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Our understanding of erosive tooth wear and its contributing factors has evolved considerably over the last decades. New terms have been continuously introduced, which frequently describe the same aspects of this condition, whereas other terms are being used inappropriately. This has led to unnecessary confusion and miscommunication between patients, professionals, and researchers. A group of 15 experts, selected by the European Organization for Caries Research (ORCA) and the Cariology Research Group of the International Association for Dental Research (IADR), participated in a 2-day workshop to define the most commonly used terms in erosive tooth wear. A modified Delphi method was utilized to reach consensus. At least 80% agreement was achieved for all terms discussed and their definitions related to clinical conditions and processes, basic concepts, diagnosis, risk, and prevention and management of erosive tooth wear. Use of the terms agreed on will provide a better understanding of erosive tooth wear and intends to enable improved communication on this topic., (© 2019 S. Karger AG, Basel.)

Dentine hypersensitivity (DH) is a common, painful dental condition with a multi-factorial aetiology. The hydrodynamic mechanism theory to explain dentine sensitivity also appears to fit DH: lesions exhibiting large numbers of open dentinal tubules at the surface and patent to the pulp. By definition, DH can only occur when dentine becomes exposed (lesion localisation) and tubules opened (lesion initiation), thus permitting increased fluid flow in tubules on stimulation. Erosion, particularly from dietary acids appears to play a dominant role in both processes. Toothbrushing with most toothpaste products alone cause clinically insignificant wear of enamel but are additive, even synergistic, to erosive enamel loss. Additionally, toothbrushing with toothpaste is implicated in 'healthy' gingival recession. Toothbrushing with most toothpastes removes the smear layer to expose tubules and again can exacerbate erosive loss of dentine. These findings thereby implicate toothbrushing with toothpaste in the aetiology of DH. Management of the condition should have secondary prevention at the core of treatment and therefore, must consider first and foremost the aetiology. Fluoride toothpaste at present appears to provide little primary or secondary preventive benefits to DH; additional ingredients can provide therapeutic benefits. Potassium-based products to block pulpal nerve response have caused much debate and are considered by many as unproven, which should not translate to ineffective. Several toothpaste technologies formulated to block tubules are from studies in vitro, in situ and controlled clinical trials considered proven for the treatment of DH., (Copyright © 2013 S. Karger AG, Basel.)

Because of the difficulties in measuring erosion in vivo, a number of in vitro and in situ models have been developed and validated. These models are flexible and informative, allowing single as well as multiple variables to be examined under specific conditions using accurate measurement techniques over defined timelines, thus yielding useful data without harmful effects on individuals. This information, together with clinical findings, is essential for clinicians advising susceptible patients appropriately regarding the management of their condition. Little guidance is available, however, on the standardisation of in vitro and in situ protocols for erosive tooth wear studies, so it is difficult to make meaningful comparisons between investigations as experimental variables differ widely from study to study. The aim of this review was to collate the available data on models designed to assess erosive challenges which are severe enough to cause tissue loss as opposed to just softening of the surface structure. The different types of models, with their merits and pitfalls, are documented. Test substrates, disinfecting regimens and ethical considerations are discussed. The aims of this paper are to give guidance to the researcher on evidence-based in vitro and in situ erosive tooth wear methodology and to suggest best practice given current knowledge., (Copyright © 2011 S. Karger AG, Basel.)

Dentine hypersensitivity is a common oral complaint, affecting the teeth of many individuals. The aetiology is multifactorial; however, over recent years the role of erosion has become more and more important. For dentine hypersensitivity to occur, the lesion must first be localised on the tooth surface and then initiated to exposed dentine tubules which are patent to the pulp. The short, sharp pain symptoms are thought to be derived from the hydrodynamic theory of pain. This episodic pain condition is likely to become a more frequent dental complaint in the future due to the increase in longevity of the dentition and the rise in tooth wear. However, conclusive evidence of successful treatment regimens still eludes us despite a multitude of products available for treatment. In explanation, pain studies are notoriously difficult to conduct due to the subjective nature of pain and the complexity of pain assessment. The basic principles of treatment are altering fluid flow in the dentinal tubules with tubule occlusion or modifying or blocking pulpal nerve response, chemically with agents like potassium or physically.

The palatal aspect of upper anterior teeth appears to be one site of predilection for erosion. This raises the question of whether abrasion of softened enamel and dentine by the tongue has a role in this process. The aim of this study in vitro was to determine whether enamel and dentine specimens licked by the tongue after exposure to acid lost more tissue than when exposed to acid alone. Flat enamel and dentine specimens were prepared from human third molars and taped to expose a window of tissue. Three groups of specimens were exposed to citric acid for 10 min followed by 60 s tongue licking, ultrasonication or immersion in water. Two further groups of enamel specimens were placed in a low erosive drink for 10 min with or without licking. At the end of 5, 10 and 15 treatment cycles tissue loss was measured by profilometry. Enamel loss was significantly greater with licking and ultrasonication compared to water immersion. Dentine loss was greater with licking and ultrasonication compared to water immersion, but differences only reached significance for ultrasonication. The low erosive drink produced one third of the citric acid erosion and licking had no effect. The results suggest that the tongue could exert an abrasive effect on dental tissues softened by erosion, thereby increasing the overall loss of tooth substance., (2004 S. Karger AG, Basel.)

The aim of this study was to use ultrasonication and profilometry as methods to study de- and remineralisation of citric acid-eroded enamel at different pH values. Seventy-eight polished human enamel samples were divided into three test and three control groups of 13 specimens each. Three specimens of each group were chosen for SEM examination. The samples were exposed to 0.3% citric acid at pH 2.54, 3.2 or 4.5 for 2 h. The depths of the resulting lesions were measured by profilometry. The test groups were placed in artificial saliva and the control groups were stored in saline (0.9% NaCl) for 24 h and new profiles recorded. Finally all specimens were ultrasonicated in water for 5, 30, 120, 240 and 480 s with profilometric measurements at each time point. Ultrasonication of the test groups after remineralisation showed little effect on the lesion depth, whereas the control groups had an enamel loss of 2.1 microm at pH 2.54, 2.9 microm at pH 3.2 and 0.4 microm at pH 4.5 after 30-second ultrasonication. These differences from respective test groups were statistically significant at pH 2.54 and 3.2 but not at pH 4.5. Ultrasonication of control pH 2.54 and 3.2 specimens removed an amorphous covering layer to reveal a flattened surface with prisms outlined by prism boundaries. It can be concluded that remineralisation in artificial saliva stabilises the surface softened enamel against ultrasonication.

The aim of this study was to use ultrasonication as a method to measure subsurface demineralisation of enamel. Polished human enamel samples with surface profiles within +/-0.3 microm were divided into 6 groups of 10 specimens. The groups of specimens were exposed to 0. 3% citric acid (pH 3.2) for 30 min, 1, 2, 3 or 4 h. The depths of the resulting lesions were measured using a profilometer. A control group was stored in water for 4 h. Ultrasonication in water was performed on the specimen groups for 5, 30, 120, 240 and 480 s with profilometric measurements at each time point. The depth of the erosion increased linearly with the exposure time. Most of the additional loss of enamel occurred with the 5-second ultrasonication. The 30-min and 1-hour erosion lesions were further deepened by approximately 1 microm with 5 s of ultrasonication. The 2-, 3- and 4-hour lesions were deepened by 2-4 microm with 5 s of ultrasonication. There were no changes in the control group. It is concluded that ultrasonication removed softened enamel from the surface of the eroded enamel. Ultrasonication together with accurate measurement of lesion depth by profilometry offers a useful method for studying the depth of enamel softening associated with erosion.