Decreased Bone Mineral Density Research Articles

Biomimetic Extracellular Vesicles Containing Biominerals for Targeted Osteoporosis Therapy.

Osteoporosis (OP) is a systemic skeletal disorder characterized by decreased bone mineral density and a heightened risk of fractures. Therapies for OP have primarily focused on balancing bone formation and bone resorption, but enhancing the remineralization of osteoporotic bone is also a key strategy for effective repair. Recent insights into biomineralization mechanisms have highlighted the essential role of mineral-containing extracellular vesicles (EVs) secreted by osteoblasts in promoting bone marrow mesenchymal stromal/stem cell (BMSC) differentiation and initiating matrix mineralization. Drawing from these principles, we developed a biomimetic approach to replicate the structure and function of the osteoblast-derived EVs by engineering biomimetic mitochondrial minerals with bone marrow homing cell membranes (CMs). This bone-targeted biomimetic system exhibits excellent biocompatibility, enhancing osteogenic differentiation and stimulating angiogenesis by regulating cellular energy metabolism. Additionally, the CM-coated structure shows affinity for collagen fibrils, effectively enhancing intrafibrillar collagen mineralization, thereby facilitating osteoporotic bone repair. Overall, the biomimetic system offers a safe and efficient therapeutic alternative, positioning it as a platform for bone tissue engineering and regenerative medicine.

Effects of Anti-obesity Strategies on Bone Mineral Density: A Comprehensive Meta-analysis of Randomized Controlled Trials.

Although an appropriate weight management strategy is essential for obese individuals, weight loss can have adverse effects on bone mineral density (BMD). We conducted a systematic review of randomized controlled trials to evaluate changes in BMD after the implementation of various weight loss strategies. The PubMed, Embase, Web of Science, and Cochrane Library databases were searched to find articles published from database inception until June 2023. Randomized controlled trials of various treatments for obese patients that reported changes in BMD were selected. The primary outcome was BMD of the whole body, lumbar spine, and total hip, measured using dual X-ray absorptiometry. Eighteen randomized controlled trials involving 2,510 participants with obesity were included in the analysis. At follow-up examination, the BMD of the lumbar spine decreased significantly after metabolic surgery (mean difference [MD]=-0.40 g/cm2; 95% confidence interval [CI], -0.73 to -0.07; I2=0%); lifestyle and pharmacological interventions did not result in a significant decrease in BMD at any location. Metabolic surgery also produced the most substantial difference in weight, with an MD of -3.14 (95% CI, -3.82 to -2.47). This meta-analysis is the first to examine the effects of all categories of anti-obesity strategies, including the use of anti-obesity medications, on BMD. Bariatric metabolic surgery can have adverse effects on BMD. Moreover, medications can be used as a treatment for weight loss without compromising bone quality.

Association of caffeine intake and sleep duration with bone mineral density: a cross-sectional study from National Health and Nutrition Examination Survey between 2011 and 2018

ObjectiveThe association between sleep duration, caffeine intake, and bone mineral density (BMD) is not well understood, with previous studies providing controversial results. This study explores the associations among caffeine intake, sleep duration, and BMD.MethodsData were sourced from the National Health and Nutrition Examination Survey (NHANES) from 2011 to 2018, including 13,457 participants who self-reported sleep duration and caffeine intake, with BMD measured via dual X-ray absorptiometry. Multivariable linear regression models, adjusted for confounders, were used alongside restricted cubic splines to examine dose-response association.ResultsOf all participants, 6821 (50.7%) were males and 6636 were females (49.3%). The mean caffeine intake and sleep duration were 93.4 mg/day and 7.19 h, respectively. RCS results showed that BMD increased with the increase in caffeine intake, especially in the low dose range of 0-200 mg/day. The dose-response association between sleep duration and BMD showed that sleep durations of 0–6 h may promote the increase of BMD, but after sleep durations greater than 6 h, BMD decreases. After adjustment for potential confounders, compared to the lowest referent quartile, individuals with caffeine intake in quartiles 2, 3, and 4 had a positive correlation with BMD (0.62 95% CI: 0.24–1.37; 0.51 95% CI: 0.22–1.13; 0.75 95% CI: 0.41–1.46; P for trend < 0.05). In covariate-adjusted linear regression models, compared with those sleeping 6 h or less per night, the difference in BMD among those sleeping 6–7 h, 7–8 h, and 8–14.5 h per night were 1.81 (95% CI: 0.4122.71), 1.25 (95% CI: 0.55–2.93), and 0.87 (95% CI: 0.38–1.69). Associations of caffeine intake, sleep duration, and BMD stratified by sex and age failed to reach statistical significance.ConclusionsAssociation might exist between the consumption of caffeine, sleep duration, and BMD; however, when stratified by sex and age, the association did not reach statistical significance.

