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Objective: The aim of this study was to determine the response of the residual epithelial network following traumatic breakdown of the periodontal ligament (PDL)., Methods: Mandibular incisor sections with PDL (experimental) and sections denuded of PDL (control) from 4- to 6-week-old Wistar-Furth rats were transplanted into the defects created in the frontal bone of the recipient syngeneic rats. At intervals, the defects with implanted teeth roots were collected and processed for histological and biochemical examination. Immunolocalization of epithelial cells was performed to monitor their phenotypic changes during transplantation healing period., Results: (1) Histological observation of the experimental sample revealed the sequence of cellular response characterized by an initial degeneration of PDL followed by a proliferation of granulation tissue. There was also a marked odontoblastic reaction with extensive deposition of regular dentine within the pulp chambers. In the control group, initial signs of bony fusion with dentine led to an extensive ankylosis and bone replacement between roots and defects. (2) Immunostaining indicated that, in experimental groups, the pattern of regularly spaced epithelial cells lying in close approximation to the root surface was distinct 10 days post-transplantation but became diminished afterwards. The immunoreaction against epithelial cells was negative in the control., Conclusion: Residual PDL is essential to prevent ankylosis after trauma and epithelial cells may facilitate the re-establishment of root-PDL-bone complex by transforming into mesenchymal cells.

Dental trauma represents one of the few situations where dentists are called upon to make unscheduled diagnostic and treatment decisions in an area that is outside their routine experience. Since patients who sustain an avulsion present infrequently, except in child-oriented or emergency-based practices, clinicians often make diagnostic and management decisions based upon their previous rare treatment experiences. Clinicians also rely on published guidelines for this aspect of their practice and expect these standards to be up-to-date and based on current research information. None of the current protocols has been tested by a prospective longitudinal outcome study in humans. Nevertheless, current guidelines have become the standard for clinical practice around the world. An effort must be made to develop treatment protocols that are based upon the biological mechanisms that underlie periodontal wound healing.

Previous studies have indicated that inflammatory resorption and ankylosis, which are frequent sequela after delayed tooth replantation, can be greatly reduced by treating the root surface with 1% solutions of stannous fluoride and tetracycline. However, the SnF2 conditioning leaves a long-standing inflammatory reaction in the periodontal ligament. To examine whether a more dilute SnF2 solution would reduce postoperative inflammation without jeopardizing any beneficial effects, anterior teeth in three young adult beagles were extracted and allowed to air-dry for 45 min. They were then immersed in 0.1% SnF2 for 5 min, rinsed in saline, immersed in 1% doxycycline HCl for 5 min, rinsed, and replanted. Control teeth were air-dried and replanted without further treatment. Block biopsies were harvested after 4 wk of healing and processed for histometric analysis. In experimental teeth, 85% of the root surface area showed normal healing, compared to 33% in control teeth. Conversely, resorption and ankylosis were more frequent in controls than in experimental teeth. A persisting inflammatory reaction either adjacent to or at a distance from the root surface was seen in limited areas in both experimental and control teeth. Compared to preceding studies, the findings indicate that reducing the strength of the SnF2 solution from 1% to 0.1% may result in less persistent inflammation, at the cost, however, of less complete prevention of inflammatory resorption and ankylosis.

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.