Osteoporosis Research Articles

Comprehensive Overview - Outcomes and Challenges of Bariatric Surgery - Physical, Psychological and Nutritional Considerations

Obesity, defined by excessive and abnormal body fat accumulation, leads to various health conditions such as diabetes, cardiovascular diseases, and certain cancers, significantly affecting the health and increasing the risk of mortality. Bariatric surgery offers a treatment for severe obesity, with restrictive and malabsorptive methods like sleeve gastrectomy (SG), adjustable gastric banding (AGB), Roux-en-Y gastric bypass (RYGB), biliopancreatic diversion (BPD). While bariatric surgery is effective for weight loss and health improvement, it is not without complications. Postoperative challenges include surgical complications, bone loss, nutritional deficiencies and changes in metabolism. Post-bariatric surgery patients may face psychological challenges such as emotional dysregulation, eating disorders like loss of control eating or binge eating, and body image concerns related to excess skin. This article explores the various impacts of bariatric surgery, addressing both physical and psychological challenges. It emphasizes the importance of holistic patient care, considering both physical outcomes and mental health post-surgery, to ensure long-term success. Materials and methodsThe article is a result of the review of the scientific literature searched by keywords “bariatric surgery”, “negative outcomes”, “obesity’’ available in Pubmed database. This overview does not cover all possible postoperative complications in bariatric surgery, but focuses on selected issues important for a comprehensive strategy for managing obesity. Aim of the studyThe aim of the study is to review the various complications and long-term effects of bariatric surgery, with a particular focus on specific issues that are important for a holistic approach to obesity treatment.

PRKD2 as a novel target for targeting the diabetes–osteoporosis nexus

Diabetes mellitus (DM) and osteoporosis (OP) co-morbidity (DMOP) pose major health challenges owing to their complex pathophysiological interactions. The aim of this study was to identify and validate key genes implicated in the pathogenesis of both conditions. By employing the Mfuzz time-series gene clustering method combined with transcriptome sequencing of patient serum, we systematically delineated gene expression patterns during the transition from a healthy state through DM to DMOP. These findings were further validated using external datasets, and a series of functional enrichment analyses, gene set enrichment analyses, and immune cell infiltration studies were conducted. Our analyses revealed a distinct progression pattern from a normal state through DM to DMOP, characterized by dynamic gene expression changes. Notably, PRKD2 emerged as a significantly downregulated gene in DMOP, highlighting its crucial role in disease pathogenesis. Further analyses revealed the involvement of PRKD2 in key signaling pathways, especially the Wnt and IL-18 pathways, which are critical for bone and glucose metabolism. Validation in cellular and animal models confirmed the role of PRKD2 in apoptosis and bone metabolism, emphasizing its therapeutic potential. In conclusion, our findings establish PRKD2 as a pivotal molecule in DMOP, offering fresh insights into its mechanisms and affirming its value as a therapeutic target.

A case–control study based on the National Health and Nutrition Examination Survey to evaluate the effects of human papilloma virus on bone health in women

BackgroundHuman papillomavirus (HPV) infection and osteoporosis (OP) are global health concerns, with higher prevalence observed in women compared to men. However, the impact of HPV infection on bone health remains uncertain.MethodsThis case–control study utilized data from the National Health and Nutrition Examination Survey (NHANES). Comparable datasets were created using nearest neighbor propensity score matching (PSM) at a ratio of 1:1. The association between HPV infection and bone mineral density (BMD) was analyzed using the Welch two-sample t-test. Furthermore, linear mixed models were employed for validation purposes. Restricted cubic spline (RCS) analysis and Kendall’s tau-b tests were performed to explore the effect of different types of HPV infection on BMD.ResultsIndividuals with HPV infection (mean age 38.11 ± 11.32 years) had lower BMD in the femur and lumbar spine compared to uninfected individuals (mean age 37.92 ± 11.42 years). RCS analysis revealed that an increasing number of cooccurring HPV types in women was associated with lower BMD. Specifically, four HPV types were negatively associated with femur BMD, while 14 HPV types were negatively associated with lumbar spine BMD. Additionally, HPV types 53, 59, and 89 exhibited effects on both femur and lumbar spine BMD.ConclusionsHPV infection is associated with a decrease in BMD, and co-infection with multiple types of HPV implies even lower BMD. Appropriately designed trials are needed to determine if interventions targeted at preventing HPV infection can have a protective effect on BMD.

