Increase In Bone Mineral Density Research Articles

Effects of 18 Months of Growth Hormone Replacement Therapy on Bone Mineral Density in Patients with Adult Growth Hormone Deficiency: A Retrospective Study.

The effect of physiological dose growth hormone (GH) replacement therapy on bone mineral density (BMD) in adults with growth hormone deficiency (GHD) is not well defined. We aimed to investigate the effects of 18 months of treatment with recombinant human growth hormone (rhGH) at physiological doses on BMD, body composition (BC), and quality of life (QoL). Sixty-eight patients diagnosed with adult growth hormone deficiency (AGHD) in our hospital were included in this retrospective study. All patients received individualized rhGH replacement to maintain normal serum insulin-like growth factor-1 (IGF-1) levels. BMD and BC measurements were performed by dual energy X-ray absorptiometry (DXA). Excluding those with incomplete follow-up data, we analyzed BMD in 68 patients, as well as BC and QoL in 36 of them. Compared with the baseline, lumbar spine BMD decreased by 0.008 g/cm2 (P=0.006) and increased by 0.011 g/cm2 (P=0.045) at month 18, and total hip BMD decreased by 0.005 g/cm2 (P=0.008) and did not change significantly from the baseline at month 18. The changes in BMD did not differ by sex, and the increase in BMD was more pronounced in patients with low Z-scores at the baseline (lumbar spine: P=0.005 and total hip: P=0.018). The percentage change from the baseline in BMD was greater for the lumbar spine than for the total hip (P=0.003). Lean body mass (LBM) increased significantly (P=0.012), total body fat ratio (TBF%) decreased significantly (P=0.011), visceral adipose tissue (VAT) decreased significantly (P=0.016), and QoL improved significantly (P < 0.001). Within 18 months of treatment, bone resorption manifested first, BMD decreased to a nadir at month 6, and then it increased. The increase in BMD was greater in the lumbar spine than in the hip, and the increase was more pronounced in patients with low BMD. Eighteen months of rhGH replacement therapy significantly improved lumbar spine BMD and improved BC and QoL.

Synergistic Effects of Combined Concurrent Training and Eri-Polyunsaturated Fatty Acid Supplementation on Bone Mineral Density, Muscle Strength, and Inflammation.

Obesity has been associated with lower bone mineral density (BMD) and rapid muscle weakness. Regular exercise and polyunsaturated fatty acid (PUFA) consumption have been recognized as nonpharmaceutical approaches to increase BMD and ameliorate muscle weakness. This study aimed to determine the effects of concurrent training (CCT) and Eri-PUFA supplementation on BMD, muscular strength, and inflammation in obese adults. A total of 33 obese participants were randomly assigned to one of three groups (n=11 per group): (1) a placebo group; (2) an Eri-PUFA ingestion group (ERI); or (3) a CCT and Eri-PUFA ingestion group (CCT+ERI). The ERI and CCT+ERI groups received approximately 2.5 g of linolenic acid per day from Eri silkworm pupae. The exercise program included aerobic and resistance exercises performed under supervision three times per week for 8 weeks. Before and after the 8-week intervention, BMD, muscular strength, and inflammatory markers were measured. Only the CCT+ERI group showed a significant increase in lumbar spine BMD (5.1%, P<0.01) and upper-body muscle strength (16.9%, P<0.01) after the intervention, with differences between the groups. After the intervention, both the ERI and CCT+ERI groups showed a significant decrease in the monocyte-to-lymphocyte ratio (-25%, P<0.01 and -21.4%, P<0.05, respectively) and tumor necrosis factor-alpha (-21.6%, P<0.05 and -19.4%, P<0.05, respectively). These findings demonstrate that combining CCT and Eri-PUFA supplementation increases BMD and upper-body muscular strength and decreases inflammation. Although Eri-PUFA consumption did not affect BMD or muscle strength directly, it may have an additive effect on BMD by reducing inflammation.

