Bone Fracture Risk Research Articles

Trunk-to-leg-volume ratio is not associated with bone density or fracture risk in middle-aged adults: results from the National Health and Nutrition Examination Survey.

Body mass index (BMI) and waist circumference (WC) are commonly used to predict bone health, which is typically assessed via bone mineral density (BMD). Trunk-to-leg-volume ratio (TLVR), a relatively novel measure, predicts cardiometabolic outcomes, but its relationships with BMD and fracture remain unstudied. This study evaluated these anthropometric measures' associations with BMD and fracture in Americans aged 40-60years. Analyses of middle-aged adults from the 2013-2014 to 2017-2018 National Health and Nutrition Examination Survey were conducted. Whole-body, dual-energy X-ray absorptiometry was used to quantify TLVR as well as BMD at the lumbar spine, while a femur-specific scan was used to quantify femoral neck BMD. Fracture history was self-reported. Linear and logistic regression models were constructed with age, diabetes, smoking, race/ethnicity, education, and physical activity as confounding variables. TLVR was generally not associated with BMD, while WC and BMI showed positive associations with femoral neck BMD. Odds of osteopenia/osteoporosis at the femoral neck were ~ 65-80% lower among participants in the highest tertile of BMI and WC versus the lowest (p < 0.001). There were no statistically significant associations between anthropometric predictors and fracture. Women in tertiles 2 or 3 of TLVR (p = 0.097 and 0.079, respectively) did have 2.66 times the odds of wrist fracture than women in tertile 1, but this was not significant. As shown in previous research, BMI and WC show positive associations with femoral BMD. In contrast, the more novel anthropometric marker TLVR shows no association with femoral BMD, and no clear association with fracture.

A novel non-invasive method for predicting bone mineral density and fracture risk using demographic and anthropometric measures

Fractures are costly to treat and can significantly increase morbidity. Although dual-energy x-ray absorptiometry (DEXA) is used to screen at risk people with low bone mineral density (BMD), not all areas have access to one. We sought to create a readily accessible, inexpensive, high-throughput prediction tool for BMD that may identify people at risk of fracture for further evaluation. Anthropometric and demographic data were collected from 492 volunteers (♂275, ♀217; [44 ​± ​20] years; Body Mass Index (BMI) = [27.6 ​± ​6.0] kg/m2) in addition to total body bone mineral content (BMC, kg) and BMD measurements of the spine, pelvis, arms, legs and total body. Multiple-linear-regression with step-wise removal was used to develop a two-step prediction model for BMC followed by BMC. Model selection was determined by the highest adjusted R2, lowest error of estimate, and lowest level of variance inflation (α ​= ​0.05). Height (HTcm), age (years), sexm=1, f=0, %body fat (%fat), fat free mass (FFMkg), fat mass (FMkg), leg length (LLcm), shoulder width (SHWDTHcm), trunk length (TRNKLcm), and pelvis width (PWDTHcm) were observed to be significant predictors in the following two-step model (p ​< ​0.05). Step1: BMC (kg) = (0.006 3 × HT) ​+ ​(−0.002 4 × AGE) ​+ ​(0.171 2 × SEXm=1, f=0) ​+ ​(0.031 4 × FFM) ​+ ​(0.001 × FM) ​+ ​(0.008 9 × SHWDTH) ​+ ​(−0.014 5 × TRNKL) ​+ ​(−0.027 8 × PWDTH) - 0.507 3; R2 ​= ​0.819, SE ​± ​0.301. Step2: Total body BMD (g/cm2) = (−0.002 8 × HT) ​+ ​(−0.043 7 × SEXm=1, f=0) ​+ ​(0.000 8 × %FAT) ​+ ​(0.297 0 × BMC) ​+ ​(−0.002 3 × LL) ​+ ​(0.002 3 × SHWDTH) ​+ ​(−0.002 5 × TRNKL) ​+ ​(−0.011 3 × PWDTH) ​+ ​1.379; R2 ​= ​0.89, SE ​± ​0.054. Similar models were also developed to predict leg, arm, spine, and pelvis BMD (R2 ​= ​0.796–0.864, p ​< ​0.05). The equations developed here represent promising tools for identifying individuals with low BMD at risk of fracture who would benefit from further evaluation, especially in the resource or time restricted setting.

