Abstract

Otitis medium (OM) with mucoid effusion is a form of OM that usually progresses to chronic OM in young children. It is characterised by mucous cell metaplasia/hyperplasia in the middle ear cleft and thick fluid accumulation in the middle ear canal. The development of OM with mucoid effusion is influenced by a number of variables, particularly problems with mucin synthesis brought on by middle ear bacterial infection and Eustachian tube dysfunction. By examining cellular and molecular processes such mucin formation and mucous cell differentiation in the middle ear mucosa with OM, we will analyse several aspects of this condition in this review. Infectious diseases, factors that cause the formation of mucin, and pertinent signalling pathways will also be covered.

Mucous cell metaplasia, which causes mucous hyper secretion and the condition to persist, is a major problem in otitis media. The molecular pathways behind mucous cell metaplasia in otitis media are not well understood, yet. Atonal homolog 1 (Atoh1), a basic helix-loop-helix (bHLH) transcription factor, has been demonstrated to be crucial for the differentiation of intestinal goblet cells in numerous studies of intestinal epithelial homeostasis. On the other hand, it has been suggested that the "Ets" transcription factor family member SAM-pointed domain-containing Ets transcription factor (SPDEF), causes asthma or lung viral illnesses to cause mucous cell metaplasia. Recent research have shown the relationship between these variables, proving that Spdef works downstream of Atoh1. Due to the fact that the pulmonary and middle ear epithelia both come from the same respiratory tract, we could use the advantages of these results to further our understanding of otitis media. When it comes to treating otitis media with mucous cell metaplasia, which is usually referred to as "intractable" in clinical settings, Atoh1 and SPDEF may be the best therapeutic targets.