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Published in: Clinical Oral Investigations 1/2013

Open Access 01-03-2013 | Review

Dentin hypersensitivity: pain mechanisms and aetiology of exposed cervical dentin

Authors: N. X. West, A. Lussi, J. Seong, E. Hellwig

Published in: Clinical Oral Investigations | Special Issue 1/2013

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Abstract

Objectives

The paper’s aim is to review dentin hypersensitivity (DHS), discussing pain mechanisms and aetiology.

Materials and methods

Literature was reviewed using search engines with MESH terms, DH pain mechanisms and aetiology (including abrasion, erosion and periodontal disease).

Results

The many hypotheses proposed for DHS attest to our lack of knowledge in understanding neurophysiologic mechanisms, the most widely accepted being the hydrodynamic theory. Dentin tubules must be patent from the oral environment to the pulp. Dentin exposure, usually at the cervical margin, is due to a variety of processes involving gingival recession or loss of enamel, predisposing factors being periodontal disease and treatment, limited alveolar bone, thin biotype, erosion and abrasion.

Conclusions

The current pain mechanism of DHS is thought to be the hydrodynamic theory. The initiation and progression of DHS are influenced by characteristics of the teeth and periodontium as well as the oral environment and external influences. Risk factors are numerous often acting synergistically and always influenced by individual susceptibility.

Clinical relevance

Whilst the pain mechanism of DHS is not well understood, clinicians need to be mindful of the aetiology and risk factors in order to manage patients’ pain and expectations and prevent further dentin exposure with subsequent sensitivity.
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Metadata
Title
Dentin hypersensitivity: pain mechanisms and aetiology of exposed cervical dentin
Authors
N. X. West
A. Lussi
J. Seong
E. Hellwig
Publication date
01-03-2013
Publisher
Springer-Verlag
Published in
Clinical Oral Investigations / Issue Special Issue 1/2013
Print ISSN: 1432-6981
Electronic ISSN: 1436-3771
DOI
https://doi.org/10.1007/s00784-012-0887-x

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