Bacterial Infections and Osteoclastogenesis Regulators in Men and Women with Cholesteatoma
2016 (English)In: Archivum Immunologiae et Therapiae Experimentalis, ISSN 0004-069X, E-ISSN 1661-4917, Vol. 64, no 3, 241-247 p.Article, review/survey (Refereed) PublishedText
One of the most distinct features of middle ear cholesteatoma is bone destruction. Aetiology of cholesteatoma is thought to be multifactorial. Endotoxins produced by bacteria are thought to initiate the inflammation process in the middle ear leading to cholesteatoma. There are physiological differences in bone metabolism between men and women. The aim of our study was the immunohistochemical evaluation of the contents of two key components of the OPG/RANK/RANKL triad-RANKL and OPG in cholesteatoma, to analyse if there are any differences between the sexes and to evaluate the bacteria species isolated from cholesteatoma just before surgical treatment and to evaluate their plausible influence on the expression of OPG and RANKL in cholesteatoma. Twenty-one adult patients with acquired cholesteatoma who underwent surgery were analysed. There were no statistically significant differences in the expression of both regulators of osteoclastogenesis between the sexes. In 38.1 % patients cholesteatoma was not infected, whereas in 61.9 % patients various bacterial infections or mycosis were found. The most frequently isolated species was Pseudomonas aeruginosa (14.29 % infections) followed by Staphylococcus aureus (9.52 % infections). There were no statistically significant differences in expression of both OPG and RANKL between uninfected and infected cholesteatomas.
Place, publisher, year, edition, pages
SPRINGER BASEL AG , 2016. Vol. 64, no 3, 241-247 p.
Cholesteatoma; Osteoprotegerin; RANKL; Bacterial infection; Sexes
IdentifiersURN: urn:nbn:se:liu:diva-129139DOI: 10.1007/s00005-015-0373-7ISI: 000376060200005PubMedID: 26584851OAI: oai:DiVA.org:liu-129139DiVA: diva2:936069
Funding Agencies|Medical University of Silesia in Katowice, Poland [KNW-1-096/P/2/0]2016-06-132016-06-132016-06-13