The otic capsule consists of dense highly mineralized compact bone. Inner ear osteoprotegerin (OPG) effectively inhibits perilabyrinthine remodeling and otic capsular bone turnover is very low compared to other bone. Consequently, degenerative changes like dead osteocytes and microcracks accumulate around the inner ear. Osteocytes are connected via canaliculi and need a certain connectivity to sustain life. Consequently, stochastic osteocyte apoptosis may disrupt the osteocytic network in unsustainable patterns leading to widespread cell death. When studying bulk-stained undecalcified human temporal bone, large clusters of dead osteocytes have been observed. Such “cellular voids” may disrupt the perilabyrinthine OPG mediated remodeling inhibition possibly leading to local remodeling. In the common ear disease otosclerosis pathological bone remodeling foci are found exclusively in the otic capsule. We believe the pathogenesis of otosclerosis is linked to the unique bony dynamics of perilabyrinthine bone and cellular voids may represent a starting point for otosclerotic remodeling. This study aims to identify and characterize cellular voids of the human otic capsule. This would allow future cellular void quantification and comparison of void and otosclerotic distribution to further elucidate the yet unknown pathogenesis of otosclerosis.