The comparison of age- and sex-specific alteration in pubic bone microstructure: A cross-sectional cadaveric study

Jadžić, Jelena; Mijucic, Jovana; Nikolić, Slobodan; Djurić, Marija; Djonić, Danijela

doi:10.1016/j.exger.2021.111375

Cited by 10 publications

(6 citation statements)

References 38 publications

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“…Our histomorphometric analysis showed a significant association between the severity of liver tissue disturbance associated with ALC and osteocytic Cx43 and sclerostin expression levels in investigated femoral and vertebral bone samples (Figure 4). These findings suggest that the staging of liver disease could significantly contribute to ALC‐induced bone loss (Figure 5), which was previously indicated by various studies dealing with individuals with alcoholic and nonalcoholic liver disease (Culafić et al, 2014; Jadzic, Cvetkovic, Tomanovic, et al, 2020; Jadzic, et al, 2021; Schmidt et al, 2021). However, the assessed osteocytic lacunar network parameters and bone marrow adiposity parameters in lumbar vertebrae did not significantly correlate with the HAI values of the ALC group.…”

Section: Discussionsupporting

confidence: 67%

The altered osteocytic expression of connexin 43 and sclerostin in human cadaveric donors with alcoholic liver cirrhosis: Potential treatment targets

et al. 2022

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Previous studies suggested that osteocyte lacunar network disruption could play a role in the complex pathophysiology of bone changes in aging and disease. Considering that particular research interest is lacking, we aimed to assess alcoholic liver cirrhosis (ALC)–induced changes in osteocyte lacunar network and bone marrow adiposity. Immunohistochemistry was conducted to assess changes in the micro‐morphology of osteocyte lacunar network and bone marrow adiposity, and expression of connexin 43 and sclerostin in vertebral and femoral samples collected from 40 cadaveric men (age range between 44 and 70 years) divided into ALC group (n = 20) and control group (n = 20). Furthermore, the assessment of the potential association between bone changes and the severity of the hepatic disorder (given by Knodell's pathohistologic scoring) was conducted. Our data revealed fewer connexin 43‐positive osteocytes per vertebral and femoral bone area (p < 0.01), suggesting defective signal transduction among osteocytes in ALC individuals. Moreover, we found an ALC‐induced increase in the number of adipocytes in the vertebral bone marrow (p = 0.038). Considering significant associations between the severity of liver tissue disturbances and impaired functionality of osteocyte lacunar network (Pearson's correlation analyses, p < 0.05), we may assume that timely treatment of the liver disease may delay bone impairment. ALC induced an increase in osteocytic sclerostin expression (p < 0.001), suggesting its role in mediating low bone formation among ALC individuals. Hence, medicaments targeting low bone formation may be beneficial to attenuate the bone changes among ALC patients. However, future clinical studies are required to verify the therapeutic utility of these findings.

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Section: Discussionsupporting

confidence: 67%

The altered osteocytic expression of connexin 43 and sclerostin in human cadaveric donors with alcoholic liver cirrhosis: Potential treatment targets

et al. 2022

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“…The risk of bone fracture of osteoporotic patients is associated with a decrease in trabecular bone density and a deterioration of the bone micro-architecture, with a particular diminution in the total number of trabecular and an increase in the number of their perforations [ 36 ]. The analysis of Micro-CT found that bone loss in the OVX rats was increased as assessed by BMD and the number of trabecular [ 37 ]. The BMD and trabecular number were increased, trabecular thickness was not altered, and trabecular separation was decreased in the JTG treated OVX rats, suggesting that enhanced bone mineral density by JTG might be due to the increase in trabecular number, but not the trabecular thickness.…”

Section: Discussionmentioning

confidence: 99%

Jin-Tian-Ge ameliorates ovariectomy-induced bone loss in rats and modulates osteoblastogenesis and osteoclastogenesis in vitro

