Background and Objectives. The pathogenesis of otitis media (OM) involves a number of factors related to the anatomy, pathology, and cell biology of the middle ear, the mastoid, the Eustachian tube, and the nasopharynx. Although some issues of pathogenesis are fairly well established, others are only marginally indicated by current knowledge, and yet others remain undisclosed. The objective of this article is to provide a state-of-the-art review on recent scientific achievements in the pathogenesis of OM, as related to anatomy, pathology, and cell biology. Data Sources. PubMed, Ovid Medline, and Cochrane Library. Review Methods. Articles published on the pathogenesis of OM and the anatomy, pathology, and cell biology of the middle ear, the mastoid, the Eustachian tube, and the nasopharynx between January 2007 and June 2011 were identified. Among almost 1900 abstracts, the authors selected 130 articles for full article review and inclusion in this report. Results. New knowledge on a number of issues emerged, including cell-specific expression and function of fluid transportation and innate immune system molecules, mucous cell metaplasia, mucin expression, bacterial adherence, and epithelial internalization, as well as the occurrence, composition, dynamics, and potential role of bacterial biofilm. In addition, the potential role of gastroesophageal reflux disease and cigarette smoke exposure has been explored further. Conclusions and Implications for Practice. Over the past 4 years, considerable scientific progress has been made on the pathogenesis of OM, as related to issues of anatomy, pathology, and cell biology. Based on these new achievements and a sustained lack of essential knowledge, suggestions for future research are outlined.
|Original language||English (US)|
|Journal||Otolaryngology - Head and Neck Surgery (United States)|
|Issue number||4 SUPPL.|
|State||Published - Apr 2013|
Bibliographical noteFunding Information:
Competing interests: Lauren Bakaletz, GlaxoSmithKline Biologicals, Inc, sponsored research funding. Sponsorships: None. Funding source: None. Abbreviations AI, autoinducer; AMP, antimicrobial peptide; AOM, acute otitis media; AQP, aquaporin; Bcl, B-cell lymphoma; CCR, chemokine receptor; COM(E), chronic otitis media (with effusion); CSOM, chronic suppurative otitis media; DC, dendritic cell; EGFR, epidermal growth factor receptor; iNOS, induction nitric oxide synthase; ET, Eustachian tube; GABAR, γ-aminobutyric acid receptor; GalNAc, galactose N-acetylgalactosamine; GAS, group A streptococci; IL, interleukin; LOS: lipo-oligosaccharide; MCP, monocyte chemoattractant protein; MMP, matrix metalloproteinase; NET, neutrophil extracellular traps; NF-κB, nuclear factor-kappa beta; NKCC, Na(+)-K(+)-2Cl(-) co-transporter; NTHi, nontypeable Haemophilus influenzae ; OM, otitis media; OME, otitis media with effusion; PCho: phosphorylcholine; SPDEF, SAM pointed domain ETS factor; TGF, transforming growth factor; TLR, toll-like receptor; TM, tympanic membrane; TNF, tumor necrosis factor; rtPCR: real-time polymerase chain reaction. Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article.
- Cell biology
- Otitis media