ReviewEFORT open reviews2026
Current advances of bone homeostasis imbalance in the cause of hereditary metabolic bone diseases.
Review in EFORT open reviews, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
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
5 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Posterior spinal fusion with pedicle screw-based constructs in osteogenesis imperfecta: a systematic review of surgical and radiographic outcomes.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2026Pooled it
- Engineering high-fidelity bone organoids: Operational classification, multilineage crosstalk, biofabrication evidence, and translational validation.Materials today. Bio · 2026Article
- Heme Oxygenase-1 in Bone Remodeling: Molecular Mechanisms and Therapeutic Implications.Biomolecules · 2026Review
- HDAC4 regulates hASC osteogenesis and bone regeneration by mediating SMAD4 via histone acetylation.Stem cell reports · 2026Article
- The recent progression of extracellular vesicles application in osteoporosis.Frontiers in pharmacology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bone homeostasis, a dynamic equilibrium essential for skeletal development and repair, is coordinately regulated by osteoclasts, osteoblasts, and osteocytes. Hereditary metabolic bone diseases arise from genetic mutations that impair the function of these key bone cells, disrupting the homeostatic balance. This review specifically addresses four prevalent hereditary metabolic bone diseases: osteogenesis imperfecta, Paget's disease of bone, hypophosphatemic rickets, and osteopetrosis. Dysfunction in major signaling pathways - notably the Wnt/β-catenin, RANK/RANKL/OPG, and TGF-β/BMP pathways - plays a central role in the aberrant bone remodeling underlying these disorders. Elucidating the molecular mechanisms involving these cells and pathways is fundamental to understanding disease pathogenesis and is crucial for the development of novel therapeutic interventions, presenting significant promise for future research.
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What OpenQuestion holds
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.