Bone Reports最新文献

{"title":"High rate of progression to symptomatic multiple myeloma in patients with smoldering myeloma and isolated osteoporotic vertebral fracture","authors":"Kevin Chevalier ,&nbsp;Sabrina Hamroun ,&nbsp;Samuel Bitoun ,&nbsp;Julien Henry ,&nbsp;Christian Roux ,&nbsp;Karine Briot ,&nbsp;Rakiba Belkhir ,&nbsp;Xavier Mariette ,&nbsp;Raphaèle Seror","doi":"10.1016/j.bonr.2024.101755","DOIUrl":"https://doi.org/10.1016/j.bonr.2024.101755","url":null,"abstract":"<div><p>Multiple myeloma (MM) frequently causes vertebral fractures (VF). Some are lytic lesions and others have the aspect of benign osteoporotic fractures not requiring anti-myeloma treatment. We explored outcome of these patients with smoldering myeloma (SM) and osteoporotic VF.</p><p>In this retrospective bi-centric study, patients were identified using a systematic keyword search on electronic medical records. Patients with SM and isolated VF of osteoporotic aspect without indications for myeloma-specific therapy were included.</p><p>Overall, 13 (7 %) of the 184 identified patients had SM and VF confirmed to be osteoporotic (median number of VF was 3). During follow-up, 12 (92 %) patients evolved to symptomatic MM, 7 (54 %) of them within 18 months (early progressors). Myeloma defining events were new lytic bone lesions in 7 patients (53.8 %). The serum calcium level was significantly higher in the early progressor group (median 2.35 IQR [2.31–2.38] and 2.28 IQR [2.21–2.29] respectively, <em>p</em> = 0.003). Early progressors had a higher number of VF at diagnosis (3.0 [2.0–5.5] vs 1.0 [1.0–2.5], <em>p</em> = 0.18) and more frequently evolved to symptomatic MM because of lytic bone lesions (5 [71 %] vs 2 [33 %], <em>p</em> = 0.13) compared to late progressors.</p><p>VF of osteoporotic appearance in the context of SM is a rare situation but at high risk of rapid progression to symptomatic MM, suggesting that they may represent bone fragility linked to MM infiltration rather than solely osteoporotic fractures. Further studies are needed to assess if earlier treatment might be beneficial in this population.</p></div>","PeriodicalId":9043,"journal":{"name":"Bone Reports","volume":"21 ","pages":"Article 101755"},"PeriodicalIF":2.5,"publicationDate":"2024-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352187224000226/pdfft?md5=afe87f7f94161630eeb982607eb0b5b0&pid=1-s2.0-S2352187224000226-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140290845","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lessons learned from the real-world diagnosis and management of hereditary hypophosphatemic rickets","authors":"Deepti Chaturvedi ,&nbsp;Taif EmadEldin Mehasi ,&nbsp;Assia Benbrahim ,&nbsp;Lubna ElDeeb ,&nbsp;Asma Deeb","doi":"10.1016/j.bonr.2024.101753","DOIUrl":"10.1016/j.bonr.2024.101753","url":null,"abstract":"<div><p>Hypophosphatemic rickets, which is often hereditary, is still under- or misdiagnosed in both children and adults, denying these individuals access to optimal management and genetic counseling. There have been recent calls to compile real-world data and share best practice on these rare conditions to guide clinical decision-making. Here we present eight clinical vignettes of patients with hypophosphatemic rickets encountered in our tertiary pediatric endocrinology practice. We describe the clinical features, genetics, and management of four cases of X-linked hypophosphatemia (<em>PHEX</em> mutations), one each of autosomal recessive hypophosphatemic rickets (<em>DMP1</em> mutation) and autosomal recessive vitamin D-dependent rickets type 1A (<em>CYP27B1</em> mutation), and two cases of distal renal tubular acidosis with <em>FOXI1</em> mutation-associated hypophosphatemic rickets. Our cases prompt consideration of the (i) frequent misdiagnosis of hypophosphatemic rickets in clinical practice and the importance of comprehensive genetic testing; (ii) variable expressivity of the causative mutations; and (iii) a lack of responsiveness and/or compliance to conventional therapy and the value of burosumab in modern management, provided access is equitable. These cases highlight common real-world themes and challenges to managing patients presenting with these diverse conditions, especially the burden of disease hidden by misdiagnosis. In sharing these cases, we hope to raise awareness of these conditions, promote best practice in genetic diagnosis and management, and further advocate for reimbursement equity for the best available therapies.