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X-ray image of a 71 years old woman with aortic calcifications, low bone density and a vertebral fracture.
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Vascular Calcification (VC), low bone mass and fragility fractures are frequently observed in ageing subjects. Although this clinical observation could be the mere coincidence of frequent age-dependent disorders, clinical and experimental data suggest that VC and bone loss could share pathophysiological mechanisms. Indeed, VC is an active process o...
Citations
... Результаты и их обсуждение Кальцификация сосудов, гипотиреоз и остеопороз являются процессами, ассоциированными со старением [10][11][12][13]. К настоящему моменту известны результаты множества исследований, подтверждающих наличие связи между остеопорозом и гипотиреозом [14], гипотиреозом и кальцификацией сосудов [15] и кальцификацией сосудов и остеопорозом [16]. ...
Introduction. There are about 16 million people aged 50 or older in the Russian Federation, who are affected by osteoporosis. At the same time, significantly many of these individuals undergo mammography, a diagnostic procedure that effectiently detects vascular calcifications. Aim. To assess the serum biochemistry parameters reflecting the bone turnover, as well as the bone densitometry values and fracture risk in women, depending on the degree of breast vascular calcifications found in mammography. Materials and Methods. We observed 56 women aged 39-81 years (average age: 63.66±1.24) sent to screening mammography in 2018. Results and Discussion. Patients who had newly discovered vascular calcifications showed a significant increase (6.98%) in their total serum calcium levels as compared to women without calcifications. Among women with calcifications, those with grade 3-4 calcifications had the highest median levels of both medium and maximum thyrostimulating hormone (TSH). Additionally, women with grade 1-2 calcifications had the highest median levels of maximum total serum calcium, which were significantly (3.7%) higher than those in women without calcifications and significantly (6.8%) higher than those in women with grade 3-4 calcifications. In women with 3-4 degree calcifications, both the mean and minimum values of the median T-test for L1-L4 vertebral body mineral density were 91% lower than in the group with grade 1-2 grade calcifications. Furthermore, they were 34% lower than in women without calcifications. Patients with grade 1-2 calcifications had the lowest risk of major fractures, as assessed by the FRAX index. At the same time, median of the minimum FRAX value during the follow-up period for patients with grade 1-2 calcifications was significantly (61%) lower than in women without calcifications. Furthermore, it was also significantly (70%) lower than in women with grade 3-4 calcifications.Conclusions. Detecting evident (grades 3-4 according to the classification we have proposed) breast vascular calcifications found in mammography is associated with the lower values of lumbar bone mineral density, indicating osteoporosis. This phenomenon primarily reflects the prospective fracture risk changes rather than retrospective ones, i.e. they precede the increase in the risk of osteoporotic fractures to the critical threshold.
... Несмотря на то, что в ряде исследований найдена взаимосвязь между низкой МПК в проксимальном отделе бедра (ПОБ) и состоянием сосудистой стенки, характеризующимся такими параметрами, как толщина КИМ, АСБ, СРПВ и индекс аугментации [20,21,[35][36][37], многие зарубежные и отечественные эксперты склоняются к мнению, что именно процесс кальцификации в большей степени является объединяющим звеном в механизмах развития ОП и АС [38][39][40][41]. Получены сведения о том, что кальцификация сосудов может влиять на ремоделирование костной ткани и способствовать снижению костной массы [42,43]. Тем не менее последовательность и взаимодействие процессов атеросклеротической кальцификации артерий, остеогенеза и костной резорбции остаются недостаточно изученными [44][45][46]. ...
We analyzed modern publications on the relationship between cardiovascular diseases (CVDs) and osteoporosis and, in particular, their preclinical manifestations. Most of the papers on this issue are observational, cross-sectional, or study associations of preclinical markers with disease risk or outcomes. However, the results of these studies do not always coincide and are contradictory. Therefore, it is not possible to define cause-effect relationship between vascular changes and decreased bone mass, as well as persistence of its relationship. Due to the difficulties in management of prospective studies, in the last decade only a few studies have appeared with long-term follow-up of patients without symptoms with subsequent assessment of preclinical manifestations. A strong relationship has been demonstrated between intima-media thickness, plaque presence, coronary artery calcification and low bone density of the spine and proximal femur, as well as between vascular stiffness (pulse wave velocity) and proximal femur bone density. The data obtained indicate combined disorders of vascular wall morphology and bone tissue, not only in postmenopausal women, but also in elderly men, and can be used to justify indications for screening for decreased bone density in patients with CVD. At the same time, larger-scale prospective studies to explore associations between markers of preclinical manifestations of CVD and decreased bone mass, including in the Russian population, are required.
... Also, some of them can promote or inhibit vascular smooth muscle cells calcification. MiRNAs are stable in plasma supporting their potential role as biomarkers for the early diagnosis of alterations in bone and vasculature health [65,66]. ...
