Fracture, bone mineral density, and the effects of calcitonin receptor gene in postmenopausal Koreans
Summary In a candidate gene association study, we found that the variations of calcitonin receptor (CALCR) gene were related to the risk of vertebral fracture and increased bone mineral density (BMD). Introduction Calcitonins through calcitonin receptors inhibit osteoclast-mediated bone resorption a...
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| creator | Lee, H.-J Kim, S.-Y Kim, G. S Hwang, J.-Y Kim, Y.-J Jeong, B Kim, T.-H Park, E. K Lee, S. H Kim, H.-L Koh, J.-M Lee, J.-Y |
| description | Summary In a candidate gene association study, we found that the variations of calcitonin receptor (CALCR) gene were related to the risk of vertebral fracture and increased bone mineral density (BMD). Introduction Calcitonins through calcitonin receptors inhibit osteoclast-mediated bone resorption and modulate calcium ion excretion by the kidney and also prevent vertebral bone loss in early menopause. Methods To identify genetically susceptible factors of osteoporosis, we discovered the variations in CALCR gene, genotyped in Korean postmenopausal women (n = 729), and examined the potential involvement of seven single-nucleotide polymorphism (SNPs) and their haplotypes in linkage disequilibrium block (BL_hts). Results The SNPs, +43147G > C (intron 7), +60644C > T (exon13, 3' untranslated region), and their haplotypes, BL2_ht1 and BL2_ht2, showed a significant association with risk of vertebral fracture (p = 0.048-0.004) and BL2_ht1 showed a highly significant protective effect. Moreover, the polymorphism +60644C > T showed a highly significant association with BMD at both lumbar spine and femoral neck. The subjects carrying CC and CT genotypes with the SNP, +60644C > T, had higher BMD values at the lumbar spine (p = 0.01-0.001) and femoral neck (p = 0.025-0.009). Conclusion These results indicate that the CALCR gene may regulate bone metabolism, and +60644C > T in the CALCR gene may genetically modulate bone phenotype. |
| doi_str_mv | 10.1007/s00198-009-1106-8 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_754870052</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>754870052</sourcerecordid><originalsourceid>FETCH-LOGICAL-c456t-fccdadc750e0cac9b3a76cde828d419f59f83bdd88f1c3158a4163cf4f1f7c1f3</originalsourceid><addsrcrecordid>eNqFkU1rFTEUhoMo9rb6A9xoEIqbjiaT76UUq2LBhRbchdzk5DplJhmTmUX_vSlzseBCV4Hked-c5EHoBSVvKSHqXSWEGt0RYjpKiez0I7SjnLGuN1I8RjtimOoMpz9O0Gmtt6RljFFP0Qk1hkup-A7BVXF-WQtc4H1OgKchQXEjDpDqsNxdYJcCXn4ChhjBLxXniL0b_bDkNCRcwMO85IIP0MJtY851mSDl2a211XzJBVyqz9CT6MYKz4_rGbq5-vD98lN3_fXj58v3153nQi5d9D644JUgQLzzZs-ckj6A7nXg1ERhomb7ELSO1DMqtONUMh95pFF5GtkZerP1ziX_WqEudhqqh3F0CfJarRJcK0JE_3-SMdkbznkjX_9F3ua1pPYMKwlTQvSKNohukC-51gLRzmWYXLmzlNh7V3ZzZZsre-_K6pZ5eSxe9xOEh8RRTgPOj4Cr7c9jcckP9Q_XM8K0MKJx_cbVdpQOUB4m_Nftr7ZQdNm6Q2nFN996QhmhWvZSGfYb0fe1-Q</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>603755271</pqid></control><display><type>article</type><title>Fracture, bone mineral density, and the effects of calcitonin receptor gene in postmenopausal Koreans</title><source>MEDLINE</source><source>SpringerNature Journals</source><creator>Lee, H.-J ; Kim, S.-Y ; Kim, G. S ; Hwang, J.-Y ; Kim, Y.-J ; Jeong, B ; Kim, T.-H ; Park, E. K ; Lee, S. H ; Kim, H.-L ; Koh, J.-M ; Lee, J.-Y</creator><creatorcontrib>Lee, H.-J ; Kim, S.-Y ; Kim, G. S ; Hwang, J.-Y ; Kim, Y.-J ; Jeong, B ; Kim, T.-H ; Park, E. K ; Lee, S. H ; Kim, H.-L ; Koh, J.-M ; Lee, J.