<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Soerensen M</submitter><funding>National Institute of Health, National Institute on Aging</funding><funding>European Union's Seventh Framework Programme</funding><funding>NIA NIH HHS</funding><funding>Fabrikant Vilhelm Pedersen og Hustrus Legat</funding><funding>Velux Fonden</funding><funding>Danish Agency for Science and Higher Education</funding><funding>Danish Agency for Science, Technology and Innovation</funding><funding>Novo Nordisk Fonden</funding><funding>National Institute on Aging</funding><funding>Fabrikant Vilhelm Pedersen og Hustrus Legat on recommendation by the Novo Nordisk Foundation</funding><pagination>e70204</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12507416</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>24(10)</volume><pubmed_abstract>Osteoporosis is driven by skeletal aging and increases the risk of fragility fractures. Skeletal aging is influenced by epigenetic mechanisms; however, the link to the epigenetic clocks, that is, the suggested biomarkers of biological aging intensively studied within aging research, remains largely unexplored. We investigated the association of eight epigenetic clocks-Horvath, IEAA, Hannum, EEAA, PhenoAge, GrimAge, DunedinPoAm, DunedinPACE-and methylation-based telomere length (mTL) measured at intake (1997, 2007, or 2008-11) with register-based incident fracture and osteoporosis diagnoses in 310 (Discovery cohort), and 777 (Replication cohort) twins, derived from nationwide population-based surveys (end-of-follow-up: 2022). For the 288 youngest twins, bone mineral density (BMD), and bone </pubmed_abstract><journal>Aging cell</journal><pubmed_title>Epigenetic Clocks as Biomarkers for Bone Aging: Evidence From a Twin Study.</pubmed_title><pmcid>PMC12507416</pmcid><funding_grant_id>P01 AG008761</funding_grant_id><funding_grant_id>09‐063256</funding_grant_id><funding_grant_id>P01 AG08761</funding_grant_id><funding_grant_id>09-063256</funding_grant_id><funding_grant_id>259679</funding_grant_id><funding_grant_id>NNF21OC0067839</funding_grant_id><pubmed_authors>Christensen K</pubmed_authors><pubmed_authors>Soerensen M</pubmed_authors><pubmed_authors>Figeac F</pubmed_authors><pubmed_authors>Kassem M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Epigenetic Clocks as Biomarkers for Bone Aging: Evidence From a Twin Study.</name><description>Osteoporosis is driven by skeletal aging and increases the risk of fragility fractures. Skeletal aging is influenced by epigenetic mechanisms; however, the link to the epigenetic clocks, that is, the suggested biomarkers of biological aging intensively studied within aging research, remains largely unexplored. We investigated the association of eight epigenetic clocks-Horvath, IEAA, Hannum, EEAA, PhenoAge, GrimAge, DunedinPoAm, DunedinPACE-and methylation-based telomere length (mTL) measured at intake (1997, 2007, or 2008-11) with register-based incident fracture and osteoporosis diagnoses in 310 (Discovery cohort), and 777 (Replication cohort) twins, derived from nationwide population-based surveys (end-of-follow-up: 2022). For the 288 youngest twins, bone mineral density (BMD), and bone </description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Oct</publication><modification>2026-06-04T08:48:01.821Z</modification><creation>2026-05-07T03:12:31.459Z</creation></dates><accession>S-EPMC12507416</accession><cross_references><pubmed>40947307</pubmed><doi>10.1111/acel.70204</doi></cross_references></HashMap>