Response of bone mineral density and balance performance in post-burn patients with selected Qigong training: A single-blind randomized controlled trial

BackgroundDecreased bone mineral density (BMD) is a common condition after a burn with significant complications that would be a global health problem. Also, balance can further worsen due to burning complications. Therefore, this study aims to analyze the additive effects of selected Qigong training exercises for 2 months to the standard physiotherapy regimen on bone mineral density and balance control post-thermal burn injuries. Methods110 participants (75 males and 35 females), aged 25–50, with deep second and third-degree thermal burns affecting the trunk and lower extremities, and a total body surface area (TBSA) of 30–45%, allocated randomly into two equal groups of 55. Group A has Qigong training along with its standard physiotherapy regimen, and the control group (Group B) has only a standard physiotherapy regimen. For eight weeks, the interventions were used four times a week. The bone mineral density (BMD), T-score of the lumbar spine, the overall stability index (OSI), and the dynamic limits of stability (DLOS) were assessed pre-intervention and after eight weeks of intervention. ResultsA two-way mixed MANOVA showed that there was a significant increase in BMD, T-score, and DLOS and a significant decrease in OSI in a favor of the Qigong training group after eight weeks of treatment compared with that of the control group. Both groups showed a significant improvement in BMD, T- score, DLOS, and OSI post-treatment compared with that at the baseline. There were statistical significances in the favor of the Qigong training group after eight weeks of treatment (P < 0.001). ConclusionIn patients with repaired second and third-degree thermal burns of the trunk and lower legs, Qigong training activities combined with a standard physiotherapy regimen for 2 months were more helpful in increasing bone mineral density and improving balance control than the standard physiotherapy regimen alone.

Novel mutation in LRP5 gene cause rare osteosclerosis: cases studies and literature review

To study the effects of low-density lipoprotein receptor-related protein 5 (LRP5) gene mutations on bone, and to open up our view of LRP5 and Wnt pathways on bone mass regulation. Three patients with increased bone mineral density or thickened bone cortex were included, who were 30-year-old, 22-year-old and 50-year-old men, respectively. The latter two patients were son and father of a same family. The characteristics of bone X-rays were evaluated in detail. Bone turnover markers were detected, such as procollagen type 1 amino-terminal peptide (P1NP), alkaline phosphatase (ALP), and type 1 collagen carboxyl terminal peptide (β-CTX). Dual energy X-ray absorptiometry (DXA) was used to measure the bone mineral density (BMD) at lumbar spine and proximal femur of the patients. The targeted next-generation sequencing (NGS) technology was used to detect pathogenic gene mutations, which were further verified by Sanger sequencing. Moreover, the gene mutation spectrum and phenotypic characteristics of reported patients with LRP5 gain-of-function mutations were summarized by reviewing the literature. The main characteristics of the first patient were headache, facial paralysis, high BMD (lumbar vertebrae 1–4: 1.877 g/cm2, Z-score: 5.8; total hip: 1.705 g/cm2, Z-score: 5.7), slightly increased P1NP (87.0 ng/mL) and β-CTX (0.761 ng/mL) level, and with thickened bone cortex, especially the cranial vault. The latter two patients showed enlargement of the mandible and enlarged osseous prominence of the tours palatinus. X-rays showed that the bone cortex of skull and long bones were thickened. The bone turnover markers and BMD were normal. All three cases carried novel missense mutations in LRP5 gene, which were mutation in exon 3 (c.586 T > G, p.Trp196Gly) of the first patient, and mutation in exon 20 (c.4240C > A, p.Arg1414Ser) of the latter two patients. Combined with the reported literature, a total of 19 gain-of-function mutations in LRP5 were detected in 113 patients from 33 families. Hotspot mutations included c.724G > A, c.512G > T and c.758C > T. Furthermore, mutations in the exon 3 of LRP5 may cause severe phenotypes. LRP5 gain-of-function mutations can lead to rare autosomal dominant osteosclerosis type Ι (ADO Ι), which was characterized by increased bone mass and thickened bone cortex. In-depth research on the Wnt pathway will be benefit for discovering important mechanisms of bone mass regulation.

