Prevent Bone Loss Research Articles

Benefits of the Phytoestrogen Resveratrol for Perimenopausal Women

Endometriosis, characterized by macroscopic lesions in the ovaries, is a serious problem for women who desire conception. Damage to the ovarian cortex is inevitable when lesions are removed via surgery, which finally decreases the ovarian reserve, thereby accelerating the transition to the menopausal state. Soon after cessation of ovarian function, in addition to climacteric symptoms, dyslipidemia and osteopenia are known to occur in women aged >50 years. Epidemiologically, there are sex-related differences in the frequencies of dyslipidemia, hypertension, and osteoporosis. Females are more susceptible to these diseases, prevention of which is important for healthy life expectancy. Dyslipidemia and hypertension are associated with the progression of arteriosclerosis, and arteriosclerotic changes in the large and middle blood vessels are one of the main causes of myocardial and cerebral infarctions. Osteoporosis is associated with aberrant fractures in the spine and hip, which may confine the patients to the bed for long durations. Bone resorption is accelerated by activated osteoclasts, and rapid bone remodeling reduces bone mineral density. Resveratrol, a plant-derived molecule that promotes the function and expression of the sirtuin, SIRT1, has been attracting attention, and many reports have shown that resveratrol might exert cardiovascular protective effects. Preclinical reports also indicate that it can prevent bone loss and endometriosis. In this review, I have described the possible protective effects of resveratrol against arteriosclerosis, osteoporosis, and endometriosis because of its wide-ranging functions, including anti-inflammatory and antioxidative stress functions. As ovarian function inevitably declines after 40 years, intake of resveratrol can be beneficial for women with endometriosis aged <40 years.

Durability and delayed treatment effects of zoledronic acid on bone loss after spinal cord injury: a randomized, controlled trial.

A single infusion of zoledronic acid (ZOL) after acute spinal cord injury (SCI) attenuates bone loss at the hip (proximal femur) and knee (distal femur and proximal tibia) for at least 6 months. The objective of this study was to examine the effects of timing and frequency of ZOL over 2 years. In this double-blind, placebo-controlled trial, we randomized 60 individuals with acute SCI (<120 days of injury) to receive either ZOL 5-mg infusion (n=30) or placebo (n=30). After 12 months, groups were again randomized to receive ZOL or placebo, resulting in four treatment groups for year 2: (i) ZOL both years; (ii) ZOL year 1, placebo year 2; (iii) placebo year 1, ZOL year 2; and (iv) placebo both years. Our primary outcome was bone loss at 12 months; compared to placebo, a single infusion of ZOL attenuated bone loss at the proximal femur, where median changes relative to baseline were -1.7% to -2.2% for ZOL versus -11.3% to -12.8% for placebo (p < 0.001). Similarly, the distal femur and proximal tibia showed changes of -4.7% to -9.6% for ZOL versus -8.9% to -23.0% for placebo (p ≤ 0.042). After 24 months, differences were significant at the proximal femur only (-3.2% to -6.0% for ZOL vs. -16.8% to -21.8% for placebo; p ≤ 0.018). Although not statistically significant, median bone density losses suggested some benefit from two annual infusions compared to a single baseline infusion, as well as from a single infusion 12 months after baseline compared to 2 years of placebo; therefore, further investigation in the 12-month to 24-month treatment window is warranted. No unanticipated adverse events associated with drug treatment were observed. In summary, ZOL 5-mg infusion after acute SCI was well-tolerated and may provide an effective therapeutic approach to prevent bone loss in the first few years following SCI. © 2021 American Society for Bone and Mineral Research (ASBMR).

