Bone remodeling is highly inhibited around the inner ear space, most likely by the anti-resorptive action of the inner ear cytokine osteoprotegerin (OPG) entering perilabyrinthine bone through the lacuno-canalicular porosity (LCP). This extracellular signaling pathway depends on the viability of individual osteocytes. The objective of this study was to evaluate the patency of the LCP at different ages. Sixty-five bulk-stained undecalcified human temporal bones and 19 ribs were selected to span the ages from the 30th gestational week to 95 years. Osteocytes from inside a 2-mm wide perilabyrinthine zone of bone were identified by 3D vector calculations and the numerical densities estimated with an optical dissector and compared to age-matched ribs. From a high fetal count of 90,000 cells/mm(3), the density of viable capsular osteocytes declined rapidly to 73,000 cells/mm(3) at three years of age, and non-viable osteocytes increased inversely. After 3 years, this decline/increase continued at a much slower rate. The densities of viable as well as non-viable osteocytes and the rates of change were much higher in perilabyrinthine bone compared to ribs. Only after the age of 80 years had the density of viable capsular osteocytes declined to the level of ribs. The bi-phasic osteocyte kinetics reflects different development stages. The high initial density of viable osteocytes may secure a life-long anatomical route for inner-ear OPG despite the unique accumulation of non-viable osteocytes. Clustering of non-viable osteocytes may cause local aberrations in the signaling system by closure of the LCP.