Development, Establishment, and Validation of a Model for the Mineralization of Periodontium Remodelling Cells: Cementoblasts.

Chronic kidney disease (CKD) patients undergoing dialysis are at high risk of bone fractures. CKD-induced mineral and bone disorder is extended to periodontal disease due to changes in the ionic composition of saliva in CKD patients, dysregulating mineralization, hindering regeneration and thereby promoting the progression of dental complications. Despite the importance of cementum for overall oral health, the mechanisms that regulate its development and regeneration are not well comprehended, and a lack of sufficient in vitro experimental models has hindered research progress. In this study, the impact of experimental conditions on the calcification of cementoblasts was systematically investigated, aimed at establishing a standardized and validated model for the calcification of cementoblasts. The effects of phosphate, calcium, ascorbic acid, β-glycerolphosphate, dexamethasone, and fetal calf serum on the calcification process of cementoblasts were analyzed over a wide range of concentrations and time points by investigating calcium content, cell viability, gene expression and kinase activity. Cementoblasts calcified in a concentration- and time-dependent manner with higher concentrations of supplements cause a higher degree of calcification but decreased cell viability. Phosphate and calcium have a significantly stronger effect on cementoblast calcification processes compared to osteogenic supplements: ascorbic acid, β-glycerolphosphate, and dexamethasone induce calcification over a wide range of osteogenic signalling pathways, with osteopontin being a central target of gene regulation. Conversely, treatment with ascorbic acid, β-glycerolphosphate, and dexamethasone leads to activating only selected pathways, especially promoting bone sialoprotein expression. The developed and validated cementoblast calcification protocol, incubating up to 60% confluent cementoblasts with 1.9 mmol L-1 of phosphate supplementation for a reasonable, multi-pathway calcification induction and 10 mmol L-1 β-glycerolphosphate, 75 µmol L-1 ascorbic acid and 10 nmol L-1 dexamethasone for a reasonable osteogenic differentiation-based calcification induction, provides standard in vitro experimental models for better understanding cementoblast function and regeneration.

Evaluation of bone mineral density, microarchitecture, and detection of fractures on young patients living with human immunodeficiency virus: when and how to screen?

People living with the human immunodeficiency virus (PLWH) developed higher life expectancy along with chronic bone disease over the past years. Our purpose is to evaluate bone mineral density, bone microarchitecture and fractures in young PLWH and understand the disease's contribution to bone derangements and fracture risk. Eighty-one HIV-infected and 54 control young (20-50 years) male and female subjects were enrolled in this study. Methods for patient evaluation included DXA-VFA (dual energy X-rays and vertebral fracture assessment), HR-pQCT (high resolution peripheral quantitative computed tomography), biochemistry and FRAX. Fifty participants from each group completed all exams. Median age was 40 (25-49) vs. 36.5 (22-50) for the HIV and control groups, respectively (p 0.120). Ethnicity, body mass index, serum phosphorus, 25-hydroxyvitamin D, PTH and CTX were similar between groups, although ALP and OC suggested higher bone turnover in PLWH. VFA identified morphometric vertebral fractures in 12% of PLWH. PLWH had lower values for lumbar spine areal BMD and Z score, volumetric BMD, trabecular bone fraction (BV/TV) and trabecular number measured at the distal tibia by HR-pQCT; as a consequence, trabecular separation and heterogeneity were higher (all p < 0.05). The FRAX-estimated risk for hip and major osteoporotic fractures was statistically higher in PLWH (p < 0.001). Our results confirm severe bone impairment and fractures associated with HIV in young patients. Thus, we developed a screening protocol for young PLWH to detect bone fragility, reduce skeletal disease progression and morbimortality, decrease fracture risk, and increase quality of life.

