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Dentin hypersensitivity is a relatively common condition. [4] [3] Due to differences in populations studied and methods of detection, the reported incidence ranges from 4-74%. [3] Dentists may under-report dentin hypersensitivity due to difficulty in diagnosing and managing the condition. [4]
Epidemiological surveys have shown that dentine hypersensitivity arises when the dentinal tubules are both exposed and patent. It was proposed that if the hydrodynamic fluid flow was responsible for hypersensitivity, then there must be higher numbers of dentinal tubules exposed at the surface of the root and patent to the dental pulp.
Hypersensitivity is most commonly caused by a lack of insulation from the triggers in the mouth due to gingival recession (receding gums) exposing the roots of the teeth, although it can occur after scaling and root planing or dental bleaching, or as a result of erosion. [19] The pulp of the tooth remains normal and healthy in dentin ...
Tertiary dentin is only formed by an odontoblast directly affected by a stimulus; therefore, the architecture and structure depend on the intensity and duration of the stimulus, e.g., if the stimulus is a carious lesion, there is extensive destruction of dentin and damage to the pulp, due to the differentiation of bacterial metabolites and toxins.
Your tooth's enamel, cementum, and dentin usually protect the pulp, but if any of those layers are damaged or irritated, the pulp can get inflamed. Cue the pain.
If the attrition is severe, the enamel can be completely worn away leaving underlying dentin exposed, resulting in an increased risk of dental caries and dentin hypersensitivity. It is best to identify pathological attrition at an early stage to prevent unnecessary loss of tooth structure as enamel does not regenerate.
Frictional keratosis: This typically presents as white plaques on the oral mucosa due to mechanical trauma. When the cause of frictional keratosis is removed the white patch may resolve. Hyperplastic reactive lesions or nodular swellings: These occur in the oral mucosa due to low grade inflammation or trauma. They develop where the mucosa is ...
In the case of an infection breaching the dentin to or very near the pulp, or in the instance of odontoblast death due to other attack (e.g. chemical or physical), undifferentiated mesenchymal cells can differentiate into odontoblast-like cells which then secrete another type, reparative dentin, underneath the site of attack.