The Effect of Concavity Restoration on Glenohumeral Stability in a Glenoid Bone Loss Model: Comparing Distal Tibial Allograft Reconstruction to Classic Latarjet.

Distal tibial allograft (DTA) reconstruction for glenoid bone loss (GBL) has gained popularity. While recent studies have demonstrated that glenoid concavity is an important factor in native glenohumeral stability, there remains a paucity of data regarding concavity restoration during reconstructive procedures for GBL and its biomechanical effect. To compare the restoration of anterior glenohumeral stability and glenoid concavity after DTA and classic Latarjet procedures. Controlled laboratory study. Nine human cadaveric specimens (mean age, 62.2 years; range, 52-69 years) underwent pretesting computed tomography (CT) to assess native glenoid concavity as determined by the glenoid depth and bony shoulder stability ratio (BSSR). GBL was created so the DTA and Latarjet graft could restore 100% of the native glenoid width. The rotator cuff tendons were loaded, and anterior stability testing was performed using a KUKA robot to apply a controlled anterior force with the shoulder in 90° of abduction and neutral external rotation. A motion capture system recorded humeral head translation. The following conditions were tested: intact, soft tissue Bankart lesion; bone loss model with DTA reconstruction; classic Latarjet procedure without conjoint tendon loaded; and classic Latarjet procedure with conjoint tendon loaded (sling effect). All specimens underwent posttesting CT to measure the BSSR of the DTA and Latarjet reconstructions. A repeated-measures analysis of variance was performed to compare the BSSR and anterior translations between the DTA and Latarjet reconstructions. DTA produced greater concavity than the Latarjet procedure (BSSR: 0.45 vs 0.35; P < .001). There was no difference in anterior translation between the DTA and Latarjet procedures with the sling effect (5.1 mm vs 4.7 mm; P > .999). However, maximum anterior translation was decreased after the DTA procedure when compared with the Latarjet technique without the sling effect (5.1 mm vs 10.3 mm; P = .045). DTA produces a more concave reconstruction and decreased anterior translation compared with the flatter reconstruction produced by the classic Latarjet procedure without the sling effect. DTA and the classic Latarjet procedure with conjoint tendon loading, however, yielded equivalent reductions in anterior translation. Distal tibial allograft reconstruction is a biomechanically equivalent alternative to the classic Latarjet due to the restoration of glenoid concavity in addition to glenoid width. Surgeons should consider the role of concavity when addressing glenohumeral instability with bone loss.

Paracrine activity of Smurf1-silenced mesenchymal stem cells enhances bone regeneration and reduces bone loss in postmenopausal osteoporosis

BackgroundOsteoporosis (OP), characterized by reduced bone mass and mineral density, is a global metabolic disorder that severely impacts the quality of life in affected individuals. Although current pharmacological treatments are effective, their long-term use is often associated with adverse effects, highlighting the need for safer, more sustainable therapeutic strategies. This study investigates the pro-osteogenic and anti-resorptive potential of the secretome from Smurf1-silenced mesenchymal stem cells (MSCs) as a promising cell-free therapy for bone regeneration.MethodsConditioned media (CM) from Smurf1-silenced rat (rCM-Smur1) and human MSCs (hCM-Smurf1) was collected and analyzed. Pro-osteogenic potential was assessed by measuring in vitro mineralization in human and rat MSCs cultures. In vivo, studies were conducted using a rat ectopic bone formation model and a post-menopausal osteoporotic mouse model. Additionally, primary human osteoporotic MSCs were preconditioned with hCM-Smurf1, and their osteogenic capacity was compared to that induced by BMP2 treatment. Ex vivo, human bone explants were treated with hCM-Smurf1 to assess anti-resorptive effects. Proteomic analysis of the soluble and vesicular CM fractions identified key proteins involved in bone regeneration.ResultsCM from Smurf1-silenced MSCs significantly enhanced mineralization in vitro and bone formation in vivo. Preconditioning human osteoporotic MSCs with hCM-Smurf1 significantly increases in vitro mineralization, with levels comparable to those achieved with BMP2 treatment. Additionally, in ex vivo human bone cultures, treatment with hCM-Smurf1 significantly reduced RANKL expression without affecting OPG levels, indicating an anti-resorptive effect. In vivo, CM from Smurf1-silenced MSCs significantly increased bone formation in a rat ectopic model, and its local administration reduced trabecular bone loss by 50% in a post-menopausal osteoporotic mouse model after a single administration within just four weeks. Proteomic analysis revealed both soluble and vesicular fractions of hCM-Smurf1 were enriched with proteins essential for ossification and extracellular matrix organization, enhancing osteogenic differentiation.ConclusionsThe Smurf1-silenced MSCs' secretome shows potent osteogenic and anti-resorptive effects, significantly enhancing bone formation and reducing bone loss. This study provides compelling evidence for the therapeutic potential of Smurf1-silenced MSC-derived secretome as a non-toxic and targeted treatment for osteoporosis. These findings warrant further in vivo studies and clinical trials to validate its therapeutic efficacy and safety.

