Calcific metamorphosis of pulp after extrusive luxation

Background/Aim The literature on the pathogenesis of extrusive dental luxation has been focused on periodontal tissue responses, with little attention given to the pulp. The aim of this study was to evaluate the response of dental pulp of teeth following extrusive luxation in a rat model. Material a...

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Published in:Dental traumatology Vol. 35; no. 2; pp. 87 - 94
Main Authors: Queiroz, Alfredo Franco, Hidalgo, Mirian Marubayashi, Consolaro, Alberto, Panzarini, Sônia Regina, França, Alline Batistussi, Pires, Willian Ricardo, Poi, Wilson Roberto
Format: Journal Article
Language:English
Published: Denmark Wiley Subscription Services, Inc 01-04-2019
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Summary:Background/Aim The literature on the pathogenesis of extrusive dental luxation has been focused on periodontal tissue responses, with little attention given to the pulp. The aim of this study was to evaluate the response of dental pulp of teeth following extrusive luxation in a rat model. Material and Methods The maxillary right central incisors of 30 rats were extrusively luxated and repositioned after 5 minutes. The animals were euthanized after 7, 15, and 30 days to provide three groups: I, II, and III, respectively (n = 10). Histological sections were stained with H and E for histomorphometric analysis of the odontoblast layer, reparative dentin deposition, Hertwig's epithelial root sheath, pulp necrosis, and periapical inflammatory infiltrate. Results In most cases, new vascular formation occured in association with reparative dentin deposition on the root walls and within the pulp. In some cases, dentin deposition occupied the entire pulp space over time, with no other types of non‐odontogenic hard tissues being observed. Pulp necrosis with the presence of periapical inflammatory infiltrate was also observed in a few cases. No statistical differences were observed among the studied groups. Conclusions Following extrusive luxation, calcific metamorphosis of the pulp is very likely to occur.
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ISSN:1600-4469
1600-9657
DOI:10.1111/edt.12456