ReviewCurrent osteoporosis reports2021
Current Analysis of Skeletal Phenotypes in Down Syndrome.
Review in Current osteoporosis reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Genetic analysis of triplicated genes affecting sex-specific skeletal deficits in Down syndrome model mice.G3 (Bethesda, Md.) · 2026Article
- Genetic analysis of triplicated genes affecting sex-specific skeletal deficits in Down syndrome model mice.bioRxiv : the preprint server for biology · 2025Article
- Telomere Biology, Erosion, and Age-Related Conditions: Insights from Down Syndrome and Other Telomere-Associated Disorders.Molecular neurobiology · 2025Review
- Cardiopulmonary and Immune Alterations in the Ts65Dn Mouse Model of Down Syndrome and Modulation by Epigallocatechin-3-Gallate-Enriched Green Tea Extract.Pharmaceutics · 2025Article
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- Skeletal health inFrontiers in neuroscience · 2024Review
- RUN(X) out of blood: emerging RUNX1 functions beyond hematopoiesis and links to Down syndrome.Human genomics · 2023Review
- Dissection of a Down syndrome-associated trisomy to separate the gene dosage-dependent and -independent effects of an extra chromosome.Human molecular genetics · 2023Article
- Genetic dissection of triplicated chromosome 21 orthologs yields varying skeletal traits in Down syndrome model mice.Disease models & mechanisms · 2023Article
- Green Tea Catechins Modulate Skeletal Development with Effects Dependent on Dose, Time, and Structure in a down Syndrome Mouse Model.Nutrients · 2022Article
- Incidence of fractures in people with intellectual disabilities over the life course: a retrospective matched cohort study.EClinicalMedicine · 2022Article
- Low bone mass and impaired fracture healing in mouse models of Trisomy21 (Down syndrome).Bone · 2022Article
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Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
purposeDown syndrome (DS) is caused by trisomy 21 (Ts21) and results in skeletal deficits including shortened stature, low bone mineral density, and a predisposition to early onset osteoporosis. Ts21 causes significant alterations in skeletal development, morphology of the appendicular skeleton, bone homeostasis, age-related bone loss, and bone strength. However, the genetic or cellular origins of DS skeletal phenotypes remain unclear. RECENT
findingsNew studies reveal a sexual dimorphism in characteristics and onset of skeletal deficits that differ between DS and typically developing individuals. Age-related bone loss occurs earlier in the DS as compared to general population. Perturbations of DS skeletal quality arise from alterations in cellular and molecular pathways affected by the overexpression of trisomic genes. Sex-specific alterations occur in critical developmental pathways that disrupt bone accrual, remodeling, and homeostasis and are compounded by aging, resulting in increased risks for osteopenia, osteoporosis, and fracture in individuals with DS.
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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.