</p></div>","PeriodicalId":9043,"journal":{"name":"Bone Reports","volume":"21 ","pages":"Article 101753"},"PeriodicalIF":2.5,"publicationDate":"2024-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352187224000202/pdfft?md5=6dfd2cc5b734f76a4a725d477b1c9e6d&pid=1-s2.0-S2352187224000202-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140279518","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microvascular disease not type 2 diabetes is associated with increased cortical porosity: A study of cortical bone microstructure and intracortical vessel characteristics","authors":"Maximilian T. Löffler ,&nbsp;Po-hung Wu ,&nbsp;Amir M. Pirmoazen ,&nbsp;Gabby B. Joseph ,&nbsp;Jay M. Stewart ,&nbsp;Isra Saeed ,&nbsp;Jing Liu ,&nbsp;Anne L. Schafer ,&nbsp;Ann V. Schwartz ,&nbsp;Thomas M. Link ,&nbsp;Galateia J. Kazakia","doi":"10.1016/j.bonr.2024.101745","DOIUrl":"https://doi.org/10.1016/j.bonr.2024.101745","url":null,"abstract":"<div><h3>Introduction</h3><p>Fracture risk is elevated in type 2 diabetes (T2D) despite normal or even high bone mineral density (BMD). Microvascular disease (MVD) is a diabetic complication, but also associated with other diseases, for example chronic kidney disease. We hypothesize that increased fracture risk in T2D could be due to increased cortical porosity (Ct.Po) driven by expansion of the vascular network in MVD. The purpose of this study was to investigate associations of T2D and MVD with cortical microstructure and intracortical vessel parameters.</p></div><div><h3>Methods</h3><p>The study group consisted of 75 participants (38 with T2D and 37 without T2D). High-resolution peripheral quantitative CT (HR-pQCT) and dynamic contrast-enhanced MRI (DCE-MRI) of the ultra-distal tibia were performed to assess cortical bone and intracortical vessels (outcomes). MVD was defined as ≥1 manifestation including neuropathy, nephropathy, or retinopathy based on clinical exams in all participants. Adjusted means of outcomes were compared between groups with/without T2D or between participants with/without MVD in both groups using linear regression models adjusting for age, sex, BMI, and T2D as applicable.</p></div><div><h3>Results</h3><p>MVD was found in 21 (55 %) participants with T2D and in 9 (24 %) participants without T2D. In T2D, cortical pore diameter (<span>Ct.Po.Dm</span><svg><path></path></svg>) and diameter distribution (<span>Ct.Po.Dm.SD</span><svg><path></path></svg>) were significantly higher by 14.6 μm (3.6 %, 95 % confidence interval [CI]: 2.70, 26.5 μm, <em>p</em> = 0.017) and by 8.73 μm (4.8 %, CI: 0.79, 16.7 μm, <em>p</em> = 0.032), respectively. In MVD, but not in T2D, cortical porosity was significantly higher by 2.25 % (relative increase = 12.9 %, CI: 0.53, 3.97 %, <em>p</em> = 0.011) and cortical BMD (Ct.BMD) was significantly lower by −43.6 mg/cm³ (2.6 %, CI: −77.4, −9.81 mg/cm³, <em>p</em> = 0.012). In T2D, vessel volume and vessel diameter were significantly higher by 0.02 mm³ (13.3 %, CI: 0.004, 0.04 mm³, <em>p</em> = 0.017) and 15.4 μm (2.9 %, CI: 0.42, 30.4 μm, <em>p</em> = 0.044), respectively. In MVD, vessel density was significantly higher by 0.11 mm⁻³ (17.8 %, CI: 0.01, 0.21 mm⁻³, <em>p</em> = 0.033) and vessel volume and diameter were significantly lower by −0.02 mm³ (13.7 %, CI: −0.04, −0.004 mm³, <em>p</em> = 0.015) and − 14.6 μm (2.8 %, CI: −29.1, −0.11 μm, <em>p</em> = 0.048), respectively.</p></div><div><h3>Conclusions</h3><p>The presence of MVD, rather than T2D, was associated with increased cortical porosity. Increased porosity in MVD was coupled with a larger number of smaller vessels, which could indicate upregulation of neovascularization triggered by ischemia. It is unclear why higher variability and average diameters of pores in T2D were accompanied by larger vessels.