Effective Brief, Low-impact, High-intensity Osteogenic Loading in Postmenopausal Osteoporosis.

Osteoporosis is characterized by reduced bone mineral density (BMD) and disrupted microarchitecture estimated by trabecular bone score (TBS), resulting in increased bone fracture risk. "Osteostrong®" is a bone-strengthening system implementing 4 devices and incorporating brief (10-minute), weekly, low-impact, and high-intensity osteogenic loading exercises. We evaluated the efficacy of the Osteostrong® intervention in postmenopausal osteoporotic women. 147 postmenopausal osteoporotic women were separated into two groups: Group A comprised 74 women receiving Osteostrong® intervention (mean age 58.8 years, 56.6-61 years 95% CI), and was subdivided into G1 receiving no antiresorptive medication, and G2 on such medication. Group B comprised 73 women that received no Osteostrong® intervention (mean age 61.8 years, 59.4-64.1 95% CI) and was subdivided into G3 on no antiresorptive therapy, and G4 on such treatment. All participants underwent a physical examination and had an assessment for secondary osteoporosis. Dual-energy X-ray absorptiometry (DXA) examinations (Horizon W [S/N 300472M]) were performed at the time of trial inclusion and 12 months later. Statistically significant increases were observed in the following parameters: i) BMD of the lumbar spine (L1-L4) in G1(p=0.0039), G2(p<0.001), and G4(p=0.0059): ii) TBS in G2(p=0.0078): iii) BMD of the right femoral neck in G1(p=0.0382) and G4(p=0.032): iv) BMD of the left femoral neck G2(p=0.0089) and in G4(p=0.0498) and total femur in G2(p=0.0162). Osteostrong® improved BMD of the lumbar spine in women with osteoporosis both off and on antiresorptive treatment. Furthermore, Osteostrong® enhanced the effect of antiresorptive therapy on BMD and TBS of the spine, hip and femoral neck.

Identifying rare variants in genes related to bone phenotypes in a cohort of postmenopausal women.

We aimed to evaluate whether extreme values of bone mineral density (BMD) in a population-based cohort of postmenopausal women (BARCOS) could be determined by rare genetic variants in genes related to monogenic bone disorders. A panel of 127 genes related to different skeletal phenotypes was designed. Massive sequencing by targeted capture of these genes was performed in 104 DNA samples from those women of the BARCOS cohort that exhibited the highest (HZ group) and lowest (LZ group) LS Z-scores, ranging from + 0.70 to + 3.80 and from - 2.35 to - 4.26, respectively. 5'UTR, 3'UTR, splice region, missense, nonsense, and short indel variants with MAF < 0.01 were annotated with CADD version 1.6 and considered in the analysis. After filtering those variants with CADD > 25 and present only in one of the groups (either LZ or HZ), six variants were detected, most of which (5/6) were in the LZ group in TCIRG1, COL1A2, SEC24D, LRP4, and ANO5 genes, while only one, in the LMNA gene, was in the HZ group. According to the ClinVar database, the COL1A2 variant, causative of a recessive form of osteogenesis imperfecta, is described as pathogenic, while the other variants are considered of uncertain significance (VUS). The variant identified in COL1A2 in a woman from the LZ group highlights the genetic overlap between monogenic diseases such as osteogenesis imperfecta and complex diseases like osteoporosis. However, the other variants were not clearly associated with the extreme BMD, suggesting that there is little contribution of rare variants to postmenopausal osteoporosis.

