ArticleAging cell2025
Epigenetic Clocks as Biomarkers for Bone Aging: Evidence From a Twin Study.
Article in Aging cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Bone aging: a paradigm of multiscale degeneration and targeted rejuvenation.Bone research · 2026Review
- Aging Biology of Bone-to-Tendon Healing and the Epigenetic Clock: A Biological-Age Readout of Rotator Cuff Healing Capacity.Biomedicines · 2026Review
- Causal relationship between aging-related biomarkers and osteoporosis: A bidirectional two-sample Mendelian randomization study.The Journal of international medical research · 2026Article
Corrections and comments
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Authors and funding
4 authors.
Funding
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 turnover markers C-terminal telopeptide (CTX) and amino pro-collagen type 1 N-terminal propeptide (P1NP) were available. Analyses were conducted at both the individual and twin-pair levels, reducing genetic and environmental confounding. A consistent pattern emerged: increased epigenetic age, faster pace of aging, and shorter mTL associated with a higher risk of fractures, or osteoporosis. Notably, DunedinPoAm, DuninPACE, and GrimAge demonstrated the most robust associations. DuninPACE displayed the largest effects; hazard ratios ranging from 1.29 to 3.17, reflecting a 29%-217% increased hazard for diagnosis pr. one standard deviation increase in DuninPACE. The same directions of effects were seen for decreasing CTX and P1NP levels, suggesting bone remodeling impairment for individuals with higher biological age. Lastly, sex- and age-specific analysis of BMD indicated the same direction of effect for DunedinPoAm, and GrimAge in older females. These findings suggest that epigenetic clocks may serve as biomarkers for bone aging.
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Registered trials
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