</p></div>","PeriodicalId":9043,"journal":{"name":"Bone Reports","volume":"20 ","pages":"Article 101745"},"PeriodicalIF":2.5,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352187224000123/pdfft?md5=3d14966779ac86845812bdf76c953c7e&pid=1-s2.0-S2352187224000123-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139992577","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In vivo imaging of bone collagen dynamics in zebrafish","authors":"Hiromu Hino,&nbsp;Shigeru Kondo,&nbsp;Junpei Kuroda","doi":"10.1016/j.bonr.2024.101748","DOIUrl":"https://doi.org/10.1016/j.bonr.2024.101748","url":null,"abstract":"<div><p>Type I collagen plays a pivotal role in shaping bone morphology and determining its physical properties by serving as a template for ossification. Nevertheless, the mechanisms underlying bone collagen formation, particularly the principles governing its orientation, remain unknown owing to the lack of a method that enables continuous in vivo observations. To address this challenge, we constructed a method to visualize bone collagen by tagging with green fluorescent protein (GFP) in zebrafish and observed the interactions between osteoblasts and collagen fibers during bone formation in vivo. When collagen type I alpha 2 chain (Col1a2)-GFP was expressed under the control of the osteoblast-specific promoters <em>osx</em> or <em>osc</em> in zebrafish, bone collagen was observed clearly enough to identify its localization, whereas collagen from other organs was not. Therefore, we determined that this method was of sufficient quality for the detailed in vivo observation of bone collagen. Next, bone collagen in the scales, fin rays, and opercular bones of zebrafish was observed in detail, when bone formation is more active. High-magnification imaging showed that Col1a2-GFP can visualize collagen sufficiently to analyze the collagen fiber orientation and microstructure of bones.</p><p>Furthermore, by simultaneously observation of bone collagen and osteoblasts, we successfully observed dynamic changes in the morphology and position of osteoblasts from the early stages of bone formation. It was also found that the localization pattern and orientation of bone collagen significantly differed depending on the choice of the expression promoter. Both promoters (<em>osx</em> and <em>osc</em>) used in this study are osteoblast-specific, but their Col1a2-GFP localizing regions within the bone were exclusive, with <em>osx</em> region localizing mainly to the outer edge of the bone and <em>osc</em> region localizing to the central area of the bone. This suggests the existence of distinct osteoblast subpopulations with different gene expression profiles, each of which may play a unique role in osteogenesis.</p><p>These findings would contribute to a better understanding of the mechanisms governing bone collagen formation by osteoblasts.</p></div>","PeriodicalId":9043,"journal":{"name":"Bone Reports","volume":"20 ","pages":"Article 101748"},"PeriodicalIF":2.5,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352187224000159/pdfft?md5=cb08f47d26cb5827c6314da29d639ff8&pid=1-s2.0-S2352187224000159-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140137962","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Disruption of FLNB leads to skeletal malformation by interfering with skeletal segmentation through the HOX gene","authors":"Qiming Xu ,&nbsp;Lijia Cui ,&nbsp;Yude Lin ,&nbsp;Leigh-Anne Cui ,&nbsp;Weibo Xia","doi":"10.1016/j.bonr.2024.101746","DOIUrl":"https://doi.org/10.1016/j.bonr.2024.101746","url":null,"abstract":"<div><p>Filamin B (FLNB) plays an important role in skeletal development. Mutations in <em>FLNB</em> can lead to skeletal malformation such as an abnormal number of ossification centers, indicating that the skeletal segmentation in the embryonic period may be interfered with. We established a mouse model with the pathogenic point mutation <em>FLNB</em> NM_001081427.1: c.4756G &gt; A (p.Gly1586Arg) using CRISPR-Cas9 technology. Micro-CT, HE staining and whole skeletal preparation were performed to examine the skeletal malformation. <em>In situ</em> hybridization of embryos was performed to examine the transcription of <em>HOX</em> genes during embryonic development. The expression of <em>FLNB</em> was downregulated in <em>FLNB</em>^{<em>G1586R/G1586R</em>} and <em>FLNB</em>^{<em>WT/G1586R</em>} mice, compared to <em>FLNB</em>^{<em>WT/WT</em>} mice. Fusions in tarsal bones were found in <em>FLNB</em>^{<em>G1586R/G1586R</em>} and <em>FLNB</em>^{<em>WT/G1586R</em>} mice, indicating that the skeletal segmentation was interfered with. In the embryo of <em>FLNB</em>^{<em>G1586R</em>/<em>G1586R</em>} mice (E12.5), the transcription levels of <em>HOXD10</em> and <em>HOXB2</em> were downregulated in the carpal region and cervical spine region, respectively. This study indicated that the loss-of-function mutation G1586R in <em>FLNB</em> may lead to abnormal skeletal segmentation, and the mechanism was possibly associated with the downregulation of <em>HOX</em> gene transcription during the embryonic period.</p></div>","PeriodicalId":9043,"journal":{"name":"Bone Reports","volume":"20 ","pages":"Article 101746"},"PeriodicalIF":2.5,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352187224000135/pdfft?md5=728bb9d200c17274480dd8ba735f03ab&pid=1-s2.0-S2352187224000135-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140030727","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The multi-faceted nature of age-associated osteoporosis","authors":"A.E. Smit ,&nbsp;O.C. Meijer ,&nbsp;E.M. Winter","doi":"10.1016/j.bonr.2024.101750","DOIUrl":"https://doi.org/10.1016/j.bonr.2024.101750","url":null,"abstract":"<div><p>Age-associated osteoporosis (AAOP) poses a significant health burden, characterized by increased fracture risk due to declining bone mass and strength. Effective prevention and early treatment strategies are crucial to mitigate the disease burden and the associated healthcare costs. Current therapeutic approaches effectively target the individual contributing factors to AAOP. Nonetheless, the management of AAOP is complicated by the multitude of variables that affect its development. Main intrinsic and extrinsic factors contributing to AAOP risk are reviewed here, including mechanical unloading, nutrient deficiency, hormonal disbalance, disrupted metabolism, cognitive decline, inflammation and circadian disruption. Furthermore, it is discussed how these can be targeted for prevention and treatment. Although valuable as individual targets for intervention, the interconnectedness of these risk factors result in a unique etiology for every patient. Acknowledgement of the multifaceted nature of AAOP will enable the development of more effective and sustainable management strategies, based on a holistic, patient-centered approach.</p></div>","PeriodicalId":9043,"journal":{"name":"Bone Reports","volume":"20 ","pages":"Article 101750"},"PeriodicalIF":2.5,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352187224000172/pdfft?md5=39c67a98f90cb657a8bae1bf1149b52d&pid=1-s2.0-S2352187224000172-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140191265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Case report: Death caused by multi-organ metastatic calcifications as a result of intramuscular injections with paraffin oil","authors":"Søren Reinhold Jakobsen ,&nbsp;Marta Diaz-delCastillo ,&nbsp;Martin Blomberg Jensen ,&nbsp;Thomas Levin Andersen ,&nbsp;Ebbe Eldrup ,&nbsp;Trine Skov Nielsen","doi":"10.1016/j.bonr.2024.101749","DOIUrl":"https://doi.org/10.1016/j.bonr.2024.101749","url":null,"abstract":"<div><p>In this forensic case report, we present autopsy findings from a young male in his thirties who had been self-injecting paraffin oil into his upper extremities 8 years prior to death. The injections induced an inflammatory response, leading to granuloma formation. This, in turn, resulted in severe hypercalcemia. The external autopsy examination revealed gross macroscopic ulcerations and enlargement of upper extremities, while calcifications of ligaments, heart, kidneys and dura mater was revealed on postmortem CT-scans. Histopathological examination showed extensive multiorgan metastatic calcifications in several tissues including the lungs, heart and kidney. Cause of death was estimated to be the extensive calcific deposits in the heart likely resulting in cardiac arrest. To our knowledge this is the first case reporting findings from an autopsy in which the cause of death was linked to cosmetic oil injections.