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Zhiyan Yu Department of Endocrinology, Shanghai Fifth People’s Hospital, Fudan University, Shanghai, China

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Yueyue Wu Department of Endocrinology, Shanghai Fifth People’s Hospital, Fudan University, Shanghai, China

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Rui Zhang Department of Endocrinology, Shanghai Fifth People’s Hospital, Fudan University, Shanghai, China

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Yue Li Department of Endocrinology, Shanghai Fifth People’s Hospital, Fudan University, Shanghai, China

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Shufei Zang Department of Endocrinology, Shanghai Fifth People’s Hospital, Fudan University, Shanghai, China

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Jun Liu Department of Endocrinology, Shanghai Fifth People’s Hospital, Fudan University, Shanghai, China

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Background

This study aimed to investigate the association of non-alcoholic fatty liver disease (NAFLD) and liver fibrosis with osteoporosis in postmenopausal women and men over 50 years of age with type 2 diabetes (T2DM).

Methods

In this study, 1243 patients with T2DM (T2DM with coexistent NAFLD, n  = 760; T2DM with no NAFLD, n  = 483) were analysed. Non-invasive markers, NAFLD fibrosis score (NFS) and fibrosis index based on four factors (FIB-4), were applied to evaluate NAFLD fibrosis risk.

Results

There was no significant difference in bone mineral density (BMD) between the NAFLD group and the non-NAFLD group or between males and females after adjusting for age, BMI and gender. In postmenopausal women, there was an increased risk of osteoporosis (odds ratio (OR): 4.41, 95% CI: 1.04–18.70, P = 0.039) in the FIB-4 high risk group compared to the low risk group. Similarly, in women with high risk NFS, there was an increased risk of osteoporosis (OR: 5.98, 95% CI: 1.40–25.60, P = 0.043) compared to the low risk group. Among men over 50 years old, there was no significant difference in bone mineral density between the NAFLD group and the non-NAFLD group and no significant difference between bone mineral density and incidence of osteopenia or osteoporosis among those with different NAFLD fibrosis risk.

Conclusion

There was a significant association of high risk for NAFLD liver fibrosis with osteoporosis in postmenopausal diabetic women but not men. In clinical practice, gender-specific evaluation of osteoporosis is needed in patients with T2DM and coexistent NAFLD.

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Nancy Martini Laboratorio de Investigaciones en Osteopatías y Metabolismo Mineral (LIOMM-UNLP-CICPBA), Facultad de Ciencias Exactas, Universidad Nacional de La Plata, La Plata, Argentina

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Lucas Streckwall Laboratorio de Investigaciones en Osteopatías y Metabolismo Mineral (LIOMM-UNLP-CICPBA), Facultad de Ciencias Exactas, Universidad Nacional de La Plata, La Plata, Argentina

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Antonio Desmond McCarthy Laboratorio de Investigaciones en Osteopatías y Metabolismo Mineral (LIOMM-UNLP-CICPBA), Facultad de Ciencias Exactas, Universidad Nacional de La Plata, La Plata, Argentina

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In post-menopausal women, aged individuals, and patients with diabetes mellitus or chronic renal disease, bone mineral density (BMD) decreases while the vasculature accumulates arterial calcifications (ACs). AC can be found in the tunica intima and/or in the tunica media. Prospective studies have shown that patients with initially low BMD and/or the presence of fragility fractures have at follow-up a significantly increased risk for coronary and cerebrovascular events and for overall cardiovascular mortality. Similarly, patients presenting with abdominal aorta calcifications (an easily quantifiable marker of vascular pathology) show a significant decrease in the BMD (and an increase in the fragility) of bones irrigated by branches of the abdominal aorta, such as the hip and lumbar spine. AC induction is an ectopic tissue biomineralization process promoted by osteogenic transdifferentiation of vascular smooth muscle cells as well as by local and systemic secreted factors. In many cases, the same regulatory molecules modulate bone metabolism but in reverse. Investigation of animal and in vitro models has identified several potential mechanisms for this reciprocal bone–vascular regulation, such as vitamin K and D sufficiency, advanced glycation end-products–RAGE interaction, osteoprotegerin/RANKL/RANK, Fetuin A, oestrogen deficiency and phytooestrogen supplementation, microbiota and its relation to diet, among others. Complete elucidation of these potential mechanisms, as well as their clinical validation via controlled studies, will provide a basis for pharmacological intervention that could simultaneously promote bone and vascular health.