Genome-wide association study identifies genetic variants which predict the response of bone mineral density to teriparatide therapy

ObjectivesTeriparatide (TPTD) is an effective treatment for osteoporosis but the individual response to therapy is variable for reasons that are unclear. This study aimed to determine whether the response to...

For premenopausal women, does calcium with or without vitamin D increase bone mineral density (BMD)?

For premenopausal women, does calcium with or without vitamin D increase bone mineral density (BMD)?

Microfibril-Associated Glycoprotein-2 Promoted Fracture Healing via Integrin αvβ3/PTK2/AKT Signaling

Fracture healing is a complex physiological process in which angiogenesis plays an essential role. Microfibril-associated glycoprotein-2 (MAGP2) has been reported to possess a proangiogenic activity via integrin αvβ3, yet its role in bone repair is unexplored. In this study, a critical-sized femoral defect (2 mm) was created in mice, followed by the delivery of an adenovirus-based MAGP2 overexpression vector or its negative control at the fracture site. At days 7, 14, 21, and 28 postfracture, bone fracture healing was evaluated by radiography, micro-computed tomography, and histopathologic analysis. Adenovirus-based MAGP2 overexpression vector–treated mice exhibited increased bone mineral density and bone volume fraction. MAGP2 overexpression contributed to an advanced stage of endochondral ossification and induced cartilage callus into the bony callus. Further analysis indicated that MAGP2 was associated with enhanced angiogenesis, as evidenced by marked MAGP2 and integrin αvβ3 costaining and increased endothelial cell markers such as endomucin and CD31 levls, as well as elevated phosphorylation of protein tyrosine kinase 2 (PTK2) and AKT serine/threonine kinase 1 (AKT) in the callus. In vitro, recombinant human MAGP2 treatment enhanced the viability, migration, and tube formation ability of human microvascular endothelial cells, which was partially reversed by integrin αvβ3 inhibition or MK-2206, a specific AKT inhibitor. Inhibition of integrin αvβ3 abolished MAGP2-induced PTK2 and AKT activation. Taken together, our data provide the first evidence that MAGP2 promotes angiogenesis and bone formation by activating the integrin αvβ3/PTK2/AKT signaling pathway.

Effect of Lumbar Spinal Stenosis on Treatment of Osteoporosis: Comparison of Three Oral Bisphosphonate Therapies

(1) Background: Lumbar spinal stenosis (LSS) causes uncomfortable neuropathic symptoms, which can negatively affect osteoporosis. The aim of this study was to investigate the effect of LSS on bone mineral density (BMD) in patients treated with one of three oral bisphosphonates (ibandronate, alendronate and risedronate) for initially diagnosed osteoporosis. (2) Methods: We included 346 patients treated with oral bisphosphonates for three years. We compared annual BMD T-scores and BMD increases between the two groups according to symptomatic LSS. The therapeutic efficacies of the three oral bisphosphonates in each group were also evaluated. (3) Results: Annual and total increases in BMD were significantly greater in group I (osteoporosis) compared to group II (osteoporosis + LSS). The total increase in BMD for three years was significantly greater in the ibandronate and alendronate subgroups than that in the risedronate subgroup (0.49 vs. 0.45 vs. 0.25, p < 0.001). Ibandronate showed a significantly greater increase in BMD than that of risedronate in group II (0.36 vs. 0.13, p = 0.018). (4) Conclusions: Symptomatic LSS may interfere with the increase in BMD. Ibandronate and alendronate were more effective in treating osteoporosis than risedronate. In particular, ibandronate was more effective than risedronate in patients with both osteoporosis and LSS.

Factors associated with bone response to teriparatide in young postmenopausal women with osteoporosis.

