This study aimed to compare the efficacy of the proximal femoral bionic nail (PFBN), proximal femoral nail antirotation (PFNA), and InterTan in the treatment of intertrochanteric fractures. This network meta-analysis was conducted in accordance with the PRISMA 2020 statement and was registered in PROSPERO (CRD420216376949). PubMed, Embase, and Web of Science Core Collection were searched from inception to February 2026. Meta-analysis was performed using Stata 18.0 and R 4.6.0. A total of 29 studies involving 3173 patients were included, divided into three groups: PFNA, InterTan, and PFBN. There was no significant difference in surgical time or 12-month Harris score among the three surgeries in pairwise comparisons (95

Orthopedic degenerative diseases, including osteoarthritis (OA), intervertebral disc degeneration (IVDD), and osteoporosis (OP), are major causes of chronic pain and functional decline in aging populations worldwide. The senescence-associated secretory phenotype (SASP), a downstream but central effector of cellular senescence, has emerged as a key pathogenic mediator that links senescent cell accumulation to tissue degeneration in the musculoskeletal system. Comprising pro-inflammatory cytokines, chemokines, matrix-degrading enzymes, growth factors, and extracellular vesicle-associated signals, SASP disrupts orthopedic tissue homeostasis through several interconnected mechanisms, including chronic sterile inflammation, extracellular matrix (ECM) catabolism, paracrine senescence propagation, stem/progenitor cell dysfunction, and, in selected contexts, aberrant neurovascular remodeling. In this review, we focus on the tissue-specific roles of SASP in major orthopedic degenerative diseases and organize current evidence according to mechanism-to-disease and mechanism-to-therapy relationships. We further summarize mechanism-linked therapeutic strategies, including senolytics, senomorphics, autophagy-based interventions, and emerging gene-/RNA-targeted approaches, while distinguishing between established preclinical avenues and exploratory modalities. Finally, we highlight key barriers to clinical translation, including tissue heterogeneity, biomarker selection, delivery specificity, safety, and trial design, to provide a more clinically actionable framework for future mechanistic and translational research.

There are few studies on the association between nighttime sleep duration and sleep quality with low back pain (LBP) in the Chinese population. This study aimed to investigate the longitudinal associations between middle-aged and older adults in China. This study is a large-sample longitudinal cohort study and the data used in this study were from the China Health and Retirement Longitudinal Study (CHARLS) survey. Nighttime sleep duration was obtained from the self-reported of the participants and was divided into five groups of < 6 h, 6 to < 7 h, 7 to < 8 h, 8 to < 9 h, and ≥ 9 h. Sleep quality was defined as days of restless sleep during the past week and was divided into four groups of < 1 day, 1–2 days, 3–4 days, and 5–7 days. Multiple logistic regression models were used to analyze the relationship between nighttime sleep duration and sleep quality with LBP. Restricted cubic spline (RCS) was used to construct a dose-response relationship between nighttime sleep duration and LBP. A total of 11,233 participants were included in this study, and after 4 years of follow-up, the incidence of LBP was 9.51

Spinal degeneration, spinal deformity, and spinal cord injury (SCI) are classically managed as discrete biomechanical or neurological entities. However, emerging evidence reveals them as an interconnected pathological continuum. This mini-review introduces the “ferroptosis-mediated domino effect” as the core metabolic driver linking these conditions. The cascade initiates within the avascular intervertebral disc, where aberrant mechanotransduction (e.g., via Piezo1) provokes severe oxidative stress and subsequent ferroptosis, leading to extracellular matrix degradation and structural collapse. The ensuing spinal deformity chronically compresses the spinal microvasculature, disrupting the blood-spinal cord barrier (BSCB) and facilitating localized iron deposition. This chronic ischemic insult generates a metabolically “primed” spinal cord characterized by extreme vulnerability. Upon secondary acute trauma, the sudden influx of heme and labile iron ignites an uncontrollable “ferroptotic storm,” synergizing with neuroinflammation to drive irreversible neural loss. Finally, we evaluate cutting-edge translational interventions—including reactive oxygen species (ROS)-responsive nanoparticles and nanozyme-loaded hydrogels—that offer spatiotemporal precision to halt this pathological crosstalk. By dismantling disciplinary silos, this framework advocates for next-generation, dual-action therapeutic strategies that simultaneously restore biomechanical stability and mitigate metabolic collapse.

