Ten Years Experience with Fluoride in Otosclerotic (Otospongiotic) Patients

Moderate dosage of sodium fluoride (NaF) (40 to 60 mg daily) has been used for ten years in more than 4,000 patients with active otospongiosis of the cochlear capsule. Initially the indication for this therapy was a positive Schwartze sign in a patient with progressive sensorineural impairment after successful fenestration or stapes surgery. Beginning in 1965 positive polytomographic evidence of a demineralized focus in the cochlear capsule has been the indication. Of the more than 4,000 patients that have received this treatment half were in Chicago and half in Beziers, France, the treatment lasting from one to as long as eight years in a few cases. Stabilization of the sensorineural component of loss, recalcification of the focus by polytomography and fading of a positive Schwartze sign are evidences of a favorable result. The results in surgically confirmed stapedial fixation otospongiosis and in pure cochlear otospongiosis are fairly uniform and consistent in the patients treated in Beziers and those treated in Chicago. A few patients have experienced a slight but significant recovery of sensorineural hearing. About 80% show stabilization of the sensorineural component of loss, while the remainder continue to show slow progression in the sensorineural loss. A smaller control group of cases that for one reason or another did not receive the medication show that progression in the sensorineural loss occurred in a much higher percentage than in the treated cases. Of interest were cases initially stabilized after fluoride therapy with improved appearance of the cochlear capsule by polytomography. The fluoride was then stopped, with reactivation of the focus two to seven years later as demonstrated by polytomography, resumption of the sensorineural progression and in some cases a positive Schwartze sign. A maintenance dose of 20 mg daily is now advised the rest of the patient's life. Our current practice is to prescribe one 20 mg enteric coated tablet of NaF after breakfast and supper with a half gram of calcium gluconate chewed up before each of these meals, and one multivitamin tablet daily to supply 400 units of Vitamin D. This is continued for two years when polytomography is repeated, the Schwartze sign is determined and the hearing tested. If the process is not arrested, the fluoride is increased to 60 mg daily for two years. A bone survey at the onset of therapy is repeated every two years to detect any beginning skeletal fluorosis. A small number of patients do not tolerate the medication due to side effects. In another small group the process continues to progress despite therapy. Our conclusion is that moderate dosage NaF is effective in 80% of cases in stabilizing the sensorineural component of loss by causing a vascular spongy expanding focus to become mature, recalcified and inactive. The toxic enzymes liberated by the active focus appear to be the mechanism of the sensorineural deterioration. Sodium fluoride acts partly as an enzyme inhibitor and partly to decrease osteoclastic resorption and to increase calcification of the focus thus arresting its activity.