Clinical risk factors caused by third molar levelling following extraction of a mandibular second molar.

Mandibular second molar (MdM2) is often lost, and its space is filled with a bridge or implant. MdM2 extraction followed by orthodontic treatment protracting mandibular third molar (MdM3) towards the MdM2 position may overcome the missing of MdM2. The objectives of our study were to describe the outcome of the procedure and examined clinical risk factors such as external apical root resorption (EARR) and alveolar bone loss (ABL), as the indicators of poor orthodontic treatment outcomes. This retrospective study included 70 cases in 56 patients who received orthodontic treatment at Tokyo Medical and Dental University Hospital between 2007 and 2018. Multi-bracket appliances were used in all patients for MdM3 protraction. Using linear mixed effects models, EARR and ABL were regressed on various factors, including panoramic and cephalometric variables. With the mean treatment duration of 1040.4 ± 441.8 days, MdM2 space closure was achieved in 92.8% (65 cases). The ANB angle (P = .023) and the use of temporary anchorage devices (TADs) (P = .021) were significantly associated with the greater EARR, while the mandibular plane angle (P = .033) was associated with the greater ABL. MdM3 protraction using the fixed appliances resulted in the closure of MdM2 space in > 90% of cases without evident root resorption. There is a possibility of residual confounding due to the nature of observational study. Orthodontic treatment of MdM3 protraction may be a feasible strategy to close the space of the missing MdM2.

FoxA1 knockdown promotes BMSC osteogenesis in part by activating the ERK1/2 signaling pathway and preventing ovariectomy-induced bone loss

The influence of deep learning in the medical and molecular biology sectors is swiftly growing and holds the potential to improve numerous crucial domains. Osteoporosis is a significant global health issue, and the current treatment options are highly restricted. Transplanting genetically engineered MSCs has been acknowledged as a highly promising therapy for osteoporosis. We utilized a random walk-based technique to discern genes associated with ossification. The osteogenic value of these genes was assessed on the basis of information found in published scientific literature. GO enrichment analysis of these genes was performed to determine if they were enriched in any certain function. Immunohistochemical and western blot techniques were used to identify and measure protein expression. The expression of genes involved in osteogenic differentiation was examined via qRT‒PCR. Lentiviral transfection was utilized to suppress the expression of the FOXA1 gene in hBMSCs. An in vivo mouse model of ovariectomy was created, and radiographic examination was conducted to confirm the impact of FOXA1 knockdown on osteoporosis. The osteogenic score of each gene was calculated by assessing its similarity to osteo-specific genes. The majority of the genes with the highest rankings were linked with osteogenic differentiation, indicating that our approach is useful for identifying genes associated with ossification. GO enrichment analysis revealed that these pathways are enriched primarily in bone-related processes. FOXA1 is a crucial transcription factor that controls the process of osteogenic differentiation, as indicated by similarity analysis. FOXA1 was significantly increased in those with osteoporosis. Downregulation of FOXA1 markedly augmented the expression of osteoblast-specific genes and proteins, activated the ERK1/2 signaling pathway, intensified ALP activity, and promoted mineral deposition. In addition, excessive expression of FOXA1 significantly reduced ALP activity and mineral deposits. Using a mouse model in which the ovaries were surgically removed, researchers reported that suppressing the FOXA1 gene in bone marrow stem cells (BMSCs) prevented the loss of bone density caused by ovariectomy. This finding was confirmed by analyzing the bone structure via micro-CT. Furthermore, our approach can distinguish genes that exhibit osteogenic differentiation characteristics. This ability can aid in the identification of novel genes associated with osteogenic differentiation, which can be utilized in the treatment of osteoporosis. Computational and laboratory evidence indicates that reducing the expression of FOXA1 enhances the process of bone formation in bone marrow-derived mesenchymal stem cells (BMSCs) and may serve as a promising approach to prevent osteoporosis.

