(0947) Mechanisms of Cellular Injury in the Setting of Cochlear Implants: A Systematic Review

Introduction: The objective of this study is to assess mechanisms of cellular injury in the context of cochlear implants (CI) for optimization of hearing outcomes. At the conclusion of this presentation, the participants should be able to identify mechanisms of cellular injury in the context of cochlear implants.

Methods: Studies were identified through the following search phrases: “cochlear implants” OR “cell death” AND “ototoxicity” in: Ovid Medline, PubMed-NCBI, CINAHL, Cochrane Library, Web of Science, and clinicaltrials.gov.

Results: Literature search yielded 2,315 results. Of them, 1,000 studies were removed due to duplication. Screening of the remaining 1,315 studies was conducted by three independent reviewers. Abstract screening yielded 73 included studies. Full text screening yielded 18 included studies. Of the included studies, 6 were completed in human patients. Of these, 3 found evidence to support reactive oxygen species (ROS), two supported fibrosis, and three supported inflammation as mechanisms of cell death during CI. The remaining 12 included studies were completed in animal models, which showed congruent mechanisms of cell death with those in humans. Of these, five supported inflammation, four supported ROS, three supported apoptosis, and two supported fibrosis as mechanisms of cellular injury during CI.

Conclusions: Data exploring cell death in the setting of CI suggests a range of mechanisms that were supported by both human and animal models. Mechanisms included in this review are reactive oxygen species, fibrosis, inflammation, and apoptosis. Targeted therapy against evidence-identified CI cell death mechanisms offers the possibility of more precisely targeting cell death mechanisms and potentially improving CI outcomes impacted by cell death in the cochlea. There remains a need to understand these mechanisms and implement specific interventions to limit cell death during CI.