Pub Date : 2016-07-20eCollection Date: 2016-01-01DOI: 10.1038/bonekey.2016.52
Kathrin Sinningen, Sylvia Thiele, Lorenz C Hofbauer, Martina Rauner
Milk fat globule-epidermal growth factor 8 (MFG-E8) is a glycoprotein that is abundantly expressed in various tissues and has a pivotal role in the phagocytic clearance of apoptotic cells. However, MFG-E8 has also gained significant attention because of its wide range of functions in autoimmunity, inflammation and tissue homeostasis. More recently, MFG-E8 has been identified as a critical regulator of bone homeostasis, being expressed in both, osteoblasts and osteoclasts. In addition, it was shown that MFG-E8 fulfils an active role in modulating inflammatory processes, suggesting an anti-inflammatory role of MFG-E8 and proposing it as a novel therapeutic target for inflammatory diseases. This concise review focusses on the expression and regulation of MFG-E8 in the context of inflammatory bone diseases, highlights its role in the pathophysiology of osteoimmune diseases and discusses the therapeutic potential of MFG-E8.
{"title":"Role of milk fat globule-epidermal growth factor 8 in osteoimmunology.","authors":"Kathrin Sinningen, Sylvia Thiele, Lorenz C Hofbauer, Martina Rauner","doi":"10.1038/bonekey.2016.52","DOIUrl":"https://doi.org/10.1038/bonekey.2016.52","url":null,"abstract":"<p><p>Milk fat globule-epidermal growth factor 8 (MFG-E8) is a glycoprotein that is abundantly expressed in various tissues and has a pivotal role in the phagocytic clearance of apoptotic cells. However, MFG-E8 has also gained significant attention because of its wide range of functions in autoimmunity, inflammation and tissue homeostasis. More recently, MFG-E8 has been identified as a critical regulator of bone homeostasis, being expressed in both, osteoblasts and osteoclasts. In addition, it was shown that MFG-E8 fulfils an active role in modulating inflammatory processes, suggesting an anti-inflammatory role of MFG-E8 and proposing it as a novel therapeutic target for inflammatory diseases. This concise review focusses on the expression and regulation of MFG-E8 in the context of inflammatory bone diseases, highlights its role in the pathophysiology of osteoimmune diseases and discusses the therapeutic potential of MFG-E8. </p>","PeriodicalId":72441,"journal":{"name":"BoneKEy reports","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4954605/pdf/bonekey201652.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34350931","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}
Pub Date : 2016-07-20eCollection Date: 2016-01-01DOI: 10.1038/bonekey.2016.48
Hiroshi Kaji
The links between muscle and bone have been recently examined because of the increasing number of patients with osteoporosis and sarcopenia. Myokines are skeletal muscle-derived humoral cytokines and growth factors, which exert physiological and pathological functions in various distant organs, including the regulation of glucose, energy and bone metabolism. Myostatin is a crucial myokine, the expression of which is mainly limited to muscle tissues. The inhibition of myostatin signaling increases bone remodeling, bone mass and muscle mass, and it may provide a target for the treatment of both sarcopenia and osteoporosis. As myostatin is involved in osteoclast formation and bone destruction in rheumatoid arthritis, myostatin may be a target myokine for the treatment of accelerated bone resorption and joint destruction in rheumatoid arthritis. Numerous other myokines, including transforming growth factor-β, follistatin, insulin-like growth factor-I, fibroblast growth factor-2, osteoglycin, FAM5C, irisin, interleukin (IL)-6, leukemia inhibitory factor, IL-7, IL-15, monocyte chemoattractant protein-1, ciliary neurotrophic factor, osteonectin and matrix metalloproteinase 2, also affect bone cells in various manners. However, the effects of myokines on bone metabolism are largely unknown. Further research is expected to clarify the interaction between muscle and bone, which may lead to greater diagnosis and the development of the treatment for muscle and bone disorders, such as osteoporosis and sarcopenia.