To investigate the factors associated with changes in vertebral bone mineral density during teriparatide treatment. Single centre, longitudinal study involving 145 osteoporotic postmenopausal women treated with teriparatide. Clinical evaluation, bone mineral density (BMD) measurements assessment and laboratory analyses were performed at baseline then after 12 and 18months of treatment. Bone non-response to treatment was defined as no significant increase in BMD at 18months as compared to baseline. Of the 145 women initially included, 109 completed the 18-month course of the treatment. 75% of them had a history of prior osteoporotic treatment. Baseline mean age was 60 ± 8years. Mean baseline vertebral T-score was -3.7 ± 0.7 and 83 (76%) women had suffered at least one vertebral fracture. At the end of treatment, 18 women (17%) were classified as non-responders. In the responder group (n = 91), vertebral BMD increased by 0.091 ± 0.04g/cm2 (12.2 ± 5.3%). Clinical characteristics, baseline BMDs and the percentage of women previously treated with bisphosphonates as well as the duration of prior treatment did not significantly differ between the two groups of responders and non-responders. At baseline, non-responders had significant mean lower C-terminal fragment of type 1 collagen (CTX) values than responders (p < 0.01). Only baseline CTX values (r = 0.30 p < 0.01) were independently correlated to vertebral BMD changes during teriparatide treatment. A minority of treated women had no vertebral densitometric gain after 18months of teriparatide therapy. Low levels of baseline bone remodeling were the main factor associated with poor response to treatment.

Denosumab in pediatric bone disorders and the role of RANKL blockade: a narrative review.

Denosumab is a valuable and safe therapy for skeletal disorders in adults and has received regulatory approval to treat osteoporosis and bone metastases. However, denosumab is not licensed for pediatric use due to a lack of high-quality prospective research on children. This study aimed to describe and discuss the benefits and disadvantages of denosumab in treating bone diseases in children and to summarize the current understanding of the role of denosumab therapy in children. A narrative review was conducted using the literature retrieved from the PubMed, Embase, and Cochrane Library databases. In children with type 6 osteogenesis imperfecta (OI), juvenile Paget disease (JPD), and secondary osteoporosis who show poor response to bisphosphonate, the use of denosumab has been reported to improve osteoporosis and increase bone mineral density (BMD). Moreover, for those with relapse, progressive and refractory aneurysmal bone cyst (ABC), fibrous dysplasia (FD), giant cell tumor of bone (GCTB), and central giant cell granuloma (CGCG) lesions, denosumab can improve pain symptoms, control disease progression, and reduce serious adverse events. Although there have been sporadic reports of adverse events such as hypocalcemia during medication and rebound hypercalcemia after discontinuation, early prevention, monitoring, and timely intervention can prevent children from experiencing severe adverse events. The published data indicate that denosumab has efficacy in alleviating disease in multiple refractory bone lesions in children.

Epidermal growth factor receptor inhibition prevents vascular calcifying extracellular vesicle biogenesis.

Chronic kidney disease (CKD) increases the risk of cardiovascular disease, including vascular calcification, leading to higher mortality. The release of calcifying extracellular vesicles (EVs) by vascular smooth muscle cells (VSMCs) promotes ectopic mineralization of vessel walls. Caveolin-1 (CAV1), a structural protein in the plasma membrane, plays a major role in calcifying EV biogenesis in VSMCs. Epidermal growth factor receptor (EGFR) colocalizes with and influences the intracellular trafficking of CAV1. Using a diet-induced mouse model of CKD followed by a high-phosphate diet to promote vascular calcification, we assessed the potential of EGFR inhibition to prevent vascular calcification. Furthermore, we computationally analyzed 7,651 individuals in the Multi-Ethnic Study of Atherosclerosis (MESA) and Framingham cohorts to assess potential correlations between coronary artery calcium and single-nucleotide polymorphisms (SNPs) associated with elevated serum levels of EGFR. Mice with CKD developed widespread vascular calcification, associated with increased serum levels of EGFR. In both the CKD mice and human VSMC culture, EGFR inhibition significantly reduced vascular calcification by mitigating the release of CAV1-positive calcifying EVs. EGFR inhibition also increased bone mineral density in CKD mice. Individuals in the MESA and Framingham cohorts with SNPs associated with increased serum EGFR exhibit elevated coronary artery calcium. Given that EGFR inhibitors exhibit clinical safety and efficacy in other pathologies, the current data suggest that EGFR may represent an ideal target to prevent pathological vascular calcification in CKD.NEW & NOTEWORTHY Here, we investigate the potential of epidermal growth factor receptor (EGFR) inhibition to prevent vascular calcification, a leading indicator of and contributor to cardiovascular morbidity and mortality. EGFR interacts and affects the trafficking of the plasma membrane scaffolding protein caveolin-1. Previous studies reported a key role for caveolin-1 in the development of specialized extracellular vesicles that mediate vascular calcification; however, no role of EGFR has been reported. We demonstrated that EGFR inhibition modulates caveolin-1 trafficking and hinders calcifying extracellular vesicle formation, which prevents vascular calcification. Given that EGFR inhibitors are clinically approved for other indications, this may represent a novel therapeutic strategy for vascular calcification.

