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Background The cells of the entire body, including the skeletal system, especially of young animals, may derive from the bone marrow in which they multiply. Therefore, it is important to assess whether the diet and quality of life of deer have a significant impact on the elemental composition of bone and bone marrow, which can directly affect their health and growth. The aim of this study was to determine the concentrations of macro- (Ca, calcium, P, phosphorus, Mg, magnesium, K, potassium, Na, sodium) and microelements (Li, lithium, Cr, chromium, Mn, manganese, Co, cobalt, Cu, copper, Zn, zinc, Se, selenium, Mo, molybdenum, and Sn, tin) accumulated in the bone marrow and bones of deer ( Cervus elaphus ). The study was carried out on 15 young stags divided into two groups: farmed and wild animals. The concentrations of macro- and microelements were analysed using the inductively coupled plasma mass spectrometry technique. This research expands our knowledge on this topic, which so far has not been extensively studied. Results The mean content of K, Na, Zn and Se in the bone marrow of farmed animals was significantly higher than in wild deer, whereas the mean content of Ca, P, Mg, K, Na and Li in the bones was higher in wild animals than in farmed individuals ( p  < 0.05). In addition, the mean concentration of Cr, Mn, Cu, Se and Mo in the bones of the analysed animals differed significantly ( p  < 0.05) and was higher in the farmed deer. The mean concentration of Se in the bone marrow of wild deer decreased with the increase of the body weight ( p  < 0.05). In turn, the mean content of Mn in the bone marrow and of Mo in the bones of the animals was significantly positively correlated with the animals’ body weight ( p  < 0.05). Conclusions The obtained results indicated different levels of micro- and macro-components in the body of farmed and wild deer, though without clear and strong variations. Generally, the higher level of macronutrients in the bones of wild deer may be related to the higher physiological importance of these minerals for life activities in the natural environment and to the limited supply of balanced food. On the other hand, the higher levels of microelements in the tissues of farmed animals may result from their significantly better nutritional status in the first year of life, achieved through appropriate nutrition as well as diet supplementation of adult females.

The gut microbiome is a key regulator of bone health that affects postnatal skeletal development and skeletal involution. Alterations in microbiota composition and host responses to the microbiota contribute to pathological bone loss, while changes in microbiota composition that prevent, or reverse, bone loss may be achieved by nutritional supplements with prebiotics and probiotics. One mechanism whereby microbes influence organs of the body is through the production of metabolites that diffuse from the gut into the systemic circulation. Recently, short-chain fatty acids (SCFAs), which are generated by fermentation of complex carbohydrates, have emerged as key regulatory metabolites produced by the gut microbiota. This Review will focus on the effects of SCFAs on the musculoskeletal system and discuss the mechanisms whereby SCFAs regulate bone cells.

Background Continuous subcutaneous insulin infusion (CSII) for the treatment of type 2 diabetes (T2D) can improve the structure and strength of femur of rats, but the effect of CSII treatment on the lumbar spine of T2D rats is unknown. The purpose of this study is to investigate the effects of CSII on the microstructure, multi-scale mechanical properties and bone mineral composition of the lumbar spine in T2D rats. Methods Seventy 6-week-old male Sprague–Dawley (SD) rats were divided into two batches, each including Control, T2D, CSII and Placebo groups, and the duration of insulin treatment was 4-week and 8-week, respectively. At the end of the experiment, the rats were sacrificed to take their lumbar spine. Microstructure, bone mineral composition and nanoscopic-mesoscopic-apparentand-macroscopic mechanical properties were evaluated through micro-computed tomography (micro-CT), Raman spectroscopy, nanoindentation test, nonlinear finite element analysis and compression test. Results It was found that 4 weeks later, T2D significantly decreased trabecular thickness (Tb.Th), nanoscopic-apparent and partial mesoscopic mechanical parameters of lumbar spine ( P  < 0.05), and significantly increased bone mineral composition parameters of cortical bone ( P  < 0.05). It was shown that CSII significantly improved nanoscopic-apparent mechanical parameters ( P  < 0.05). In addition, 8 weeks later, T2D significantly decreased bone mineral density (BMD), bone volume fraction (BV/TV) and macroscopic mechanical parameters ( P  < 0.05), and significantly increased bone mineral composition parameters of cancellous bone ( P  < 0.05). CSII treatment significantly improved partial mesoscopic-macroscopic mechanical parameters and some cortical bone mineral composition parameters ( P  < 0.05). Conclusions CSII treatment can significantly improve the nanoscopic-mesoscopic-apparent-macroscopic mechanical properties of the lumbar spine in T2D rats, as well as the bone structure and bone mineral composition of the lumbar vertebrae, but it will take longer treatment time to restore the normal level. In addition, T2D and CSII treatment affected bone mineral composition of cortical bone earlier than cancellous bone of lumbar spine in rat. Our study can provide evidence for clinical prevention and treatment of T2D-related bone diseases.