{"title":"Effects of myokines on bone.","authors":"Hiroshi Kaji","doi":"10.1038/bonekey.2016.48","DOIUrl":"https://doi.org/10.1038/bonekey.2016.48","url":null,"abstract":"<p><p>The links between muscle and bone have been recently examined because of the increasing number of patients with osteoporosis and sarcopenia. Myokines are skeletal muscle-derived humoral cytokines and growth factors, which exert physiological and pathological functions in various distant organs, including the regulation of glucose, energy and bone metabolism. Myostatin is a crucial myokine, the expression of which is mainly limited to muscle tissues. The inhibition of myostatin signaling increases bone remodeling, bone mass and muscle mass, and it may provide a target for the treatment of both sarcopenia and osteoporosis. As myostatin is involved in osteoclast formation and bone destruction in rheumatoid arthritis, myostatin may be a target myokine for the treatment of accelerated bone resorption and joint destruction in rheumatoid arthritis. Numerous other myokines, including transforming growth factor-β, follistatin, insulin-like growth factor-I, fibroblast growth factor-2, osteoglycin, FAM5C, irisin, interleukin (IL)-6, leukemia inhibitory factor, IL-7, IL-15, monocyte chemoattractant protein-1, ciliary neurotrophic factor, osteonectin and matrix metalloproteinase 2, also affect bone cells in various manners. However, the effects of myokines on bone metabolism are largely unknown. Further research is expected to clarify the interaction between muscle and bone, which may lead to greater diagnosis and the development of the treatment for muscle and bone disorders, such as osteoporosis and sarcopenia. </p>","PeriodicalId":72441,"journal":{"name":"BoneKEy reports","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4954587/pdf/bonekey201648.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34350933","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}
Pub Date : 2016-07-20eCollection Date: 2016-01-01DOI: 10.1038/bonekey.2016.50
Jonathan A Mitchell, Diana L Cousminer, Babette S Zemel, Struan F A Grant, Alessandra Chesi
Osteoporosis is one of the most common chronic forms of disability in postmenopausal women and represents a major health burden around the world. Bone fragility is affected by bone mineral density (BMD), and, one of the most important factors in preventing osteoporosis is optimizing peak bone mass, which is achieved during growth in childhood and adolescence. BMD is a complex trait resulting from environmental and genetic factors. Genome-wide association studies have discovered robust genetic signals influencing BMD in adults, and similar studies have also been conducted to investigate the genetics of BMD in the pediatric setting. These latter studies have revealed that many adult osteoporosis-related loci also regulate BMD during growth. These investigations have the potential to profoundly impact public health and will allow for the eventual development of effective interventions for the prevention of osteoporosis.
{"title":"Genetics of pediatric bone strength.","authors":"Jonathan A Mitchell, Diana L Cousminer, Babette S Zemel, Struan F A Grant, Alessandra Chesi","doi":"10.1038/bonekey.2016.50","DOIUrl":"https://doi.org/10.1038/bonekey.2016.50","url":null,"abstract":"<p><p>Osteoporosis is one of the most common chronic forms of disability in postmenopausal women and represents a major health burden around the world. Bone fragility is affected by bone mineral density (BMD), and, one of the most important factors in preventing osteoporosis is optimizing peak bone mass, which is achieved during growth in childhood and adolescence. BMD is a complex trait resulting from environmental and genetic factors. Genome-wide association studies have discovered robust genetic signals influencing BMD in adults, and similar studies have also been conducted to investigate the genetics of BMD in the pediatric setting. These latter studies have revealed that many adult osteoporosis-related loci also regulate BMD during growth. These investigations have the potential to profoundly impact public health and will allow for the eventual development of effective interventions for the prevention of osteoporosis. </p>","PeriodicalId":72441,"journal":{"name":"BoneKEy reports","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4954586/pdf/bonekey201650.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34350932","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}
Pub Date : 2016-06-29eCollection Date: 2016-01-01DOI: 10.1038/bonekey.2016.30
Constance B Hilliard
This ecological correlation study explores the marked differential in osteoporosis susceptibility between East and West Africans. African tsetse belt populations are lactase non-persistent (lactose intolerant) and possess none of the genetic polymorphisms carried by lactase persistent (lactose tolerant) ethnic populations. What appears paradoxical, however, is the fact that Niger-Kordofanian (NK) West African ethnicities are also at minimal risk of osteoporosis. Although East Africans share a genetic affinity with NK West Africans, they display susceptibility rates of the bone disorder closer to those found in Europe. Similar to Europeans, they also carry alleles conferring the lactase persistence genetic traits. Hip fracture rates of African populations are juxtaposed with a global model to determine whether it is the unique ecology of the tsetse-infested zone or other variables that may be at work. This project uses MINITAB 17 software for regression analyses. The research data are found on AJOL (African Journals Online), PUBMED and JSTOR (Scholarly Journal Archive). Data showing the risk of osteoporosis to be 80 times higher among East Africans with higher levels of lactase persistence than lactase non-persistence West Africans are compared with global statistics. Hip fracture rates in 40 countries exhibit a high Pearson's correlation of r=0.851, with P-value=0.000 in relation to dairy consumption. Lower correlations are seen for hip fracture incidence vis-à-vis lactase persistence, per capita income and animal protein consumption. Ethnic populations who lack lactase persistence single-nucleotide polymorphisms may be at low risk of developing osteoporosis.