Serum phosphate is associated with increased risk of bone fragility fractures in haemodialysis patients.

Bone fragility fractures are associated with high morbidity and mortality. This study analysed the association between the current biochemical parameters of chronic kidney disease-mineral and bone disorders (CKD-MBD) and bone fragility fractures in the COSMOS (Current management Of Secondary hyperparathyroidism: a Multicentre Observational Study) project. COSMOS is a 3-year, multicentre, open cohort, prospective, observational study carried out in 6797 haemodialysis patients (227 centres from 20 European countries). The association of bone fragility fractures (outcome) with serum calcium, phosphate and parathyroid hormone (PTH) (exposure), was assessed using standard Cox proportional hazards regression and Cox proportional hazards regression for recurrent events. Additional analyses were performed considering all-cause mortality as a competitive event for bone fragility fracture occurrence. Multivariable models were used in all strategies, with the fully adjusted model including a total of 24 variables. During a median follow-up of 24months, 252 (4%) patients experienced at least one bone fragility fracture (incident bone fragility fracture rate 28.5 per 1000 patient-years). In the fractured and non-fractured patients, the percentage of men was 43.7% and 61.4%, mean age 68.1 and 63.8years and a haemodialysis vintage of 55.9 and 38.3months, respectively. Baseline serum phosphate >6.1mg/dL (reference value 4.3-6.1mg/dL) was significantly associated with a higher bone fragility fracture risk in both regression models {hazard ratio (HR) 1.53 [95% confidence interval (CI) 1.10-2.13] and HR 1.44 (95% CI 1.02-2.05)}. The significant association persisted after competitive risk analysis [subHR 1.42 (95% CI 1.02-1.98)] but the finding was not confirmed when serum phosphate was considered as a continuous variable. Baseline serum calcium showed no association with bone fragility fracture risk in any regression model. Baseline serum PTH >800pg/mL was significantly associated with a higher bone fragility fracture risk in both regression models, but the association disappeared after a competitive risk analysis. Hyperphosphatemia was independently and consistently associated with an increased bone fracture risk, suggesting serum phosphate could be a novel risk factor for bone fractures in haemodialysis patients.

Suppression of TLR4 prevents diabetic bone loss by regulating FTO-mediated m6A modification.

Toll-like receptor-4 (TLR4) has been implicated in the development and progression of diabetic osteoporosis. However, the mechanisms underlying TLR4-regulated bone metabolism in diabetes are yet to be fully understood. Epigenetic modifications have been indicated as a possible mechanism leading to increased risk of osteoporosis and bone fracture. As N6-methyladenosine (m6A) is the most common epigenetic modification in eukaryotic mRNAs, we hypothesized that TLR4 regulates m6A modification in bone tissues of diabetic rats, thereby potentially explaining the pathogenesis of diabetic bone loss. m6A sequencing (m6A-seq) was performed in samples of the femur of TLR4-wild type (TLR4WT) and TLR4-knockout (TLR4KO) diabetic rats to identify genes with differential m6A modifications that may be associated with the bone loss phenotype. We found that in TLR4KO rats, the rapid weight loss of diabetic rats was prevented, and bone mineral density (BMD) was significantly increased. m6A-seq and Gene Ontology enrichment analysis revealed that m6A-modified genes in the femur of TLR4KO diabetic rats were associated with regulation of biological processes such as osteoclast differentiation. qRT-PCR analysis on the expression levels of the m6A-modified methyltransferases and demethylases demonstrated that only the m6A demethylase fat mass and obesity-associated protein（FTO）was decreased. Using an osteoclast cell model, we confirmed that TLR4-mediated osteoclast differentiation was induced by glycolipid toxicity via inhibition of FTO expression. Taken together, these results suggest that inhibition of TLR4 may prevent diabetic bone loss via regulation of FTO-mediated m6A modification.