Co-encapsulation of combinatorial flavonoids in biodegradable polymeric nanoparticles for improved anti-osteoporotic activity in ovariectomized rats

In our study a novel nanocombination of flavonoids was synthesized for anti-osteoporotic therapeutics. We chose 2 flavonoids, quercetin and curcumin to be encapsulated in polylactic-co-glycolic acid (PLGA) for anti-osteoporotic activity in induced ovariectomized rats. The synthesized flavonoids co-encapsulated PLGA nanoparticles were analysedfor morphological changes with electron micrography and its zeta potential along with PDI was determined. The encapsulation and loading efficiency studies were performed along with in vitro release studies. Cytotoxicity of the synthesized nanoparticles was evaluated with primary bone cells. The administration of the flavonoid co-encapsulated nanoparticles was done intragastrically after which the physical parameters of the femur, compression test of lumbar vertebra were studied. Weight of ash, % of ash and ash calcium of femoral bone were calculated along with biochemical characterization of serum. The histopathological examination of femur was done too. The synthesized flavonoids co-encapsulated PLGA nanoparticles were small enough (110–135 nm) and exhibited homogeneous distribution. The high encapsulation and loading efficiencies demonstrated a favourable nanocombination. The cytotoxicity results exhibited the cytocompatibility of the nanoparticles. From the in-vivo studies, it was seen that the flavonoids co-encapsulated PLGA nanoparticles inhibited trabecular bone loss and significantly improved bone mineral density and bone microarchitecture. The flavonoids loaded PLGA nanoparticles augmented the protective effect to prevent bone loss after ovariectomy. This study may be furthered for novel therapeutic management of osteoporosis. • Quercetin and curcumin encapsulated in PLGA nanoparticles. • Encapsulation and loading efficiency studies with in-vitro release. • in-vivo studies show inhibited trabecular bone loss and improved bone density. • The protective effect on bone loss got augmented after ovariectomy.

Raloxifene in the Treatment of Osteoporosis in Postmenopausal Women with End-Stage Renal Disease: A Systematic Review and Meta-Analysis.

As a selective estrogen receptor modulator (SERM), raloxifene is used in healthy postmenopausal women to prevent bone loss and reduce fractures. However, the benefit of raloxifene is uncertain in the treatment of osteoporosis among patients with end-stage renal disease (ESRD) or those who require maintenance dialysis. We assessed the safety and efficacy of raloxifene in this particular population. Studies were selected from PubMed, Springer, CNKI (Chinese National Knowledge Infrastructure) and Wanfang Database. Randomized controlled trials (RCTs) and prospective studies with control/placebo groups were included. Five studies were included with a total of 244 participants (121 patients in the raloxifene group and 123 patients in the placebo/control group). The median duration of treatment was 12 months. The incidence rate of side effects of raloxifene was 0/121 (0%). There was a significant improvement of lumbar spine bone mineral density (BMD) levels in the raloxifene group compared with the placebo group (MD: 33.88, 95% CI: 10.93, 56.84, p=0.004). There was no significant difference concerning the improvement of femoral neck BMD (MD: 8.42, 95% CI: -10.21, 27.04, p=0.38), intact parathyroid hormone (iPTH) (MD: -12.62, 95% CI: -35.36, 10.13, p=0.28), calcium (MD: -0.08, 95% CI: -0.61, 0.44, p=0.76), phosphorus (MD: 0.18, 95% CI: -0.12, 0.48, p=0.23) or bone alkaline phosphatase (BAP) (MD: -4.33, 95% CI: -14.44, 5.79, p=0.40). Raloxifene seems to be effective in improving the lumbar spine BMD in postmenopausal women with ESRD. More large RCTs are necessary to evaluate the long-term safety of raloxifene in uremic patients.

Tenofovir Modulates Semaphorin 4D Signaling and Regulates Bone Homeostasis, Which Can Be Counteracted by Dipyridamole and Adenosine A2A Receptor.