-Y</creatorcontrib><description>Summary In a candidate gene association study, we found that the variations of calcitonin receptor (CALCR) gene were related to the risk of vertebral fracture and increased bone mineral density (BMD). Introduction Calcitonins through calcitonin receptors inhibit osteoclast-mediated bone resorption and modulate calcium ion excretion by the kidney and also prevent vertebral bone loss in early menopause. Methods To identify genetically susceptible factors of osteoporosis, we discovered the variations in CALCR gene, genotyped in Korean postmenopausal women (n = 729), and examined the potential involvement of seven single-nucleotide polymorphism (SNPs) and their haplotypes in linkage disequilibrium block (BL_hts). Results The SNPs, +43147G > C (intron 7), +60644C > T (exon13, 3' untranslated region), and their haplotypes, BL2_ht1 and BL2_ht2, showed a significant association with risk of vertebral fracture (p = 0.048-0.004) and BL2_ht1 showed a highly significant protective effect. Moreover, the polymorphism +60644C > T showed a highly significant association with BMD at both lumbar spine and femoral neck. The subjects carrying CC and CT genotypes with the SNP, +60644C > T, had higher BMD values at the lumbar spine (p = 0.01-0.001) and femoral neck (p = 0.025-0.009). Conclusion These results indicate that the CALCR gene may regulate bone metabolism, and +60644C > T in the CALCR gene may genetically modulate bone phenotype.</description><identifier>ISSN: 0937-941X</identifier><identifier>EISSN: 1433-2965</identifier><identifier>DOI: 10.1007/s00198-009-1106-8</identifier><identifier>PMID: 19946674</identifier><language>eng</language><publisher>London: London : Springer-Verlag</publisher><subject>Absorptiometry, Photon ; Adult ; Aged ; Asian people ; Biological and medical sciences ; Bone density ; Bone Density - genetics ; CALCR ; Chromosome Mapping ; Diseases of the osteoarticular system ; Endocrinology ; Female ; Femur Neck - physiopathology ; Fracture ; Fractures ; Genetic Association Studies - methods ; Genotype ; Genotype & phenotype ; Humans ; Injuries of the limb. Injuries of the spine ; Investigative techniques, diagnostic techniques (general aspects) ; Linkage Disequilibrium ; Lumbar Vertebrae - physiopathology ; Medical sciences ; Medicine ; Medicine & Public Health ; Menopause ; Middle Aged ; Original Article ; Orthopedics ; Osteoarticular system. Muscles ; Osteoporosis ; Osteoporosis, Postmenopausal - genetics ; Osteoporosis, Postmenopausal - physiopathology ; Osteoporosis. Osteomalacia. Paget disease ; Osteoporotic Fractures - genetics ; Osteoporotic Fractures - physiopathology ; Phenotype ; Polymorphism ; Polymorphism, Single Nucleotide ; Postmenopause ; Radiodiagnosis. Nmr imagery. Nmr spectrometry ; Receptors, Calcitonin - genetics ; Rheumatology ; SNP ; Spinal Fractures - genetics ; Spinal Fractures - physiopathology ; Traumas. Diseases due to physical agents</subject><ispartof>Osteoporosis international, 2010-08, Vol.21 (8), p.1351-1360</ispartof><rights>International Osteoporosis Foundation and National Osteoporosis Foundation 2009</rights><rights>2015 INIST-CNRS</rights><rights>International Osteoporosis Foundation and National Osteoporosis Foundation 2010</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c456t-fccdadc750e0cac9b3a76cde828d419f59f83bdd88f1c3158a4163cf4f1f7c1f3</citedby><cites>FETCH-LOGICAL-c456t-fccdadc750e0cac9b3a76cde828d419f59f83bdd88f1c3158a4163cf4f1f7c1f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00198-009-1106-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00198-009-1106-8$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23038595$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19946674$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lee, H.-J</creatorcontrib><creatorcontrib>Kim, S.-Y</creatorcontrib><creatorcontrib>Kim, G. S</creatorcontrib><creatorcontrib>Hwang, J.-Y</creatorcontrib><creatorcontrib>Kim, Y.-J</creatorcontrib><creatorcontrib>Jeong, B</creatorcontrib><creatorcontrib>Kim, T.-H</creatorcontrib><creatorcontrib>Park, E. K</creatorcontrib><creatorcontrib>Lee, S. H</creatorcontrib><creatorcontrib>Kim, H.