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Updated: Jun 8, 2026

Analysis and Imaging of Osteocytes
Published on: November 29, 2024
The viability and spatial distribution of osteocytes in the human labyrinthine capsule: a quantitative study using
Sune Land Bloch1, Mads Sølvsten Sørensen
1Rigshospitalet, University of Copenhagen, Department of Otorhinolaryngology, Blegdamsvej 9, 2100 Copenhagen, Denmark. sunebloch@hotmail.com
Background:
Bone remodeling is highly inhibited around the labyrinthine space, most likely by the action of the anti-resorptive cytokine osteoprotegerin (OPG). Inner ear OPG may enter the bony otic capsule through the lacuno-canalicular porosity (LCP). The aim of the study was to investigate the patency of this extracellular signaling pathway by exploring the viability, age dependency and spatial distribution of capsular osteocytes.
Methods:
Sixty-five bulk-stained undecalcified human temporal bones were selected to span the ages from 30th gestational week to 95 years. Osteocytes within 1000 μm wide iso-concentric perilabyrinthine zones of bone were identified by 3-D vector calculations and the number of cells per unit of bone volume estimated within each zone by optical dissectors.
Results:
From a high initial numerical density and a centripetal distribution of viable osteocytes, the density declined over time. This effect was higher towards the inner ear space and shifted viable osteocytes into to a centrifugal distribution with age. Contrary to this, non-viable osteocytes accumulated centripetally around the inner ear space and accounted for 50% of all lacunae at 80 years of age. Non-viable osteocytes were heterogeneously distributed forming islets of varying size surrounded by the intact and viable parts of the LCP.
Conclusion:
The simultaneous presence of high numbers of non-viable osteocytes within a dense network of viable osteocytes is unique for the bony otic capsule. Viable osteocytes may sustain a life-long anti-resorptive signaling pathway for inner ear OPG. Clustering of non-viable osteocytes may locally impede the effect of OPG leaving the ghost regions unprotected against focal bone remodeling, as in human otosclerosis.
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