Current Osteoporosis Reports最新文献

{"title":"Inflammasomes and the IL-1 Family in Bone Homeostasis and Disease","authors":"Hsu‐Wen Tseng, S. Samuel, K. Schroder, J. Lévesque, Kylie A Alexander","doi":"10.1007/s11914-022-00729-8","DOIUrl":"https://doi.org/10.1007/s11914-022-00729-8","url":null,"abstract":"","PeriodicalId":11080,"journal":{"name":"Current Osteoporosis Reports","volume":"20 1","pages":"170 - 185"},"PeriodicalIF":4.3,"publicationDate":"2022-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49029775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Osteoporosis Diagnosis, Management, and Referral Practice After Fragility Fractures","authors":"Phillip Snodgrass, Anthony Zou, U. Gruntmanis, I. Gitajn","doi":"10.1007/s11914-022-00730-1","DOIUrl":"https://doi.org/10.1007/s11914-022-00730-1","url":null,"abstract":"","PeriodicalId":11080,"journal":{"name":"Current Osteoporosis Reports","volume":"20 1","pages":"163 - 169"},"PeriodicalIF":4.3,"publicationDate":"2022-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47543188","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sfrp4 and the Biology of Cortical Bone.","authors":"Ruiying Chen, Roland Baron, Francesca Gori","doi":"10.1007/s11914-022-00727-w","DOIUrl":"10.1007/s11914-022-00727-w","url":null,"abstract":"<p><strong>Purpose of review: </strong>Periosteal apposition and endosteal remodeling regulate cortical bone expansion and thickness, both critical determinants of bone strength. Yet, the cellular characteristics and local or paracrine factors that regulate the periosteum and endosteum remain largely elusive. Here we discuss novel insights in cortical bone growth, expansion, and homeostasis, provided by the study of Secreted Frizzled Receptor Protein 4 (Sfrp4), a decoy receptor for Wnt ligands.</p><p><strong>Recent findings: </strong>SFRP4 loss-of function mutations cause Pyle disease, a rare skeletal disorder characterized by cortical bone thinning and increased fragility fractures despite increased trabecular bone density. On the endosteal surface, Sfrp4-mediated repression of non-canonical Wnt signaling regulates endosteal resorption. On the periosteum, Sfrp4 identifies as a critical functional mediator of periosteal stem cell/progenitor expansion and differentiation. Analysis of signaling pathways regulating skeletal stem cells/progenitors provides an opportunity to advance our understanding of the mechanisms involved in cortical bone biology.</p>","PeriodicalId":11080,"journal":{"name":"Current Osteoporosis Reports","volume":"20 2","pages":"153-161"},"PeriodicalIF":4.2,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9098678/pdf/nihms-1784024.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9227985","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Finite Element Models of Osteocytes and Their Load-Induced Activation","authors":"T. Smit","doi":"10.1007/s11914-022-00728-9","DOIUrl":"https://doi.org/10.1007/s11914-022-00728-9","url":null,"abstract":"","PeriodicalId":11080,"journal":{"name":"Current Osteoporosis Reports","volume":"20 1","pages":"127 - 140"},"PeriodicalIF":4.3,"publicationDate":"2022-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48652418","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aberrant Bone Regulation in Albright Hereditary Osteodystrophy dueto Gnas Inactivation: Mechanisms and Translational Implications","authors":"P. McMullan, E. Germain-Lee","doi":"10.1007/s11914-022-00719-w","DOIUrl":"https://doi.org/10.1007/s11914-022-00719-w","url":null,"abstract":"","PeriodicalId":11080,"journal":{"name":"Current Osteoporosis Reports","volume":"20 1","pages":"78 - 89"},"PeriodicalIF":4.3,"publicationDate":"2022-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45109096","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bioenergetic Metabolism In Osteoblast Differentiation.","authors":"Leyao Shen,&nbsp;Guoli Hu,&nbsp;Courtney M Karner","doi":"10.1007/s11914-022-00721-2","DOIUrl":"https://doi.org/10.1007/s11914-022-00721-2","url":null,"abstract":"<p><strong>Purpose of review: </strong>Osteoblasts are responsible for bone matrix production during bone development and homeostasis. Much is known about the transcriptional regulation and signaling pathways governing osteoblast differentiation. However, less is known about how osteoblasts obtain or utilize nutrients to fulfill the energetic demands associated with osteoblast differentiation and bone matrix synthesis. The goal of this review is to highlight and discuss what is known about the role and regulation of bioenergetic metabolism in osteoblasts with a focus on more recent studies.