{"title":"High osteoporosis risk among East Africans linked to lactase persistence genotype.","authors":"Constance B Hilliard","doi":"10.1038/bonekey.2016.30","DOIUrl":"10.1038/bonekey.2016.30","url":null,"abstract":"<p><p>This ecological correlation study explores the marked differential in osteoporosis susceptibility between East and West Africans. African tsetse belt populations are lactase non-persistent (lactose intolerant) and possess none of the genetic polymorphisms carried by lactase persistent (lactose tolerant) ethnic populations. What appears paradoxical, however, is the fact that Niger-Kordofanian (NK) West African ethnicities are also at minimal risk of osteoporosis. Although East Africans share a genetic affinity with NK West Africans, they display susceptibility rates of the bone disorder closer to those found in Europe. Similar to Europeans, they also carry alleles conferring the lactase persistence genetic traits. Hip fracture rates of African populations are juxtaposed with a global model to determine whether it is the unique ecology of the tsetse-infested zone or other variables that may be at work. This project uses MINITAB 17 software for regression analyses. The research data are found on AJOL (African Journals Online), PUBMED and JSTOR (Scholarly Journal Archive). Data showing the risk of osteoporosis to be 80 times higher among East Africans with higher levels of lactase persistence than lactase non-persistence West Africans are compared with global statistics. Hip fracture rates in 40 countries exhibit a high Pearson's correlation of r=0.851, with P-value=0.000 in relation to dairy consumption. Lower correlations are seen for hip fracture incidence vis-à-vis lactase persistence, per capita income and animal protein consumption. Ethnic populations who lack lactase persistence single-nucleotide polymorphisms may be at low risk of developing osteoporosis. </p>","PeriodicalId":72441,"journal":{"name":"BoneKEy reports","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4926535/pdf/bonekey201630.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34663725","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}
Pub Date : 2016-06-29eCollection Date: 2016-01-01DOI: 10.1038/bonekey.2016.49
Silvia Marino, Katherine Ann Staines, Genevieve Brown, Rachel Anne Howard-Jones, Magdalena Adamczyk
Ex vivo explant culture models are powerful tools in bone research. They allow investigation of bone and cartilage responses to specific stimuli in a controlled manner that closely mimics the in vivo processes. Because of limitations in obtaining healthy human bone samples the explant growth of animal tissue serves as a platform to study the complex physico-chemical properties of the bone. Moreover, these models enable preserving important cell-cell and cell-matrix interactions in order to better understand the behaviour of cells in their natural three-dimensional environment. Thus, the use of bone ex vivo explant cultures can frequently be of more physiological relevance than the use of two-dimensional primary cells grown in vitro. Here, we describe isolation and ex vivo growth of different animal bone explant models including metatarsals, femoral heads, calvaria, mandibular slices and trabecular cores. We also describe how these explants are utilised to study bone development, cartilage and bone metabolism, cancer-induced bone diseases, stem cell-driven bone repair and mechanoadaptation. These techniques can be directly used to understand mechanisms linked with bone physiology or bone-associated diseases.