Clinical experience with denosumab discontinuation.

Discontinuing denosumab (DMAb) rapidly decreases bone mineral density (BMD) and increases the risk of multiple vertebral fractures. We wanted to examine if the recommendation stated in the ECTS position paper on DMAb discontinuation can prevent the bone loss in a clinical setting. We conducted a retrospective cohort study based on medical records of patients referred for DMAb discontinuation. We administered zoledronate (ZOL) 6 months after the last DMAb injection and 3, 6, 12, and 24 months thereafter if p-C-terminal collagen crosslinks (CTX) increased above 0.5 μg/l or BMD decreased (≥ 5% at the hip, ≥ 3% at the spine) at months 12 and 24. We included 66 women and men discontinuing DMAb after a mean treatment duration of 6.7 ± 2.7 (mean ± SD) years. BMD decreased 12 months after the initial ZOL treatment by 2.5 ± 4.2% and 1.9 ± 2.5% at the LS and TH, respectively (n = 44) (p ≤ 0.001 for all). There was no significant change in FNBMD (0.0 ± 5.1) (p > 0.05). No significant change in BMD was seen from month 12 to month 24 at any site (p > 0.05 for all). Thirty percent and twenty-two percent of patients experienced flu-like symptoms after the first and second ZOL infusion. No fractures occurred during the study period. Adhering to the recommendation in the ECTS position statement, a mean of 3 infusions of ZOL limited the bone loss 12 and 24 months after DMAb discontinuation, thereby preserving most of the BMD gained during DMAb treatment. The frequent occurrence of flu-like symptoms after ZOL proves to be a challenge, showing that routine prophylaxis against acute phase responses should be considered in patients treated with ZOL after discontinuing DMAb.

History of Health at Cayo Santiago-An Investigation of Environmental and Genetic Influences on the Skeletal Remains of the Introduced Rhesus Macaque (Macaca mulatta) Colony.

The Cayo Santiago rhesus macaque colony is a renowned primate population that has experienced significant natural and anthropogenic ecological variation in their 85-year history. Demographic and familial information is also tracked and collated for the majority of monkeys. Thus, the health history of rhesus macaques at Cayo Santiago should reflect the impacts of both environmental and genetic factors. In this study, we utilized a sample of skeletal remains comprised of 2787 individuals (1571 females, 1091 males), born between 1938 and 2017 from the derived skeletal collection of the primate colony to assess variation in survivorship, pathology, bone mineral density (BMD), and dental eruption status, in the context of hurricane impacts, nutritional fluctuations, and matriline genealogy. Results demonstrated that rhesus macaques at Cayo Santiago exhibit a range of skeletal pathologies that encompass biomedical and archaeological significance, multiple etiologies, severities, locations, and types, in addition to a secular trend of declining BMD that is hypothesized to reflect decreasing physical activity levels under increasing population densities. Specifically, hurricane impacts were found to increase the rate of systemic disease, decrease BMD in young adults, and delay eruption of the primary dentition. Certain matrilines exhibited heightened levels of systemic disease at early ages while others exhibited greater rates of congenital disease. Early-life adversity, through the experience of major hurricanes, may enhance inflammatory pathways, heightening the risk of disease and accelerating the aging process leading to reduced BMD. Such impacts may underly greater levels of observed infection post-hurricane through intensification of pathogen transmission and disease rates brought on by hurricane-adaptive social strategies that favor closer proximity. Familial susceptibility to disease indicates heritable host genetic factors are likely influencing disease patterning in the population. A cluster of congenital diseases may most convincingly illustrate this, or alternatively reflects low levels of genetic diversity in the population.