Intervertebral disc degeneration (IVDD) is a well-known major contributor to lower back pain and has become a significant challenge in the field of public health. Kaempferol (KAE) is a naturally occurring flavonoid compound found in various herbs and plant families, known for its potent anti-inflammatory and antioxidant pharmacological effects. Ferroptosis is a recently discovered form of cell death characterized by iron dependence and the uncontrollable accumulation of lipid peroxides. Studies have reported that the activity of nucleus pulposus (NP) cells in IVDD is influenced by ferroptosis, which is one of the contributing factors to IVDD. As of now, the therapeutic effects and mechanisms of KAE in IVDD remain unclear. To elucidate the therapeutic effects and potential mechanisms of KAE in IVDD, we established an in vitro NP cell degeneration model and found that KAE could delay the degeneration process of NP cells. Then we performed transcriptome sequencing and identified that ferroptosis and the p38 MAPK pathway might be potential targets through which KAE exerts its therapeutic effects. Further in vitro experiments revealed that KAE could inhibit ROS production, thereby suppressing the p38 MAPK pathway to delay the progression of NP cell ferroptosis, thus protecting NP cells from degeneration. We then used molecular docking to validate the tight binding of KAE to ferroptosis-related targets. Finally, we further confirmed the potential of KAE in protecting against IVDD in vivo. In summary, our study demonstrates that KAE may be a promising candidate drug for the treatment of IVDD.

Based on the theory of ″Qu-Zhi-Bu-Yi″, this study aimed to investigate the optimal compatibility ratio of Angelicae Pubescentis Radix and Taxilli Herba for preventing and treating pressure-induced human nucleus pulposus(NP) cell apoptosis, and to elucidate the mechanisms. A human NP cell apoptosis model was established using abnormal mechanical pressure at 1.0 MPa. The concentration ratios of quercetin, osthole, and columbianadin were screened by the orthogonal experimental design. Cell proliferation and apoptosis were determined using the cell counting kit-8(CCK-8) assay and Annexin V-APC/PI double staining, respectively. Western blot was performed to detect apoptosis-related proteins, as well as key protein expressions in the phosphatase and tensin homolog(PTEN)-induced putative kinase 1(PINK1)/Parkin-mediated mitophagy pathway, and the nuclear factor erythroid 2-related factor 2(Nrf2)-mediated antioxidant pathway. Mitochondrial ultrastructure was observed by transmission electron microscopy(TEM). Mitochondrial membrane potential was measured using the JC-1 staining. Oxidative stress markers were evaluated by the enzyme-linked immunosorbent assay(ELISA). Energy metabolism was quantified using colorimetry. Reactive oxygen species(ROS) levels were detected using the 2',7'-dichlorodihydrofluorescein diacetate(DCFH-DA) fluorescent probe. The Nrf2 overexpression and knockdown model construction efficacy in NP cells was validated by quantitative real-time polymerase chain reaction(qRT-PCR). Additionally, rescue experiments were designed to validate the mechanism of the above pathways. Based on the results, the optimal combination of quercetin at 50 μmol·L~(-1), osthole at 6.25 μmol·L~(-1), and columbianadin at 12.5 μmol·L~(-1) significantly promoted NP cell proliferation and inhibited apoptosis. The components enhanced mitophagy by activating the PINK1/Parkin pathway and alleviated oxidative stress by activating the Nrf2 pathway. Rescue experiments showed that the anti-apoptotic effects of the traditional Chinese medicine(TCM) components could be reversed by mitophagy inhibition and Nrf2 knockdown. In conclusion, the Angelicae Pubescentis Radix-Taxilli Herba components inhibit pressure-induced NP cell apoptosis by synergistically activating PINK1/Parkin-mediated mitophagy and Nrf2-mediated antioxidant response. These findings provide experimental evidence for intervertebral disc degeneration treatment.