Semaphorin 4D (Sema4D) is a neurotrophin that is secreted by osteoclasts and binds to its receptor PlexinB1 on osteoblasts to inhibit their differentiation and function. Adenosine A2A activation inhibits osteoclast Sema4D-mediated secretion, diminishes inflammatory osteolysis and prevents bone loss following tenofovir (one of the most used antivirals in HIV). Therefore, tenofovir might activate Sema4D signaling to alter bone turnover. Female C57Bl/6/A2AKO mice were ovariectomized and treated with saline (control), tenofovir 75 mg/Kg/day, dipyridamole 25 mg/Kg/day or a combination for 5 weeks and long bones were prepared for histology. Primary murine-induced osteoclast/osteoblast were challenged with tenofovir/dipyridamole 1 μM each, and the expression of Sema4D/PlexinB1, RhoA/ROCK/IGF1R was studied by RT-PCR, Western blot and immunostaining. In vivo tenofovir showed an increased expression of Sema4D when compared to control mice, and dipyridamole reverted the expression in an A2A-dependent manner. In vitro, tenofovir increases Sema4D expression and secretion in osteoclast precursors, and pre-treatment with dipyridamole reverted this effect. pRhoA and ROCK1 activation were increased and IRS1/IGF1R expression was diminished by tenofovir in the Vav3/ARHGAP18 mechanism in osteoblast precursors and reverted by dipyridamole in an A2A-dependent manner. This suggests that tenofovir increases bone loss by activation of Sema4D/PlexinB1 signaling, which inhibits osteoblast differentiation. Agents that increase local adenosine concentrations, such as dipyridamole, might prevent bone loss following the inhibition of this pathway.

Bisphosphonate-enoxacin inhibit osteoclast formation and function by abrogating RANKL-induced JNK signalling pathways during osteoporosis treatment.

Osteoporosis is an age‐related disease characterized by low mineral density, compromised bone strength and increased risk of fragility fracture. Most agents for treating osteoporosis focus primarily on anti‐resorption by inhibiting osteoclast activity. Bisphosphonate (BP) is a potent anti‐resorptive agent that has been used clinically for decades and is proven to be effective. However, BP has a variety of side effects and is far from being an ideal anti‐osteoporosis agent. BP selectively binds to calcium crystals, which are subsequently taken up or released by osteoclasts. Based on the action of BP, we previously demonstrated the inhibitory effect of a novel bone‐targeting BP derivative, bisphosphonate‐enoxacin (BE). In the current study, we used bone marrow‐derived osteoclast cultures to further assess the inhibitory effect of BE on osteoclastogenesis and employed reverse transcription PCR and real‐time PCR to examine expression of osteoclast‐specific genes. Additionally, we used bone resorption and F‐actin immunofluorescence assays to evaluate the effect of BE on osteoclast function and investigated the potential mechanisms affecting osteoclast differentiation and function in vitro. Furthermore, an ovariectomized (OVX) rat model was established to evaluate the therapeutic effects of BE on preventing bone loss. Results showed that BE exerted potent inhibitory effects on osteoclast formation and bone resorption by specifically abrogating RANKL‐induced JNK signalling, and that it preserved OVX rat bone mass in vivo without any notable side effects. Collectively, these results indicated that the BP derivative BE may have significant potential as a treatment for osteoporosis and other osteolytic diseases.

Role of Polyphenols in the Metabolism of the Skeletal System in Humans and Animals – A Review

Abstract Polyphenols are a group of compounds arousing enormous interest due to their multiple effects on both human and animal health and omnipresence in plants. A number of in vitro and animal model studies have shown that all polyphenols exhibit anti-inflammatory and antioxidant activities, and play a significant role against oxidative stress-related pathologies. They also exert gut promotory effects and prevent chronic degenerative diseases. However, less attention has been paid to the potential influence of polyphenols on bone properties and metabolism. It is well known that proper growth and functioning of the organism depend largely on bone growth and health. Therefore, understanding the action of substances (including polyphenols) that may improve the health and functioning of the skeletal system and bone metabolism is extremely important for the health of the present and future generations of both humans and farm animals. This review provides a comprehensive summary of literature related to causes of bone loss during ageing of the organism (in both humans and animals) and possible effects of dietary polyphenols preventing bone loss and diseases. In particular, the underlying cellular and molecular mechanisms that can modulate skeletal homeostasis and influence the bone modeling and remodeling processes are presented.

The association between serum vitamin D and body composition in South African HIV-infected women.