The role of oxidative stress in bone tissue in the pathogenesis of osteopenia in patients with chronic lymphocytic leukemia

Introduction. A decrease in bone mineral density (BMD), the development of osteopenia and osteoporosis is observed in patients with chronic lymphocytic leukemia (CLL). Patients with CLL are at a higher risk of developing fractures due to osteoporosis compared to healthy age-matched individuals. The pathogenesis of the osteodestructive process in CLL has been poorly studied and may be associated with excessive generation of reactive oxygen species and/or inhibition of antioxidant defense.Aim: to investigate the relationship between indicators of oxidative stress in bone tissue and indicators of osteopenia in patients with CLL.Materials and methods. The study included 48 male patients with CLL aged 50–70 years, divided into group 1 (n = 34) without signs of osteopenia and group 2 (n = 14) with signs of osteopenia based on osteodensitometry (T-score from –1.0 SD to –2.5 SD). BMD, T- and Z-scores were assessed in the lumbar spine, proximal femoral neck (PFC), and proximal femur. In the bone tissue homogenate, the content of products of oxidative modification of proteins (OMP) was determined spectrophotometrically in spontaneous and metal-catalyzed modes, reserve-adaptation potential, and general antioxidant status.Results. Osteopenia was detected in 30 % of patients with CLL according to osteodensitometry in the neck of the proximal femur. In patients with CLL and osteopenia, signs of oxidative stress were observed in the bone tissue: early OMP products of a neutral and basic nature, late products of a neutral nature accumulated in the spontaneous detection mode; early and late OMP products of a neutral and basic nature accumulated in the induced mode; reserve-adaptive potential, the general antioxidant status decreased. Signs of osteopenia in the PFC in patients with CLL in the femoral neck increased as the content of early and late OMP products in the bone tissue increased in spontaneous and metal-induced detection modes, and the general antioxidant status in the bone tissue decreased.Conclusion. Based on the data obtained, it is possible to modernize diagnostic criteria and therapeutic approaches.

Modification of bone architecture following sleeve gastrectomy: a 5-year follow-up.

Bariatric surgery induces a decrease in areal bone mineral density (aBMD), but the long-term effect on trabecular and cortical volumetric bone mineral density (vBMD) has not been well assessed. The main aim of this 5-year longitudinal study was to investigate the changes following sleeve gastrectomy (SG) in aBMD, bone turnover markers and trabecular and cortical vBMD. Forty-five patients with obesity were assessed before and 1, 2 and 5years after SG. Trabecular and cortical vBMD, cortical thickness and structural parameters were assessed by 3D-Shaper® software at hip. Values of bone turnover markers peaked after 1year and decreased after 2 and 5years, but without returning to baseline values. aBMD decreased mostly at femoral neck(-9.7%) and total hip(-10.7%) over the 5years, with the greatest loss occurring at 1year(-5.9% and -6.3%, respectively). A similar profile of decrease was observed for integral hip vBMD with significant decreases of 6.6%, 7.7% and 10.7% after 1, 2 and 5years, mainly due to a reduction in the trabecular (10.5%, 12.0% and 17.2%, respectively) rather than cortical (1.4%, 1.9% and 2.9%, respectively) component. A modest decrease in mean cortical thickness (2.5%, 2.8% and 3.9%, respectively) and an alteration in the structural parameters were concomitantly observed. Older age and greater body weight loss were the factors most associated with an increased loss of aBMD and vBMD. In conclusion, the study demonstrates that SG induces not only an alteration in bone turnover and aBMD, but also a reduction in vBMD at hip, predominantly due to trabecular component deterioration as determined by 3D-Shaper® software. The maintenance of bone deterioration for at least 5years - that is, after 4years of relative body weight stabilization or minimal weight regain - suggests the need for a therapeutic approach to preserve bone health in patients who undergo SG.

