Aetiology and risk factors
The aetiology of dentin hypersensitivity is based primarily
on in vitro and in situ data, case report data and epidemio-
logical surveys, not randomised controlled clinical studies.
For dentin hypersensitivity to occur, the dentin surface of a
tooth must be exposed (lesion localisation) and a number of
dentin tubules in close proximity to each other must be
patent from the pulp to the oral environment (lesion initia-
tion) [10]. There is no evidence that there is a differentiation
between coronal and radicular dentin hypersensitivity. How-
ever, another name for the condition was coined by the 2002
Workshop of the European Federation of Periodontology
[43], root sensitivity, without evidence to support a different
diagnosis and management strategy. Nevertheless, there are
interesting differences in the dentin of crown and root, and
throughout its structure. In the crown, the tubules follow a
double curved course but in the root and beneath the incisal
tips, the tubules take a straighter course [44]. The circum-
ference of the dentin at the peripheral part of the root or
crown is much greater then nearer the pulp, leading to the
columnar appearance of the odontoblasts as they are
squashed together especially over the pulp horns [45]; the
convergence of this unique structural organisation estimated
at 4:1 [46] or 3:1 [47]. The number of tubules per unit area
and radius of the tubules increases from enamel-cemental
junction (~20,000 per mm2) to the pulp (~45,000 per mm2),