BackgroundHIV and antiretroviral therapy (ART) alter vitamin D metabolism, and may be associated with bone loss.ObjectivesThe aim of this study was to determine the association between serum 25-hydroxyvitamin D (25(OH)D) and body composition in postmenopausal South African women living with HIV and on ART.MethodIn this 2-year longitudinal study on 120 women conducted in the North West province of South Africa, serum 25(OH)D concentration, bone mineral density (BMD) at three sites, lean mass and percentage of body fat (%BF) were measured by dual-energy X-ray absorptiometry (DXA). Multivariable linear mixed models were used to assess the association between serum 25(OH)D and body composition over 2 years. Linear mixed models were also used to determine the longitudinal association between lean mass, %BF and BMD.ResultsVitamin D deficiency and insufficiency increased from baseline (10.2% and 19.5%) to 11.5% and 37.5%, respectively, after 2 years. Serum 25(OH)D decreased significantly, however, with a small effect size of 0.39 (P = 0.001), whilst total BMD (effect size 0.03, P = 0.02) and left hip femoral neck (FN) BMD (effect size 0.06, P = 0.0001) had significant small increases, whereas total spine BMD did not change over the 2 years. Serum 25(OH)D had no association with any BMD outcomes. Lean mass had a stronger positive association with total spine and left FN BMD than %BF.ConclusionSerum 25(OH)D was not associated with any BMD outcomes. Maintenance of lean mass could be important in preventing bone loss in this vulnerable group; however, longer follow-up may be necessary to confirm the association.

Magnesium Picolinate Improves Bone Formation by Regulation of RANK/RANKL/OPG and BMP-2/Runx2 Signaling Pathways in High-Fat Fed Rats.

Magnesium (Mg) deficiency may affect bone metabolism by increasing osteoclasts, decreasing osteoblasts, promoting inflammation/oxidative stress, and result in subsequent bone loss. The objective of the present study was to identify the molecular mechanism underlying the bone protective effect of different forms of Mg (inorganic magnesium oxide (MgO) versus organic magnesium picolinate (MgPic) compound) in rats fed with a high-fat diet (HFD). Forty-two Wistar albino male rats were divided into six group (n = 7): (i) control, (ii) MgO, (iii) MgPic, (iv) HFD, (v) HFD + MgO, and (vi) HFD + MgPic. Bone mineral density (BMD) increased in the Mg supplemented groups, especially MgPic, as compared with the HFD group (p < 0.001). As compared with the HFD + MgO group, the HFD + MgPic group had higher bone P (p < 0.05) and Mg levels (p < 0.001). In addition, as compared to MgO, MgPic improved bone formation by increasing the levels of osteogenetic proteins (COL1A1 (p < 0.001), BMP2 (p < 0.001), Runx2 (p < 0.001), OPG (p < 0.05), and OCN (p < 0.001), IGF-1 (p < 0.001)), while prevented bone resorption by reducing the levels of RANK and RANKL (p < 0.001). In conclusion, the present data showed that the MgPic could increase osteogenic protein levels in bone more effectively than MgO, prevent bone loss, and contribute to bone formation in HFD rats.

Fractions of Shen-Sui-Tong-Zhi Formula Enhance Osteogenesis Via Activation of β-Catenin Signaling in Growth Plate Chondrocytes.

