Does chronic low-dose aspirin use benefit bone health? A cross-sectional study on patients with type 2 diabetes mellitus.

INTRODUCTION: Numerous studies have reported the striking result that aspirin use is associated with higher bone mineral density (BMD), suggesting its potential as a population-wide osteoporosis prevention measure. Therefore, this study aimed to examine the impact of chronic low-dose aspirin use on bone remodeling biomarkers and BMD in an aging population. MATERIALS AND METHODS: Between September and November of 2019, clinical data regarding the medication use, serum bone remodeling biomarkers, and BMD of 567 consecutively hospitalized patients, a minimum of 50 years old with type 2 diabetes mellitus (T2DM), were collected. The cross-sectional associations between chronic low-dose aspirin use and serum concentrations of bone remodeling biomarkers and BMD were estimated separately using linear regression. Potential confounding variables were controlled for, including age, sex, and comorbidities. RESULTS: Low-dose aspirin users had significantly lower serum bone alkaline phosphatase (BAP) concentrations than non-users (82.44 ± 28.03 U/L vs 90.71 ± 32.79 U/L, p = 0.025). On the other hand, low-dose aspirin users had insignificantly higher vertebral BMD (0.95 ± 0.19 vs 0.91 ± 0.21, p = 0.185), femoral neck BMD (0.80 ± 0.15 vs 0.78 ± 0.17, p = 0.309) and Ward's triangle BMD (0.46 ± 0.14 vs 0.44 ± 0.13, p = 0.209), regardless of adjustment. CONCLUSIONS: This cross-sectional study demonstrated that chronic use of low-dose aspirin was associated with significantly lower serum concentrations of BAP in hospitalized patients with T2DM. The mechanism causing the insignificantly higher BMD observed in chronic aspirin users in this study and the significant increments in BMD reported in previous studies requires further clarification in other clinical trials.

Percutaneous cortical bone trajectory screw fixation versus traditional open pedicle screw fixation for type A thoracolumbar fractures without neurological deficit.

Retrospective matched-cohort comparative study. Cortical bone trajectory screw (CBT) technique is a new insertion technique in terms of fixation strength and less invasiveness. The purposes of this study were to compare the clinical and radiological outcomes of percutaneous CBT fixation (PCBT) with traditional open posterior pedicle screw fixation (OPPS) technique. Between September 2019 and October 2020, patients undergoing posterior stabilization were matched for age, sex, diagnosis, fractured level, and AO classification. 24 control patients with OPPS were identified and appropriately matched to 24 consecutive patients with PCBT technique. Clinical outcomes and radiographic assessments including vertebral wedge angle (VWA) and sagittal index were recorded and compared between the two groups. Incision length, intraoperative blood loss and hospital stay in the PCBT group were significantly better than the OPPS group (P < 0.05). The VAS scores 5 days after operation for PCBT patients were significantly lower than those for OPPS patients (P = 0.003), but these differences lost significance at last follow-up. There was no significant difference in VWA and sagittal index between OPPS and PCBT group (P > 0.05). While no complications were noted in the PCBT group, there were four cases with complications in the traditional OPPS group. The present study showed that PCBT is a safe and feasible method for the treatment of thoracolumbar fractures without neurological deficits. This new surgical treatment was more minimally invasive, yet yielded equivalent or superior clinical and radiographic outcomes compared to the traditional open pedicle screw fixation surgery.

Potential Adverse Effect of Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) on Bisphosphonate Efficacy: An Exploratory Post Hoc Analysis From a Randomized Controlled Trial of Clodronate.

Nonsteroidal anti-inflammatory drugs (NSAIDs) have been reported to have weak but beneficial effects on bone health, including fracture risk, but many epidemiological studies are likely confounded. We explored the relationship between NSAIDs and fracture risk in a post hoc analysis of a well-documented, randomized, placebo-controlled study of the bisphosphonate, clodronate, in which treatment reduced osteoporotic fracture risk by 23%. Concurrent medication use at baseline was used to identify those prescribed oral NSAIDs. Only verified, incident fractures were included in the analysis. A total of 1082 (20.8%) women reported use of NSAIDs at baseline. They were slightly, but significantly, younger (mean 79 versus 80 years, p = 0.004), heavier (mean 66.7 versus 64.7 kg, p < 0.001) than nonusers, with slightly higher femoral neck bone mineral density (FN-BMD, 0.66 versus 0.64 g/cm2 , p < 0.001). In an adjusted model, NSAID use was associated with a significant increase in osteoporotic fracture risk over the 3-year study period (hazard ratio [HR] 1.27; 95% confidence interval [CI], 1.01-1.62; p = 0.039). However, this increase in risk was not statistically significant in the placebo group (HR 1.11; 95% CI, 0.81-1.52). In women receiving clodronate, the effect of the bisphosphonate to reduce osteoporotic fracture risk was not observed in those receiving NSAIDs (HR 0.95; 95% CI, 0.65-1.41; p = 0.81) in contrast to those not using NSAIDs (HR 0.71; 95% CI, 0.58-0.89; p = 0.002). In a subset with hip BMD repeated at 3 years, BMD loss during clodronate therapy was greater in those women receiving NSAIDs than in nonusers (eg, total hip -2.75% versus -1.27%, p = 0.078; femoral neck -3.06% versus -1.12%, p = 0.028), and was not significantly different from that observed in women receiving placebo. The efficacy of the bisphosphonate, clodronate, to reduce fracture risk was largely negated in those receiving NSAIDs. Although the mechanism is unclear, this clinically significant observation requires exploration in studies of commonly used bisphosphonates. © 2022 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR).

[Effects of neurogenesin 1 gene on functional recovery of spinal cord injury in rats and its mechanism].

OBJECTIVE: To explore the effects of Neurogenesin 1 (Ng1) gene on functional recovery after spinal cord injury (SCI) and its mechanism. METHODS: Thirty-six rats (aging 4 months, weighing 230 g and being male or female), were randomly divided into two groups: experimental group (n=18) and control group (n=18). After spinal cord contusive injury at T10 level was made in all these rats using modified Allen's method, Ng1 recombinant plasmid and blank plasmid were transfected into the damaged areas of experimental group and control group respectively by Alzet pumps. At 1 day, 1 week, 2 weeks, 3 weeks, and 4 weeks after SCI, Basso-Beattle-Bresnahan (BBB) Rating Scale was used to observe the recovery of motor function. At 1 week after injury, the expressions of Ng1 mRNA and protein in injured spinal cord were detected by RT-PCR and Western blot techniques. And at 2 and 4 weeks, double immunofluorescence and histopathologic examinations were performed to study the proliferation of the adult endogenous neural stem cells and pathological change after SCI. RESULTS: At 1-4 weeks after SCI, the BBB scores in the experimental group was significantly higher than that in control group (P < 0.05), and at 4 weeks the BBB score of the experimental group (16.80 +/- 1.79) was significantly higher than that of the control group (9.60 +/- 1.67), (P < 0.01). RT-PCR and Western blot showed that the mRNA and protein expressions of Ng1 were observed in the experimental group and no expression was seen in the control group. Histologic observation showed that the morphology of spinal cord and neurons in the experimental group was better than that in the control group and was close to the normal tissue. The mean number of Nestin+/BrdU+ newborn endogenous neural stem cells in the experimental group was significantly more than that in control group (P < 0.05). CONCLUSION: Ng1 gene could promote the proliferation of endogenous neural stem cells and protect the injured neurons, which enhances the repair of the motor function after SCI.