{"title":"Models of ex vivo explant cultures: applications in bone research.","authors":"Silvia Marino, Katherine Ann Staines, Genevieve Brown, Rachel Anne Howard-Jones, Magdalena Adamczyk","doi":"10.1038/bonekey.2016.49","DOIUrl":"10.1038/bonekey.2016.49","url":null,"abstract":"<p><p>Ex vivo explant culture models are powerful tools in bone research. They allow investigation of bone and cartilage responses to specific stimuli in a controlled manner that closely mimics the in vivo processes. Because of limitations in obtaining healthy human bone samples the explant growth of animal tissue serves as a platform to study the complex physico-chemical properties of the bone. Moreover, these models enable preserving important cell-cell and cell-matrix interactions in order to better understand the behaviour of cells in their natural three-dimensional environment. Thus, the use of bone ex vivo explant cultures can frequently be of more physiological relevance than the use of two-dimensional primary cells grown in vitro. Here, we describe isolation and ex vivo growth of different animal bone explant models including metatarsals, femoral heads, calvaria, mandibular slices and trabecular cores. We also describe how these explants are utilised to study bone development, cartilage and bone metabolism, cancer-induced bone diseases, stem cell-driven bone repair and mechanoadaptation. These techniques can be directly used to understand mechanisms linked with bone physiology or bone-associated diseases. </p>","PeriodicalId":72441,"journal":{"name":"BoneKEy reports","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4926536/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34663726","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}
Pub Date : 2016-06-15eCollection Date: 2016-01-01DOI: 10.1038/bonekey.2016.42
Zhanna E Belaya, Alexander V Iljin, Galina A Melnichenko, Alexander G Solodovnikov, Liudmila Y Rozhinskaya, Larisa K Dzeranova, Ivan I Dedov
The aim of this study was to evaluate the diagnostic performance of osteocalcin (OC), as measured by automated electrochemiluminescence immunoassay (ECLIA), in identifying Cushing's syndrome (CS) in two separate populations: among obese and overweight subjects and among women of postmenopausal age with osteoporosis. Among the 106 referral patients with obesity, CS was confirmed in 42 cases. The patients of the referred population provided late-night salivary cortisol (LNSC), underwent low-dose dexamethasone suppression testing (DST) and were further evaluated until CS was pathologically confirmed. A threshold of OC-8.3 ng ml(-1) differentiated CS among obese and overweight subjects with a sensitivity of 73.8% (95% confidence interval (CI) 58.9-84.7) and a specificity of 96.9% (95% CI 89.3-99.1). The total area under the receiver operating characteristic curve (AUC) was 0.859 (95% CI 0.773-0.945), which was lower than LNSC or DST (P=0.01). In the retrospective portion of the study, the OC levels were evaluated in 67 subjects with newly diagnosed postmenopausal osteoporosis and in 23 patients (older than 45) with newly diagnosed CS and osteoporosis (presence of low traumatic fractures or T-score P-2.5). The diagnostic performance of OC for osteoporosis due to CS was within an AUC of 0.959 (95% CI 0.887-1.00). A threshold for OC of 8.3 ng ml-1 yielded a sensitivity of 95.4% (95% CI 78.2-99.2%) and a specificity of 98.5% (95% CI 92.0-99.7%). Thus, osteocalcin could be used in the diagnostic testing for endogenous hypercortisolism in patients referred to exclude CS and to identify CS among patients of postmenopausal age with osteoporosis.
本研究的目的是评估骨钙素(OC)的诊断性能,通过自动电化学发光免疫测定(ECLIA)测量,在两个不同的人群中识别库欣综合征(CS):肥胖和超重受试者和绝经后骨质疏松症妇女。106例转诊肥胖患者中,42例确诊CS。患者提供了深夜唾液皮质醇(LNSC),进行了低剂量地塞米松抑制试验(DST),并进一步评估,直到病理证实CS。OC-8.3 ng ml(-1)区分肥胖和超重受试者CS的阈值敏感性为73.8%(95%可信区间(CI) 58.9-84.7),特异性为96.9% (95% CI 89.3-99.1)。受试者工作特征曲线下总面积(AUC)为0.859 (95% CI 0.773 ~ 0.945),低于LNSC和DST (P=0.01)。在研究的回顾性部分,评估了67名新诊断的绝经后骨质疏松症患者和23名新诊断的CS和骨质疏松症患者(年龄大于45岁)(存在低创伤性骨折或t评分P-2.5)的OC水平。OC对CS所致骨质疏松的诊断价值在0.959以内(95% CI 0.887-1.00)。OC的阈值为8.3 ng ml-1,敏感性为95.4% (95% CI 78.2-99.2%),特异性为98.5% (95% CI 92.0-99.7%)。因此,骨钙素可用于排除CS的内源性高皮质醇血症患者的诊断检测,也可用于绝经后骨质疏松症患者的CS诊断。
{"title":"Diagnostic performance of osteocalcin measurements in patients with endogenous Cushing's syndrome.","authors":"Zhanna E Belaya, Alexander V Iljin, Galina A Melnichenko, Alexander G Solodovnikov, Liudmila Y Rozhinskaya, Larisa K Dzeranova, Ivan I Dedov","doi":"10.1038/bonekey.2016.42","DOIUrl":"https://doi.org/10.1038/bonekey.2016.42","url":null,"abstract":"<p><p>The aim of this study was to evaluate the diagnostic performance of osteocalcin (OC), as measured by automated electrochemiluminescence immunoassay (ECLIA), in identifying Cushing's syndrome (CS) in two separate populations: among obese and overweight subjects and among women of postmenopausal age with osteoporosis. Among the 106 referral patients with obesity, CS was confirmed in 42 cases. The patients of the referred population provided late-night salivary cortisol (LNSC), underwent low-dose dexamethasone suppression testing (DST) and were further evaluated until CS was pathologically confirmed. A threshold of OC-8.3 ng ml(-1) differentiated CS among obese and overweight