ReviewThe journals of gerontology. Series A, Biological sciences and medical sciences2013
Pathogenesis of age-related bone loss in humans.
Review in The journals of gerontology. Series A, Biological sciences and medical sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers, 2 of them syntheses that pooled it.
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
126 citing papers in PubMed, 2 syntheses or guidelines pooled it, 217 citations in OpenAlex.
- Prevalence and risk factors of postmenopausal osteoporosis: a systematic review and meta-analysis based on multivariate logistic regression.Frontiers in endocrinology · 2026Pooled it
- The effect of physical exercise on bone density in middle-aged and older men: a systematic review.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2013Pooled it
- Radiographic Peri-Implant Bone Changes in Osteoporotic Women Treated With a Ti-Zr, Bone Level Tapered Implant With a Hydrophilic Surface: A 12-Month Prospective Case-Series.Clinical oral implants research · 2025Trial
- Unmasking Indolent Systemic Mastocytosis in Patients with Unexplained or Treatment-Refractory Osteoporosis: A Case Series with Diagnostic and Therapeutic Implications.Biomolecules · 2026Article
- Bone microarchitecture and material properties decline differently across midlife for male and female F344 × BN F1 rats.bioRxiv : the preprint server for biology · 2026Article
- Sex differences in potassium regulation: evidence, molecular mechanisms and clinical implications.Biology of sex differences · 2026Review
- Sustained and reversible effects of a dietary phosphate intake on bone and mineral metabolism during aging.GeroScience · 2026Article
- Age-related differences in BMD response during three years of denosumab treatment.Frontiers in aging · 2026Article
- Mathematical modeling of bone remodeling after surgical menopause.Frontiers in systems biology · 2026Article
- Extracellular vesicles from antler blastema progenitor cells reverse bone loss and mitigate aging-related phenotypes in mice and macaques.Nature aging · 2025Article
- Testosterone Delays Bone Microstructural Destruction via Osteoblast-Androgen Receptor-Mediated Upregulation of Tenascin-C.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- CCN Proteins as Matricellular Regulators of Bone in Aging and Disease.Current osteoporosis reports · 2025Review
- Associations of Habitual Skeletal Loading with Bone Changes during the Menopausal Transition: A Follow-Up Study.Medicine and science in sports and exercise · 2025Article
- Protective Effect of Methyl Sulfonyl Methane on the Progression of Age-Induced Bone Loss by Regulating Oxidative Stress-Mediated Bone Resorption.Antioxidants (Basel, Switzerland) · 2025Article
- Polyphenols, aging, and health: What can we expect from the food industry in the technology era?Frontiers in medicine · 2025Review
- Effect of Tai Chi on Bone Mineral Density in Middle-Aged and Older Adults: A Meta-Analysis.Orthopedic reviews · 2025Article
- Decoding senescence of aging single cells at the nexus of biomaterials, microfluidics, and spatial omics.npj aging · 2024Review
- Article
- The updated understanding of advanced maternal age.Fundamental research · 2024Review
- Sex-specific trisomic Dyrk1a-related skeletal phenotypes during development in a Down syndrome model.Disease models & mechanisms · 2024Article
66 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
backgroundAlthough data from rodent systems are extremely useful in providing insights into possible mechanisms of age-related bone loss, concepts evolving from animal models need to ultimately be tested in humans.
methodsThis review provides an update on mechanisms of age-related bone loss in humans based on the author's knowledge of the field and focused literature reviews.
resultsNovel imaging, experimental models, biomarkers, and analytic techniques applied directly to human studies are providing new insights into the patterns of bone mass acquisition and loss as well as the role of sex steroids, in particular estrogen, on bone metabolism and bone loss with aging in women and men. These studies have identified the onset of trabecular bone loss at multiple sites that begins in young adulthood and remains unexplained, at least based on current paradigms of the mechanisms of bone loss. In addition, estrogen appears to be a major regulator of bone metabolism not only in women but also in men. Studies assessing mechanisms of estrogen action on bone in humans have identified effects of estrogen on RANKL expression by several different cell types in the bone microenvironment, a role for TNF-α and IL-1β in mediating effects of estrogen deficiency on bone, and possible regulation of the Wnt inhibitor, sclerostin, by estrogen.
conclusionsThere have been considerable advances in our understanding of age-related bone loss in humans. However, there are also significant gaps in knowledge, particularly in defining cell autonomous changes in bone in human studies to test or validate concepts emerging from studies in rodents. Decision Editor: Luigi Ferrucci, MD, PhD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.