The Role of Inflammatory and Nutritional Indices in Postmenopausal Osteoporosis: A Retrospective Study.

Background: Postmenopausal osteoporosis is characterized by impaired bone metabolism, inflammation, and nutritional deficiencies. This study aimed to evaluate the potential of inflammatory and nutritional markers in identifying decreased bone mineral density (BMD) in postmenopausal women. Methods: This cross-sectional study retrospectively analyzed postmenopausal women from January 2018 and December 2023. A total of 368 women were divided into three groups based on T-scores: 61 women with osteoporosis (T-score ≤ -2.5), 153 women with osteopenia (-1 > T-score > -2.5), and 154 women with normal BMD (T-score > -1). Inflammatory and nutritional biomarkers included the neutrophil/lymphocyte ratio (NLR), platelet/lymphocyte ratio (PLR), monocyte/lymphocyte ratio (MLR), systemic immune-inflammation index (SII), systemic inflammation response index (SIRI), pan-immune inflammation value (PIV), geriatric nutritional risk index (GNRI), triglycerides, total cholesterol, and body weight index (TCBI), prognosis nutritional index (PNI), hemoglobin, albumin, lymphocyte, and platelet (HALP) score, 25-OH Vitamin D level, Na, K, Ca, Mg, and their ratios. Results: The GNRI was significantly lower in the osteoporosis group compared to the control group. The NLR, PLR, SII, SIRI, PIV, TCBI, PNI, and HALP were similar between the groups. The GNRI and TCBI showed a positive correlation with T-scores. The Mg level was lower in the osteoporosis group than in the control group and osteopenia group, and the Na/Mg ratio was higher. Additionally, the Ca/Mg ratio was lower in the osteoporosis group than in the control group. The T-score was positively correlated with Mg and Ca/Mg, while the Na/Mg ratio showed a significant negative correlation. Vitamin D, other minerals, and their ratios did not show significant differences between the groups. Conclusions: Our findings suggest that the GNRI could serve as a useful indicator for assessing bone health and the risk of osteoporosis. Furthermore, maintaining appropriate levels of Mg and balanced Na/Mg and Ca/Mg ratios appears crucial for BMD.

The Application of L-Serine-Incorporated Gelatin Sponge into the Calvarial Defect of the Ovariectomized Rats.

Osteoporosis, characterized by decreased bone mineral density due to an imbalance between osteoblast and osteoclast activity, poses significant challenges in bone healing, particularly in postmenopausal women. Current treatments, such as bisphosphonates, are effective but associated with adverse effects like medication-related osteonecrosis of the jaw, necessitating safer alternatives. This study investigated the use of L-serine-incorporated gelatin sponges for bone regeneration in calvarial defects in an ovariectomized rat model of osteoporosis. Thirty rats were divided into three groups: a control group, a group treated with a gelatin sponge containing an amino acid mixture, and a group treated with a gelatin sponge containing L-serine. Bone regeneration was assessed using micro-computed tomography (micro-CT) and histological analyses. The L-serine group showed a significant increase in bone volume (BV) and bone area compared to the control and amino acid groups. The bone volume to total volume (BV/TV) ratio was also significantly higher in the L-serine group. Immunohistochemical analysis demonstrated that L-serine treatment suppressed the expression of cathepsin K, a marker of osteoclast activity, while increasing serine racemase activity. These findings suggest that L-serine-incorporated gelatin sponges not only enhance bone formation but also inhibit osteoclast-mediated bone resorption, providing a promising and safer alternative to current therapies for osteoporosis-related bone defects. Further research is needed to explore its clinical applications in human patients.

Fluoxetine inhibited RANKL-induced osteoclastic differentiation in vitro.