The gut microbiota (GM) modulates the hosts metabolism and immune system. Probiotic bacteria are defined as live microorganisms which when administered in adequate amounts confer a health benefit on the host and can alter the composition of the GM. Germ-free mice have increased bone mass associated with reduced bone resorption indicating that the GM also regulates bone mass. Ovariectomy (ovx) results in bone loss associated with altered immune status. The purpose of this study was to determine if probiotic treatment protects mice from ovx-induced bone loss. Mice were treated with either a single Lactobacillus (L) strain, L. paracasei DSM13434 (L. para) or a mixture of three strains, L. paracasei DSM13434, L. plantarum DSM 15312 and DSM 15313 (L. mix) given in the drinking water during 6 weeks, starting two weeks before ovx. Both the L. para and the L. mix treatment protected mice from ovx-induced cortical bone loss and bone resorption. Cortical bone mineral content was higher in both L. para and L. mix treated ovx mice compared to vehicle (veh) treated ovx mice. Serum levels of the resorption marker C-terminal telopeptides and the urinary fractional excretion of calcium were increased by ovx in the veh treated but not in the L. para or the L. mix treated mice. Probiotic treatment reduced the expression of the two inflammatory cytokines, TNFα and IL-1β, and increased the expression of OPG, a potent inhibitor of osteoclastogenesis, in cortical bone of ovx mice. In addition, ovx decreased the frequency of regulatory T cells in bone marrow of veh treated but not probiotic treated mice. In conclusion, treatment with L. para or the L. mix prevents ovx-induced cortical bone loss. Our findings indicate that these probiotic treatments alter the immune status in bone resulting in attenuated bone resorption in ovx mice.

Introduction This study aimed to investigate the effects of quercetin (a plant-based flavonoid) supplementation over 90 days on prominent bone turnover markers (BTMs), inflammatory markers, bone mineral density (BMD), body composition, and physical function in postmenopausal women. Materials and Methods Thirty-three healthy postmenopausal women were recruited to participate in a double-blind, placebo-controlled investigation. Participants were randomized into one of two supplement groups: (1) 500 mg of quercetin (QUE) once daily or (2) 500 mg of methylcellulose (placebo; PLB) once daily. Pre- and post-testing visits included assessments of BTMs (i.e., osteocalcin [OC], procollagen type I N-terminal propeptide [PINP], and type I collagen cross-linked C-terminal telopeptide [CTX]), inflammatory markers (i.e., interleukin [IL]-6, tumor necrosis factor-alpha [TNF-α], and C-reactive protein [CRP]), BMD measurements, body composition measurements, and physical function including timed up and go and handgrip strength. Results The QUE group increased OC ( p  = 0.016; d  = 0.89), PINP ( p  = 0.030; d  = 0.64), and CTX ( p  = 0.023; d  = 0.91) levels and decreased IL-6 ( p  = 0.045; d  = 0.73) and TNF-α ( p  = 0.021; d  = 0.90) levels compared to PLB. CRP ( p  = 0.448; d  = 0.34), body composition ( p  > 0.05), and physical function ( p  > 0.05) remained unchanged. Conclusion The results suggest that QUE may better assist in controlling a normal bone turnover cycle by mediating bone formation and decreasing pro-inflammatory cytokines. However, although within the accepted range, there was an increase in the bone resorption marker and therefore, it is unclear if QUE will protect against future bone loss. Nonetheless, additional research is necessary to evaluate the bone-conserving properties of QUE among postmenopausal women. Clinical Trail Registration The ClinicalTrials.gov ID number: NCT05371340.

Haematological malignancies were previously thought to be driven solely by genetic or epigenetic lesions within haematopoietic cells. However, the niches that maintain and regulate daily production of blood and immune cells are now increasingly being recognized as having an important role in the pathogenesis and chemoresistance of haematological malignancies. Within haematopoietic cells, the accumulation of a small number of recurrent mutations initiates malignancy. Concomitantly, specific alterations of the niches, which support haematopoietic stem cells and their progeny, can act as predisposition events, facilitating mutant haematopoietic cell survival and expansion as well as contributing to malignancy progression and providing protection of malignant cells from chemotherapy, ultimately leading to relapse. In this Perspective, we summarize our current understanding of the composition and function of the specialized haematopoietic niches of the bone marrow during health and disease. We discuss disease mechanisms (rather than malignancy subtypes) to provide a comprehensive description of key niche-associated pathways that are shared across multiple haematological malignancies. These mechanisms include primary driver mutations in bone marrow niche cells, changes associated with increased hypoxia, angiogenesis and inflammation as well as metabolic reprogramming by stromal niche cells. Consequently, remodelling of bone marrow niches can facilitate immune evasion and activation of survival pathways favouring malignant haematopoietic cell maintenance, defence against excessive reactive oxygen species and protection from chemotherapy. Lastly, we suggest guidelines for the handling and biobanking of patient samples and analysis of the niche to ensure that basic research identifying therapeutic targets can be more efficiently translated to the clinic. The hope is that integrating knowledge of how bone marrow niches contribute to haematological disease predisposition, initiation, progression and response to therapy into future clinical practice will likely improve the treatment of these disorders.This Perspective outlines our current understanding of how the bone marrow niche contributes to both the initiation and the progression of haematological malignancies and suggests guidelines for the field which might help to overcome existing research challenges.