Emerging evidence suggests a link between gut microbiota and intervertebral disc diseases (IDDs); however, the causal relationships remain unclear. This study aimed to evaluate the causal effects of gut microbiota on the risk of cervical disc disorders (CDD), other intervertebral disc disorders (OIDD), pyogenic intervertebral disc infections, and discitis, shedding light on the potential “gut-disc axis”. Genetic variation data for 202 gut microbiota taxa were obtained from the Dutch Microbiome Project, and disease outcome data were sourced from the FinnGen consortium. A Mendelian Randomization (MR) approach was employed to assess causal relationships, using genetic variants as instrumental variables. Sensitivity analyses, including tests for pleiotropy, heterogeneity, and reverse causation, ensured robust findings. The study identified 20 gut microbial taxa with significant associations to IDDs. Notably, taxa within the Erysipelotrichaceae family showed consistent protective effects against OIDD after Bonferroni correction (P < 0.05). Associations between several species and specific diseases, such as Alistipes senegalensis with CDD and Ruminococcus lactaris with discitis, were also observed. Sensitivity analyses confirmed no evidence of confounding or reverse causation. This study provides evidence of causal relationships between specific gut microbiota and IDDs, supporting the existence of a “gut-disc axis.” The findings suggest that microbial dysbiosis may influence spinal health through systemic inflammation and immune regulation. These insights open new possibilities for microbiota-targeted interventions, such as probiotics or dietary modifications, to prevent or manage IDDs. However, further research is required to validate these therapeutic strategies.

[This corrects the article DOI: 10.3389/fphar.2025.1619687.].

ETHNOPHARMACOLOGICAL RELEVANCE:Shenqi Yanshen Granule (SYG), a traditional Chinese medicine formulation, is clinically used for chronic kidney disease-mineral bone and disorder (CKD-MBD) by tonifying the kidney, activating blood, eliminating toxins, and dispelling turbidity. However, its mechanism remains unclear. AIM OF THE STUDY:This study aimed to elucidate the therapeutic mechanism of SYG in CKD-MBD using an integrated approach combining proteomics and bioinformatics. MATERIALS AND METHODS:Forty-four CKD-MBD patients were divided into a treatment group (TG, n = 23) receiving standard therapy plus SYG (30g, twice daily), or a control group (CG, n = 21) receiving standard therapy alone. A normal group (NG, n = 20) served as healthy controls. After 8 weeks, renal function, mineral-bone metabolism parameters, and bone mineral density (BMD) were evaluated. Plasma proteomics was used to identify potential targets, followed by network pharmacology, molecular docking, and dynamics simulations to predict bioactive compounds. Finally, RANKL-stimulated RAW264.7 cells were conducted to validate the therapeutic targets and bioactive compounds. RESULTS:After 8 weeks of treatment in a small cohort, preliminary improvements were observed in renal function (Scr, BUN), mineral-bone metabolism markers (Ca, iPTH, 25(OH)VD, b-ALP, β-CTX), and BMD in CKD-MBD patients. Plasma proteomics indicated that SYG downregulated PAK2 and CRKL within the MAPK pathway. Network pharmacology identified icariin as a constituent capable of binding both targets, which was supported by molecular docking and dynamics simulations showing stable complex formation under static and dynamic conditions. In vitro, both SYG and icariin significantly suppressed PAK2 and CRKL expression at mRNA and protein levels during RANKL-induced osteoclast differentiation in RAW264.7 cells. CONCLUSION:This study suggests that PAK2 and CRKL are potential therapeutic targets of SYG for ameliorating CKD-MBD, and icariin may be an important active ingredient. These findings provide a foundational mechanistic hypothesis that warrants further validation in larger-scale clinical trials.

