Evidence map›Paper›PMID 39669499›Full record

ReviewFrontiers in endocrinology2024

Poor bone health in Duchenne muscular dystrophy: a multifactorial problem beyond corticosteroids and loss of ambulation.

Amelia Hurley-Novatny, David Chang, Katsuhiro Murakami, Ling Wang, Hongshuai Li

Abstract readReview
In one paragraph

Review in Frontiers in endocrinology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed.

  1. Article
  2. [Association analysis between dystrophin gene polymorphism and non-syndromic cleft lip with or without cleft palate].Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Fat embolism syndrome in Duchenne muscular dystrophy: an underdiagnosed complication.Acta myologica : myopathies and cardiomyopathies : official journal of the Mediterranean Society of Myology · 2025
    Article
  10. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Amelia Hurley-NovatnyDepartment of Orthopedics and Rehabilitation, University of Iowa, Iowa City, IA, United States.
David ChangMedical Scientist Training Program, Carver College of Medicine, University of Iowa, Iowa City, IA, United States.
Katsuhiro MurakamiDepartment of Orthopedics and Rehabilitation, University of Iowa, Iowa City, IA, United States.
Ling WangDepartment of Orthopedics and Rehabilitation, University of Iowa, Iowa City, IA, United States.
Hongshuai LiDepartment of Orthopedics and Rehabilitation, University of Iowa, Iowa City, IA, United States.

Funding

Storage Lesion in Banked Blood Due to Disruption of Nitric Oxide HomeostasisR01HL098032 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Mark T Gladwin · 2009 to 2026
$12.5M
Medical Scientist Training ProgramT32GM139776 · NIGMS · UNIVERSITY OF IOWA · PI Gordon F Buchanan · 2021 to 2026
$6.4M
Role of FGF21 in DMDR01AR083398 · NIAMS · UNIVERSITY OF IOWA · PI Hongshuai Li · 2024 to 2026
$1.7M
Targeting Nitrate-Nitrite-NO pathway for Ameliorating Muscle and Bone Comorbidities in Duchenne Muscular DystrophyR01AR076357 · NIAMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI LI, HONGSHUAI · 2020 to 2024
$1.6M
NHLBI NIH HHS R01 HL098032NIAMS NIH HHS R01 AR076357NIAMS NIH HHS R01 AR083398NIGMS NIH HHS T32 GM139776
6 · The paper itself

Abstract

Duchenne muscular dystrophy (DMD) is a progressive, fatal muscle wasting disease caused by X-linked mutations in the dystrophin gene. Alongside the characteristic muscle weakness, patients face a myriad of skeletal complications, including osteoporosis/osteopenia, high susceptibility to vertebral and long bone fractures, fat embolism post-fracture, scoliosis, and growth retardation. Those skeletal abnormalities significantly compromise quality of life and are sometimes life-threatening. These issues were traditionally attributed to loss of ambulation and chronic corticosteroid use, but recent investigations have unveiled a more intricate etiology. Factors such as vitamin D deficiency, hormonal imbalances, systemic inflammation, myokine release from dystrophic muscle, and vascular dysfunction are emerging as significant contributors as well. This expanded understanding illuminates the multifaceted pathogenesis underlying skeletal issues in DMD. Present therapeutic options are limited and lack specificity. Advancements in understanding the pathophysiology of bone complications in DMD will offer promising avenues for novel treatment modalities. In this review, we summarize the current understanding of factors contributing to bone problems in DMD and delineate contemporary and prospective multidisciplinary therapeutic approaches.

Indexed as

Adrenal Cortex HormonesMuscular Dystrophy, DuchenneBone and BonesBone Diseases, MetabolicHumansOsteoporosisAdrenal Cortex HormonesDMDmuscle and bone crosstalkmyokinesosteoporosisskeletal abnormality

Identifiers

PMID39669499
PMCPMC11634624

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.