et al. 2022

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Background Tiger bone, which had been one of the most famous traditional Chinese medicine for 2000 years, was originate from the skeleton of Panthera tigris L., and had the actions of anti-inflammatory, analgesic, immune-regulatory and promoting healing of bone fracture, and was used for the treatment of osteoporosis and rheumatoid arthritis. Jin-Tian-Ge (JTG), the artificial tiger bone powder, were prepared from skeletons of several farmed animals to substitute the natural tiger bone, and has been used for the treatment of osteoporosis in clinical practice. However, the characteristic and mechanism of action of JTG for the therapy of osteoporosis need to be further evidenced by using modern pharmacological methods. The aim of this work is to investigate the bone-protective effects of JTG, and explore the possible underlying mechanism. Methods Ovariectomy (OVX) rats were orally administrated JTG or estradiol valerate (EV) for 12 weeks. We investigated the pharmacodynamic effects of JTG on anti-bone loss in OVX rats, and also investigated the role of JTG in promoting osteogenesis and inhibiting osteoclast differentiation. Results JTG increased the bone mineral density (BMD), improved the bone microarchitecture and biomechanical properties in ovariectomized rast, whereas reversed the bone high turnover in OVX rats as evidenced by serum biochemical markers in OVX rats. JTG increased osteogenic differentiation of BMSCs in vitro, and up-regulated the expression of the key proteins of BMP and Wnt/β-catenin pathways. JTG also inhibited the osteoclastogenesis of BMM as evidenced by the alteration of the TRAP activity, F-actin construction and the expression of nuclear factor of activated T-cells cytoplasmic 1 (NFATc1), c-Fos, Cathepsin K (Ctsk) and matrix metallopeptidase 9 (MMP9) of OCs induced with RANKL and LPS, reduced the expression and phosphorylation of NF-κB in OCs. Conclusions JTG prevented bone loss in OVX rats and increased osteogenic differentiation of BMSCs through regulation of the BMP and Wnt/β-catenin pathway, inhibited osteoclastogenesis by suppressing the NF-κB pathway, suggesting that JTG had the potentials for prevention and treatment of osteoporosis by modulating formation and differentiation of osteoblast and osteoclast.

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“…Namely, the aging-related trabecular micro-architectural decline is presented as a loss of trabecular elements, declined trabecular connectivity coupled with trabecular thinning observed at the proximal femora, vertebral bodies, the radius and tibia of aged individuals (64-66). Along with trabecular micro-architectural bone loss (Figure 2), increased cortical porosity (originating from accumulation of incompletely closed osteons and resorption cavities) and cortical thinning are proven to contribute to bone fragility in aged individuals (11,64) and individuals with chronic liver diseases (29) and renal disorders (55). Moreover, it is becoming clear that spatial distribution of skeletal alterations and decline in intrinsic bone properties contribute to increased susceptibility to bone fracture in a site-specific manner (7,67).…”

Section: Multi-scale Bone Analysis: Review Of Current Liter Ature And...mentioning

confidence: 99%

“…Bone fractures in aged individuals most frequently appear at the femoral neck, radius, and vertebral column, with a predilection to affect postmenopausal women (9)(10)(11). Moreover, bone fractures in these individuals commonly occur due to low-energy trauma (predomi-nantly due to a fall from a standing height) (12,13).…”

Section: Introductionmentioning

confidence: 99%

Structural basis of increased bone fragility in aged individuals: Multi-scale perspective

Jadžić,

Đurić

2024

Medicinska istraživanja

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Numerous epidemiological studies have shown that increased bone fragility and a higher risk of fractures are present in the aged, which reduces their quality of life and represents a significant socio-economic burden for the healthcare system. However, morphological and structural determinants underlying increased bone fragility have yet to be fully explained. This paper aimed to provide an overview of modern studies that dealt with determinants of increased bone fragility, analyzing different hierarchical levels of bone tissue organization (macro-, micro-, and nano-levels) in aged individuals and individuals with chronic comorbidities (mainly in individuals with chronic liver disease, renal disorders, and type 2 diabetes mellitus). Also, variable frequency of fractures at different skeletal sites in aged persons and individuals with chronic diseases was shown, indicating that aging-related bone loss is not a uniform process. A complete understanding of the spatial pattern of impaired bone quality can aid in the targeted evaluation of individualized fracture risk. Establishing a firm connection between the results of the clinical assessment of bone status and the analysis of numerous structural and mechanical bone properties (on various hierarchical levels) can represent a solid base for developing adequate guidelines and algorithms for prevention and treatment of increased bone fragility in aged individuals and individuals with chronic diseases.

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The comparison of age- and sex-specific alteration in pubic bone microstructure: A cross-sectional cadaveric study

Cited by 10 publications

References 38 publications

The altered osteocytic expression of connexin 43 and sclerostin in human cadaveric donors with alcoholic liver cirrhosis: Potential treatment targets

The altered osteocytic expression of connexin 43 and sclerostin in human cadaveric donors with alcoholic liver cirrhosis: Potential treatment targets

Jin-Tian-Ge ameliorates ovariectomy-induced bone loss in rats and modulates osteoblastogenesis and osteoclastogenesis in vitro

Structural basis of increased bone fragility in aged individuals: Multi-scale perspective

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