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Souad Daamouch Department of Medicine III and Center for Healthy Aging, Technische Universität Dresden, Dresden, Germany

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Sylvia Thiele Department of Medicine III and Center for Healthy Aging, Technische Universität Dresden, Dresden, Germany

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Lorenz Hofbauer Department of Medicine III and Center for Healthy Aging, Technische Universität Dresden, Dresden, Germany

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Martina Rauner Department of Medicine III and Center for Healthy Aging, Technische Universität Dresden, Dresden, Germany

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The link between obesity and low bone strength has become a significant medical concern. The canonical Wnt signaling pathway is a key regulator of mesenchymal stem cell differentiation into either osteoblasts or adipocytes with active Wnt signaling promoting osteoblastogenesis. Our previous research indicated that Dickkopf-1 (Dkk1), a Wnt inhibitor, is upregulated in bone tissue in obesity and that osteoblast-derived Dkk1 drives obesity-induced bone loss. However, Dkk1 is also produced by adipocytes, but the impact of adipogenic Dkk1 on bone remodeling and its role in obesity-induced bone loss remain unclear. Thus, in this study, we investigated the influence of adipogenic Dkk1 on bone homeostasis and obesity-induced bone loss in mice. To that end, deletion of Dkk1 in adipocytes was induced by tamoxifen administration into 8-week-old male Dkk1fl/fl;AdipoQcreERT2 mice. Bone and fat mass were analyzed at 12 and 20 weeks of age. Obesity was induced in 8-week-old male Dkk1fl/fl;AdipoQcre mice with a high-fat diet (HFD) rich in saturated fats for 12 weeks. We observed that 12-week-old male mice without adipogenic Dkk1 had a significant increase in trabecular bone volume in the vertebrae and femoral bones. While histological and serological bone formation markers were not different, the number of osteoclasts and adipocytes was decreased in the vertebral bones of Dkk1fl/fl;AdipoQcre-positive mice. Despite the increased bone mass in 12-week-old male mice, at 20 weeks of age, there was no difference in the bone volume between the controls and Dkk1fl/fl;AdipoQcre-positive mice. Also, Dkk1fl/fl;AdipoQcre-positive mice were not protected from HFD-induced bone loss. Even though mRNA expression levels of Sost, another important Wnt inhibitor, in bone from Dkk1-deficient mice fed with HFD were decreased compared to Dkk1-sufficient mice on an HFD, this did not prevent the HFD-induced suppression of bone formation. In conclusion, adipogenic Dkk1 may play a transient role in bone mass regulation during adolescence, but it does not contribute to bone homeostasis or obesity-induced bone loss later in life.

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Rong Xu Center for Endocrine Metabolism and Immune Diseases, Lu He Hospital, Capital Medical University, Beijing, China
Beijing Key Laboratory of Diabetes Research and Care, Beijing, China

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Difei Lian Center for Endocrine Metabolism and Immune Diseases, Lu He Hospital, Capital Medical University, Beijing, China
Beijing Key Laboratory of Diabetes Research and Care, Beijing, China

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Yan Xie Center for Endocrine Metabolism and Immune Diseases, Lu He Hospital, Capital Medical University, Beijing, China
Beijing Key Laboratory of Diabetes Research and Care, Beijing, China

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Lin Mu Center for Endocrine Metabolism and Immune Diseases, Lu He Hospital, Capital Medical University, Beijing, China
Beijing Key Laboratory of Diabetes Research and Care, Beijing, China

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Yali Wu Center for Endocrine Metabolism and Immune Diseases, Lu He Hospital, Capital Medical University, Beijing, China
Beijing Key Laboratory of Diabetes Research and Care, Beijing, China

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Zhilei Chen Center for Endocrine Metabolism and Immune Diseases, Lu He Hospital, Capital Medical University, Beijing, China
Beijing Key Laboratory of Diabetes Research and Care, Beijing, China

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Baoyu Zhang Center for Endocrine Metabolism and Immune Diseases, Lu He Hospital, Capital Medical University, Beijing, China
Beijing Key Laboratory of Diabetes Research and Care, Beijing, China

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Osteoporosis (OP) is a systemic bone disease in which bone density and quality decrease and bone fragility increases due to a variety of causes, making it prone to fractures. The development of OP is closely related to oxidative stress. Uric acid (UA) is the end product of purine metabolism in the human body. Extracellular UA has antioxidant properties and is thought to have a protective effect on bone metabolism. However, the process of UA degradation can lead to intracellular oxidative stress, which together with UA-induced inflammatory factors, leads to increased bone destruction. In addition, UA can inhibit vitamin D production, resulting in secondary hyperparathyroidism and further exacerbating UA-associated bone loss. This review summarizes the relationship between serum UA levels and bone mineral density, bone turnover markers, and so on, in the hope of providing new insights into the pathogenesis and treatment of OP.