The Effect of Denosumab in Elderly Patients Regarding Bone Density and Fracture Risk.

With an aging population, the importance of treating and diagnosing osteoporosis is increasing. Osteoporosis, previously known as a resorptive change primarily related to endocrinological mechanisms, is also being approached as a phenomenon of senile change. Denosumab is gaining popularity among osteoporosis medications due to its ability to increase bone mineral density (BMD) and the economic benefit arising from the 6-month cycle. In line with previous literature, this study aimed to examine the BMD-augmenting effect of denosumab through which it reduces fracture risk in individuals aged over 80 years. We reviewed patients who received denosumab between 2018 and 2022 with a minimum clinical observation period of 12 months. BMD was measured every 12 months, and patients were classified per their period of denosumab use. Fracture risk was evaluated using the fracture risk assessment tool (FRAX) and fracture incidence during the observation period were assessed. Among 155 patients, a significant increase in BMD was observed at 3 sites: the lumbar spine, femoral neck, and total hip (p<0.001, p<0.001, and p=0.001, respectively). The patients were divided according to the length of clinical follow-up they received, and similar results were found in all subgroups. Fracture risk assessment was performed using FRAX and the incidence of fracture events during follow-up. FRAX significantly decreased in all subgroups except those who received 24 months of follow-up (p=0.003, p=0.41, p=0.001 in the 12, 24, and ≥36 months groups, respectively). Denosumab use resulted in long-term BMD increase and reduced fracture risk in individuals aged 80 and above.

Selected musculoskeletal disorders in patients with thyroid dysfunction, diabetes, and obesity.

Many medical conditions affect the skeletal system and constitute independent risk factors for fractures. The action of thyroid hormones is necessary to maintain adequate development, mineralization, and bone strength. Untreated hyperthyroidism can lead to a decrease in bone mineral density (BMD), osteoporosis, and pathological fractures. In hypothyroidism, the changes in the quality of bone structure lead to an increase in the frequency of fractures. Excessive body weight negatively impacts fracture risk, increases the risk of osteoarthritis and accelerates the development of rheumatoid arthritis and osteoporosis. Type 1 and type 2 diabetes are associated with an increased risk of bone fractures despite different etiopathogenesis due to the duration of the disease and the pro-inflammatory state, the incorporation of advanced glycation end products (AGEs) into the bone matrix, and microvascular disorders. This study summarizes the current literature on the influence of thyroid dysfunction, obesity, and diabetes on the skeletal system.

Are there associations between hip geometry and bone quality? An analysis on 3074 adults from a general population

IntroductionPatients with reduced bone mineral density and altered hip geometry are susceptible for hip pathologies. Knowledge on associations between bone properties and hip geometric parameters might facilitate identification of patients at risk for hip pathologies. The aim of the present study was to identify associations of bone properties assessed by quantitative ultrasound (QUS) at the heel and hip geometric parameters like center-edge angle (CE), neck-shaft angle (NSA) and alpha angle.Materials and methodsHip geometric parameters (CE, NSA and alpha angle) of 3074 participants from the population-based Study of Health in Pomerania were assessed on magnetic resonance imaging. QUS was performed on both calcanei providing broadband ultrasound attenuation (BUA), speed of sound (SOS) and stiffness-index. Based on the stiffness-index the individual osteoporotic fracture risk (low, moderate or high) was determined. Associations between QUS-based and hip geometric parameters were calculated in linear regression models adjusted for age, sex, body height and weight. Interactions of QUS markers with age and sex on hip geometric parameters were tested.ResultsSignificant inverse associations between BUA (β = − 0.068), SOS (β = − 0.024) as well as stiffness-index (β = − 0.056) and CE were present, while fracture risk was positively associated with CE (β for high = 1.28 and moderate = 2.54 vs. low fracture risk). Interactions between BUA and sex as well as between SOS and age were detected in the models for CE. Furthermore, there was an inverse relation between fracture risk and NSA that was restricted to the moderate risk (β for moderate vs. low fracture risk = − 0.60). There were no significant associations between QUS parameters and alpha angle.ConclusionsIn the general population, several associations between QUS-based bone properties or fracture risk and hip geometry are present. Less dysplastic hips had a lower stiffness-index and a higher fracture risk, whereas more valgus hips had a lower fracture risk.

