This animal experimental study (144 cats) was designed to allow observation of the healing processes at the oval window following stapedectomy during the first two postoperative weeks. The first 61 animals (Series I) had no oval window cover except for a blood clot which might form spontaneously. The second 64 animals (Series II) had Gelfoam® as a cover to the oval window following stapedectomy. A third series of 19 animals had temporalis fascia used as the oval window cover, and these ears were studied histologically for up to nine weeks. The unoperated ear acted as a control for the operated ear in all animals and after the animals were killed, both temporal bones were decalcified, imbedded in celloidin, serially sectioned at 20μ, and every tenth section stained and mounted for histologic study. It was observed that oval window closure was effected by endosteal, periosteal, and fibrous tissue proliferation from the traumatized tissues about the oval window fenestra, and that this process was facilitated by the presence of some type of scaffolding material such as a blood clot or Gelfoam®. Temporalis fascia placed in the oval window was observed to be rapidly incorporated into a much thicker oval window neomembrane and to seal the fenestra promptly. Partial removal of the footplate also facilitated more rapid closure of the smaller oval window fenestra, but fibrous tissue and new bone formation was noted to form about bony fragments still attached at the oval window level. Free bony fragments within the vestibule were not observed to stimulate new bone formation. Suppuration was observed most frequently in Series I (no oval window cover), with 67.8% of these animals having some degree of otitis media. In Series II (Gelfoam® cover) 20.6% had otitis media, and in Series III (temporalis fascia) 21% had middle ear infection. Suppuration markedly impaired but did not completely prevent the oval window reparative processes. Animals having some type of oval window cover were noted to have a lesser incidence of suppurative labyrinthine involvement when otitis media was present. Other labyrinthine complications were observed, including endolymphatic hydrops, Wittmaack's hypotonic atrophy, as well as RBC, fibrin, and albuminous precipitates in the labyrinth. Hypotonic atrophy was observed in a high incidence of animals having rupture of one or more endolymphatic structures, suggesting a mechanical mechanism as one possible explanation for this condition. Hypotonic atrophy may represent the end-stage (collapse) in the fluctuant endolymphatic ballooning of hydrops which is seen when saccular or Reissner's membrane ruptures have occurred.
18F-NaF PET/CT imaging of bone formation induced by bioactive glass S53P4 after mastoid obliteration