Background: Shen-sui-tong-zhi formula (SSTZF) has been used to treat osteoporosis for decades and shows excellent clinical efficacy. This article aims to explore the optimal anti-osteoporotic ingredient and its precise mechanisms in mice models. Methods: In this study, we first screened the optimal anti-osteoporosis fraction of SSTZF extract in vivo, and then further explored the mechanism of its effects both in vivo and in vitro. Ten-week-old female C57BL/6J mice were administrated with each fraction of SSTZF. At 10 weeks after ovariectomy (OVX), femurs were collected for tissue analyses, including histology, micro-CT, biomechanical tests, and immunohistochemistry for ALP, FABP4, and β-catenin. Additionally, we also evaluated the mRNA expression level of ALP and FABP4 and the protein expression level of β-catenin after being treated with SSTZF extract in C3H10T1/2 cells. Moreover, we investigated the anti-osteoporosis effect of SSTZF extract on mice with β-catenin conditional knockout in growth plate chondrocytes (β-catenin Gli1ER mice) through μCT, histology, and immunohistochemistry analyzes. Results: At 10 weeks after treatment, osteoporosis-like phenotype were significantly ameliorated in SSTZF n-butanol extract (SSTZF-NB) group mice, as indicated by increased trabecular bone area and ALP content, and decreased lipid droplet area and FABP4 content. No such improvements were observed after being treated with other extracts, demonstrating that SSTZF-NB is the optimal anti-osteoporosis fraction. Additionally, the elevated β-catenin was revealed in both OVX mice and C3H10T1/2 cells with SSTZF-NB administered. Furthermore, a significant osteoporosis-like phenotype was observed in β-catenin Gli1ER mice as expected. However, SSTZF-NB failed to rescue the deterioration in β-catenin Gli1ER mice, no significant re-upregulated ALP and downregulated FABP4 were observed after being treated with SSTZF-NB, demonstrating that SSTZF-NB prevents bone loss mainly via β-catenin signaling. Conclusion: SSTZF-NB enhances osteogenesis mainly via activation of β-catenin signaling in growth plate chondrocytes. SSTZF-NB is the optimal anti-osteoporosis fraction of SSTZF and it can be considered a salutary alternative therapeutic option for osteoporosis.

First-in-class humanized FSH blocking antibody targets bone and fat

The authors report the generation, structure and function of a fully humanized, humanized antibody that profoundly inhibits follicle-stimulating hormone (FSH) actions in cell-based assays. Administration of the antibody to ovariectomized mice prevented bone loss and also accumulation of adipose tissue when fed a high-fat diet (HFD).

Extract and fraction of Musa paradisiaca flower have osteogenic effect and prevent ovariectomy induced osteopenia

BackgroundOsteoporosis is an asymptomatic bone disorder leading to altered bone microarchitecture, mineralization and strength. Musa paradisiaca has been reported to have antioxidant and anti-inflammatory effects in various diseases. Its impact on postmenopausal osteoporosis has not been investigated yet. PurposeThe intention of the current study was to evaluate the bone regeneration and osteoprotective potential of extract and fraction of M. paradisiaca flower in ovariectomized (Ovx) Sprague Dawley (SD) rats, a model of post-menopausal bone loss. The study also aims to identify osteogenic compounds from active fraction. MethodsEthanolic extract (MFE) and butanolic fraction (MFE-Bu) from flower of M. paradisiaca were prepared and their efficacy was tested in rat femur osteotomy model at different doses. Effective dose from both extract (250 mg/kg) and fraction (50 mg/kg) were taken for study in osteopenic bone loss model. PTH was taken as reference standard (20 µg/kg/twice a week). Bones were harvested at autopsy for dynamic and static histomorphometry. Serum was collected for ELISA. Pure compounds were isolated from butanolic fraction (MFE-Bu), and were assessed for their osteogenic effect. ResultsMFE and MFE-Bu were observed for their potential in bone healing and prevention of bone loss. Both MFE and MFE-Bu promoted new bone regeneration at injury site as assessed by microCT and calcein dye labeling studies. These also led to restoration of bone microarchitecture deteriorated as a result of osteopenia and improved bone biomechanical properties. Extract as well as the fraction exhibited dual bone anabolic and anti-resorptive properties where they elevated serum procollagen type I N-terminal propeptide (P1NP), a bone formation marker and suppressed serum C-telopeptide of type I collagen (CTX-1), a bone resorption marker. As many as four osteogenic compounds were isolated from MFE-Bu. Oleracein-E was found to be the most potent osteogenic agent based on osteoblast differentiation, mineralization assays, qPCR and protein expression studies. ConclusionOur studies demonstrates that ethanolic extract from the flower of M. paradisiaca and its butanolic fraction exhibit dual osteogenic and anti-resorptive potential, and have an advantage over PTH which though promotes bone formation but is also bone catabolic in nature.