</p></div>","PeriodicalId":9043,"journal":{"name":"Bone Reports","volume":"20 ","pages":"Article 101749"},"PeriodicalIF":2.5,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352187224000160/pdfft?md5=6b914088738b4d5b9a9cb3218298485d&pid=1-s2.0-S2352187224000160-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140052131","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Craniofacial disorders and dysplasias: Molecular, clinical, and management perspectives","authors":"Sunday O. Akintoye ,&nbsp;Akinyele O. Adisa ,&nbsp;Chukwubuzor U. Okwuosa ,&nbsp;Mel Mupparapu","doi":"10.1016/j.bonr.2024.101747","DOIUrl":"10.1016/j.bonr.2024.101747","url":null,"abstract":"<div><p>There is a wide spectrum of craniofacial bone disorders and dysplasias because embryological development of the craniofacial region is complex. Classification of craniofacial bone disorders and dysplasias is also complex because they exhibit complex clinical, pathological, and molecular heterogeneity. Most craniofacial disorders and dysplasias are rare but they present an array of phenotypes that functionally impact the orofacial complex. Management of craniofacial disorders is a multidisciplinary approach that involves the collaborative efforts of multiple professionals. This review provides an overview of the complexity of craniofacial disorders and dysplasias from molecular, clinical, and management perspectives.</p></div>","PeriodicalId":9043,"journal":{"name":"Bone Reports","volume":"20 ","pages":"Article 101747"},"PeriodicalIF":2.5,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352187224000147/pdfft?md5=3eb5e2d20d111d0f05106554a74f4249&pid=1-s2.0-S2352187224000147-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140084645","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Real world fracture prediction of fracture risk assessment tool (FRAX), osteoporosis self-assessment tool for Asians (OSTA) and one-minute osteoporosis risk test: An 11-year longitudinal study","authors":"Yueh-Hsuan Sheng ,&nbsp;Tai-Yin Wu ,&nbsp;Chen-Kun Liaw ,&nbsp;Sheng-Huang Hsiao ,&nbsp;Kuan-Liang Kuo ,&nbsp;Ching-Yao Tsai","doi":"10.1016/j.bonr.2024.101742","DOIUrl":"https://doi.org/10.1016/j.bonr.2024.101742","url":null,"abstract":"<div><h3>Introduction</h3><p>Fractures affect people's quality of life especially in the elders. One of the most important risk factors is osteoporosis. There are many screening tools to predict osteoporosis and fractures. We aimed to compare the predictive validity of three commonly used screening tools: fracture risk assessment tool (FRAX), osteoporosis self-assessment tool for Asians (OSTA) and one-minute osteoporosis risk test. Among them, OSTA and one-minute osteoporosis risk test were originally developed to predict osteoporosis risks and FRAX was to predict fracture risks.</p></div><div><h3>Methods</h3><p>This is an 11-year longitudinal study. We enrolled 708 senior people from health examinees in Taiwan in 2010. A standardized questionnaire and blood tests were provided. Annual telephone interview was conducted to assess the real fracture status. We calculated risk scores of FRAX, OSTA, and one-minute osteoporosis risk test and compared with real-world fracture records.