ReviewThe application of clinical genetics2015
Progressive osseous heteroplasia: diagnosis, treatment, and prognosis.
Review in The application of clinical genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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
45 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Progressive osseous heteroplasia in a 5-year-old boy with a novel mutation in exon 2 of GNAS: a case presentation and literature review.BMC musculoskeletal disorders · 2023Pooled it
- Article
- When Bone Forms Where It Shouldn't: Heterotopic Ossification in Muscle Injury and Disease.International journal of molecular sciences · 2025Review
- Article
- Late-Onset Progressive Osseous Heteroplasia: 2 Unrelated Cases and Use of Positron Emission Tomography for Diagnosis.JCEM case reports · 2025Article
- Heterotopic ossification: Current developments and emerging potential therapies.Chinese medical journal · 2025Review
- Insights Gained From an Ultrarare Case of Progressive Osseous Heteroplasia With Severe Complications.Cureus · 2025Article
- Cutaneous Calcified Mass of Foot in Pseudohypoparathyoidism: Case Report.Medicina (Kaunas, Lithuania) · 2024Article
- Progressive osseous heteroplasia in a five-month-old boy with a mutation in exon 9 ofAmerican journal of translational research · 2024Article
- Role of hedgehog signaling in the pathogenesis and therapy of heterotopic ossification.Frontiers in cell and developmental biology · 2024Review
- Progressive osseous heteroplasia: A case report with an unexpected trigger.Bone reports · 2023Article
- A Novel De Novo Frameshift Pathogenic Variant in the FAM111B Resulting in Progressive Osseous Heteroplasia Phenotype.Calcified tissue international · 2023Article
- Review
- Aggressive atraumatic myositis ossificans in a toddler.Radiology case reports · 2022Article
- Insights into skeletal stem cells.Bone research · 2022Review
- Identification of Risk Factors in the Development of Heterotopic Ossification After Primary Total Hip Arthroplasty.The Journal of clinical endocrinology and metabolism · 2022Article
- Cancellous bone-like tissue replacement from calcinosis in patients with systemic sclerosis with multiple external root resorption.Bone reports · 2022Article
- Aberrant Bone Regulation in Albright Hereditary Osteodystrophy dueto Gnas Inactivation: Mechanisms and Translational Implications.Current osteoporosis reports · 2022Review
- Frequency ofFrontiers in endocrinology · 2022Article
- Case Report: Everolimus reduced bone turnover markers but showed no clinical benefit in a patient with severe progressive osseous heteroplasia.Frontiers in pediatrics · 2022Article
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
Abstract
Progressive osseous heteroplasia (POH) is an ultrarare genetic condition of progressive ectopic ossification. Most cases of POH are caused by heterozygous inactivating mutations of GNAS, the gene encoding the alpha subunit of the G-stimulatory protein of adenylyl cyclase. POH is part of a spectrum of related genetic disorders, including Albright hereditary osteodystrophy, pseudohypoparathyroidism, and primary osteoma cutis, that share common features of superficial ossification and association with inactivating mutations of GNAS. The genetics, diagnostic criteria, supporting clinical features, current management, and prognosis of POH are reviewed here, and emerging therapeutic strategies are discussed.
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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.