Selective serotonin reuptake inhibitor correlates with decreased bone mineral density and impedes orthodontic tooth movement. The present study aimed to examine the effects of fluoxetine on osteoclast differentiation and function. Human peripheral blood mononuclear cells (hPBMCs) and murine RAW264.7 cells were cultured with RANKL to stimulate osteoclast differentiation. The resulting multinucleated cells displayed characteristics of mature osteoclasts. Fluoxetine at 0.01-1 μM did not impact cellular viability or oxidative stress. However, 10 μM fluoxetine significantly reduced clonal growth, cell viability, and increased cytotoxicity and lipid peroxidation in RAW 264.7 cells. Further, application of 0.1 μM fluoxetine potently suppressed osteoclast differentiation of both RAW264.7 and hPBMCs, with reduced osteoclast numbers and downregulation of osteoclastic genes matrix metalloproteinase-9, cathepsin K, and integrin β3 at mRNA and protein levels. Fluoxetine also disrupted F-actin ring formation essential for osteoclast resorptive function. Mechanistically, fluoxetine inhibited NF-kB signaling by reducing phosphorylation of pathway members IκBα and p65, preventing IκBα degradation and blocking p65 nuclear translocation. In conclusion, this study demonstrates fluoxetine suppressing osteoclast differentiation in association with disrupting NF-kB activation, providing insight into orthodontic treatment planning for patients taking fluoxetine.

The study of risk factors for osteoporosis with prolonged use of anticonvulsants: intermediate results

The mechanisms of anticonvulsant effects on bone metabolism are not studied sufficiently. This determines the relevance of research on factors that influence the development of osteoporosis in patients taking long-term anticonvulsants. The aim of the study to evaluate the effect of modifiable and non-modifiable osteoporosis risk factors on changes in bone mineral density during long-term therapy with anticonvulsants. Materials and methods. The study included 100 adult patients receiving anticonvulsants for moren12 months and 58 healthy volunteers. All participants underwent a clinical screening with assessment of factors affecting bone metabolism and a densitometric study using quantitative computed tomography at three points (L1, L2 and femoral neck). Results. CT-densitometry results showed decrease bone mineral density in the most part of the participants in both study groups. According to the data of the analysis of the influence of osteoporosis risk factors on bone mineral density values, it was found that the presence of fractures in the anamnesis and low level of motor activity increased the risk of osteoporosis development in patients taking long-term anticonvulsants (p (χ2) &lt; 0.001). Conclusion. The results of the study confirm the importance of continuing research on factors affecting bone metabolism and developing a set of preventive measures to prevent the development of osteoporosis.

Association Between Dietary Tryptophan Intake and Bone Health: A Cross-Sectional Study

The relationship between dietary tryptophan intake and the risk of low bone mineral density (LBMD) has not been thoroughly evaluated. This study aimed to examine the relationship between dietary tryptophan intake and LBMD. A total of 12,003 participants aged 50 years and older with complete data on bone mineral density (BMD) and tryptophan intake from the National Health and Nutrition Examination Survey (NHANES) 2005 to 2020 were included in this cross-sectional study. The median dietary tryptophan intake among the 12,003 participants was 1822.14 mg/day, with significantly lower levels observed in individuals with LBMD compared to those with normal bone mass (1740.45 mg/day vs. 2041.39 mg/day, p < 0.001). For every 2.7-fold increase in dietary tryptophan intake, the risk of low BMD decreases by 22%. When dietary tryptophan intake was categorized into quartiles, significantly lower risks of LBMD were observed in the third [Odds Ratio (OR) = 0.68, 95% confidence interval (CI): 0.51–0.91] and fourth (OR = 0.65, 95% CI: 0.49–0.87) quartiles compared to the reference group after multivariable adjustment. Moreover, the restricted cubic spline (RCS) results revealed a negative nonlinear relationship between dietary tryptophan intake and LBMD (p for overall < 0.001, p for nonlinear < 0.05), with this correlation remaining consistent across various population subgroups and exhibiting no significant interaction according to stratification variables. Sensitivity analyses further substantiated these findings. Overall, we found that increased dietary tryptophan intake may be associated with a lower risk of LBMD among individuals aged ≥ 50 years, highlighting the importance of optimizing tryptophan nutrition for reducing osteoporosis risk.

