ReviewCureus2025
Genetic Influences and Targeted Treatments in Osteoporosis: A Systematic Review.
Review in Cureus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Bone as a Biomarker of Ageing and Senescence: Connecting Musculoskeletal Health to Longevity via Diet, Nutrition and Exercise.Biology · 2026Review
- Causal genes for osteoporosis: Mendelian randomization analysis with multilayer xQTL data.Medicine · 2026Article
- Letter to the editor regarding: 'Hypocalcemia following denosumab in osteoporosis: Incidence and risk factors in a Saudi cohort'.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2026Article
- Real-World Assessment of Osteoporosis-Related Polymorphisms: Negative Findings for Osteoporosis and an Exploratory Association with Vitamin D.Life (Basel, Switzerland) · 2026Article
- Osteoporosis After Menopause and After Drug Therapy: The Molecular Mechanism of Bone Loss and Its Treatment.International journal of molecular sciences · 2026Review
- PBX1 promotes osteoporosis by upregulating HMGB1 to suppress osteogenic differentiation of bone marrow mesenchymal stem cells.Stem cell research & therapy · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoporosis is a chronic skeletal disorder marked by reduced bone mineral density (BMD) and increased fracture risk, posing a substantial global health burden. Traditionally considered multifactorial, growing evidence highlights a significant genetic contribution across both early-onset monogenic and adult-onset polygenic forms. Understanding the molecular and genetic architecture of osteoporosis is crucial for guiding targeted diagnostics and developing personalised therapeutic strategies. This review aimed to: (1) identify and summarise genetic mutations and polymorphisms associated with osteoporosis, classifying them into monogenic and multifactorial causes; (2) distinguish between syndromic and non-syndromic forms of genetically influenced osteoporosis; (3) evaluate how specific genetic variations influence the risk, onset, and severity of osteoporosis, particularly in postmenopausal populations; (4) examine current anti-resorptive and anabolic treatments in the context of genetic backgrounds; and (5) identify gaps in knowledge to guide future research into genetics-based screening and individualised treatment. A comprehensive literature search was conducted across PubMed, Embase, CINAHL, and the Cochrane Library for studies published between 2000 and 2025. Medical Subject Headings (MeSH) and free-text keywords were used to retrieve peer-reviewed articles, clinical trials, genetic association studies, and systematic reviews. Eligible studies explored genetic variants, bone signalling pathways (e.g., WNT/β-catenin, Notch), or pharmacological therapies in relation to BMD, fracture incidence, or osteogenesis. Data were extracted and thematically analysed under the following three core domains: genetic and molecular mechanisms, osteogenesis and bone remodelling, and treatment responses linked to genetic profiles. The review identified a wide spectrum of genetic contributors to osteoporosis. Monogenic forms, often syndromic, were linked to mutations in genes such as
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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.