Osteoradionecrosis of the Temporal Bone
Joseph B. Nadol, Jr.
Although the effects of radiation on bone have been known for many years (1), its effects on the temporal bone and labyrinth received little attention before 1950. Radiation-induced damage has been described in the external auditory canal, middle ear, ossicular chain, mastoid, petrous apex, and membranous labyrinth. Osteoradionecrosis of the temporal bone may be defined as death and sequestration of the bone following radiation therapy to the temporal bone or surrounding structures, such as the nasopharynx. Ramsden et al. (2) described two distinct clinical forms of osteoradionecrosis: localized, involvement of the tympanic bone that resolves after separation of sequestration; and diffuse, necrosis of the temporal bone resulting in secondary injury to brain, labyrinth, facial nerve, and carotid artery. Clinical signs of osteoradionecrosis may occur many years following administration of radiation.
RADIATION EFFECTS ON THE TEMPORAL BONE
External and Middle Ear
Isolated lesions induced by radiation therapy may be seen in the external ear canal and, less commonly, in the middle ear. Borsanyi (3) described necrosis of the skin of the external ear canal in approximately 10% of 100 patients who received radiation therapy for nasopharyngeal carcinoma and other tumors in the head and neck. In a study of 29 patients with osteoradionecrosis, Ramsden et al. (2) found that the most common manifestation of osteoradionecrosis of the temporal bone was necrosis of tympanic bone of the floor or anterior wall of the external auditory canal. Osteoradionecrosis of the ossicles has also been described (4, 5, 6).
Labyrinth
Hearing loss, which may be severe to profound, may occur months or years after radiation therapy to the temporal bone (7,8). The incidence of sensorineural loss may reach 36% of patients who have received a full course of radiation (7), and in some cases vestibular damage has also been described. The effect of radiation on the membranous labyrinth as studied in an animal model (9) includes delayed degeneration of sensory and supporting cells in the organ of Corti and loss of auditory neurons. In this animal model of radiation labyrinthitis, a linear relationship between radiation dose and the percent of missing outer hair cells and supporting cells was found. In addition, significant loss of myelinated nerve fibers was seen in areas unassociated with hair cell loss, suggesting that degenerative neuropathy may be an additional and primary effect.
Mastoid and Petrous Apex
More diffuse osteoradionecrosis of the temporal bone may occur, resulting in intracranial complications (2). Although this diffuse form is most common in individuals with radiation therapy directed primarily at lesions within the temporal bone (2), diffuse and progressive osteoradionecrosis may occur in cases in which the temporal bone was not the primary focus of radiation (10,11). The incidence of diffuse osteoradionecrosis increases with radiation dose. Cole (12) found clinical evidence of osteoradionecrosis in 19% of 21 patients treated with radiation therapy for glomus jugulare tumors. In a series of 20 patients treated with surgery and postoperative radiation therapy (13), osteoradionecrosis was described in 25%. Wang and Doppke (14) reported that osteoradionecrosis may be minimized by limiting the radiation dose to 2,000 rets (nominal standard dose equivalent to 7,400 rads in 37 fractions at a rate of 5 fractions per week). Nadol and Schuknecht (10) described an incidence of osteoradionecrosis of 42% in cases of squamous cell carcinoma of the temporal bone that were treated with surgery resulting in an open mastoid cavity, followed by full-course radiation therapy, whereas in another group of patients receiving an average dose of 4,610 rads, no osteoradionecrosis occurred despite an open cavity technique, suggesting both a positive correlation with radiation dosage and the possibility of a threshold phenomenon.
RADIOBIOLOGY AND HISTOPATHOLOGY OF OSTEORADIONECROSIS
Ewing (1) described three clinical situations that predisposed to osteoradionecrosis: (i) proximity of bone to the body surface, (ii) superinfection or trauma, and (iii) poor blood supply. The primary response appears to be a vasculitis and inhibition of mitosis. There is evidence of progressive vascular damage over time, including endarteritis, thrombosis, and progressive ischemia (15), with no evidence of spontaneous microvascularization with time. Hence, the risk of osteoradionecrosis increases continuously after radiation therapy.