Women's perspectives regarding osteoporosis, fracture risk, and pharmacologic treatment: a cross-sectional study.

Bisphosphonate medications can prevent the substantial bone loss that occurs during early menopause, but little is known about whether women would accept bisphosphonate treatment at this time in their life, when imminent fracture risk is low. We assessed women's perspectives regarding bone loss, fracture risk, and preventative pharmacotherapy in early menopause. In this cross-sectional study, Canadian women aged ≥ 45years were recruited via Facebook advertisement to complete an electronic survey. Primary outcome was the proportion of early menopausal respondents (≤ 5years since final menstrual period) who were worried about bone loss and fractures. Secondary outcomes were the proportionof early menopausal women willing to accept pharmacologic intervention aimed at preventingeither bone loss or future fractures. We compared responses between early menopausal women and older women (> 5years since final menstrual period). 2033 women responded to the Facebook advertisement, 1195 eligible women (aged: 45 to 89years) started the survey, and 966 completed it. Among early menopausal respondents (N = 98), 38 (42%) were worried about future fractures and 9 of 25 (36%) who had a prior bone mineral density scan were worried about their results. A total of 42 (47%) were willing to start medication to prevent fractures, and 48 (54%) would start medication to prevent bone loss. Responses were comparable between early menopausal women and older women. Menopausal women are concerned about bone loss and fractures. Many women would consider early menopausal pharmacotherapy, with the goals of preserving bone health and lowering their risk of fractures.

Effect of sodium-glucose transporter 2 inhibitors on bone

Diabetes mellitus is a common illness, and the number of people affected by this condition is expected to increase significantly. Complications associated with type 2 diabetes mellitus, such as cataracts, retinopathy, neuropathy, and orthostatic hypotension, can increase the risk of falls and subsequent bone fractures. Canagliflozin, dapagliflozin, empagliflozin, ertugliflozin, and ipragliflozin are a group of medications known as sodium-glucose cotransporter-2 inhibitors (SGLT-2i), which are oral drugs used to treat type 2 diabetes mellitus. This group of medications is a recent addition to the current treatment options for this condition. There are concerns about the impact of SGLT-2 inhibitors on bone health. Although drugs in this category have similarities in reducing blood glucose and preventing cardiovascular disease, they can have varying effects on bone metabolism. The effect of SGLT-2 inhibitors (SGLT-2is)-induced weight loss on bone mineral density (BMD) and bone turnover is significant and cannot be disregarded. Although SGLT-2 inhibitors were initially predicted to increase the likelihood of bone fractures, clinical evidence contradicts this assumption. It is noteworthy to emphasize that empagliflozin and dapagliflozin did not indicate an increased risk of fractures. It is also interesting to note that SGLT2i drugs positively affect heart function and can reduce the incidence of heart failure, which can lead to a decrease in osteoporosis and bone fractures. Based on clinical trials and real-world evidence, there does not appear to be a link between the administration of SGLT2 inhibitors and the risk of fractures. However, caution should still be exercised when prescribing these drugs to patients with advanced disease or kidney complications who may be at higher risk of bone fractures. It is always important to consider individual patient factors and potential risks before making treatment decisions.