Intervertebral disc degeneration (IVDD) is a prevalent condition contributing to various spinal disorders, posing a significant global health burden. Mitophagy plays a crucial role in maintaining mitochondrial quantity and quality and is closely associated with the onset and progression of IVDD. Well-documented region-specific mitophagy mechanisms in IVDD are guiding the development of therapeutic strategies. In the nucleus pulposus (NP), impaired mitochondria lead to apoptosis, oxidative stress, senescence, extracellular matrix degradation and synthesis, excessive autophagy, inflammation, mitochondrial instability, and pyroptosis, with key regulatory targets including AMPK, PGC-1α, SIRT1, SIRT3, Progerin, p65, Mfn2, FOXO3, NDUFA4L2, SLC39A7, ITGα5/β1, Nrf2, and NLRP3 inflammasome. In the annulus fibrosus (AF), mitochondrial damage induces apoptosis and oxidative stress mediated by PGC-1α, while in the cartilage endplate (CEP), mitochondrial dysfunction similarly triggers apoptosis and oxidative stress. These mechanistic insights highlight therapeutic strategies such as activating Parkin-dependent and Ub-independent mitophagy pathways for NP, enhancing Parkin-dependent mitophagy for AF, and targeting Parkin-mediated mitophagy for CEP. These strategies include the use of natural ingredients, hormonal modulation, gene editing technologies, targeted compounds, and manipulation of related proteins. This review summarizes the mechanisms of mitophagy in different regions of the intervertebral disc and highlights therapeutic approaches using mitophagy modulators to ameliorate IVDD. It discusses the complex mechanisms of mitophagy and underscores its potential as a therapeutic target. The objective is to provide valuable insights and a scientific basis for the development of mitochondrial-targeted drugs for anti-IVDD.

The aim of this study was to describe the technique of percutaneous paravertebral endoscopic decompression for the treatment of far-out syndrome and to analyze the early clinical results of this technique. From April 2021 to June 2023, a retrospective study was conducted on patients with far-out syndrome who underwent percutaneous paravertebral endoscopic decompression at Hospital of Chengdu University of Traditional Chinese Medicine. The Visual Analogue Scale (VAS), Oswestry Disability Index (ODI), and modified MacNab criteria were utilized for the assessment of leg pain, quality of life, and clinical efficacy, respectively. Clinical outcomes were assessed at the day before surgery, 1 day, 1 month, 3 months, 6 months after surgery, and the last follow-up. Meanwhile, the incidence rate of foraminal stenosis, surgery time, and complications were recorded for comprehensive evaluation. This study included a cohort of 16 patients, with a mean age at the time of surgery of 70.94 ± 4.04 years. The average duration of symptoms was 10.81 ± 5.13 months, while the mean follow-up period lasted for 16.69 ± 5.84 months. The results revealed significant improvements in VAS scores and ODI scores at each time point following the operation (P < 0.05). According to the modified MacNab criteria, excellent or good outcomes were observed in 15 cases (93.70

OBJECTIVE:To develop a predictive model for infection risk in elderly rheumatoid arthritis (RA) patients using laboratory markers, particularly erythrocyte sedimentation rate (ESR), albumin (ALB), and C-reactive protein (CRP). METHODS:This retrospective study included 452 elderly RA patients admitted to the Hospital of Chengdu University of Traditional Chinese Medicine between January 2021 and June 2024. The patients were randomly divided into a training group (271 patients) and a validation group (181 patients) at a 6:4 ratio. Key clinical and laboratory data were collected, including ESR, ALB, CRP, and others. Lasso regression and multivariable logistic regression were employed to identify infection-related factors. Model performance was evaluated using receiver operating characteristic (ROC) curves, calibration curves, and decision curve analysis (DCA). RESULTS:The study identified ALB<33.75 g/L, CRP≥32.75 mg/L, and ESR≥51.50 mm/h as independent risk factors for infection in elderly RA patients. A predictive model incorporating these three markers demonstrated high diagnostic accuracy, with an AUC of 0.909 in the training group and 0.880 in the validation group. DCA further confirmed the clinical utility of the model. CONCLUSIONS:This study successfully developed a predictive model combining ESR, ALB, and CRP to assess infection risk in elderly RA patients. This model has significant potential to enhance early infection detection and support clinical decision-making, offering a valuable tool for managing this vulnerable population.