Exogenous melatonin prevents type 1 diabetes mellitus\u2013induced bone loss, probably by inhibiting senescence

SummaryExogenous melatonin inhibited the senescence of preosteoblast cells in type 1 diabetic (T1D) mice and those cultured in high glucose (HG) by multiple regulations. Exogenous melatonin had a protective effect on diabetic osteoporosis, which may depend on the inhibition of senescence.IntroductionSenescence is thought to play an important role in the pathophysiological mechanisms underlying diabetic bone loss. Increasing evidence has shown that melatonin exerts anti-senescence effects. In this study, we investigated whether melatonin can inhibit senescence and prevent diabetic bone loss.MethodsC57BL/6 mice received a single intraperitoneal injection of 160 mg/kg streptozotocin, followed by the oral administration of melatonin or vehicle for 2 months. Then, tissues were harvested and subsequently examined. MC3T3-E1 cells were cultured under HG conditions for 7 days and then treated with melatonin or not for 24 h. Sirt1-specific siRNAs and MT1- or MT2-specific shRNA plasmids were transfected into MC3T3-E1 cells for mechanistic study.ResultsThe total protein extracted from mouse femurs revealed that melatonin prevented senescence in T1D mice. The micro-CT results indicated that melatonin prevented bone loss in T1D mice. Cellular experiments indicated that melatonin administration prevented HG-induced senescence, whereas knockdown of the melatonin receptors MT1 or MT2 abolished these effects. Sirt1 expression was upregulated by melatonin administration but significantly reduced after MT1 or MT2 was knocked down. Knockdown of Sirt1 blocked the anti-senescence effects of melatonin. Additionally, melatonin promoted the expression of CDK2, CDK4, and CyclinD1, while knockdown of MT1 or MT2 abolished these effects. Furthermore, melatonin increased the expression of the polycomb repressive complex (PRC), but knockdown of MT1 or MT2 abolished these effects. Furthermore, melatonin increased the protein levels of Sirt1, PRC1/2 complex–, and cell cycle–related proteins.ConclusionThis work shows that melatonin protects against T1D-induced bone loss, probably by inhibiting senescence. Targeting senescence in the investigation of diabetic osteoporosis may lead to novel discoveries.

Anti-Osteoporotic Activity of Pueraria lobata Fermented with Lactobacillus paracasei JS1 by Regulation of Osteoblast Differentiation and Protection against Bone Loss in Ovariectomized Mice

Osteoporosis is the most common bone disease associated with low bone mineral density. It is the process of bone loss and is most commonly caused by decreased estrogen production in women, particularly after menopause. Pueraria lobata, which contains various metabolites, especially isoflavone, is widely known as regulator for bone mineral contents. In this study, the effects of the P. lobata extract (PE) with or without fermentation with Lactobacillus paracasei JS1 (FPE) on osteoporosis were investigated in vitro and in vivo. The effects of PE and FPE on human osteoblastic MG63 cells, RAW 264.7 cells, and ovariectomized (OVX)-induced model mice were analyzed at various ratios. We found that FPE increased calcium deposition and inhibited bone resorption by in vitro assay. Furthermore, treatment with PE and FPE has significantly restored destroyed trabecular bone in the OVX-induced bone loss mouse model. Overall, FPE demonstrated bioactivity to prevent bone loss by decreasing bone turnover.

A Multi-Institutional Randomized Controlled Trial to Investigate Whether Zoledronate Prevents Bone Loss After Discontinuation of Denosumab: The Study Protocol of Denosumab Sequential Therapy (DST) Trial.