Moringa oleifera leaf attenuate osteoporosis in ovariectomized rats by modulating gut microbiota composition and MAPK signaling pathway

Moringa oleifera leaf (MLP) contains abundant complex nutrients with anti-osteoporosis potential. However, its efficacy and mechanisms against osteoporosis remain unknown. The purpose of this research is to investigate MLP's anti-osteoporotic effects and mechanisms. Animal experiments were used in this work to validate MLP's anti-osteoporotic efficacy. We investigated the mode of action of MLP, analyzed its impact on the gut microbiota, and predicted and validated its anti-osteoporosis-related molecular targets and pathways through network pharmacology, molecular docking, and western blotting. In an ovariectomized osteoporosis rat model, MLP significantly increased bone mineral density and improved bone metabolism-related indicators, bone microstructure, and lipid profile. Moreover, it improved gut microbiota composition and increased the expression of Occludin and Claudin-1 protein in the duodenum. Network pharmacology identified a total of 97 active ingredients and 478 core anti-osteoporosis targets. Of these, MAPK1 (also known as ERK2), MAPK3 (also known as ERK1), and MAPK8 (also known as JNK) were successfully docked with the active constituents of MLP. Interestingly, MLP increased ERK and VAV3 protein expression and decreased p-ERK and JNK protein expression in the femur. These findings confirm MLP's anti-osteoporotic efficacy, which could be mediated via regulation of gut microbiota and MAPK signaling.

Bone modifying agents in postmenopausal breast cancer patients treated with aromatase inhibitors: beyond bone protection?

Estrogen-receptor positive tumours represent the majority of breast cancers in postmenopausal women. Adjuvant endocrine therapy with aromatase inhibitors (AIs), continued for up to 10 years in high-risk patients, reduces by 40% the risk of recurrence. However, this therapy, among other side effects, is burdened with a higher incidence of osteoporotic bone fractures. To date, both bisphosphonates and denosumab are recognized as first-line drugs in the primary prevention of osteoporotic fractures in patients treated with AIs. They have demonstrated their effectiveness in increasing bone mineral density and in reducing the incidence of fractures, but they have also been shown to improve disease free survival (DFS).

Allolobophora caliginosa coelomic fluid and extract alleviate glucocorticoid-induced osteoporosis in mice by suppressing oxidative stress and regulating osteoblastic/osteoclastic-related markers

