Understanding the aetiology and resolution of chronic otitis media from animal and human studies

Mahmood F. Bhutta, Ruth B. Thornton, Lea Ann S. Kirkham, Joseph E. Kerschner, Michael T. Cheeseman

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Inflammation of the middle ear, knownclinicallyas chronic otitis media, presents in different forms, such as chronic otitis media with effusion (COME; glue ear) and chronic suppurative otitis media (CSOM). These are highly prevalent diseases, especially in childhood, and lead to significant morbidity worldwide. However, much remains unclear about this disease, including its aetiology, initiation and perpetuation, and the relative roles of mucosal and leukocyte biology, pathogens, and Eustachian tube function. Chronic otitis media is commonly modelled in mice but most existing models only partially mimic human disease and manyare syndromic. Nevertheless, these models have provided insights into potential disease mechanisms, and have implicated altered immune signalling, mucociliary function and Eustachian tube function as potential predisposing mechanisms. Clinical studies of chronic otitis media have yet to implicate a particular molecular pathway or mechanism, and current human genetic studies are underpowered. We also do not fully understand how existing interventions, such as tympanic membrane repair, work, nor how chronic otitis media spontaneously resolves. This Clinical Puzzle article describes our current knowledge of chronic otitis media and the existing research models for this condition. It also identifies unanswered questions about its pathogenesis and treatment, with the goal of advancing our understanding of this disease to aid the development of novel therapeutic interventions.

Original languageEnglish
Pages (from-to)1289-1300
Number of pages12
JournalDMM Disease Models and Mechanisms
Volume10
Issue number11
DOIs
Publication statusPublished - 1 Nov 2017

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Otitis Media
Animals
Eustachian Tube
Glues
Suppurative Otitis Media
Pathogens
Otitis Media with Effusion
Tympanic Membrane
Medical Genetics
Repair
Adhesives
Ear
Membranes
Leukocytes
Morbidity
Research

Cite this

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title = "Understanding the aetiology and resolution of chronic otitis media from animal and human studies",
abstract = "Inflammation of the middle ear, knownclinicallyas chronic otitis media, presents in different forms, such as chronic otitis media with effusion (COME; glue ear) and chronic suppurative otitis media (CSOM). These are highly prevalent diseases, especially in childhood, and lead to significant morbidity worldwide. However, much remains unclear about this disease, including its aetiology, initiation and perpetuation, and the relative roles of mucosal and leukocyte biology, pathogens, and Eustachian tube function. Chronic otitis media is commonly modelled in mice but most existing models only partially mimic human disease and manyare syndromic. Nevertheless, these models have provided insights into potential disease mechanisms, and have implicated altered immune signalling, mucociliary function and Eustachian tube function as potential predisposing mechanisms. Clinical studies of chronic otitis media have yet to implicate a particular molecular pathway or mechanism, and current human genetic studies are underpowered. We also do not fully understand how existing interventions, such as tympanic membrane repair, work, nor how chronic otitis media spontaneously resolves. This Clinical Puzzle article describes our current knowledge of chronic otitis media and the existing research models for this condition. It also identifies unanswered questions about its pathogenesis and treatment, with the goal of advancing our understanding of this disease to aid the development of novel therapeutic interventions.",
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Understanding the aetiology and resolution of chronic otitis media from animal and human studies. / Bhutta, Mahmood F.; Thornton, Ruth B.; Kirkham, Lea Ann S.; Kerschner, Joseph E.; Cheeseman, Michael T.

In: DMM Disease Models and Mechanisms, Vol. 10, No. 11, 01.11.2017, p. 1289-1300.

Research output: Contribution to journalArticle

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