Association between lipid accumulation products and mortality outcomes in patients with osteoporosis and osteopenia.

Osteoporosis (OP) and osteopenia are metabolic bone disorders associated with increased fragility and fracture risk. While lipid accumulation products (LAP) are emerging as potential markers of metabolic health, their prognostic significance in patients with OP or osteopenia remains unclear. The objective of this study is to elucidate the relationship between lipid accumulation products (LAP) and all-cause as well as cardiovascular mortality in individuals diagnosed with either condition. Data from the 2007-2018 National Health and Nutrition Examination Survey (NHANES) were retrospectively analyzed. Kaplan-Meier survival curves, multivariable Cox proportional hazards regression, and restricted cubic spline plots were used to evaluate the association between LAP and mortality outcomes in patients with OP or osteopenia. Subgroup and threshold analyses were also conducted. This study included 4959 patients diagnosed with OP or osteopenia, followed over a comprehensive duration of 12years, during which 800 instances of all-cause mortality and 194 deaths attributed to cardiovascular diseases were documented. A linear negative correlation was identified between LAP and both all-cause and cardiovascular mortality among patients with OP or osteopenia. Notably, at an LAP level of 3.69, the risk ratio reached 1, indicating a transition in mortality risk from high to low. Subgroup analyses revealed a more pronounced association between LAP and mortality. Our study revealed a significant linear negative correlation between the lipid accumulation product (LAP) and both all-cause and cardiovascular mortality in patients diagnosed with osteoporosis (OP) and osteopenia.

UTE MRI technical developments and applications in osteoporosis: a review

Osteoporosis (OP) is a metabolic bone disease that affects more than 10 million people in the USA and leads to over two million fractures every year. The disease results in serious long-term disability and death in a large number of patients. Bone mineral density (BMD) measurement is the current standard in assessing fracture risk; however, the majority of fractures cannot be explained by BMD alone. Bone is a composite material of mineral, organic matrix, and water. While bone mineral provides stiffness and strength, collagen provides ductility and the ability to absorb energy before fracturing, and water provides viscoelasticity and poroelasticity. These bone components are arranged in a complex hierarchical structure. Both material composition and physical structure contribute to the unique strength of bone. The contribution of mineral to bone’s mechanical properties has dominated scientific thinking for decades, partly because collagen and water are inaccessible using X-ray based techniques. Accurate evaluation of bone requires information about its components (mineral, collagen, water) and structure (cortical porosity, trabecular microstructure), which are all important in maintaining the mechanical integrity of bone. Magnetic resonance imaging (MRI) is routinely used to diagnose soft tissue diseases, but bone is “invisible” with clinical MRI due to its short transverse relaxation time. This review article discusses using ultrashort echo time (UTE) sequences to evaluate bone composition and structure. Both morphological and quantitative UTE MRI techniques are introduced. Their applications in osteoporosis are also briefly discussed. These UTE-MRI advancements hold great potential for improving the diagnosis and management of osteoporosis and other metabolic bone diseases by providing a more comprehensive assessment of bone quantity and quality.

Melatonin alleviates senile osteoporosis by regulating autophagy and enhancing fracture healing in aged mice.

In our previous research, we have found that melatonin (MEL) affects the osteoporotic process. By balancing bone remoulding, autophagy is involved in age-related bone loss. However, as a regulator of autophagy, whether MEL influences senile osteoporosis via regulating autophagy remains unclear. Cellular, radiological, and histopathological evaluations were performed on 36 16-month-old male C57BL6/L mice or aged bone marrow-derived mesenchymal stem cells. A MEL-gelatin methacrylamide system was constructed to aid osteoporotic fracture healing. In this study, we found that bone loss, low level of MEL, and decreased autophagy coexisted in aged C57BL6/L mice. A physiological (low, 10 nM but not 100 nM) concentration of MEL restored bone loss, transformed the cytokine framework, and increased the autophagic level in aged mice, whereas inhibition of autophagy unfavourably reduced the positive effects of MEL on bone mass. The autophagy-conducted increased osteogenic lineage commitment and extracellular matrix mineralization, but not matrix synthesis of aged bone marrow-derived mesenchymal stem cells, was responsible for MEL anabolic effects on bone. PIK3C-AKT-MTOR signal was tested to be a main pathway that is involved in MEL-induced autophagy. Our data suggest that the application of MEL can restore degenerative osteogenesis of aged bone marrow-derived mesenchymal stem cells, and has the potential to regain bone mass in aged mice through activating autophagy via the PIK3C-AKT-MTOR pathway. MEL therefore may serve as a potential clinical therapy to treat senile osteoporosis.

