This article discusses a series of delayed secondary lesions triggered by cochlear hair cell death. In the early stages of outer hair cell destructions, the Deiters’ cells are immediately expanded to plug the perforations on the surface of the organ of Corti. The expansion of Deiters’ cells can effectively prevent the infiltration of high potassium endolymph into the internal space of the organ of Corti to protect remaining outer hair cells and support cells from potassium toxicity. The expanded Deiters’ cells then differentiate into tall columnar cells to support the overall shape of the organ of Corti. In the location of sporadic missing of outer hair cells, the tall columnar cells converted from former Dieter’s cells permanently support the structure of the organ of Corti, which allows the remaining survival outer hair cells to continue function of amplifying and converting the acoustic vibration signals to maintain the residual hearing. In the cochlear injury model with extensive outer hair cell death, the former Deiters’ cells transformed into tall columnar cells die 30 days after redifferentiation, which subsequently leads to the collapse of the entire structure of the organ of Corti and the death of inner hair cells and support cells. Finally, only a layer of flat epithelium remains on the cochlear basilar membrane. Whether in an experimental model of both inner and outer hair cells missing or in an experimental model of massive death of outer hair cells followed by collapse of supporting structures and death of inner hair cells, cochlear efferent nerves and afferent fibers on the cochlear basilar membrane are destroyed within few weeks after hair cell missing. The spiral ganglion neurons in the Rosenthal’s canal of modiolus subsequently initiate the delayed spiral ganglion death due to loss of nerve stimulation signals and lack of neurotrophic factors. The death of the spiral ganglion neurons causes irreversible destruction of the axons at the central end of the auditory nerve connecting the cochlear nucleus, and eventually leading to permanent interruption of the nerve connections between the pericochlear system and the central auditory system.