BackgroundLumbar disc herniation (LDH) is a common disease, and most cases can be satisfactorily treated with conservative therapy. Chuzhen therapy, a non-surgical, non-pharmacological, and non-invasive therapy, can be performed at home, making it more acceptable to patients. However, evidence supporting the efficacy of this therapy for the treatment of acute LDH is limited.Case presentationWe report a 50-year-old male who presented with lower back pain, persistent radiating pain, and numbness in the lower extremities. Computed tomography (CT) imaging revealed a large right-sided protruding nucleus pulposus (PNP) at the L5/S1 level, compressing the nerve root. The patient experienced significant symptomatic relief after 1 month of outpatient Chuzhen therapy followed by 3 years of home-based Chuzhen therapy. Follow-up imaging conducted 3 years later showed a remarkable regression of the herniated nucleus pulposus, with a substantial 64.8% reduction in its size. Concurrently, the patient's LDH classification was downgraded from MSU3-AB to MSU2-A.ConclusionsWe report for the first time a case of LDH treated at home with Chuzhen therapy, which resulted in disc retraction. In this case, Chuzhen therapy was safe and effective as a monotherapy, but more conclusive and effective evidence is needed to elucidate its specific therapeutic mechanism.

Neck pain (NP) is a common musculoskeletal disorder that significantly diminishes patients' quality of life. While nonsteroidal anti-inflammatory drugs (NSAIDs) are frequently prescribed for neck pain management, their use can result in side effects, such as peptic ulcers. Consequently, non-pharmacological treatments like acupuncture and massage serve as effective alternatives. Chuzhen therapy, an adaptation of the traditional Chinese Nine Needles, is a non-invasive treatment that combines the therapeutic benefits of acupuncture and massage by stimulating meridians and acupoints through specific techniques. This approach provides a safe and effective option for neck pain treatment. This paper outlines a comprehensive method for Chuzhen therapy application in neck pain treatment, detailing acupoint selection, material preparation, treatment duration, procedural steps, and safety precautions. The Visual Analogue Scale (VAS), Neck Disability Index (NDI), and Short Form 36 Health Survey (SF-36) are employed as assessment tools to evaluate this method's efficacy. Findings demonstrate that Chuzhen therapy effectively alleviates neck pain, improves patients' quality of life, and does not produce adverse effects.

OBJECTIVE: To investigate the effect of pestle needle therapy(PNT) on the posterior cervical muscle(PCM) in a rabbit model of cervical spondylosis(CS) and explore the underlying mechanisms. METHODS: Rabbits were divided into control, CS models Ⅰ and Ⅱ(CS1 and CS2), electroacupuncture(EA), PNT Ⅰ and Ⅱ(PN1 and PN2), activator(AVT), and PNT combined with activator(C-AVT) groups. A long-term neck immobilization technique was used to establish a rabbit model of CS. Following completion of modeling, the EA group received electroacupuncture intervention, whereas the CS1, CS2, and C-AVT groups received PNT intervention. The AVT and C-AVT groups received local 740 Y-P injections into the PCM daily. The inflammatory injury to PCM was evaluated based on pain threshold, morphological changes, and interleukin(IL)-1β, IL-6, and tumor necrosis factor(TNF)-α levels. PCM fibrosis was evaluated by measuring the positive area(PA) of collagen fibrils(CFs) and collagen type 1 alpha 1(Col1α1) using Masson's and immunohistochemical staining. Terminal deoxynucleotidyl transferase-mediated d UTP nick-end labeling assay and transmission electron microscopy were used to identify apoptotic cells and assess autophagy, respectively. Western blotting was used to determine B-cell lymphoma-2(Bcl-2), Bcl-2 associated X protein(Bax), cysteine aspartate-specific protease(caspase)-3, sequestosome-1(P62), microtubuleassociated protein light chain 3(LC3-Ⅰ/Ⅱ), phosphatidylinositol 3-kinase(PI3K), protein kinase B(AKT), and mammalian target of rapamycin(mTOR) levels. Real-time quantitative polymerase chain reaction was used to determine mRNA expression levels of PI3K, AKT, mTOR, autophagy protein(ATG), and ATG7. RESULTS: PNT alleviated PCM cell degeneration and necrosis, inhibited inflammatory cell infiltration, decreased IL-1β, IL-6, and TNF-α levels, and decreased the PA of CFs and Col1α1. In the PN1 group, cell apoptosis in the PCM decreased, autophagy increased, Bcl-2 and LC3-Ⅱ/Ⅰ levels increased, Bax, Caspase-3, and P62 levels decreased, and the mRNA expression of ATG5 and ATG7 increased. PNT inhibits protein and mRNA expression of PI3K, AKT, and mTOR. Finally, the trend in the results of the rescue experiment was consistent with previous results. CONCLUSION: PNT inhibited apoptosis and promoted autophagy of PCM cells in CS rabbits and alleviated inflammation and fibrosis injury of PCM by inhibiting the PI3K/AKT/mTOR pathway.

