ArticleJournal of orthopaedic research : official publication of the Orthopaedic Research Society2022
Osteochondroma formation is independent of heparanase expression as revealed in a mouse model of hereditary multiple exostoses.
Article in Journal of orthopaedic research : official publication of the Orthopaedic Research Society, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 10 citations in OpenAlex.
- Article
- Clinical Characteristics and Outcomes of Surgical Treatment of Solitary Osteochondromas in Children: A 11-Year Retrospective Study.Medical sciences (Basel, Switzerland) · 2026Article
- The Pathophysiological Functions of Heparanases: From Evolution, Structural and Tissue-Specific Perspectives.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Review
- Ulnar lengthening in the treatment of forearm deformity caused by hereditary multiple exostoses in children.World journal of orthopedics · 2025Review
- Review
- Clinical survey of a pedigree with hereditary multiple exostoses and identification of EXT‑2 gene deletion mutation.Molecular medicine reports · 2022Article
- Hinge positioning method of Ilizarov apparatus in correcting radial head luxation caused by multiple hereditary exostoses.Joint diseases and related surgery · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Hereditary multiple exostoses (HME) is a rare, pediatric disorder characterized by osteochondromas that form along growth plates and provoke significant musculoskeletal problems. HME is caused by mutations in heparan sulfate (HS)-synthesizing enzymes EXT1 or EXT2. Seemingly paradoxically, osteochondromas were found to contain excessive extracellular heparanase (Hpse) that could further reduce HS levels and exacerbate pathogenesis. To test Hpse roles, we asked whether its ablation would protect against osteochondroma formation in a conditional HME model consisting of mice bearing floxed Ext1 alleles in Agr-CreER background (Ext1
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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.