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Endolymphatic Hydrops in Otologic Syphilis: A Temporal Bone Study

Miller, Mia E.*; Makary, Chadi; Lopez, Ivan A.*; Ishiyama, Akira*

doi: 10.1097/MAO.0b013e3181dbb7e4
Basic Science

Hypothesis: Endolymphatic hydrops in temporal bones with otologic syphilis directly relates to osteitis, new bone formation, and/or resorption along the course of the endolymphatic system.

Background: Ménière's disease and otosyphilis both cause progressive endolymphatic hydrops, and the mechanism of hydrops formation in each disease process remains unclear. Traditionally, osteitic changes of the labyrinthine capsule were thought to lead to endolymphatic hydrops in syphilitic temporal bones. More recently, authors have suggested that microgummata and inflammatory change obliterating the endolymphatic duct and sac may cause endolymphatic hydrops in otosyphilis.

Methods: This is a histopathologic study of 11 temporal bones from patients with otosyphilis. Gathered data include presence/absence of endolymphatic hydrops of the cochlea, saccule, and utricle; bony changes involving the endolymphatic duct and sac; a description of bony changes throughout the temporal bone; and the degree of atrophy of the organ of Corti, spiral ganglion, and stria vascularis.

Results: The presence of osteitic changes surrounding the endolymphatic duct and sac and whether the endolymphatic system was obliterated did not directly correlate with the presence of endolymphatic hydrops in this study.

Conclusion: We reject the hypothesis that otologic syphilis is directly related to osteitis, new bone formation, and/or resorption along the course of the endolymphatic duct and sac. Although a change in the endolymphatic system may contribute to the formation of endolymphatic hydrops in otologic syphilis, it is not the only cause. Whether otosyphilis and Ménière's disease share a common mechanism of endolymphatic hydrops formation remains unclear, and the relationship between these causes of hydrops should be investigated further.

*University of California-Los Angeles Division of Head and Neck Surgery, Los Angeles, California; and †Massachusetts Eye and Ear Infirmary, Boston, Massachusetts, U.S.A.

Address correspondence and reprint requests to Akira Ishiyama, M.D., UCLA Division of Head and Neck Surgery, 10833 Le Conte Ave. CHS 62-158, Los Angeles, CA 90095; E-mail:

This work was supported in part by the Otopathology Mini-Travel Fellowship Program of the National Institute on Deafness and Other Communication Disorders Temporal Bone, Hearing and Balance Pathology Resource Registry. This also was funded in part by the National Institutes of Health Grants NIDCD R01 DC-06-001, DC 008635, DC 005028, and DC 005187.

© 2010 Otology & Neurotology, Inc.