewer software were used to visualize the knowledge network of countries, institutions, authors, references, and keywords in this field. SPSS and Microsoft Excel software were used for curve fitting and correlation analysis.Results: A total of 3,259 articles and reviews were included. The number of publications about gout significantly increased yearly. Publications were mainly concentrated in North America, Europe, Oceania, and East Asia. The USA contributed most with 1,025 publications, followed by China and New Zealand. After adjusting for publications by population size and Gross Domestic Product (GDP), New Zealand ranked in the first place. GDP and international collaboration were significantly correlated with scientific productivity for gout research. University of Auckland and Professor Dalbeth Nicola were the most prolific institutions and influential authors, respectively. Rheumatology was the most productive journal for gout research. Gout research hotspots have shifted over time in the following order: clinical features, pathological mechanisms, complications, gouty arthritis, epidemiology, and dual-energy computed tomography to drug clinical trials, which can be observed from the keyword analysis and co-cited reference cluster analysis.Conclusions: This study found that research on gout is flourishing. The development and experimentation of drugs for the prevention and treatment of gouty arthritis would be the focus of current research and developmental trends in future research.

Osteoporosis remains a clinical challenge. Teriparatide is an anabolic drug and alendronate is an antiresorptive agent; both are used in the treatment of osteoporosis. Comprehensive reviews investigating the comparative safety and efficacy of teriparatide versus alendronate are scarce. Therefore, we conducted a systematic review and meta-analysis of randomized controlled trials (RCTs) to evaluate the safety and efficacy of teriparatide versus alendronate for the treatment of postmenopausal osteoporosis. We conducted a comprehensive literature review of the PubMed, EMBASE, Cochrane Controlled Trials Registry, and the China Academic Journal Network Publishing databases for relevant RCTs of teriparatide versus alendronate in postmenopausal osteoporosis patients. Outcome measures were percentage change in lumbar spine and femoral neck bone mineral density (BMD) and incidence of vertebral and nonvertebral fractures. Effect size was reported as weighted mean differences (WMDs) for continuous outcomes and odds ratios (OR) for dichotomous outcomes, with associated 95% confidence intervals (CIs). Six trials involving 618 patients were included. The meta-analysis demonstrated a significant increase in lumbar spine BMD (WMD: 3.46, 95% CI: 2.15–4.77, P < .00001), but not femoral neck BMD (WMD = 1.50, 95% CI: 0.04–2.95, P = .04), in postmenopausal osteoporosis patients treated with teriparatide compared with alendronate for 6 to 18 months. These beneficial effects were apparent in the lumbar spine at 12 months of treatment (WMD: 4.49, 95% CI: 2.57–6.40, P < .01). Teriparatide was not superior to alendronate in reducing fracture risk (OR: −0.03, 95% CI: −0.12 to 0.07; P = .52). Teriparatide may be superior to alendronate for increasing lumbar spine BMD in postmenopausal osteoporosis. The efficacy and safety of long-term teriparatide and alendronate treatment in postmenopausal osteoporosis should be further investigated in clinical trials.

This study assessed the application of metagenomic next-generation sequencing in pathogen detection of periprosthetic joint infections. A total of 95 cases who previously had undergone hip and knee replacement undergoing revision from January 2018 to January 2021 were included in this study. Specimens of synovial fluid and deep-tissue were collected for culture and metagenomic next-generation sequencing, and patients were retrospectively categorized as infected or aseptic using the Musculoskeletal Infection Society criteria after revision surgery. The sensitivity, specificity, positive and negative predictive values were compared. A total of 36 cases had positive culture results and 59 cases had positive metagenomic next-generation sequencing results. Culture was positive in 34 infected cases (58.6%) and 2 aseptic cases (5.4%). Metagenomic next-generation sequencing was positive in 55 infected cases (94.8%) and 4 aseptic cases (10.8%). Five cases diagnosed with infection had other potential pathogens detected by metagenomic next-generation sequencing. Among the 24 culture-negative periprosthetic joint infections, metagenomic next-generation sequencing was able to identify potential pathogens in 21 cases (87.5%). From sampling to reporting, the average time needed for culture was 5.2 (95% CI 3.1–7.3) days, while that for metagenomic next-generation sequencing was 1.3 (95% CI 0.9–1.7) days. Metagenomic next-generation sequencing is more advantageous in pathogen detection of periprosthetic joint infection after total joint replacement, especially in patients with multiple infections or negative culture results.

Objective. To evaluate the association between neutrophil levels and all‐cause mortality in geriatric hip fractures. Methods. Elderly patients with hip fractures were screened between January 2015 and September 2019. Demographic and clinical characteristics of the patients were collected. Linear and nonlinear multivariate Cox regression models were used to identify the association between neutrophil levels and mortality. Analyses were performed using Empower Stats and R software. Results. A total of 2,589 patients were included in this study. The mean follow‐up period was 38.95 months. During the study period, 875 (33.80%) patients died due to various causes. Linear multivariate Cox regression models showed that neutrophil levels were associated with mortality after adjusting for confounding factors, when neutrophil concentration increased by 1∗10⁹/L, the mortality risk increased by 3% (HR = 1.03, 95% CI: 1.00–1.06, and P = 0210). Neutrophil concentration was used as a categorical variable; we only found statistically significant differences when neutrophil levels were high (HR = 1.27, 95% CI:1.05–1.52, and P = 0.0122). In addition, the results are stable in P for trend and propensity score matching sensitivity analysis. Conclusions. Neutrophil levels are associated with mortality in geriatric hip fractures and could be considered a predictor of death risk in the long‐term. This study is registered with the Chinese Clinical Trial Registry (ChiCTR) as number ChiCTR2200057323.