Effect of collagen fiber orientation on mechanical properties of bone and myofascia in hindlimb unloading rats

It is well known that the bone loss which may lead to bone fracture risk occurs under microgravity and disuse. Besides bone mineral density (BMD), the role of collagen as the main component of bone in the mechanism has unknown. In addition, myofascia, which is also mainly composed of collagen, plays an important role in the force transmission in musculoskeletal system. In this study, the collagen alternations of hindlimb tibia and myofascia in tail-suspension rats, which hindlimb unloading as a model to simulate microgravity and/or disuse, were investigated and further the correlations with the mechanical properties were analyzed. The collagen fiber orientations were observed by second-harmonic generation (SHG) microscopy and quantitatively analyzed in MATLAB. Bone mechanical properties were measured by three-point-bending test and nanoindentation. Myofascial mechanical properties were explored by tensile test. The results showed: 1) the collagen fibers orientation both in bone and myofascia were dispersed, as standard deviation of collagen fiber orientation increased .2) the mechanical properties of tibia were decreased by unloading both at macro level (maximum load, breaking load and stiffness, etc.) and micro level (hardness). In myofascia, the yield strain and ultimate strain were significantly decreased. 3) correlation analysis showed bone collagen orientation was related to bone hardness/elastic modulus, and myofascial collagen orientation was related to myofascial elastic modulus and yield limit. Additionally, myofascial mechanical properties were related to bone mechanical properties. These suggested disordered collagen orientation may be related to the deterioration of mechanical properties in both bone and myofascia under simulated microgravity. The alternation of myofascial mechanical property may have a certain impact on the deterioration of bone mechanical properties through affecting the force transmission from muscle to bone.

FOXO 1 deletion in chondrocytes rescues diabetes-impaired fracture healing by restoring angiogenesis and reducing apoptosis.

Diabetes mellitus is associated with higher risks of long bone and jaw fractures. It is also associated with a higher incidence of delayed union or non-union. Our previous investigations concluded that a dominant mechanism was the premature loss of cartilage during endochondral bone formation associated with increased osteoclastic activities. We tested the hypothesis that FOXO1 plays a key role in diabetes-impaired angiogenesis and chondrocyte apoptosis. Closed fractures of the femur were induced in mice with lineage-specific FOXO1 deletion in chondrocytes. The control group consisted of mice with the FOXO1 gene present. Mice in the diabetic group were rendered diabetic by multiple streptozotocin injections, while mice in the normoglycemic group received vehicle. Specimens were collected 16 days post fracture. The samples were fixed, decalcified, and embedded in paraffin blocks for immunostaining utilizing anti cleaved caspase-3 or CD31 specific antibodies compared with matched control IgG antibody, and apoptosis by the TUNEL assay. Additionally, ATDC5 chondrocytes were examined in vitro by RT-PCR, luciferase reporter and chromatin immunoprecipitation assays. Diabetic mice had ~ 50% fewer blood vessels compared to normoglycemic mice FOXO1 deletion in diabetic mice partially rescued the low number of blood vessels (p < 0.05). Additionally, diabetes increased caspase-3 positive and apoptotic chondrocytes by 50%. FOXO1 deletion in diabetic animals blocked the increase in both to levels comparable to normoglycemic animals (p < 0.05). High glucose (HG) and high advanced glycation end products (AGE) levels stimulated FOXO1 association with the caspase-3 promoter in vitro, and overexpression of FOXO1 increased caspase-3 promoter activity in luciferase reporter assays. Furthermore, we review previous mechanistic studies demonstrating that tumor necrosis factor (TNF) inhibition reverses impaired angiogenesis and reverses high levels of chondrocyte apoptosis that occur in fracture healing. New results presented here, in combination with recent studies, provide a comprehensive overview of how diabetes, through high glucose levels, AGEs, and increased inflammation, impair the healing process by interfering with angiogenesis and stimulating chondrocyte apoptosis. FOXO1 in diabetic fractures plays a negative role by reducing new blood vessel formation and increasing chondrocyte cell death which is distinct from its role in normal fracture healing.