Resumo Fundamento A osteoartrite é um tipo prevalente de artrite caracterizada por alterações degenerativas crônicas no sistema músculo-esquelético, que podem resultar em danos articulares e dor crônica. Objetivo Este estudo investigou as associações entre o índice de ativação e estresse endotelial (EASIX) e o aumento do risco de doença cardiovascular aterosclerótica (DCVA) e mortalidade por todas as causas entre pacientes diagnosticados com osteoartrite. Métodos O estudo de coorte abrangeu 2.028 indivíduos com idades entre 40 e 79 anos com osteoartrite, utilizando dados do banco de dados do National Health and Nutrition Examination Surveys (NHANES) abrangendo os anos de 2007 a 2018. O modelo de regressão logística ponderada univariada e o modelo de Cox ponderado foram estabelecidos, respectivamente, para rastrear possíveis fatores de confusão. Um nível de significância de p < 0,05 foi adotado para todas as análises estatísticas. Resultados O estudo revelou um risco elevado de DCVA em correlação com um log (EASIX) aumentado (razão de chances: 1,94, com intervalo de confiança de 95%: 1,57-2,41). Quando comparados a indivíduos com log (EASIX) < -1,29, aqueles com log (EASIX)>-0,78 demonstraram um risco aumentado de DCVA (razão de chances: 2,31, com intervalo de confiança de 95%: 1,68-3,18). Um valor de log (EASIX) mais alto também foi associado a um risco aumentado de mortalidade por todas as causas (razão de risco: 1,59, com intervalo de confiança de 95%: 1,14-2,23). Entre os indivíduos diagnosticados com osteoartrite, aqueles que apresentaram log (EASIX)>-0,78 apresentaram maior risco de morrer por qualquer causa, em comparação aos pacientes com log (EASIX) <-1,29. Conclusão A presença de um alto índice EASIX foi associada a um risco aumentado de DCVA e mortalidade por todas as causas entre pacientes com osteoartrite.

BACKGROUND:Osteoarthritis is a prevalent type of arthritis characterized by chronic degenerative changes in the musculoskeletal system, which can result in joint damage and chronic pain. OBJECTIVE:This study was to investigate the associations between the endothelial activation and stress index (EASIX) and the increased risk of atherosclerotic cardiovascular disease (ASCVD) and all-cause mortality among patients diagnosed with osteoarthritis. METHODS:The cohort study encompassed 2028 individuals aged 40-79 years with osteoarthritis, utilizing data from the National Health and Nutrition Examination Surveys (NHANES) database spanning the years 2007 to 2018. The univariate weighted logistic regression model and weighted Cox model were respectively established to screen possible confounders. A significance level of p < 0.05 was adopted for all statistical analyses. RESULTS:The study revealed an elevated risk of ASCVD in correlation with an increased log (EASIX) (Odds Ratio: 1.94, with 95% Confidence Interval:1.57-2.41). When compared to individuals with log (EASIX)< -1.29, those with a log (EASIX) > -0.78 demonstrated a heightened risk of ASCVD (Odds Ratio: 2.31, with 95% Confidence Interval:1.68-3.18). A higher log (EASIX) value was also linked to an increased risk of mortality from all causes (Hazard Ratio: 1.59, with 95% Confidence Interval:1.14 -2.23). Among individuals diagnosed with osteoarthritis, those exhibiting log (EASIX)> -0.78 faced a greater risk of dying from any cause, as compared to patients with log (EASIX) <-1.29. CONCLUSION:The presence of a high EASIX index was linked to an increased risk of ASCVD and all-cause mortality among patients with osteoarthritis.

