ArticleScience progress
Bone destruction in chronic otitis media is not mediated by the RANKL pathway or estrogen receptor-alpha.
Article in Science progress. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed, 2 citations in OpenAlex.
- Article
- Cholesteatoma: An Updated Review of Molecular Pathogenesis and Potential Therapeutic Directions.Current medicinal chemistry · 2026Review
- Correlation analysis between CT values of cochlear bone labyrinth and auditory function and disease progression in patients with chronic suppurative otitis media.Frontiers in medicine · 2026Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChronic otitis media with or without cholesteatoma progresses with various degrees of bone resorption and remodeling. Estrogen mediates osteoprotective effects through the receptor activator of NF-κB ligand (RANKL) pathway, which is mainly mediated by estrogen receptor-alpha (ER-α).
objectivesThe present study investigated the expression patterns of receptor activator of NF-κB (RANK), osteoprotegerin (OPG), RANKL, and ER-α in pathological tissue from patients with chronic otitis media to determine the roles of those factors in osteolytic mechanisms underlying the pathogenesis of chronic otitis media.
methodsNormal and pathological specimens from 18 patients with chronic otitis media were examined.
resultsThere were no significant differences in RANK, OPG, RANKL, or ER-α mRNA expression between normal and pathological specimens of epithelial tissue.
conclusionsOur findings suggested that RANK, OPG, RANKL, and ER-α are not associated with the bone destruction in chronic otitis media; other cytokines may directly activate the osteoclasts in chronic otitis media.
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Registered trials
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