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Research Article

Effect of denervation on healing after tooth replantation in the ferret

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Pages 379-385 | Published online: 02 Jul 2009
 

Abstract

Studies have shown that the sensory nerves participate in inflammation and immune responses and possess trophic-facilitating wound healing in general. Tooth avulsion represents a pulpal and periodontal injury, and the mechanisms involved in the healing responses subsequent to replantation of teeth are still unclear. The objective of this study was to investigate the healing responses after denervation and replantation of teeth. Unilateral denervation was performed in 15 ferrets by axotomy of the inferior alveolar nerve, 5 days before extraction of the first lower premolars. Six weeks later the mandibles were excised and processed for histological evaluation. Immunohistochemistry was performed using antibodies against the sensory neuropeptides substance P (SP) and calcitonin gene-related peptide (CGRP), and measurements of root resorption and ankylosis were performed in four sections from each replanted tooth. After 6 weeks substantial reinnervation was observed in the jaws. Immunoreactivity in the pulp was observed in only two replanted teeth on the denervated side, compared with four on the innervated side. Total pulp necrosis appeared in 10 replanted teeth on the denervated side and in 5 on the innervated, indicating that sensory nerves promote survival of the pulp after replantation. SP-immunoreactive (IR) fibers were more frequently observed in the resorptive lacunae than CGRP-IR fibers. However, resorptive areas lacking IR fibers were frequently found along the root surface. Root resorption averaged 0.062 &#45 0.029 mm2 on the innervated side compared to 0.016 &#45 0.0043 mm2 on the denervated (P < 0.02). Ankylosis was observed in four of the replanted teeth on the innervated side (169.3 &#45 49.7 µm) and in six on the denervated side (332.56 &#45 193.2 µm) (P = 1). It is concluded that the sensory nerves promote root resorption after pulpoperiodontal injuries but have less influence on the osteoblastic activity expressed by ankylosis.

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