ORL; journal for oto-rhino-laryngology and its related specialties · 2008
Intravital microlesions in the human otic capsule. Detection, classification and pathogenetic significance revisited.
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Frisch Thomas, Bretlau Poul, Sorensen Mads Solvsten
Аннотация
PURPOSE OF THE STUDY: To verify microcracks in human temporal bones by a method which distinguishes intravital lesions from artifacts, to revisit previous information derived from decalcified materials on their morphology and classification and to discuss the possible clinical significance.
PROCEDURES: Histological analysis of 210 undecalcified adult human temporal bones bulk-stained by basic fuchsin in ethanol prior to embedding in methyl methacrylate and processing by the cutting and grinding method.
RESULTS: Intravital crack lesions appeared in all specimens and could be distinguished from artifacts regardless of crack morphology and size. Particularly, large microfissures were found around the labyrinthine windows, while smaller microfissures originating at the perilymphatic space were found throughout perilabyrinthine bone. Small noncommunicating fatigue microdamage was identified for the first time. All lesions were reorganized according to morphology, topography and possible clinical significance.
CONCLUSION: Microfissures accumulate in the adult otic capsule as expected when bone remodeling is low. Any capsular microlesion may introduce a possible barrier in the recently discovered antiresorptive signaling pathway from inner ear structures via the lacunocanalicular osteocytic network to perilabyrinthine bone. For this reason intravital microfissures may interfere with in vivo inhibition of temporal bone remodeling and consequently offer another pathogenetic factor in otosclerosis.
PROCEDURES: Histological analysis of 210 undecalcified adult human temporal bones bulk-stained by basic fuchsin in ethanol prior to embedding in methyl methacrylate and processing by the cutting and grinding method.
RESULTS: Intravital crack lesions appeared in all specimens and could be distinguished from artifacts regardless of crack morphology and size. Particularly, large microfissures were found around the labyrinthine windows, while smaller microfissures originating at the perilymphatic space were found throughout perilabyrinthine bone. Small noncommunicating fatigue microdamage was identified for the first time. All lesions were reorganized according to morphology, topography and possible clinical significance.
CONCLUSION: Microfissures accumulate in the adult otic capsule as expected when bone remodeling is low. Any capsular microlesion may introduce a possible barrier in the recently discovered antiresorptive signaling pathway from inner ear structures via the lacunocanalicular osteocytic network to perilabyrinthine bone. For this reason intravital microfissures may interfere with in vivo inhibition of temporal bone remodeling and consequently offer another pathogenetic factor in otosclerosis.