The Laryngoscope · 1999
Bone modeling dynamics in acute otitis media.
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Cayé-Thomasen P, Hermansson A, Tos M, Prellner K
Аннотация
OBJECTIVE: A number of middle ear diseases are associated with pathologic bone modeling, either formative or resorptive. As such, the pathogenesis of a sclerotic mastoid has been controversial for decades. Experimental studies on acute middle ear infection have shown varying degrees of both osteoresorption and osteoneogenesis. This study presents data on the dynamics of bone modeling in a rat model of acute pneumococcal otitis media, studied longitudinally from day 1 through 6 months after inoculation.
RESULTS: Qualitative, as well as quantitative histopathology revealed initial osteoresorption, followed by increasing apposition of new bone in the middle ear cavity, initiated at the outer periosteum. Measured bone thickness in four anatomically distinct locations peaked 3 months after inoculation, followed by some degree of normalization. However, bone thickness was still massively increased 6 months after the acute incident. Except in perilymphatic spaces of the otic capsule, resorptive and formative activity were found in all bone tissue structures surrounding the middle ear cavity, including the bony external auditory canal and the ossicles.
CONCLUSION: These findings may support the existence of a perilymphatic barrier of specialized bone and suggest that even a single episode of acute infection may alter properties of ossicular chain conduction. The authors conclude that acute otitis media is accompanied by massive and progressing net osteoneogenesis, already evident at 3 days and peaking 3 months after inoculation, followed by some degree of normalization. This is conceivably in support of the environmental theory of mastoid pneumatization, claiming inflammatory disease as the cause of a sclerotic mastoid.
RESULTS: Qualitative, as well as quantitative histopathology revealed initial osteoresorption, followed by increasing apposition of new bone in the middle ear cavity, initiated at the outer periosteum. Measured bone thickness in four anatomically distinct locations peaked 3 months after inoculation, followed by some degree of normalization. However, bone thickness was still massively increased 6 months after the acute incident. Except in perilymphatic spaces of the otic capsule, resorptive and formative activity were found in all bone tissue structures surrounding the middle ear cavity, including the bony external auditory canal and the ossicles.
CONCLUSION: These findings may support the existence of a perilymphatic barrier of specialized bone and suggest that even a single episode of acute infection may alter properties of ossicular chain conduction. The authors conclude that acute otitis media is accompanied by massive and progressing net osteoneogenesis, already evident at 3 days and peaking 3 months after inoculation, followed by some degree of normalization. This is conceivably in support of the environmental theory of mastoid pneumatization, claiming inflammatory disease as the cause of a sclerotic mastoid.