Vertical and horizontal bone loss following alveolar socket preservation using bone grafts and autologous platelet concentrates vs bone grafts alone: a systematic review and meta-analysis

BackgroundSocket preservation is a proactive approach that limits bone loss after tooth extraction to maintain adequate bone volume, height and width. Many methods have proven effective in achieving socket preservation, including using various bone grafts and autologous platelet concentrates (APCs). Combining these two methods may lead to improved results in socket preservation and patient outcomes.AimsTo compare the combined use of APCs and bone grafts in socket preservation, with the use of bone grafts alone. Primary outcomes were radiographic vertical bone loss (VBL) and horizontal bone loss (HBL).MethodsA search on Pubmed, Scopus, Embase and Google Scholar databases was conducted to identify human studies using APCs in extraction sockets between January 2014 and August 2024. The inclusion criteria involved comparative human studies ranging from evidence levels II to III (Oxford Centre for Evidence-Based Medicine Levels of Evidence). For assessing bias in the included studies, the Cochrane Risk of Bias tools were used. The Grading of Recommendations Assessment, Development, and Evaluation (GRADE) approach was used to determine the quality of evidence available.ResultsA total of five randomised controlled trials (RCTs) were included in the analysis. Studies included the use of platelet rich fibrin (PRF), injectable platelet rich fibrin (i-PRF), advanced platelet rich fibrin (A-PRF), advanced platelet rich fibrin plus (A-PRF+) and concentrated growth factors (CGF). The risk of bias was judged high and moderate for two out of five RCTs. The analysis revealed a combined effect size for VBL reduction, with a standardized mean difference (SMD) of −0.83 (p < 0.001; 95% confidence interval (CI) = [−1.2, −0.57]; I² = 73.13%). For HBL reduction, the combined effect size was SMD = −0.72 (p < 0.001; 95% CI = [−1.08, −0.37]; I² = 68.34%). The overall evidence quality rating for the use of APCs in combination with bone grafts to reduce VBL during socket preservation was assessed as moderate, whereas to reduce HBL it was determined to be low.ConclusionThe current literature demonstrates the added benefits of APCs combined with bone grafts in alveolar socket preservation compared to bone grafts alone in reducing vertical and horizontal bone loss. However, based on the GRADE assessment, the quality of evidence was judged low-to-moderate. Further randomised clinical studies would increase the certainty of the evidence.

Opportunistic osteoporosis screening in intraoperative CT can accurately identify patients with low volumetric bone mineral density and osteoporosis during spine surgery.

To evaluate the accuracy of opportunistic measurements of volumetric bone mineral density (vBMD) in intraoperative multi-detector CT (MDCT) scans, using preoperative MDCT as the reference. This retrospective, single-center study included 105 patients (mean age: 73 ± 12.6 years, 53 women) who underwent spine surgery for various indications. All patients had preoperative MDCT with/without intravenous contrast and unenhanced intraoperative scans. VBMD of thoracolumbar vertebrae was automatically extracted using a convolutional neural network (CNN)-based framework with asynchronous calibration and contrast-phase correction. Vertebrae affected by artifacts, fractures, or severe degenerations were excluded. Root-mean-square errors (RMSEs) for associations between pair-wise vertebrae from preoperative and intraoperative vBMD values were calculated in linear regression models. Mean bias and 95%-limits of agreement (LOA) were calculated in Bland-Altman plots. Strong associations between preoperative and intraoperative vBMD values were observed in the thoracic (R2 = 0.94) and lumbar spine (R2 = 0.96). Intraoperative vBMD values showed high accuracy in reference to preoperative measurements with a mean bias of -1.3mg/cm3 for the thoracic spine (LOA: -18.7 to 16.1mg/cm3) and - 3.0mg/cm3 for the lumbar spine (LOA: -17.4 to 11.3mg/cm3). RMSEs between preoperative and intraoperative vBMD values slightly increased for contrast-enhanced scans (RMSEthoracic: 8.42 vs. 10.1mg/cm3; RMSElumbar: 7.75 vs. 8.87mg/cm3). Opportunistic osteoporosis screening with the presented approach is feasible and demonstrates high accuracy in reference to preoperative MDCT scans. This could enable the identification of patients with low bone mass during surgery, allowing surgeons to take measures (e.g., adapted techniques) that prevent postoperative complications and improve patient outcomes.

