Periodontal Disease

A somewhat obscure etiologic theory for facial neuralgias presumes a low-grade osteomyelitis of the jaws that produces neural degeneration with subsequent production of inappropriate pain signals. Animal investigations and treatment successes with human patients based on this theory lend it credence. The present study examined 224 tissue samples removed from alveolar bone cavities in 135 patients with trigeminal neuralgia or atypical facial neuralgia. All tissue samples demonstrated clear evidence of chronic intraosseous inflammation. The most common microscopic features included dense marrow fibrosis or “scar” formation, a sprinkling of lymphocytes in a relative absence of other inflammatory cells (especially histiocytes), and smudged, nonresorbing necrotic bone flakes. Very little healing or new bone formation was visible. These lesions were able to burrow several centimeters to initiate distant cavities. The present preliminary investigation cannot prove etiology, but the presence of intraosseous inflammation in every single jawbone specimen in these patients and certain clinical and treatment aspects of these lesions (to be reported later) has led the authors to recommend the term neuralgia-inducing cavitational osteonecrosis or NICO for these lesions.

A patient with a history of trauma to the maxillary left anterior region presented with chronic pain of unknown etiology. Root canal therapy and periradicular surgery failed to resolve the persistent pain. A second surgical procedure revealed a bone cavity superior and distopalatally to the apex of the maxillary left lateral incisor. The suspected etiology was necrotic bone removed from the bone cavity.

A 32-yr-old white North American male resident of Norway presented with an asymptomatic radiolucency first identified 3 yr after the removal of an impacted mandibular right third molar in Southern California 16 yr previously. Surgical exploration revealed an intraosseous cavity filled with a black, homogeneous, gelatinous substance thought to be foreign material, but which was diagnosed histologically as containing black yeasts. Cultivation of a microbiologic sample for 6 wk grew black yeast-like colonies. The yeast isolate was identified as an Aureobasidium species different from the typical A. pullulans. A blood sample was negative with regard to antibodies both with double diffusion technique and ELISA. Also, examination with respect to dermatologic manifestations gave negative results. Flucytocin 10 g/d was administered systemically for 30 d. Six months postoperatively bone regeneration was satisfactory radiologically.

Light and electron microscopy were used to analyze nine therapy-resistant and asymptomatic human periapical lesions, which were removed as block biopsies during surgical treatment of the affected teeth. The cases that required surgery represented about 10% of all of the cases which received endodontic treatment and root fillings during the period 1977 to 1984. These cases revealed periapical lesions when they were examined 4 to 10 yr after treatment. The biopsies were processed for correlated light and electron microscopy. Six of the nine biopsies revealed the presence of microorganisms in the apical root canal. Four contained one or more species of bacteria and two revealed yeasts. Of the four cases in which bacteria were found, only in one biopsy could they be found by light microscope. In the other three specimens, the bacterial presence could be confirmed only after repeated electron microscopic examination of the apical root canal by serial step-cutting technique. Among the three cases in which no microorganisms could be encountered, one showed histopathological features of a foreign body giant cell granuloma. These findings suggest that in the majority of root-filled human teeth with therapy-resistant periapical lesions, microorganisms may persist and may play a significant role in endodontic treatment failures. In certain instances such lesions may also be sustained by foreign body giant cell type of tissue responses at the periapex of root-filled teeth.

Clinical reports on several cases of treatment of the pain syndrome resulting from residual bone cavitiesi from extracted teeth with which etiology and symptoms are very similar to idiopathic trigeminalneuralgia or atypical facial pain. A new surgical technique is employed to successfully alleviate virtually all of the syri1ptoms and facilitates total remission of the facial pain and the “Phantom Tooth” syndrome.

One case of Garre’s osteomyelitis involving the mandible was seen, treated and documented. It was treated by extraction of the causal infected tooth with no supplement of antibiotics. The patients experienced a complete regression of the lesion within six months.

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.

Material consisting of 16 patients examined and/or treated under the diagnosis osteomyelitis is reported. A description is given of the history, etiology, clinical and radiographic findings, results of histologic and microbiologic examinations, blood chemistry, diagnostic subgroups, findings at operation and the surgical and antibiotic therapy used. The results of treatment at short-term follow-up are given. Of nine patients observed 5 months or longer, six showed signs of healing, while the result was judged as uncertain in two cases and unsuccessful in one.

A simple, one-time procedure has been employed in the treatment of localized alveolar osteitis of the mandible and maxilla. One application affords the patient significant relief from pain and promotes rapid healing.

The subject of osteomyelitis of the upper and lower jaws is very large and complicated. In this communication the general and anatomic considerations pertaining to this subject will first be discussed.