subjects with a sensitivity of 73.8% (95% confidence interval (CI) 58.9-84.7) and a specificity of 96.9% (95% CI 89.3-99.1). The total area under the receiver operating characteristic curve (AUC) was 0.859 (95% CI 0.773-0.945), which was lower than LNSC or DST (P=0.01). In the retrospective portion of the study, the OC levels were evaluated in 67 subjects with newly diagnosed postmenopausal osteoporosis and in 23 patients (older than 45) with newly diagnosed CS and osteoporosis (presence of low traumatic fractures or T-score P-2.5). The diagnostic performance of OC for osteoporosis due to CS was within an AUC of 0.959 (95% CI 0.887-1.00). A threshold for OC of 8.3 ng ml-1 yielded a sensitivity of 95.4% (95% CI 78.2-99.2%) and a specificity of 98.5% (95% CI 92.0-99.7%). Thus, osteocalcin could be used in the diagnostic testing for endogenous hypercortisolism in patients referred to exclude CS and to identify CS among patients of postmenopausal age with osteoporosis. </p>","PeriodicalId":72441,"journal":{"name":"BoneKEy reports","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4909045/pdf/bonekey201642.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34614246","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}
Pub Date : 2016-06-15eCollection Date: 2016-01-01DOI: 10.1038/bonekey.2016.40
Roland Chapurlat
In vivo evaluation of bone microstructure with high-resolution peripheral quantitative tomography (HRpQCT) has been used for a decade in research settings. In this review, we examine the value this technique could have in clinical practice. Bone microstructure parameters obtained with HRpQCT are associated with prevalent fracture in men and women. In postmenopausal women, some parameters also predict incident fracture, independently of areal bone mineral density. In specific population groups including patients with diabetes, chronic kidney disease, glucocorticosteroid therapy and rheumatic diseases, abnormal microstructure parameters from HRpQCT have been reported. Findings from HRpQCT studies may also explain ethnic differences in bone fragility. Treatment monitoring has been challenging in the various clinical trials with available HRpQCT data. The improvements were of small magnitude but tended to be proportional to the potency of antiresorptive agents. Microfinite element analysis was a better predictor of treatment efficacy than the microarchitectural parameters. In conclusion, HRpQCT remains a valuable research tool, but more work is needed to be able to use it in clinical practice.
{"title":"In vivo evaluation of bone microstructure in humans: Clinically useful?","authors":"Roland Chapurlat","doi":"10.1038/bonekey.2016.40","DOIUrl":"https://doi.org/10.1038/bonekey.2016.40","url":null,"abstract":"<p><p>In vivo evaluation of bone microstructure with high-resolution peripheral quantitative tomography (HRpQCT) has been used for a decade in research settings. In this review, we examine the value this technique could have in clinical practice. Bone microstructure parameters obtained with HRpQCT are associated with prevalent fracture in men and women. In postmenopausal women, some parameters also predict incident fracture, independently of areal bone mineral density. In specific population groups including patients with diabetes, chronic kidney disease, glucocorticosteroid therapy and rheumatic diseases, abnormal microstructure parameters from HRpQCT have been reported. Findings from HRpQCT studies may also explain ethnic differences in bone fragility. Treatment monitoring has been challenging in the various clinical trials with available HRpQCT data. The improvements were of small magnitude but tended to be proportional to the potency of antiresorptive agents. Microfinite element analysis was a better predictor of treatment efficacy than the microarchitectural parameters. In conclusion, HRpQCT remains a valuable research tool, but more work is needed to be able to use it in clinical practice. </p>","PeriodicalId":72441,"journal":{"name":"BoneKEy reports","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4909044/pdf/bonekey201640.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34614245","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}
Pub Date : 2016-05-25eCollection Date: 2016-01-01DOI: 10.1038/bonekey.2016.23
John P Kemp, Carolina Medina-Gomez, Jonathan H Tobias, Fernando Rivadeneira, David M Evans
Peak bone mass, the maximum amount of bone accrued at the end of the growth period, is an important predictor of future risk of osteoporosis and fracture. Hence, the contribution of genetic factors influencing bone accrual is of considerable interest to the osteoporosis research community. In this article, we review evidence that genetic factors play an important role in bone growth, describe the genetic loci implicated so far and briefly discuss lessons learned from the application of genome-wide association studies. Moreover, we attempt to make the case for genetic investigations of bone mineral density in paediatric and young adult populations, describing their potential to increase our knowledge of the process of bone metabolism throughout the life course, and in turn, identify novel targets for the pharmacological treatment of osteoporosis.