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Jiaxin Zhang Department of Traditional Chinese Medicine (TCM) Orthopedics, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China

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Jinlan Jiang Wenzhou Institute, University of Chinese Academy of Sciences, Wenzhou, Zhejiang, China

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Yao Qin School of Public Health, Hangzhou Medical College, Hangzhou, Zhejiang, China

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Yihui Zhang Department of Traditional Chinese Medicine (TCM) Orthopedics, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China

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Yungang Wu Department of Traditional Chinese Medicine (TCM) Orthopedics, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China

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Huadong Xu School of Public Health, Hangzhou Medical College, Hangzhou, Zhejiang, China

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Purpose

This study aims to investigate the associations of the systemic immune-inflammation index (SII) with bone mineral density (BMD) and osteoporosis in adult females from a nationally representative sample.

Methods

A cross-sectional study was performed among 4092 females aged ≥20 years from the National Health and Nutrition Examination Survey 2007–2010. Linear and logistic regressions were applied to explore the relationships of SII with BMD and the risk of osteoporosis, respectively.

Results

Linear regression analyses found that a doubling of SII levels was significantly correlated with a 1.39% (95% CI: 0.57%, 2.20%) decrease in total femur BMD, a 1.16% (95% CI: 0.31%, 2.00%) decrease in femur neck BMD, a 1.73% (95% CI: 0.78%, 2.66%) decrease in trochanter BMD, and a 1.35% (95% CI: 0.50%, 2.20%) decrease in intertrochanteric BMD among postmenopausal women, after adjusting for covariates. Logistic regression analyses showed that compared with postmenopausal women in the lowest SII quartile, those in the highest quartile had higher risks of osteoporosis in the total femur (odds ratio (OR) = 1.70, 95% CI: 1.04, 2.76), trochanter (OR = 1.86, 95% CI: 1.07, 3.38), intertrochanter (OR = 2.01, 95% CI: 1.05, 4.04) as well as overall osteoporosis (OR = 1.57, 95% CI: 1.04, 2.37). In contrast, there was no significant association between SII and BMD in premenopausal women.

Conclusions

SII levels were negatively associated with BMD levels in postmenopausal women but not in premenopausal women. Elevated SII levels could be a potential risk factor for osteoporosis in postmenopausal women.

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Demi T.c. de Winter D de Winter, Princess Máxima Center for Pediatric Oncology, Prinses Maxima Centrum voor Kinderoncologie BV, Utrecht, Netherlands

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Sebastian J.c.m.m. Neggers S Neggers, Department of Internal Medicine, section Endocrinology, Erasmus MC University Medical Center Rotterdam, Rotterdam, Netherlands

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Mm van den Heuvel-Eibrink M van den Heuvel-Eibrink, Princess Máxima Center for Pediatric Oncology, Prinses Maxima Centrum voor Kinderoncologie BV, Utrecht, Netherlands

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Jenneke E. van Atteveld J van Atteveld, Princess Máxima Center for Pediatric Oncology, Prinses Maxima Centrum voor Kinderoncologie BV, Utrecht, Netherlands

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Childhood cancer survivors are at increased risk of developing (long-term) skeletal adverse effects, such as osteonecrosis, impaired bone mineral density, and fractures. This paper provides an overview of the current understanding of bone health in these survivors, examining whether it represents a significant concern. It focuses on the challenges of assessing and managing bone health in childhood cancer survivors, highlighting diagnostic pitfalls, methods for accurately identifying those at high risk, and suggested strategies for surveillance and management of osteonecrosis and impaired bone mineral density. The need for improved surveillance strategies, particularly for high-risk survivors, alongside potential prevention and management options, including pharmacological and lifestyle interventions, is emphasised. Given the lack of consensus on optimal prevention and treatment strategies, the paper emphasises the need for further research to optimise care and improve long-term outcomes for childhood cancer survivors with bone health impairments.

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