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Parallel anatompathological and enzymatic research led to the discovery of the role played by histiocytes, actively engaged in the lytic process and containing numerous lysosomes, and thus to postulate a cellular and enzymatic concept of otospongiosis. The enzymatic experiments were continued by mico‐electrophoresis and allowed the authors to confirm this enzymatic action. In a third step, specific micro‐concentrations of trypsin and alpha‐1 antitrypsin correlated with cochlear progression, and showed an identical sudden reversal of activity. It was deduced that, when the balance of trypsinlantitrypsin is upset, cochlear deterioration can occur. Confirmation of this concept was done by experimental cytologic findings by scanning electron microscopy. Alteration or destruction of hair cells were the proof of the toxicity of the trypsin action on the inner ear, chiefly on the outer hair cells. The upset of the equilibrium of trypsin and antitrypsin in otospongiotic microfoci and resulting spreading of enzymes from the microfoci into different parts of the cochlea, provokes the peculiar response of the otic capsule with various clinical expressions according to the localization of the impairment: a clinical, stapedial one, resulting in conductive hearing loss; a cochlear one, leading to a sensorineural deafness; a vestibular one, provoking dizziness or even vertigo. The relationship of this enzymatic concept with the disease is explained in detail and leads the authors to express genetic prospects and possibilities of treatment by enzymatic inhibitors.

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