Aging is an inevitable process of our civilization. Since ancient times, scientists have tried to solve the mystery of aging. The research continues to this day. The most common diseases of old age are disorders of the musculoskeletal system. Among them, osteoporosis continues to occupy the third place in the structure of overall morbidity and mortality. Such statistical data make us think about the search for a possible cause of the disease at the molecular level. The purpose of this study was to analyze the literature data on modern directions of osteoporosis treatment, including stem-cells based bioregenerative medicine. An analytical review of literature data was conducted using the information analysis of Medline (PubMed), Web of Science and Scopus databases, Google Scholar and the Cochrane Central Register of Controlled Trials (CENTRAL) from 2018 to 2022 using the keywords “osteoporosis”, bioregenerative therapy”, “stem cell therapy”. Recent results of preclinical experimental studies have shown the effectiveness of the introduction of new bioregenerative technologies. In particular, the use of mesenchymal stem cells, exosomes and miRNAs. Preclinical studies on MSC transplantation in the treatment of osteoporosis indicate an increase in osteogenic differentiation, an increase in BMD. Exosomes also may play multiple roles in the treatment of osteoporosis: improving the disbalance between osteoclasts and osteoblasts, structural modification of exosomes and transmitters’ drug function. The promotion of bone regeneration of exosomes has been shown in animal models. Exosomes with active ingredients can treat a variety of skeletal disorders including osteoporosis and osteoporotic fractures. The results of recent research of the bone disorder treatment based on stem cells therapy have shown convincing prospects for new approaches.
... A low bone mineral content has been shown to be a risk factor for increased incidence of coronary artery disease and cardiovascular mortality [63,64]. Osteoporosis blocks the skeleton from exerting its reservoir function when positive phosphorus balance occurs, and is also associated with heterotopic mineralization [65][66][67][68]. As a direct indicator of phosphorus overload, higher serum phosphorus concentrations, even within the normal range, are independently associated with worse microvascular function, coronary artery calcification, incident CKD, and mortality in community-living individuals [69][70][71][72]. ...
Phosphorus is an essential micromineral with a key role in cellular metabolism and tissue structure. Serum phosphorus is maintained in a homeostatic range by the intestines, bones, and kidneys. This process is coordinated by the endocrine system through the highly integrated actions of several hormones, including FGF23, PTH, Klotho, and 1,25D. The excretion kinetics of the kidney after diet phosphorus load or the serum phosphorus kinetics during hemodialysis support that there is a “pool” for temporary phosphorus storage, leading to the maintenance of stable serum phosphorus levels. Phosphorus overload refers to a state where the phosphorus load is higher than is physiologically necessary. It can be caused by a persistently high-phosphorus diet, renal function decline, bone disease, insufficient dialysis, and inappropriate medications, and includes but is not limited to hyperphosphatemia. Serum phosphorus is still the most commonly used indicator of phosphorus overload. Trending phosphorus levels to see if they are chronically elevated is recommended instead of a single test when judging phosphorus overload. Future studies are needed to validate the prognostic role of a new marker or markers of phosphorus overload.
... As a commonly used drug for bone regeneration, PTH promotes osteogenesis by activating osteoblast cells and the secretion of SOST through the receptor PTHr1. 16,17 Additionally, the cost of PTH is much lower than that of bone morphogenetic proteins, making it more readily available for clinical applications. At the same time, previous studies have proven that locally delivered PTH significantly promotes bone regeneration. ...
... To test the release profiles of MgONPs in-vitro, group A and B (0.5 * 1.5 * 1.5cm) were immersed individually in 10mL of phosphate buffered solution (PBS) at 37°C and agitated at 100rpm. At 1,3,5,7,9,11,13,15,17,19,21,23,25,27, and 29d, samples were removed from the solution and rinsed three times with fresh PBS before soaking in fresh buffer solutions of the same volume. Afterwards the solutions were mixed with aqua regia solution in a 1:1 vol ratio to dissolve the MgONPs. ...
Introduction
An antibacterial and pro-osteogenic coaxially electrospun nanofiber guided bone regeneration (GBR) membrane was fabricated to satisfy the complicated and phased requirements of GBR process.
Methods
In this study, we synthesize dual-functional coaxially electrospun nanofiber GBR membranes by encapsulating parathyroid hormone (PTH) in the core layer and magnesium oxide nanoparticles (MgONPs) in the shell layer (MgONPs-PCL/PTH-PCL). Herein, the physicochemical characterization of MgONPs-PCL/PTH-PCL, the release rates of MgONPs and PTH, and antibacterial efficiency of the new membrane were evaluated. Furthermore, the pro-osteogenicity of the membranes was assessed both in-vitro and in-vivo.