NHANES data analysis of the cardiometabolic index in relation to lumbar spine bone mineral density.

to investigate the correlation between cardiometabolic index (CMI) and lumbar spine bone mineral density (LSBMD) in U.S. adults. the study selected eligible participants from the National Health and Nutrition Examination Survey (NHANES) database from 2011 to 2018. After adjusting for age, gender, race/ethnicity, body mass index (BMI), liver function markers, kidney function markers, blood routine indicators, metabolic markers, and chronic disease status, a logistic regression model combined with a restricted cubic spline model, smooth curve fitting, and threshold effect analysis was used to examine the association between CMI and LSBMD. Subgroup analysis was performed to verify the robustness of the results. among the 3,885 participants, for each unit increase in CMI, LSBMD decreased by 0.011 g/cm². Additionally, a turning point was identified at CMI = 0.797. When CMI was below 0.797, LSBMD decreased as CMI increased, showing a strong negative correlation (β = -0.077, 95 % CI: -0.097 to -0.058, p < 0.001). However, beyond this threshold, the relationship between CMI and LSBMD was no longer significant. Subgroup analysis revealed that the negative correlation between CMI and BMD was consistent across most subgroups (such as gender, BMI, hypertension, and high cholesterol), but instability was observed in subgroups such as individuals aged 51-59, Mexican Americans, non-Hispanic Blacks, and those with diabetes. there exists a non-linear inverse correlation with CMI and LSBMD, showing that CMI could be a potential contributing factor for decreased bone mineral density, with a more pronounced effect within a specific range.

Expert consensus on the diagnosis and treatment of pyruvate kinase deficiency

Pyruvate kinase deficiency (PKD) is a rare autosomal recessive disorder caused by mutations in the PKLR gene, encoding erythrocyte pyruvate kinase, which affects erythrocyte energy production, and then in turn affects erythrocyte function and longevity. PKD is characterized by chronic hemolytic anemia, and other features include chronic hemolytic complications, such as iron overload, decreased bone mineral density, and cardiopulmonary complications. The treatment of PKD requires individualized approach based on the patient's condition, including red blood cell transfusions, pyruvate kinase activators, and treatment for complications. This consensus focuses on the pathogenesis, clinical characteristics, diagnosis and treatment of PKD, and aims to provide better medical service for clinicians, such as diagnosis, treatment, monitoring, and prevention of complications for PKD patients.

Handgrip and its relation to age, fragility fractures, and BMD between sexes in a population aged 50+ years.

A decrease in bone mineral density (BMD) accompanied by muscle weakness during aging significantly increases the probability of low-energy fracture occurrence, but it can also happen in those with a non-osteoporotic score (treatment gap). To improve the identification process of those at risk, the authors proposed using the interconnectivity between bone mineral density and muscle tissue. A total of 20,776 patient records were collected from the database in the period 2008-2021. After applying inclusion criteria, a total of 7159 records were used in the study. Questionnaires regarding patients' history were collected at admission. Patients underwent lumbar spine and/or femoral neck DXA examination and handgrip testing with a handheld dynamometer. Statistical analysis was conducted using tests suitable for the distribution of the data. Osteoporosis was diagnosed in a total of 1914 patients. Depending on the diagnosis there was a significant (p < 0.001) difference in handgrip strength (HGS) between the BMD statuses (norm-osteopenia-osteoporosis). HGS was significantly (p < 0.001) correlated with both BMD neck (r = 0.2) and spine (r = 0.1) in females, and with BMD neck (r = 0.11) in the male population. In our study group HGS was significantly (p < 0.001) higher for all the analysed fractures in the no-fracture group of women. There was no such relationship in reference to the male population. Due to its relationship with BMD, its low cost, and availability, HGS might prove useful in identifying women at risk of a fragility fracture.