Allolobophora calignosa (Ac) is a folk medicine for millennia, as it possesses many biological activities. This study aimed to investigate the chemo-preventive activity of A.calignosa coelomic fluid (AcCF) and A.calignosa extract (AcE) on glucocorticoid-induced osteoporosis (GIOP) in mice. Characterization and in vitro biological activity of AcE and AcCF has been assessed. Male CD-1 mice were subcutaneously received dexamethasone (DEX) (1 mg/kg, 5 times/week) and concurrently intraperitoneally treated with either AcCF (20 mg/kg) or AcE (45 mg/kg) every other day for 28 days. Serum and bone homogenates were subjected for qPCR and biochemical analysis. AcE and AcCF treatment significantly increased bone mineral density (BMD), bone mineral content (BMC), calcium (Ca), phosphorus (P), and calcitonin levels, whereas activity of serum alkaline phosphatase (ALP), bone alkaline phosphatase (BALP), serum acidic phosphatase (ACP), bone acidic phosphatase (BACP) and parathyroid hormone (PTH) levels were significantly reduced compare with untreated GIOP mice. Treatment with AcE and AcCF modulates oxidative stress and downregulated Rank and Mmp9 expression, as well as increased glycosaminoglycan content in the organic bone matrix, resulting in osteoclastogenesis inhibition. Overall, AcCF and AcE show a chemo-preventive activity against GIOP by inhibiting oxidative stress and regulating expression and/or activity of osteoblast/osteoclast-related markers.

Bone Remodelling of the Proximal Femur After Hip Revision with a Metaphyseal-Fixation Femoral Stem Component.

Whether hip revision with a metaphyseal-fixation femoral stem component can restore the bone mass of the proximal femur remains unclear. The aims of this study were to identify whether the bone mineral density (BMD) of the proximal femur increases following hip revision with a metaphyseal-fixation femoral stem and to identify the factors associated with BMD recovery. This was a retrospective study involving 36 patients who underwent hip arthroplasty with a metaphyseal-diaphyseal fixation stem (standard length stem) and had indications for hip revision, which was performed with a proximal press-fit short-stem prosthesis for each patient. Dual-energy X-ray absorptiometry (DEXA) was used to obtain, evaluate, and compare the BMD at baseline and one year and two years postoperatively. The proximal femur was divided into several independent areas according to the Gruen zone (Gruen 1 to Gruen 7 from the greater trochanter counterclockwise to the lesser trochanter). Logistic regression analyses were used to assess potential factors significantly associated with an increase in BMD. An increased BMD was obviously identified in the proximal femur. Two years after the surgery, the BMD of the Gruen 1, Gruen 2, Gruen 6, and Gruen 7 areas had increased by 22.6%, 12.6%, 16.2% and 24.2%, respectively, relative to baseline. Three independent risk factors associated with bone mineral density recovery were identified: age (OR=1.100, 95% CI=1.005-1.203, P=0.038), osteoporosis (OR=14.921, 95% CI=1.223-182.101, P=0.034) and fair to poor hip function (OR=13.142, 95% CI=1.024-168.582, P=0.048). This study confirms that metaphyseal-fixation stem hip revision can indeed help restore bone mass in the proximal femur, especially in the Gruen 1, Gruen 2, Gruen 6 and Gruen 7 zones. It was also found that advanced age, osteoporosis, and fair to poor hip joint function were three important risk factors affecting the recovery of proximal femur bone mass after surgery. Retrospectively registered.

The association of diabetes status and bone mineral density among US adults: evidence from NHANES 2005–2018

BackgroundsWe aimed to explore the relationship between diabetes status and bone mineral density (BMD) among adults with pre-diabetes and diabetes.MethodsWe collected and analyzed five cycles (2005–2006, 2007–2008, 2009–2010, 2013–2014, and 2017–2018) data from NHANES. We removed the individuals containing missing values. The linear regression models were used to explore the relationship between diabetes status and bone mineral density. Finally, we performed subgroup analyzes by age, sex and race to find special populations.ResultFinally, 9661 participants with complete data were involved in the study. 944 were diagnosed with pre-diabetes, and 2043 were with diabetes. We found that bone mineral density in the hip, femoral neck, and lumbar spine showed an upward trend in both prediabetic and diabetic patients in the three linear regression models. Further, after subgroup analysis, we found that this trend was more prominent in whites race, women, and those over 50 years old.ConclusionUsing NHANES data from 2005 to 2018, we found that patients with abnormal glucose metabolism had increased bone mineral density.