{"title":"The case for genome-wide association studies of bone acquisition in paediatric and adolescent populations.","authors":"John P Kemp, Carolina Medina-Gomez, Jonathan H Tobias, Fernando Rivadeneira, David M Evans","doi":"10.1038/bonekey.2016.23","DOIUrl":"https://doi.org/10.1038/bonekey.2016.23","url":null,"abstract":"<p><p>Peak bone mass, the maximum amount of bone accrued at the end of the growth period, is an important predictor of future risk of osteoporosis and fracture. Hence, the contribution of genetic factors influencing bone accrual is of considerable interest to the osteoporosis research community. In this article, we review evidence that genetic factors play an important role in bone growth, describe the genetic loci implicated so far and briefly discuss lessons learned from the application of genome-wide association studies. Moreover, we attempt to make the case for genetic investigations of bone mineral density in paediatric and young adult populations, describing their potential to increase our knowledge of the process of bone metabolism throughout the life course, and in turn, identify novel targets for the pharmacological treatment of osteoporosis. </p>","PeriodicalId":72441,"journal":{"name":"BoneKEy reports","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4879864/pdf/bonekey201623.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34446508","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}
Pub Date : 2016-05-18eCollection Date: 2016-01-01DOI: 10.1038/bonekey.2016.29
Patrizia D'Amelio, Francesca Sassi
The immune system has been recognized as one of the most important regulators of bone turnover and its deregulation is implicated in several bone diseases such as postmenopausal osteoporosis and inflammatory bone loss; recently it has been suggested that the gut microbiota may influence bone turnover by modulation of the immune system. The study of the relationship between the immune system and bone metabolism is generally indicated under the term 'osteoimmunology'. The vast majority of these studies have been performed in animal models; however, several data have been confirmed in humans as well: this review summarizes recent data on the relationship between the immune system and bone with particular regard to the data confirmed in humans.
{"title":"Osteoimmunology: from mice to humans.","authors":"Patrizia D'Amelio, Francesca Sassi","doi":"10.1038/bonekey.2016.29","DOIUrl":"https://doi.org/10.1038/bonekey.2016.29","url":null,"abstract":"<p><p>The immune system has been recognized as one of the most important regulators of bone turnover and its deregulation is implicated in several bone diseases such as postmenopausal osteoporosis and inflammatory bone loss; recently it has been suggested that the gut microbiota may influence bone turnover by modulation of the immune system. The study of the relationship between the immune system and bone metabolism is generally indicated under the term 'osteoimmunology'. The vast majority of these studies have been performed in animal models; however, several data have been confirmed in humans as well: this review summarizes recent data on the relationship between the immune system and bone with particular regard to the data confirmed in humans. </p>","PeriodicalId":72441,"journal":{"name":"BoneKEy reports","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4870940/pdf/bonekey201629.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34496579","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}
L. Wright, P. Ottewell, N. Rucci, O. Peyruchaud, G. Pagnotti, A. Chiechi, J. Buijs, J. Sterling
{"title":"Murine models of breast cancer bone metastasis.","authors":"L. Wright, P. Ottewell, N. Rucci, O. Peyruchaud, G. Pagnotti, A. Chiechi, J. Buijs, J. Sterling","doi":"10.1038/BONEKEY.2016.31","DOIUrl":"https://doi.org/10.1038/BONEKEY.2016.31","url":null,"abstract":"","PeriodicalId":72441,"journal":{"name":"BoneKEy reports","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1038/BONEKEY.2016.31","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"58484323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}