</p><p><strong>Recent findings: </strong>Bioenergetic metabolism has emerged as an important regulatory node in osteoblasts. Recent studies have begun to identify the major nutrients and bioenergetic pathways favored by osteoblasts as well as their regulation during differentiation. Here, we highlight how osteoblasts obtain and metabolize glucose, amino acids, and fatty acids to provide energy and other metabolic intermediates. In addition, we highlight the signals that regulate nutrient uptake and metabolism and focus on how energetic metabolism promotes osteoblast differentiation. Bioenergetic metabolism provides energy and other metabolites that are critical for osteoblast differentiation and activity. This knowledge contributes to a more comprehensive understanding of osteoblast biology and may inform novel strategies to modulate osteoblast differentiation and bone anabolism in patients with bone disorders.</p>","PeriodicalId":11080,"journal":{"name":"Current Osteoporosis Reports","volume":"20 1","pages":"53-64"},"PeriodicalIF":4.3,"publicationDate":"2022-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9245007/pdf/nihms-1778989.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10635300","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulation of FGF23: Beyond Bone.","authors":"Petra Simic,&nbsp;Jodie L Babitt","doi":"10.1007/s11914-021-00703-w","DOIUrl":"https://doi.org/10.1007/s11914-021-00703-w","url":null,"abstract":"<p><strong>Purpose of review: </strong>Fibroblast growth factor 23 (FGF23) is a bone- and bone marrow-derived hormone that is critical to maintain phosphate homeostasis. The principal actions of FGF23 are to reduce serum phosphate levels by decreasing kidney phosphate reabsorption and 1,25-dihydroxyvitamin D synthesis. FGF23 deficiency causes hyperphosphatemia and ectopic calcifications, while FGF23 excess causes hypophosphatemia and skeletal defects. Excess FGF23 also correlates with kidney disease, where it is associated with increased morbidity and mortality. Accordingly, FGF23 levels are tightly regulated, but the mechanisms remain incompletely understood.</p><p><strong>Recent findings: </strong>In addition to bone mineral factors, additional factors including iron, erythropoietin, inflammation, energy, and metabolism regulate FGF23. All these factors affect Fgf23 expression, while some also regulate FGF23 protein cleavage. Conversely, FGF23 may have a functional role in regulating these biologic processes. Understanding the bi-directional relationship between FGF23 and non-bone mineral factors is providing new insights into FGF23 regulation and function.</p>","PeriodicalId":11080,"journal":{"name":"Current Osteoporosis Reports","volume":"19 6","pages":"563-573"},"PeriodicalIF":4.3,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8958553/pdf/nihms-1761638.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9407269","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Polygenic and Monogenic Basis of Paediatric Fractures.","authors":"S Ghatan,&nbsp;A Costantini,&nbsp;R Li,&nbsp;C De Bruin,&nbsp;N M Appelman-Dijkstra,&nbsp;E M Winter,&nbsp;L Oei,&nbsp;Carolina Medina-Gomez","doi":"10.1007/s11914-021-00680-0","DOIUrl":"10.1007/s11914-021-00680-0","url":null,"abstract":"<p><strong>Purpose of review: </strong>Fractures are frequently encountered in paediatric practice. Although recurrent fractures in children usually unveil a monogenic syndrome, paediatric fracture risk could be shaped by the individual genetic background influencing the acquisition of bone mineral density, and therefore, the skeletal fragility as shown in adults. Here, we examine paediatric fractures from the perspective of monogenic and complex trait genetics.</p><p><strong>Recent findings: </strong>Large-scale genome-wide studies in children have identified ~44 genetic loci associated with fracture or bone traits whereas ~35 monogenic diseases characterized by paediatric fractures have been described. Genetic variation can predispose to paediatric fractures through monogenic risk variants with a large effect and polygenic risk involving many variants of small effects. Studying genetic factors influencing peak bone attainment might help in identifying individuals at higher risk of developing early-onset osteoporosis and discovering drug targets to be used as bone restorative pharmacotherapies to prevent, or even reverse, bone loss later in life.