-L</creatorcontrib><creatorcontrib>Koh, J.-M</creatorcontrib><creatorcontrib>Lee, J.-Y</creatorcontrib><title>Fracture, bone mineral density, and the effects of calcitonin receptor gene in postmenopausal Koreans</title><title>Osteoporosis international</title><addtitle>Osteoporos Int</addtitle><addtitle>Osteoporos Int</addtitle><description>Summary In a candidate gene association study, we found that the variations of calcitonin receptor (CALCR) gene were related to the risk of vertebral fracture and increased bone mineral density (BMD). Introduction Calcitonins through calcitonin receptors inhibit osteoclast-mediated bone resorption and modulate calcium ion excretion by the kidney and also prevent vertebral bone loss in early menopause. Methods To identify genetically susceptible factors of osteoporosis, we discovered the variations in CALCR gene, genotyped in Korean postmenopausal women (n = 729), and examined the potential involvement of seven single-nucleotide polymorphism (SNPs) and their haplotypes in linkage disequilibrium block (BL_hts). Results The SNPs, +43147G > C (intron 7), +60644C > T (exon13, 3' untranslated region), and their haplotypes, BL2_ht1 and BL2_ht2, showed a significant association with risk of vertebral fracture (p = 0.048-0.004) and BL2_ht1 showed a highly significant protective effect. Moreover, the polymorphism +60644C > T showed a highly significant association with BMD at both lumbar spine and femoral neck. The subjects carrying CC and CT genotypes with the SNP, +60644C > T, had higher BMD values at the lumbar spine (p = 0.01-0.001) and femoral neck (p = 0.025-0.009). Conclusion These results indicate that the CALCR gene may regulate bone metabolism, and +60644C > T in the CALCR gene may genetically modulate bone phenotype.</description><subject>Absorptiometry, Photon</subject><subject>Adult</subject><subject>Aged</subject><subject>Asian people</subject><subject>Biological and medical sciences</subject><subject>Bone density</subject><subject>Bone Density - genetics</subject><subject>CALCR</subject><subject>Chromosome Mapping</subject><subject>Diseases of the osteoarticular system</subject><subject>Endocrinology</subject><subject>Female</subject><subject>Femur Neck - physiopathology</subject><subject>Fracture</subject><subject>Fractures</subject><subject>Genetic Association Studies - methods</subject><subject>Genotype</subject><subject>Genotype & phenotype</subject><subject>Humans</subject><subject>Injuries of the limb. Injuries of the spine</subject><subject>Investigative techniques, diagnostic techniques (general aspects)</subject><subject>Linkage Disequilibrium</subject><subject>Lumbar Vertebrae - physiopathology</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Menopause</subject><subject>Middle Aged</subject><subject>Original Article</subject><subject>Orthopedics</subject><subject>Osteoarticular system. Muscles</subject><subject>Osteoporosis</subject><subject>Osteoporosis, Postmenopausal - genetics</subject><subject>Osteoporosis, Postmenopausal - physiopathology</subject><subject>Osteoporosis. Osteomalacia. Paget disease</subject><subject>Osteoporotic Fractures - genetics</subject><subject>Osteoporotic Fractures - physiopathology</subject><subject>Phenotype</subject><subject>Polymorphism</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Postmenopause</subject><subject>Radiodiagnosis. Nmr imagery. Nmr spectrometry</subject><subject>Receptors, Calcitonin - genetics</subject><subject>Rheumatology</subject><subject>SNP</subject><subject>Spinal Fractures - genetics</subject><subject>Spinal Fractures - physiopathology</subject><subject>Traumas. Diseases due to physical agents</subject><issn>0937-941X</issn><issn>1433-2965</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqFkU1rFTEUhoMo9rb6A9xoEIqbjiaT76UUq2LBhRbchdzk5DplJhmTmUX_vSlzseBCV4Hked-c5EHoBSVvKSHqXSWEGt0RYjpKiez0I7SjnLGuN1I8RjtimOoMpz9O0Gmtt6RljFFP0Qk1hkup-A7BVXF-WQtc4H1OgKchQXEjDpDqsNxdYJcCXn4ChhjBLxXniL0b_bDkNCRcwMO85IIP0MJtY851mSDl2a211XzJBVyqz9CT6MYKz4_rGbq5-vD98lN3_fXj58v3153nQi5d9D644JUgQLzzZs-ckj6A7nXg1ERhomb7ELSO1DMqtONUMh95pFF5GtkZerP1ziX_WqEudhqqh3F0CfJarRJcK0JE_3-SMdkbznkjX_9F3ua1pPYMKwlTQvSKNohukC-51gLRzmWYXLmzlNh7V3ZzZZsre-_K6pZ5eSxe9xOEh8RRTgPOj4Cr7c9jcckP9Q_XM8K0MKJx_cbVdpQOUB4m_Nftr7ZQdNm6Q2nFN996QhmhWvZSGfYb0fe1-Q</recordid><startdate>20100801</startdate><enddate>20100801</enddate><creator>Lee, H.