Background Low back pain is the leading cause of productivity loss, imposes a significant economic burden on the patients and society. Oxidative stress is considered a critical factor in the complex pathophysiological process and pathogenic mechanism of low back pain. Adjustment dietary pattern can effectively increase antioxidant biomarkers levels within the body to reduce oxidative stress. The composite dietary antioxidant index (CDAI) serves a reliable scoring system for quantifying the potential dietary antioxidant capacity of daily diets. Objective We aim to investigate the potential association between CDAI and low back pain, in order to enhance the management of low back pain through dietary guidance. Methods This study included 17,682 participants from the National Health and Nutrition Examination Survey (NHANES) 1999–2000, 2001–2002, 2003–2004 and 2009–2010. The weighted logistic regression model was used to investigate the association between CDAI and low back pain, while restricted cubic spline (RCS) was employed to examine non-linear trend and cutoffs. Results After adjusting for all confounders, the results showed that there was no significant association between CDAI and low back pain. However, individuals in the highest quartile of CDAI exhibited an 11.7% less likelihood of experiencing a low back pain than those in the lowest quartile (OR = 0.883; 95% CI [0.787,0.991], P = 0.034), and the trend test was also significant (P for trend < 0.001). RCS indicated a linear relationship between CDAI and low back pain (P for non-linear = 0.876). Gender subgroup analysis showed that this negative association was significant in the female population (OR = 0.983; 95% CI [0.968, 0.998], P = 0.027), and females in the highest quartile of CDAI were 19.7% less likely to suffer low back pain than those in the lowest quartile (OR = 0.803; 95% CI [0.682,0.945], P = 0.008). Additionally, the changes in zinc (OR = 1.009; 95% CI [1.002, 1.016], P = 0.015) and selenium (OR = 0.379; 95% CI [0.164, 0.875], P = 0.023) per milligram were independently associated with low back pain. Conclusion The fully adjusted model showed no significant association between CDAI and low back pain, but it was significant in quartiles. Meanwhile, subgroup analysis by gender revealed a negative association between CDAI and low back pain in the female population. Additionally, the findings of this study also suggested that the antioxidant diets should be studied in a dietary pattern context.

Objective Glucocorticoid-induced osteoporosis (GIOP) represents a major complication arising from the long-term use of glucocorticoids, which are widely prescribed for various inflammatory and autoimmune conditions. Despite its prevalence, the current therapeutic options for GIOP are limited in terms of efficacy, safety profiles, and patient compliance. The Modified Danggui Buxue Decoction (DGBXD), a traditional Chinese herbal formulation, has shown promise in preliminary studies for its potential osteoprotective effects. The present study aimed to explore the mechanistic underpinnings of DGBXD’s action on GIOP using network pharmacology and molecular docking approaches, bridging traditional medicine with modern pharmacological insights. Method Network pharmacology is applied to screen drug-active compounds and potential core target proteins for disease treatment and to explore the drugs’ therapeutic mechanisms. Result Altogether, 78 DGBXD active compounds and 223 DGBXD-related, 146 component-disease common, and 2,168 GIOP-associated target genes were obtained. The PPI network had 43 nodes and 462 edges, and a total of 10 core target genes, including TP53, JUN and MAPK3, were identified. The results of the GO enrichment analysis implied that DGBXD might participate in biological activities, including responses to oxidative stress and nutrient levels. The outcomes of the KEGG pathway enrichment analysis showed that DGBXD may treat GIOP through TNF, IL-17, and phosphatidylinositol 3-kinase (PI3K)-Akt signaling pathways. Based on to the molecular docking results, biologically active compounds (beta-carotene, formononetin, luteolin, and isorhamnetin) exhibited good binding to AKT1 and ESR1. Conclusion DGBXD may aid in GIOP treatment by modulating multiple therapeutic targets and signaling pathways.