The bone marrow constitutes the primary site for life-long blood production and skeletal regeneration. However, its cellular and spatial organization remains controversial. Here, we combine single-cell and spatially resolved transcriptomics to systematically map the molecular, cellular and spatial composition of distinct bone marrow niches. This allowed us to transcriptionally profile all major bone-marrow-resident cell types, determine their localization and clarify sources of pro-haematopoietic factors. Our data demonstrate that Cxcl12-abundant-reticular (CAR) cell subsets (Adipo-CAR and Osteo-CAR) differentially localize to sinusoidal and arteriolar surfaces, act locally as ‘professional cytokine-secreting cells’ and thereby establish peri-vascular micro-niches. Importantly, the three-dimensional bone-marrow organization can be accurately inferred from single-cell transcriptome data using the RNA-Magnet algorithm described here. Together, our study reveals the cellular and spatial organization of bone marrow niches and offers a systematic approach to dissect the complex organization of whole organs.Baccin, Al-Sabah, Velten et al. use single-cell and spatially resolved transcriptomics to map the cellular, molecular and spatial organization of the endosteal, sinusoidal and arteriolar bone marrow niches.

In a study of diet and several exercise modes to reverse frailty and prevent weight-loss–induced reduction in muscle and bone in obese older adults, weight loss plus combined aerobic and resistance exercise was the most effective method of improving functional status. More than a third of persons 65 years of age or older in the United States are obese, 1 and this group constitutes a population vulnerable to adverse outcomes, because obesity exacerbates the age-related decline in physical function and causes frailty. 2 – 5 However, appropriate management of obesity in older adults remains controversial, given the reported reduction in relative health risks associated with increasing body-mass index in this group. 6 Moreover, an important concern is that weight loss could worsen frailty by accelerating the age-related decline in muscle and bone mass and resultant sarcopenia and osteopenia. 7 , 8 Given the positive effects of exercise . . .

Bone volume, microstructure and its material composition are maintained by bone remodelling, a cellular activity carried out by bone multicellular units (BMUs). BMUs are focally transient teams of osteoclasts and osteoblasts that respectively resorb a volume of old bone and then deposit an equal volume of new bone at the same location. Around the time of menopause, bone remodelling becomes unbalanced and rapid, and an increased number of BMUs deposit less bone than they resorb, resulting in bone loss, a reduction in bone volume and microstructural deterioration. Cortices become porous and thin, and trabeculae become thin, perforated and disconnected, causing bone fragility. Antiresorptive agents reduce fracture risk by reducing the rate of bone remodelling so that fewer BMUs are available to remodel bone. Bone fragility is not abolished by these drugs because existing microstructural deterioration is not reversed, unsuppressed remodelling continues producing microstructural deterioration and unremodelled bone that becomes more mineralized can become brittle. Anabolic agents reduce fracture risk by stimulating new bone formation, which partly restores bone volume and microstructure. To guide fracture prevention, this Review provides an overview of the structural basis of bone fragility, the mechanisms of remodelling and how anabolic and antiresorptive agents target remodelling defects.Bone turnover and risk of fracture are orchestrated by homeostatic functions of osteoclast–osteoblast bone remodelling units. Anabolic and antiresorptive drugs used to treat and prevent fractures have differing effects on remodelling defects, but which class of drug is the preferred front-line therapy?

Some compositional and structural features of mature bone mineral particles remain unclear. They have been described as calcium-deficient and hydroxyl-deficient carbonated hydroxyapatite particles in which a fraction of the PO 4 3− lattice sites are occupied by HPO 4 2− ions. The time has come to revise this description since it has now been proven that the surface of mature bone mineral particles is not in the form of hydroxyapatite but rather in the form of hydrated amorphous calcium phosphate. Using a combination of dedicated solid-state nuclear magnetic resonance techniques, the hydrogen-bearing species present in bone mineral and especially the HPO 4 2− ions were closely scrutinized. We show that these HPO 4 2− ions are concentrated at the surface of bone mineral particles in the so-called amorphous surface layer whose thickness was estimated here to be about 0.8 nm for a 4-nm thick particle. We also show that their molar proportion is much higher than previously estimated since they stand for about half of the overall amount of inorganic phosphate ions that compose bone mineral. As such, the mineral-mineral and mineral-biomolecule interfaces in bone tissue must be driven by metastable hydrated amorphous environments rich in HPO 4 2− ions rather than by stable crystalline environments of hydroxyapatite structure.