Anti-aging chitosan/gelatin film crosslinked by α-arbutin for bone regeneration by free radical scavenging to prevent osteoblast senescence

Osteoblasts play a critical role in maintaining bone homeostasis. Senescence causes by free radical-mediated oxidative stress may affect the viability and osteogenic differentiation potential of osteoblast during bone formation. To eliminate the impacts of senescent cells by free radical scavenging is an optimal option for bone regeneration in age-related bone disease, such as osteoporosis (OP) and periodontitis. In this study, we fabricated an antioxidant film (CG-ARB) by crosslinking chitosan (C) and gelatin (G) usingα-Arbutin (ARB) as a crosslinker. The morphological, physicochemical, and radical scavenging characteristics of the films were investigated. Its antioxidative ability to prevent osteoblast senescence for restoration of osteogenic differentiation was analyzedin vitro. A Sprague-Dawley rat model with critical size calvarial defect was used to evaluate the bone regeneration and biosafetyin vivo. The results demonstrated that CG-ARB formed a dense fiber membrane, allowing for the gradual and sustained release of ARB for at least 10 d. ARB exerted antioxidant effect that prevented osteoblast senescencein vitroand promote bone healingin vivo. Furthermore, CG-ARB did not cause hemolysis or organ toxicity, and was therefore, considered biosafe. These results indicated that CG-ARB film could be an ideal drug delivery system for sustained released of ARB in bone defect repair.

Assessing AI-Enhanced Learning in Bone Loss Detection among Dental Students.

Assessing AI-Enhanced Learning in Bone Loss Detection among Dental Students.

Dental implants in solid organ transplant recipients: A systematic review and meta-analysis.

It remains to be determined whether dental implantation treatment in solid organ transplant (SOT) recipients and non-organ transplant patients yields similar clinical outcomes. This review summarizes related data for existing cases and presents a meta-analysis of the outcomes of dental implants in SOT recipients and non-organ transplant patients. An electronic literature search was conducted in the PubMed, Web of Sciences, Cochrane Library and China National Knowledge Infrastructure databases covering articles published from inception to December 2024. This study was performed in accordance with the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines and was designed based on the Population, Intervention, Comparison, Outcome and Study design (PICOS) framework. The risk of bias was evaluated using the Joanna Briggs Institute (JBI) Critical Appraisal Checklist or the Newcastle-Ottawa Scale (NOS). The certainty of findings was assessed using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) criteria. Meta-analysis was performed using a fixed effects model to estimate the combined performance measures and 95% confidence intervals for the implant survival rate, marginal bone loss (MBL), and probing depth (PD). A total of 12 articles were included in the systematic review. The implant survival rate of 290 implants in 110 SOT recipients was 99.3%. The meta-analysis of four case-control studies revealed no significant differences in the implant survival rate and PD between SOT recipients and non-organ transplant patients (P=0.45 and P=0.49, respectively), while there was slightly less MBL in SOT recipients (P=0.02), possibly caused by confounding factors and bias. Organ transplantation does not impair implant survival in the short and mid-long term. Dental implantation can serve as a treatment option for tooth loss in SOT recipients.

Association between serum hemoglobin level and bone mineral density in adults: Iranian multi-center osteoporosis study (IMOS).