Background: Though denosumab is an effective treatment for osteoporosis, the rebound effect after discontinuation has drawn investigators' attention. It includes a dramatic loss of gained bone mineral density (BMD) and an increased risk of vertebral fractures. This prospective multi-institutional randomized controlled trial aims to investigate whether zoledronate prevents loss of BMD after discontinuation of denosumab. The trial was registered as Denosumab Sequential Therapy (DST) trial in March 2019 at clinicaltrials.gov, with the identifier NCT03868033.Methods: The study is conducted at National Taiwan University Hospital and its branches. Patients who have continuously received denosumab treatment for two or more years are surveyed for eligibility. Baseline characteristics and questionnaires of life quality are recorded after recruitment. BMD, circulating levels of bone turnover markers (BTMs), including serum N-terminal propeptide of type 1 collagen (P1NP) and C-terminal telopeptide (CTX), are checked before the stratified randomization to 4 groups. Biological sex and the T-scores are used to create 4 strata. The participants in group 1 adhere to regular denosumab therapy for another 2 years. All the other patients receive on-time zoledronate treatment in the first year. The participants in group 2, 3, and 4 have on-time denosumab, on-time zoledronate and drug holiday in the second year, respectively. BMDs are checked annually. Pre-scheduled checkpoints of BTMs are also arranged. For patient safety, rescue treatment with another injection of zoledronate will be applied to the patients on drug holiday if the CTX levels raise above the pre-specified threshold, 0.573 ng/mL for women and 0.584 ng/mL for men. The primary outcomes are the percentage changes of BMDs in lumbar spine, total hip and femoral neck. The secondary outcomes include the changes of serum level of the BTMs, new osteoporotic fractures, extra zoledronate injections needed in group 4 and the differences of quality of life.Discussion: We aim to provide evidence whether zoledronate prevents bone loss after denosumab cessation. To our knowledge, the study has the largest sample size. No other randomized controlled study included all the three different treatment strategies and a positive control. It is also the first associated randomized controlled trial outside Europe.

Antioxidant and Bone; Protect Your Future: A Brief Review.

The global campaign of osteoporosis has been organized by the International Osteoporosis Foundation (IOF) and them introducing World Osteoporosis Day (WOD) in 1997. The day is celebrated on October 20th each year and aimed to improve the awareness of the population about disease prevention. We present some aspects of bone health and the prevention of osteoporosis related to the use of vitamins. The presenting mini-review covers a variety of sources including PubMed, Embase, Scopus, and directory of open access journals (DOAJ) from 10 years ago (Oct 2009 to Oct 2019) for recent developments in the prevention of bone loss. The search was performed by using combinations of the following keywords and or their equivalents; osteoporosis, bones health, bone loss, and vitamin to find related articles about the prevention of osteoporosis by nutritional factors. The factors affecting bone are various and could begin from fetal periods to the end of life. Some of them are not changeable including age, and genetic; however, it is possible to modify some others such as poor nutrition and vitamin deficiency. Beyond vitamin D deficiency, consumption of other vitamins also is beneficial to maintain bone health. By considering the nutritional factors especially vitamins that affect bones, it is possible to have stronger bones to enjoy life in the elderly and protect your future.

Osteoprotective Effects of ‘Anti-Diabetic’ Polyherbal Mixture in Type 1 Diabetic Rats

Abstract Bone loss leading to osteopenia and osteoporosis is a frequent secondary complication of diabetes. This study aimed to evaluate the value of a traditionally used ‘anti-diabetic’ polyherbal mixture as a possible remedy for the prevention of this complication. Diabetes was induced in Wistar female rats with a single intraperitoneal injection of alloxan monohydrate. The animals with blood glucose higher than 20 mmol/L for 14 consecutive days were considered diabetic. For the next 14 days, animals were treated with two concentrations of the polyherbal mixture (10 and 20 g of dry plant material/ kg). Bone histopathology was evaluated using the H&amp;E and Masson’s trichrome staining. Alloxan-induced diabetes triggered bone histological changes characteristic for the development of osteopenia and osteoporosis and treatment with the polyherbal decoction restored these histopathological changes of the bones to the healthy animal level. At the same time, treatment with these tested doses has shown no adverse effects. These findings suggest that this mixture might be used as a remedy for the prevention of diabetic bone loss.

Management of osteoporosis in postmenopausal women: the 2021 position statement of The North American Menopause Society.