Results
We successfully fabricated a coaxially electrospun nanofiber MgONPs-PCL/PTH-PCL membrane with the majority of nanofibers (>65%) ranged from 0.40~0.60μm in diameter. MgONPs-PCL/PTH-PCL showed outstanding antibacterial potential against Escherichia coli (E. coli) and Staphylococcus aureus (S. aureus) through the release of MgONPs. We also discovered that the incorporation of MgONPs significantly prolonged the release of PTH. Furthermore, both the in-vivo and in-vitro studies demonstrated that high dosage of PTH promoted pro-osteogenicity of the membrane to improve bone regeneration efficacy with the presence of MgONPs.
Conclusion
The new composite membrane is a promising approach to enhance bone regeneration in periodontitis or peri-implantitis patients with large-volume bone defects.
... The mechanisms associated with bone loss are well known, including the role of pro-inflammatory cytokines, e.g., tumor necrosis factor α (TNFα), interleukin-1 (IL-1), interleukin-6 (IL-6), in activating bone resorption by osteoclasts (bone-resorbing cells) and inhibiting bone formation by osteoblasts (bone-forming cells) [15]. Bone formation occurs mainly on periosteal surfaces, whereas bone resorption is usually present at endosteal surfaces. ...
... Furthermore, estrogen loss during menopause can be consistent with an elevated expression of RANKL and reduced expression of osteoprotegerin (OPG), its natural antagonist by osteoblasts and osteocytes, thereby raising bone resorption in both trabecular and cortical bone compartments [10,17]. The role of bone formation is equally important in the process of bone fragility and is controlled by sclerostin, which is expressed by osteocytes and acts as an inhibitor of the Wnt/β-catenin signaling pathway, a strong stimulus for osteoblast differentiation [15]. Schematic representation of osteoblast and osteoclast differentiation with the involvement of selected important signaling pathways and regulators is illustrated in Figure 1. ...
Osteoporosis is considered an age-related disorder of the skeletal system, characterized primarily by decreased bone mineral density (BMD), microstructural quality and an elevated risk of fragility fractures. This silent disease is increasingly becoming a global epidemic due to an aging population and longer life expectancy. It is known that nutrition and physical activity play an important role in skeletal health, both in achieving the highest BMD and in maintaining bone health. In this review, the role of macronutrients (proteins, lipids, carbohydrates), micronutrients (minerals—calcium, phosphorus, magnesium, as well as vitamins—D, C, K) and flavonoid polyphenols (quercetin, rutin, luteolin, kaempferol, naringin) which appear to be essential for the prevention and treatment of osteoporosis, are characterized. Moreover, the importance of various naturally available nutrients, whether in the diet or in food supplements, is emphasized. In addition to pharmacotherapy, the basis of osteoporosis prevention is a healthy diet rich mainly in fruits, vegetables, seafood and fish oil supplements, specific dairy products, containing a sufficient amount of all aforementioned nutritional substances along with regular physical activity. The effect of diet alone in this context may depend on an individual’s genotype, gene-diet interactions or the composition and function of the gut microbiota.
... The regulatory system in blood maintains calcium and phosphate levels under strict control through intestinal absorption, skeletal flux, and renal excretion, but various factors such as aging, dietary pattern, and daily activity may affect serum calcium and phosphate concentrations and their interactions over the course of one's life [2,[11][12][13]. This study aimed to investigate the longitudinal effects of serum calcium and phosphate levels and their ratio on incident ischemic heart disease (IHD) in a large-scale community-dwelling Korean cohort using National Health Insurance Service data. ...
Serum calcium and phosphate levels are controlled by a regulatory system, but their individual concentration tendencies and interactions may affect long-term vascular health. This study aimed to assess the effects of serum calcium and phosphate levels on incident ischemic heart disease (IHD) in a large-scale community-dwelling Korean cohort. We evaluated 15,259 non-diabetic individuals (median age, 45 years; range, 30–85) without previous IHD or ischemic stroke using the Korean National Health Insurance data. The study population was classified based on the calcium, phosphate, and calcium/phosphate ratios. Using Cox proportional hazards regression models, we estimated hazard ratios (HRs) with 95% confidence intervals (CIs) for IHD over 50 months after baseline enrolment. The age- and sex-adjusted incidence of IHD gradually increased with serum calcium and phosphate quartiles and decreased with calcium/phosphate ratio quartiles, with an overall crude rate of 2.1% (315/15,259). After setting the lowest calcium, phosphate, and calcium/phosphate ratio quartiles as a reference group, the HRs (95% CIs) of the highest calcium, phosphate, and calcium/phosphate ratio quartiles for IHD were 1.77 (1.15–2.72), 1.73 (1.18–2.55), and 0.58 (0.39–0.87), respectively, after adjusting for potential confounding variables. Serum calcium and phosphate levels were positively associated with IHD incidence, while the serum calcium/phosphate ratio exhibited an inverse relationship. Serum calcium and phosphate homeostasis may merit serious consideration to understand the pathogenesis of coronary atherosclerosis as a risk modifier for IHD.