</p></div><div><h3>Results</h3><p>The mean age of the participants were 74.9 (SD 6.4). There were 356 (50.3 %) men. From 2010 to 2020, a total of 105 (14.8 %) persons suffered from fractures. Compared to people without fractures, people with fractures had higher FRAX major osteoporotic fracture risk scores (14.0 % ± 7.6 % vs.11.3 % ± 5.7 %), higher hip fracture risk scores, and higher OSTA risk (5.9 % ± 1.4 % vs. 5.3 % ± 1.3 %). Cox regression analysis showed that hazard ratios for fracture of high FRAX risk was 1.53 (95 % confidence interval (CI) 1.05–2.21), and for high OSTA risk was 1.37 (95 % CI 1.04–1.82).</p></div><div><h3>Conclusions</h3><p>Only OSTA and FRAX scores were satisfactory in predicting 10-year fractures.</p></div>","PeriodicalId":9043,"journal":{"name":"Bone Reports","volume":"20 ","pages":"Article 101742"},"PeriodicalIF":2.5,"publicationDate":"2024-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352187224000093/pdfft?md5=a45cf1f36c18eea7f6aa4bb709ac8450&pid=1-s2.0-S2352187224000093-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139898600","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Strontium ranelate retards disc degradation and improves endplate and bone micro-architecture in ovariectomized rats with lumbar fusion induced – Adjacent segment disc degeneration","authors":"Qi Sun ,&nbsp;Fang Liu ,&nbsp;Jiakang Fang ,&nbsp;Qiangqiang Lian ,&nbsp;Yunpeng Hu ,&nbsp;Xinyu Nan ,&nbsp;Fa-Ming Tian ,&nbsp;Guochuan Zhang ,&nbsp;Dianwen Qi ,&nbsp;Liu Zhang ,&nbsp;Jingwen Zhang ,&nbsp;Yang Luo ,&nbsp;Zuzhuo Zhang ,&nbsp;Zhuang Zhou","doi":"10.1016/j.bonr.2024.101744","DOIUrl":"10.1016/j.bonr.2024.101744","url":null,"abstract":"<div><h3>Objectives</h3><p>Adjacent segment disc degeneration (ASDD) is one of the long-term sequelae of spinal fusion, which is more susceptible with osteoporosis. As an anti-osteoporosis drug, strontium ranelate (SR) has been reported to not only regulate bone metabolism but also cartilage matrix formation. However, it is not yet clear whether SR has a reversal or delaying effect on fusion-induced ASDD in a model of osteoporosis.</p></div><div><h3>Materials and methods</h3><p>Fifth three-month-old female Sprague-Dawley rats that underwent L4-L5 posterolateral lumbar fusion (PLF) with spinous-process wire fixation 4 weeks after bilateral ovariectomy (OVX) surgery. Animals were administered vehicle (V) or SR (900 mg/kg/d) orally for 12 weeks post-PLF as follows: Sham+V, OVX + V, PLF + V, OVX + PLF + V, and OVX + PLF + SR. Manual palpation and X-ray were used to evaluate the state of lumbar fusion. Adjacent-segment disc was assessed by histological (VG staining and Scoring), histomorphometry (Disc Height, MVD, Calcification rate and Vascular Bud rate), immunohistochemical (Col-II, Aggrecan, MMP-13, ADAMTS-4 and Caspase-3), and mRNA analysis (Col<img>I, Col-II, Aggrecan, MMP-13 and ADAMTS-4). Adjacent L6 vertebrae microstructures were evaluated by microcomputed tomography.</p></div><div><h3>Results</h3><p>Manual palpation and radiographs showed clear evidence of the fused segment's immobility. After 12 weeks of PLF surgery, a fusion-induced ASDD model was established. Low bone mass caused by ovariectomy can significantly exacerbate ASDD progression. SR exerted a protective effect on adjacent segment intervertebral disc with the underlying mechanism possibly being associated with preserving bone mass to prevent spinal instability, maintaining the functional integrity of endplate vascular microstructure, and regulating matrix metabolism in the nucleus pulposus and annulus fibrosus.</p></div><div><h3>Discussion</h3><p>Anti-osteoporosis medication SR treatments not only maintain bone mass and prevent fractures, but early intervention could also potentially delay degenerative conditions linked to osteoporosis. Taken together, our results suggested that SR might be a promising approach for the intervention of fusion-induced ASDD with osteoporosis.</p></div>","PeriodicalId":9043,"journal":{"name":"Bone Reports","volume":"20 ","pages":"Article 101744"},"PeriodicalIF":2.5,"publicationDate":"2024-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352187224000111/pdfft?md5=50ecf22295faa2e1e4935399628b2a4a&pid=1-s2.0-S2352187224000111-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139884282","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}