Previous studies have investigated the relationship between hemoglobin (Hb) levels and bone mineral density (BMD) with controversial findings. This study aimed to evaluate this association using data from the 4th Iranian Multicenter Osteoporosis Study (IMOS), a population-based national survey, including a population sample aged 50 years and older. The present study was conducted as a cross-sectional data analysis derived from the fourth round of the IMOS. Demographic information, Hb levels, and BMD measurements were collected. BMD was measured with dual-energy X-ray absorptiometry (DXA). Low BMD (osteopenia/osteoporosis) and osteoporosis were defined as a T-score less than -1 and less than -2.5 at each site including hip, femoral neck, or lumbar spine, respectively. Multiple linear regression analysis was used to assess the relationship between Hb levels and BMD. This study included 1,426 participants (54.2% female) with the mean age of 62.6 ± 8.0 years. The mean Hb levels among patients with or without osteoporosis were 12.9 ± 2.0 mg/dl and 13.1 ± 1.9 mg/dl, respectively (p-value = 0.08). It was demonstrated a positive relationship between Hb levels and BMD at hip (β = 0.0079, 95% CI: 0.002- 0.0135, p-value = 0.006) and femoral neck (β = 0.0064, 95% CI: 0.0015- 0.0113, p-value = 0.01) in only men. However, there was no significant correlation between Hb levels with low BMD and osteoporosis in either gender. Our findings showed a favorable relationship between Hb levels and BMD at the hip and femoral neck, particularly in men. This highlights gender and site-specific distinctions between hematological and skeletal health..Future studies should unravel these possible associations and investigate the underlying mechanisms.

Jingui Shenqi Wan alleviates bone loss induced by primary osteoporosis by inhibiting osteoblast pyroptosis

ObjectiveThe primary objective of this study was to elucidate the underlying pharmacological mechanisms by which Jingui Shenqi Wan (JGSQW) alleviates postmenopausal osteoporosis (PMOP). Through a systematic investigation, we sought to identify the specific molecular pathways through which JGSQW modulates the progression of PMOP, thereby providing a scientific basis for its clinical application.MethodsWe established an ovariectomized (OVX) mouse model to simulate estrogen deficiency-induced PMOP. Initially, micro-CT imaging and Alcian blue hematoxylin/orange G (ABH/OG) staining were employed to assess the effects of JGSQW on bone microarchitecture and bone mass preservation. Immunohistochemistry (IHC) was then utilized to evaluate the expression of osteogenic markers, including Osterix (OSX), Runx2, and Osteopontin (OPN). Additionally, Tartrate - Resistant Acid Phosphatase (TRAP) staining was performed to visualize and quantify osteoclasts. We further investigated the potential role of JGSQW in modulating the pyroptosis pathway.ResultsJGSQW effectively alleviates the destruction of bone microstructure and the loss of bone mass caused by estrogen deficiency, an effect that appears to be mediated by promoting osteogenesis. Additionally, JGSQW significantly downregulates the expression of GSDMD in osteoblasts and mitigates the abnormal release of inflammatory factors, thereby maintaining the normal functional activities of osteoblasts.ConclusionJGSQW may effectively mitigate the progression of estrogen deficiency-induced PMOP by inhibiting the dysregulated activation of osteoblast pyroptosis.

The skeletal abnormalities and their clinical challenges in SATB2-Associated Syndrome

Abstract SATB2-Associated Syndrome (SAS) is an autosomal dominant genetic disorder caused by pathogenic variations in the special AT-rich sequence-binding protein 2 (SATB2) gene. In addition to neurodevelopmental and craniofacial defects, over 90% of patients with SAS manifest biochemical and/or radiographic skeletal abnormalities, and around one third of patients report clinical and/or radiographic fractures. SATB2 protein is a potent transcription factor that promotes osteoblast differentiation and maturation; loss-of-function pathogenic variations of the SATB2 gene result in a wide spectrum of skeletal abnormalities ranging from gross skeletal anomalies to abnormal bone turnover markers, low bone mineral density, and recurrent fractures. There is at present no known effective treatment for bone health in patients with SAS. We present an adult patient with SAS who has recurrent fractures despite long-term treatment with antiresorptive agents. We propose an alternative pharmacotherapy approach utilizing a PTH analogue to stimulate osteoblasts, hence addressing the underlying pathophysiology of bone disease in patients with SAS.