Abstract
ABSTRACT Objective: This study investigated the presence of inflammatory response in the dental pulp of rats showing hypersensitive dentin, induced by erosive episodes. Methods: Sixteen Wistar rats were fed with commercial sucrose-free pellet diet for 12 hours; whereas the food was removed during the remainder of the day, and the animals received mineral water or a lemon-based sucrose-free soft drink, according to the group to which they belonged. Eight animals consumed the soft drink to induce hypersensitivity, while the other 8 animals received mineral water (control). After six weeks, the animals were euthanized, the mandible was removed and subjected to a median incision in the sagittal plane, to obtain right and left hemimandibles. The slides stained with hematoxylin-eosin were analyzed using light microscopy. Results: Histological evaluation of the control and experimental groups revealed no inflammatory process in the pulp tissue, and the presence of inflammatory cells, such as lymphocytes, plasma cells, eosinophils and macrophages, was not observed. In addition, there was no edema or dilated and congested blood vessels. The Mann-Whitney test showed no significant difference (p = 1.000) between the experimental and the control groups. Conclusion: In the animal model used, dentin hypersensitivity does not trigger dental pulp inflammatory response.
Highlights
Dentin hypersensitivity is characterized by chronic, yet short-lasting pain, caused by thermal, osmotic, chemical or evaporative stimuli due to the exposure of the dentinal tubules to the oral environment [1,2] producing symptoms that cannot be explained by any other dental pathology [3].Among the sources responsible for the exposure of the dentin tubules is dental erosion, caused mainly by dietary or gastric acids [4]
From a pathophysiological point of view, dentin hypersensitivity has been attributed to the movement of fluid inside the dentin tubules, which would trigger the nerve endings in both the vicinity and inside the pulp tissue [1]
Based on the potential relationship between dentin hypersensitivity and pulp inflammation and considering the feasibility of employing animal models to provide such conditions, this study aimed to investigate the existence of inflammatory response in the pulp of rats upon creating dental erosion to induce dentin hypersensitivity
Summary
Dentin hypersensitivity is characterized by chronic, yet short-lasting pain, caused by thermal, osmotic, chemical or evaporative stimuli due to the exposure of the dentinal tubules to the oral environment [1,2] producing symptoms that cannot be explained by any other dental pathology [3].Among the sources responsible for the exposure of the dentin tubules is dental erosion, caused mainly by dietary or gastric acids [4]. Dental erosion has been associated with the localization and the initiation of dentin hypersensitivity [2,5]. From a pathophysiological point of view, dentin hypersensitivity has been attributed to the movement of fluid inside the dentin tubules, which would trigger the nerve endings in both the vicinity and inside the pulp tissue [1]. It has been suggested, the possibility that an inflammatory response within the dental pulp may coexist [6]. There have been, only very few initiatives in the literature that intended to investigate the pulp reactions in hypersensitive dentin [8,9,10]
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