Vertebral Compression Fractures in Very Early Onset Inflammatory Bowel Disease.

Patients with VEOIBD receiving care at a single tertiary center were prospectively enrolled in a longitudinal data repository. Retrospective chart review was performed to identify clinical characteristics and comorbidities. Those with clinically apparent vertebral compression fractures subsequently underwent an additional chart review focused on bone health. Three out of 216 (1.4%) patients with VEOIBD had symptomatic vertebral compression fractures. Of the 3 patients with vertebral compression fractures, all had Crohn's disease, 2 had monogenic inflammatory bowel disease, and all reported back pain. One patient notably had a normal dual-energy X-ray absorptiometry, highlighting a potential limitation of dual-energy X-ray absorptiometry to identify increased skeletal fragility in this population. Risk factors for suboptimal bone health included chronic inflammation secondary to poorly controlled inflammatory bowel disease, substantial glucocorticoid exposure, chronic use of other medications associated with suboptimal bone health including proton pump inhibitors and granulocyte colony-stimulating factor, and solid organ transplant. Patients treated with bisphosphonates had improved clinical outcomes, with resolution of back pain and increased bone mineral density. Vertebral compression fracture should be considered in the differential diagnosis of patients with VEOIBD and back pain, especially in those with other risk factors for suboptimal bone health. Treatment of compression fractures with bisphosphonates resulted in resolution of back pain and improved bone density.

Effect of Yi Jin Jing exercise plus Elastic Band Resistance exercise on overall bone mineral density in postmenopausal women.

This work aimed to study the effects of Yi Jin Jing plus Elastic Band Resistance exercise on bone mineral density at all parts of the body and bone metabolism index levels in postmenopausal women. Randomized controlled trial. Forty postmenopausal women were randomly assigned equally to the exercise or to the control group. The control group maintained their lifestyle behaviors unaltered, whereas the exercise group received Yi Jin Jing plus Elastic Band Resistance exercise. The primary outcome was overall bone mineral density at each part, and the secondary one was bone metabolism indicator levels and bone mineral density on both sides. The results after six months showed increased bone mineral density at all parts of the body in the exercise group (spine, P = 0.002; thighs, lumbar, and whole body, P < 0.05) and decreased bone mineral density in the control group (trunk, pelvis, and spine, P < 0.01). In particular, the decrease and increase were greater on the non-preferred (left) side than on the right side. As for bone metabolism indexes, β-Crosslaps levels reduced (P = 0.016) and a significant increase in 1,25-(OH)2-D3 (P < 0.001) can be observed in the exercise group. The results suggested that Yi Jin Jing plus Elastic Band Resistance exercise could delay the overall decrease of bone mineral density in postmenopausal women, especially on the non-preferred side. It also increased bone formation metabolite levels and inhibited bone resorption metabolite levels.

Untreated Atypical Left Femoral Shaft Fracture: A Case Report of Its Complication

Background: Bisphosphonate therapy is used to manage osteoporosis and decrease the risk of vertebral and hip fractures. These drugs act by suppressing osteoclast activity by inducing the inhibition of bone resorption and increasing bone mineral density. It has been shown that long-term use of bisphosphonate is correlated to a higher incidence of atypical femoral fractures. Case report: This is a case report of an 81-year-old female, on bisphosphonate therapy for 12 years and with chronic left thigh pain for two and a half years who developed an incomplete atypical left femur fracture. What’s special about this case is that the fracture was ignored and then progressed after three months into a complete displaced spiral fracture that required surgical fixation. Conclusion: The benefits of bisphosphonate treatment in preventing osteoporotic fractures outweigh the risk of the occurrence of these atypical fractures. Orthopedic surgeons as well as primary care physicians must keep atypical fractures in their differential diagnosis in patients presenting with prodromal symptoms and who are on long-term bisphosphonate therapy

Calcium and vitamin D for increasing bone mineral density in premenopausal women.

Calcium and vitamin D for increasing bone mineral density in premenopausal women.