Sodium butyrate enhances titanium nail osseointegration in ovariectomized rats by inhibiting the PKCα/NOX4/ROS/NF-κB pathways

BackgroundElevated levels of oxidative stress as a consequence of estrogen deficiency serve as a key driver of the onset of osteoporosis (OP). In addition to increasing the risk of bone fractures, OP can reduce the bone volume proximal to titanium nails implanted to treat these osteoporotic fractures, thereby contributing to titanium nail loosening. Sodium butyrate (NaB) is a short-chain fatty acid produced by members of the gut microbiota that exhibits robust antioxidant and anti-inflammatory properties.MethodsOP fracture model rats parameters including bone mineral density (BMD), new bone formation, and the number of bonelets around the implanted nail were analyzed via micro-CT scans, H&E staining, and Masson’s staining. The protective effects of NaB on such osseointegration and the underlying mechanisms were further studied in vitro using MC3T3-E1 cells treated with carbonyl cyanide m-chlorophenylhydrazone (CCCP) to induce oxidative stress. Techniques including Western immunoblotting, electron microscopy, flow cytometry, alkaline phosphatase (ALP) staining, and osteoblast mineralization assays were employed to probe behaviors such as reactive oxygen species production, mineralization activity, ALP activity, protein expression, and the ability of cells to attach to and survive on titanium plates.ResultsNaB treatment was found to enhance ALP activity, mineralization capacity, and Coll-I, BMP2, and OCN expression levels in CCCP-treated MC3T3-E1 cells, while also suppressing PKC and NF-κB expression and enhancing Nrf2 and HO-1 expression in these cells. NaB further suppressed intracellular ROS production and malondialdehyde levels within the cytosol while enhancing superoxide dismutase activity and lowering the apoptotic death rate. In line with these results, in vivo work revealed an increase in BMD in NaB-treated rats that was associated with enhanced bone formation surrounding titanium nails.ConclusionThese findings indicate that NaB may represent a valuable compound that can be postoperatively administered to aid in treating OP fractures through the enhancement of titanium nail osseointegration.

Design the femoral implant matched anatomical Ti64 implant and compare among lattice structures topology optimization and cylindrical pores

Trabecular bone, a porous and spongy kind of bone tissue composed of a lattice of connecting rods and/or plates, is crucial for the transfer of weight in crucial joints including the spine, hip, and knee. It is impacted by a variety of metabolic bone illnesses, such as osteoporosis, which result in bone loss, reduced bone strength, and an elevated risk of bone fracture. To promote osseointegration due to the permeable porous, we suggest, in this study, a new approach to design a femoral permeable porous implant to achieve suitable stiffness, lightweight, and biocompatibility for the bone. Accordingly, data are collected from a digital bio-model to design a femoral implant for mimics segmental bone defect (SBD) with a biocompatible material Ti6Al4V (Ti64). To do this, three lattice structures (LSs) are compared and derived from implicit surface modeling called a triply periodic minimal surface (TPMS) to obtain the LS suitable to create it within the solid inner volume of the tibia implant. Thus, performed the finite element analysis (FEA) method for the enhanced Designs and compare them in terms of stress, deformation, and lightweight.

Cardiac effects of parathyroid hormone excess; an updated mini-review

Hyperparathyroidism causes high levels of PTH, which can lead to a variety of cardiovascular problems that can pose a significant risk to an individual’s overall health. In more severe cases, such as high blood calcium levels due to primary hyperparathyroidism, the individual may also experience increased risks of kidney stones, bone fractures, and osteoporosis.

Impact of Medication Adherence on Bone Mineral Density and Fracture Risk in Patients With Osteoporosis: A Systematic Review.

