The possible role of dental and oral disease in the etiology of idiopathic trigeminal and atypical
facial neuralgias has been examined. Among thirty-eight patients with
idiopathic trigeminal neuralgia and twenty-three patients with atypical
facial neuralgia, there was in nearly all instances a close relationship between
pain experienced and the existence of cavities in alveolar bone and jawbone of the patients. The cavities were at the sites of previous
tooth extractions and, although at times more than 1 cm. in a given diameter, were usually not detectable by x-rays. A new method for their detection and localization was developed empirically, based on the observation that peripheral infiltration of
local anesthetic into or very close to the bone cavity rapidly abolished trigger and pain perception by patients during persistence of the
anesthetic action. Histopathologic examination of bone removed from cavities by
curettage revealed, in both idiopathic trigeminal and atypical
facial neuralgias, a similar pattern characterized by a highly vascular abnormal healing response of bone. Some lesions presented a mild chronic inflammatory (lymphocytic) infiltration. Preliminary microbiologic studies of material from the walls of the cavities showed the existence within them of a complex, mixed polymicrobial aerobic and anaerobic flora. Treatment consisted of vigorous
curettage of the bone cavities, repeated if necessary, plus administration of
antibiotics to induce healing and filling-in of the cavities by new bone. Responses of patients to the above treatment consisted of marked to complete
pain remissions, the longest of which has been for 9 years. Complete healing leads to complete and persistent
pain remissions. It was concluded that in both idiopathic trigeminal and atypical
facial neuralgias, dental and oral pathoses may be major etiologic factors.