Cellular Differentiation of the Middle Ear Lining

The fine surface view of the human adult eustachian tube

“…Metaplasia of the respiratory epithelium is common following repeated inflammations, the ciliated columnar cells being transformed into squamous cells or goblet cells. The islands of squamous cells at the floor of the cartilaginous portion of the tube occasionally noted in the present investigation, might be the consequence of previous inflammatioa Sade (1971) and others have pointed out that stratified keratinizing squamous epithelium is a pathological process in the human middle ear. Tos and Bak-Pedersen (1976) have described cellular changes in the mucosa of the middle ear and eustachian tube in various middle-ear diseases.…”

A new theory on the pathogenesis of acquired cholesteatoma: Mucosal traction

“…A critical step is that mucin, which has escaped from embedded mucosa, leads to the inflammation seen in the perimatrix, itself inducing keratinocyte proliferation and migration and also bone destruction . Mucous glands are also increased in density in disease states, but the density is diminished in cholesteatoma, possibly because they have become broken down and remnants embedded in the perimatrix . Ongoing coupled mucosal migration may lead to the trapping of mucosa and mucosal elements, which in turn leads to further inflammation and production of proinflammatory cytokines.…”

Etiopathogenesis of acquired cholesteatoma: Prominent theories and recent advances in biomolecular research

“…This theory claims that the precursors to cholesteatoma are retraction pockets of the pars flaccida, which compared to the pars tensa, is less fibrous and less resistant to displacement. The retraction pocket is caused by negative pressure in the middle ear, which in‐turn results from eustachian tube dysfunction (hydrops ex vacuo theory), repeated inflammation, habitual sniffing, or a mastoid of small volume . A deepening of the retraction pocket with accumulation of desquamated keratin can lead to cholesteatoma formation, which obstructs the opening of the pocket and thereby induces ingrowth expansion into the middle ear cleft.…”