To review evidence regarding osteoporosis screening, prevention, diagnosis, and management in the past decade and update the position statement published by The North American Menopause Society (NAMS) in 2010 regarding the management of osteoporosis in postmenopausal women as new therapies and paradigms have become available. NAMS enlisted a panel of clinician experts in the field of metabolic bone diseases and/or women's health to review and update the 2010 NAMS position statement and recommendations on the basis of new evidence and clinical judgement. The panel's recommendations were reviewed and approved by the NAMS Board of Trustees. Osteoporosis, especially prevalent in older postmenopausal women, increases the risk of fractures that can be associated with significant morbidity and mortality. Postmenopausal bone loss, related to estrogen deficiency, is the primary contributor to osteoporosis. Other important risk factors for postmenopausal osteoporosis include advanced age, genetics, smoking, thinness, and many diseases and drugs that impair bone health. An evaluation of these risk factors to identify candidates for osteoporosis screening and recommending nonpharmacologic measures such as good nutrition (especially adequate intake of protein, calcium, and vitamin D), regular physical activity, and avoiding smoking and excessive alcohol consumption are appropriate for all postmenopausal women. For women at high risk for osteoporosis, especially perimenopausal women with low bone density and other risk factors, estrogen or other therapies are available to prevent bone loss. For women with osteoporosis and/or other risk factors for fracture, including advanced age and previous fractures, the primary goal of therapy is to prevent new fractures. This is accomplished by combining nonpharmacologic measures, drugs to increase bone density and to improve bone strength, and strategies to reduce fall risk. If pharmacologic therapy is indicated, government-approved options include estrogen agonists/antagonists, bisphosphonates, RANK ligand inhibitors, parathyroid hormone-receptor agonists, and inhibitors of sclerostin. Osteoporosis is a common disorder in postmenopausal women. Management of skeletal health in postmenopausal women involves assessing risk factors for fracture, reducing modifiable risk factors through dietary and lifestyle changes, and the use of pharmacologic therapy for patients at significant risk of osteoporosis or fracture. For women with osteoporosis, lifelong management is necessary. Treatment decisions occur continuously over the lifespan of a postmenopausal woman. Decisions must be individualized and should include the patient in the process of shared decision-making.

English

Bone loss and osteoporosis with the resultant increase in fracture risk should be major concerns for patients and health care providers. As the population ages, the long-term effects of osteoporosis including pain, loss of independence and institutionalized care will become more prevalent. Efforts to prevent bone loss and osteoporosis should start with proper education about a healthy lifestyle, including optimal calcium and vitamin D and exercise in adolescence. This education should continue throughout life, with emphasis during times of increased bone loss such as the menopause transition. This paper reviews the cornerstone of bone health; calcium and vitamin D. Although dietary sources of both nutrients are available, most people do not receive adequate amounts for proper bone health. In addition, the heightened awareness of damaging effects of sunlight has limited vitamin D synthesis from the skin. Fortunately, supplements are available that can supply the body with amounts necessary for bone health.

The Impact of Rheumatoid Arthritis on Bone Loss: Links to Osteoporosis and Osteopenia.

Rheumatoid arthritis (RA) is an autoimmune chronic connective tissue disease that produces persistent systemic inflammation, with joint inflammation leading to function loss and joint destruction. Low bone mass causes skeletal bone loss, commonly referred to as osteopenia or osteoporosis. We conducted this literature review to examine the relationship between RA and osteoporosis and the variables contributing to this connection. We used articles from the US National Library of Medicine (PubMed), Google Scholar, Science Direct to access the required information. Eventually, our results concluded that RA could result in local periarticular and generalized bone loss. Many risk factors contribute to this association, such as chronic joints inflammation, glucocorticoid use, genetics, and estrogen hormone effects. Still, it is not clear yet whether this is due to a consequence of treatment, immobility, or the activity of the disease. There are many recommendations by the American College of Rheumatology for RA patients during the disease course to reduce the risk of osteoporosis development, which include early starts of disease-modifying anti-inflammatory drugs (DMARDs), doing a dual-energy x-ray (DXA) or quantitative ultrasound (QUS) for identifying a patient at risk of osteoporosis, taking vitamin D, calcium, and bisphosphonates. Further prospective studies and clinical trials are essential to provide a solid evidence-based recommendation that will help to prevent bone loss in RA patients.