-J</creator><creator>Kim, S.-Y</creator><creator>Kim, G. S</creator><creator>Hwang, J.-Y</creator><creator>Kim, Y.-J</creator><creator>Jeong, B</creator><creator>Kim, T.-H</creator><creator>Park, E. K</creator><creator>Lee, S. H</creator><creator>Kim, H.-L</creator><creator>Koh, J.-M</creator><creator>Lee, J.-Y</creator><general>London : Springer-Verlag</general><general>Springer-Verlag</general><general>Springer</general><general>Springer Nature B.V</general><scope>FBQ</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7TS</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope></search><sort><creationdate>20100801</creationdate><title>Fracture, bone mineral density, and the effects of calcitonin receptor gene in postmenopausal Koreans</title><author>Lee, H.-J ; Kim, S.-Y ; Kim, G. S ; Hwang, J.-Y ; Kim, Y.-J ; Jeong, B ; Kim, T.-H ; Park, E. K ; Lee, S. H ; Kim, H.-L ; Koh, J.-M ; Lee, J.-Y</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c456t-fccdadc750e0cac9b3a76cde828d419f59f83bdd88f1c3158a4163cf4f1f7c1f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Absorptiometry, Photon</topic><topic>Adult</topic><topic>Aged</topic><topic>Asian people</topic><topic>Biological and medical sciences</topic><topic>Bone density</topic><topic>Bone Density - genetics</topic><topic>CALCR</topic><topic>Chromosome Mapping</topic><topic>Diseases of the osteoarticular system</topic><topic>Endocrinology</topic><topic>Female</topic><topic>Femur Neck - physiopathology</topic><topic>Fracture</topic><topic>Fractures</topic><topic>Genetic Association Studies - methods</topic><topic>Genotype</topic><topic>Genotype & phenotype</topic><topic>Humans</topic><topic>Injuries of the limb. Injuries of the spine</topic><topic>Investigative techniques, diagnostic techniques (general aspects)</topic><topic>Linkage Disequilibrium</topic><topic>Lumbar Vertebrae - physiopathology</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Menopause</topic><topic>Middle Aged</topic><topic>Original Article</topic><topic>Orthopedics</topic><topic>Osteoarticular system. Muscles</topic><topic>Osteoporosis</topic><topic>Osteoporosis, Postmenopausal - genetics</topic><topic>Osteoporosis, Postmenopausal - physiopathology</topic><topic>Osteoporosis. Osteomalacia. Paget disease</topic><topic>Osteoporotic Fractures - genetics</topic><topic>Osteoporotic Fractures - physiopathology</topic><topic>Phenotype</topic><topic>Polymorphism</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Postmenopause</topic><topic>Radiodiagnosis. Nmr imagery. Nmr spectrometry</topic><topic>Receptors, Calcitonin - genetics</topic><topic>Rheumatology</topic><topic>SNP</topic><topic>Spinal Fractures - genetics</topic><topic>Spinal Fractures - physiopathology</topic><topic>Traumas. Diseases due to physical agents</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lee, H.-J</creatorcontrib><creatorcontrib>Kim, S.-Y</creatorcontrib><creatorcontrib>Kim, G. S</creatorcontrib><creatorcontrib>Hwang, J.-Y</creatorcontrib><creatorcontrib>Kim, Y.-J</creatorcontrib><creatorcontrib>Jeong, B</creatorcontrib><creatorcontrib>Kim, T.-H</creatorcontrib><creatorcontrib>Park, E. K</creatorcontrib><creatorcontrib>Lee, S. H</creatorcontrib><creatorcontrib>Kim, H.-L</creatorcontrib><creatorcontrib>Koh, J.-M</creatorcontrib><creatorcontrib>Lee, J.