Dentoalveolar ankylosis and associated root resorption in replanted teeth. Experimental and clinical studies in monkeys and man.

Periodontal pathology is an unavoidable complication following replantation of avulsed teeth. The present thesis focuses on the etiology, diagnosis, progression and prevention of dentoalveolar ankylosis. The experimental studies were carried out both in vitro and in vivo. Clinical studies were also performed on the progression of ankylosis. Initially, it was determined that the histomorphometrical method used in the animal studies was sufficiently accurate for the estimation of an area of a root surface showing a defined condition. In vivo studies revealed that the periodontal membrane (PDM) of a tooth prevented from drying for one hour before replantation heals without root resorption and ankylosis in a similar manner to an immediately replanted tooth. However, replantation of a tooth with a necrotic PDM results in a rapid destruction of the root by inflammatory resorption. These observations were predicted from the results of the in vitro studies, indicating that data gained from in vitro work may contribute to our understanding of periodontal healing in replanted teeth. Prevention or elimination of inflammatory resorption results in increased dentoalveolar ankylosis. Masticatory stimulation during the healing period will maximize the area of functional PDM and minimize dentoalveolar ankylosis. Antibiotics should be administered as early as possible and endodontic treatment should be performed within the first weeks after replantation to prevent inflammatory resorption. Accurate diagnosis of dentoalveolar ankylosis by assessment of percussion sound and mobility is only possible when more than 20 percent of the root surface is ankylotic. Radiographic diagnosis of ankylosis is of limited value in the early stages of replacement resorption. The rate of replacement resorption was shown to be age related. Even though replacement resorption is present, a tooth in an older individual can remain functional for a long period, possibly throughout life. Furthermore, residual infection and associated periodontal inflammation may be moderating factors in the progression of replacement resorption.