Osteoporosis is a chronic, prevalent disease marked by decreased bone mass and changes in bone anatomy associated with significant morbidity. The management of osteoporosis necessitates long-term therapy for which patient adherence is of vital importance. In the present review, we aim to collect all potential evidence from relevant studies that reported the impact of medication adherence on bone mineral density and fracture risk in patients with osteoporosis. We have conducted both electronic and manual search strategies within the potential databases and included articles and reviews to find relevant studies. We have assessed the effects of osteoporotic medication adherence on fracture rates and bone mineral density. The study participants were divided into two groups, adherent and non-adherent. Studies from the year 2010-2023 were included. Final inclusion consisted of 14 studies that showed variation in adherence rates with only three studies reporting optimal adherence followed by two studies with nearly half adherent population while the rest of the studies reported low medication adherence. The highest adherence rate reported was 82% while the lowest was 8%. Among the included studies the fracture rates varied significantly. Decreased rates of fracture were observedin the adherent population however two of the included studies were contrary to these findings. Additionally, only three studies discussed the effect of adherence on bone mineral density. Lack of medication adherence is linked to an increased risk of fracture, and low bone mineral density, further associated with more severe complications as per the evidence from the literature. However, variation in the fracture rates as observed in our findings advocates the need for further research for the generalizability of results.

Generic Platform for the Multiplexed Targeted Electrochemical Detection of Osteoporosis-Associated Single Nucleotide Polymorphisms Using Recombinase Polymerase Solid-Phase Primer Elongation and Ferrocene-Modified Nucleoside Triphosphates.

Osteoporosis is a multifactorial disease influenced by genetic and environmental factors, which contributes to an increased risk of bone fracture, but early diagnosis of this disease cannot be achieved using current techniques. We describe a generic platform for the targeted electrochemical genotyping of SNPs identified by genome-wide association studies to be associated with a genetic predisposition to osteoporosis. The platform exploits isothermal solid-phase primer elongation with ferrocene-labeled nucleoside triphosphates. Thiolated reverse primers designed for each SNP were immobilized on individual gold electrodes of an array. These primers are designed to hybridize to the SNP site at their 3'OH terminal, and primer elongation occurs only where there is 100% complementarity, facilitating the identification and heterozygosity of each SNP under interrogation. The platform was applied to real blood samples, which were thermally lysed and directly used without the need for DNA extraction or purification. The results were validated using Taqman SNP genotyping assays and Sanger sequencing. The assay is complete in just 15 min with a total cost of 0.3€ per electrode. The platform is completely generic and has immense potential for deployment at the point of need in an automated device for targeted SNP genotyping with the only required end-user intervention being sample addition.

Risk and management of osteoporosis due to inhaled, epidural, intra-articular or topical glucocorticoids

Glucocorticoids (GCs) are widely used by several specialties for the treatment of a variety of diseases and conditions. The unfavorable effect of oral GCs on bone health is well-documented. The ensuing from their use glucocorticoid-induced osteoporosis (GIOP) is the most common cause of medication-induced osteoporosis and fractures. It is uncertain, however, if, and in what extent, GCs administered by other routes affect the skeleton. In the present review, we quote current evidence on the effect of inhaled GCs, epidural and intra-articular steroid injections, and topical GCs on bone outcomes. Although evidence is limited and weak, it seems that a small proportion of the administered GCs may be absorbed, enter the systemic circulation, and adversely affect the skeleton. Potent GCs, higher doses, and longer treatment duration seem to infer the greater risk for bone loss and fractures. There are scarce data, and only for inhaled GCs, regarding the efficacy of antiosteoporotic medications in patients receiving GCs through routes other than oral. Further studies are needed to clarify the relationship between GC administration through these routes and bone outcomes and to help establishing guidelines for the optimal management of such patients.

Association between sarcopenia and obesity and its comorbidity effect on metabolic parameters and bone fracture risk score in mid-aged Korean women

Objective: The aim of this study is to investigate the association among reduced muscle mass, obesity and its comorbidity, as well as the effects of reduced muscle mass and obesity on various metabolic risk factors and fractures risk in middle age Korean women.