</p>","PeriodicalId":11080,"journal":{"name":"Current Osteoporosis Reports","volume":"19 5","pages":"481-493"},"PeriodicalIF":4.3,"publicationDate":"2021-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s11914-021-00680-0","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38879971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Energy Metabolism of Osteocytes.","authors":"Vivin Karthik,&nbsp;Anyonya R Guntur","doi":"10.1007/s11914-021-00688-6","DOIUrl":"https://doi.org/10.1007/s11914-021-00688-6","url":null,"abstract":"<p><strong>Purpose of review: </strong>In this review, we provide a recent update on bioenergetic pathways in osteocytes and identify potential future areas of research interest. Studies have identified a role for regulation of bone formation and bone resorption through osteocyte mechanosensing and osteocyte secreted factors. Nevertheless, there is a paucity of studies on the bioenergetics and energy metabolism of osteocytes, which are required for the regulation of bone remodeling.</p><p><strong>Recent findings: </strong>Osteocytes are cells of the osteoblast lineage embedded in bone. The osteocyte lacunocanalicular network within the skeletal matrix is exposed to a unique hypoxic environment. Therefore, the bioenergetic requirements of these cells could differ from other bone cells due to its location in the ossified matrix and its role in bone regulation transduced by mechanical signals. Recent findings highlighted in this review provide some evidence that metabolism of these cells is dependent on their location due to the substrates present in the microenvironment and metabolic cues from stress pathways. Both glycolysis (glucose metabolism) and oxidative phosphorylation (mitochondrial dynamics, ROS generation) affect osteocyte function and viability. In this review, we provide evidence that is currently available about information regarding bioenergetics pathways in osteocytes. We discuss published studies showing a role for hypoxia-driven glucose metabolism in regulating osteocyte bioenergetics. We also provide information on various substrates that osteocytes could utilize to fuel energetic needs, namely pyruvate, amino acids, and fatty acids. This is based on some preliminary experimental evidence that is available in literature. The role of parathyroid hormone PTH and parathryoid hormone-related peptide PTHrP in bone anabolism and resorption, along with regulation of metabolic pathways in the cells of the skeletal niche, needs to be explored further. Mitochondrial metabolism has a role in osteocyte bioenergetics through substrate utilization, location of the osteocyte in the bone cortex, and mitochondrial biogenesis. While there are limitations in studying metabolic flux in traditional cell lines, there are now novel cell lines and sophisticated tools available to study osteocyte bioenergetics to help harness its potential in vivo in the future.</p>","PeriodicalId":11080,"journal":{"name":"Current Osteoporosis Reports","volume":"19 4","pages":"444-451"},"PeriodicalIF":4.3,"publicationDate":"2021-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s11914-021-00688-6","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39005768","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Potential Role of Perilacunar Remodeling in the Progression of Osteoporosis and Implications on Age-Related Decline in Fracture Resistance of Bone.","authors":"Katharina Jähn-Rickert,&nbsp;Elizabeth A Zimmermann","doi":"10.1007/s11914-021-00686-8","DOIUrl":"https://doi.org/10.1007/s11914-021-00686-8","url":null,"abstract":"<p><strong>Purpose of review: </strong>We took an interdisciplinary view to examine the potential contribution of perilacunar/canalicular remodeling to declines in bone fracture resistance related to age or progression of osteoporosis.</p><p><strong>Recent findings: </strong>Perilacunar remodeling is most prominent as a result of lactation; recent advances further elucidate the molecular players involved and their effect on bone material properties. Of these, vitamin D and calcitonin could be active during aging or osteoporosis. Menopause-related hormonal changes or osteoporosis therapies affect bone material properties and mechanical behavior. However, investigations of lacunar size or osteocyte TRAP activity with age or osteoporosis do not provide clear evidence for or against perilacunar remodeling. While the occurrence and potential role of perilacunar remodeling in aging and osteoporosis progression are largely under-investigated, widespread changes in bone matrix composition in OVX models and following osteoporosis therapies imply osteocytic maintenance of bone matrix. Perilacunar remodeling-induced changes in bone porosity, bone matrix composition, and bone adaptation could have significant implications for bone fracture resistance.</p>","PeriodicalId":11080,"journal":{"name":"Current Osteoporosis Reports","volume":"19 4","pages":"391-402"},"PeriodicalIF":4.3,"publicationDate":"2021-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s11914-021-00686-8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39005769","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}