Isoginkgetin Inhibits RANKL-induced Osteoclastogenesis and Alleviates Bone Loss

Osteoporosis is characterized by excessive osteoclast activity leading to bone loss, decreased bone mineral density, and increased susceptibility to fractures. Through in vivo/vitro experiments, along with network pharmacology analysis, we aimed to explore the underlying mechanisms of Isoginkgetin (IGG) in inhibiting osteoclastogenesis, providing valuable insights for further research in the future. Firstly, we ascertained the safe concentration of IGG stimulation on BMMs, followed by a systematic exploration of the concentration gradient at which IGG inhibited osteoclastogenesis using TRAP analysis. An osteoporosis model was established to further validate the in vitro experimental findings by combining Micro-CT and immunohistochemical analysis. The results show that IGG did not exhibit cytotoxicity or proliferative effects on BMMs at concentrations equal to or less than 10 μM. Additionally, IGG inhibited the activity of osteoclastogenesis and bone resorption function at lower concentrations. RT-PCR and Western Blot results demonstrated that IGG could downregulate genes and proteins associated with osteoclastogenesis. The Western Blot results also showed that IGG inhibited the phosphorylation expression of P38, ERK, and P65 in the MAPK and NF-κB pathways. At the same time, it rescued the degradation of IκB-α at 15 and 60 min. IGG can also impact the relative expression levels of oxidative proteins such as SOD-1, HO-1, and catalase, thereby influencing cellular equilibrium and stress levels, ultimately inhibiting the formation of mature OC. In vivo experiments demonstrated that IGG alleviated bone loss caused by osteoclasts and improved relevant parameters of trabecular bone. So, IGG effectively attenuated osteoclastogenesis, and improved bone density, thereby portraying its role in osteoporosis management.

Forearm bone mineral density as a predictor of adjacent vertebral refracture after percutaneous kyphoplasty in patients with osteoporotic vertebral compression fracture: a retrospective analysis

BackgroundThe incidence of adjacent vertebral body re-fracture after percutaneous kyphoplasty (PKP) is associated with a number of variables, of which decreased bone mineral density is one of the major risk factors. Forearm bone mineral density (BMD) measurements are gaining attention because of their convenience and validity, but there is a lack of systematic research on the specific relationship between forearm BMD and the risk of adjacent vertebral re-fracture after PKP.PurposeTo investigate the correlation between forearm BMD and the risk of adjacent vertebral re-fracture after PKP in osteoporotic vertebral compression fractures (OVCF) patients.MethodsRetrospective evaluation of 198 OVCF patients receiving PKP was conducted in this study. The patients were divided into two groups: the no-fracture group and the re-fracture group, according to whether or not they had undergone vertebral re-fracture. Obtain basic information about the patient's age, sex, body mass index, bone cement leakage, smoking history, diabetes history, and surgical segmentation. Using computed tomography, the mean Hounsfield unit (HU) values for the BMD of the L1 lumbar spine were determined. For the dual-energy X-ray BMD test, the distal one-third lengths of the patient's nondominant forearm's radius and ulna were chosen. Receiver operating characteristic curves were utilized to evaluate the predictive value of forearm BMD versus lumbar CT values for vertebral re-fracture, and univariate and multivariate logistic regression analyses were employed to identify characteristics related with vertebral re-fracture following PKP.ResultsRe-fracture rate after PKP was 17.2% at a minimum 12-month follow-up. Significant differences were seen between the refracture and non-fracture groups in terms of hypertension, Cobb angle correction, vertebral height recovery rate, intradiscal cement leakage, forearm bone density, and vertebral HU values. In multifactorial logistic regression analysis, forearm bone density (OR 0.821; 95% CI 0.728–0.937, p = 0.008) and HU values (OR 0.815; 95% CI 0.733–0.906, p = 0.005) were independent risk factors for vertebral re-fracture. The area under the curve (AUC) for forearm BMD values and HU values predicting adjacent vertebral re-fracture were 0.956 and 0.967, respectively.ConclusionsForearm BMD is an independent risk factor for re-fracture of adjacent vertebrae after PKP. In addition, forearm BMD, as a valid indicator of postoperative re-fracture after PKP in patients with OVCF, and the HU value of lumbar spine CT were both powerful tools for predicting re-fracture.