-Y</creatorcontrib><collection>AGRIS</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Physical Education Index</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><jtitle>Osteoporosis international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lee, H.-J</au><au>Kim, S.-Y</au><au>Kim, G. S</au><au>Hwang, J.-Y</au><au>Kim, Y.-J</au><au>Jeong, B</au><au>Kim, T.-H</au><au>Park, E. K</au><au>Lee, S. H</au><au>Kim, H.-L</au><au>Koh, J.-M</au><au>Lee, J.-Y</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Fracture, bone mineral density, and the effects of calcitonin receptor gene in postmenopausal Koreans</atitle><jtitle>Osteoporosis international</jtitle><stitle>Osteoporos Int</stitle><addtitle>Osteoporos Int</addtitle><date>2010-08-01</date><risdate>2010</risdate><volume>21</volume><issue>8</issue><spage>1351</spage><epage>1360</epage><pages>1351-1360</pages><issn>0937-941X</issn><eissn>1433-2965</eissn><abstract>Summary In a candidate gene association study, we found that the variations of calcitonin receptor (CALCR) gene were related to the risk of vertebral fracture and increased bone mineral density (BMD). Introduction Calcitonins through calcitonin receptors inhibit osteoclast-mediated bone resorption and modulate calcium ion excretion by the kidney and also prevent vertebral bone loss in early menopause. Methods To identify genetically susceptible factors of osteoporosis, we discovered the variations in CALCR gene, genotyped in Korean postmenopausal women (n = 729), and examined the potential involvement of seven single-nucleotide polymorphism (SNPs) and their haplotypes in linkage disequilibrium block (BL_hts). Results The SNPs, +43147G > C (intron 7), +60644C > T (exon13, 3' untranslated region), and their haplotypes, BL2_ht1 and BL2_ht2, showed a significant association with risk of vertebral fracture (p = 0.048-0.004) and BL2_ht1 showed a highly significant protective effect. Moreover, the polymorphism +60644C > T showed a highly significant association with BMD at both lumbar spine and femoral neck. The subjects carrying CC and CT genotypes with the SNP, +60644C > T, had higher BMD values at the lumbar spine (p = 0.01-0.001) and femoral neck (p = 0.025-0.009). Conclusion These results indicate that the CALCR gene may regulate bone metabolism, and +60644C > T in the CALCR gene may genetically modulate bone phenotype.</abstract><cop>London</cop><pub>London : Springer-Verlag</pub><pmid>19946674</pmid><doi>10.1007/s00198-009-1106-8</doi><tpages>10</tpages></addata></record> |
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| subjects | Absorptiometry, Photon Adult Aged Asian people Biological and medical sciences Bone density Bone Density - genetics CALCR Chromosome Mapping Diseases of the osteoarticular system Endocrinology Female Femur Neck - physiopathology Fracture Fractures Genetic Association Studies - methods Genotype Genotype & phenotype Humans Injuries of the limb. Injuries of the spine Investigative techniques, diagnostic techniques (general aspects) Linkage Disequilibrium Lumbar Vertebrae - physiopathology Medical sciences Medicine Medicine & Public Health Menopause Middle Aged Original Article Orthopedics Osteoarticular system. Muscles Osteoporosis Osteoporosis, Postmenopausal - genetics Osteoporosis, Postmenopausal - physiopathology Osteoporosis. Osteomalacia. Paget disease Osteoporotic Fractures - genetics Osteoporotic Fractures - physiopathology Phenotype Polymorphism Polymorphism, Single Nucleotide Postmenopause Radiodiagnosis. Nmr imagery. Nmr spectrometry Receptors, Calcitonin - genetics Rheumatology SNP Spinal Fractures - genetics Spinal Fractures - physiopathology Traumas. Diseases due to physical agents |
| title | Fracture, bone mineral density, and the effects of calcitonin receptor gene in postmenopausal Koreans |
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