Risk factors for decreased bone mineral density in patients with Hodgkin’s lymphoma

BACKGROUND: Osteoporosis is a disease characterized by a decrease in bone mineral density that leads to low-energy fractures. Hodgkin’s lymphoma, which occurs mainly in young people (16–35 years), may be one of the causes of impaired bone remodeling. Given the high prevalence of osteoporosis in young patients with Hodgkin’s lymphoma, it is important to identify early predictors of the development of osteoporosis. AIM: To evaluate risk factors for decreased bone mineral density in patients with Hodgkin’s lymphoma receiving pathogenetic therapy. MATERIALS AND METHOD: The study included 63 patients with Hodgkin’s lymphoma and 30 healthy volunteers who served as controls. All participants completed a questionnaire to identify common and specific risk factors for osteoporosis. Common risk factors included sex, age, body mass index, history of fractures in the patient and immediate family, use of hormone replacement therapy, proton pump inhibitors, corticosteroids, comorbidities, amenorrhea in women, level of physical activity, and calcium intake. Specific risk factors for osteoporosis included polychemotherapy as a pathogenetic therapy for Hodgkin’s lymphoma. RESULTS: The study identified four main risk factors for the development of osteopenia/osteoporosis in young patients with Hodgkin lymphoma following pathogenetic therapy such as use of proton pump inhibitors, corticosteroids, chemotherapy-induced amenorrhea in women, and low physical activity. CONCLUSION: Methods for predicting and preventing osteoporosis have not yet been developed for young patients, as this disease is considered to be associated with old age. However, some groups of young patients are at high risk for disruption of bone microarchitecture with low-energy fractures, significantly reducing quality of life. All these factors make early detection of osteoporosis predictors important.

Bone Material Strength index is low in Patients with Cushing's Syndrome even after long-term remission.

Hypercortisolism in endogenous Cushing's syndrome (CS) results in decreased bone mineral density (BMD) and increased fracture risk. Although after remission BMD improves, fracture rate remains elevated, suggesting that BMD may not adequately reflect fracture risk in this group. The aim was to evaluate bone material properties, another component of bone quality, using Impact Microindentation (IMI) in patients with CS in remission. Cross-sectional study in 60 patients and 60 age-, sex-, and BMD-matched controls at a tertiary referral center between 2019 and 2021. Bone material strength index (BMSi) was measured by IMI using the OsteoProbe® device at the tibia. In addition, laboratory investigation, BMD, and vertebral fracture assessment were performed. By design, patients and controls were comparable for age (median age 56.5 years), sex (48 women), BMD at the lumbar spine and femoral neck. They were also comparable regarding the number of fragility fractures (21 vs. 27, p=0.22). Median time of remission in patients was 6 years (range 1 to 41). Despite comparable BMD, BMSi was significantly lower in patients compared to controls (76.2±6.7 vs 80.5±4.9, p<0.001). In patients, BMSi was negatively correlated with BMI (r= -0.354, p=0.01), but not related to the presence of fracture, physiological hydrocortisone replacement use, other pituitary insufficiencies, or time since remission. Bone material properties remain altered in patients with endogenous CS, even after long-term remission. These abnormalities, known to be associated with fractures in other populations, may play a role in the persistent bone fragility of steroid excess.

Effective pharmacotherapy of osteoporosis in perimenopause

Osteoporosis (OP) is a disease characterized by a decrease in bone mineral density (BMD) and a high risk of fractures. In perimenopausal women with a disturbed hormonal background, the risk of developing this pathology increases significantly. Special diagnostic methods and therapy that take into account the etiopathogenesis of the disease can reduce the disability rates associated with OP among patients of this group. The article provides data on the results of examination and treatment of 57 perimenopausal women with OP and reveals the potential of diagnostics that allows evaluating the effectiveness of therapy. The drug "Osteomed Forte" has shown effectiveness in reducing and closing cavities in the trabecular bone sections in patients with verified OP and androgen deficiency, and improving hormonal status in perimenopause allowed to suspend the development of OP and even achieve its partial regression.