Editing Tooth decay (section)

====Sclerotic dentin====
The structure of dentin is an arrangement of microscopic channels, called [[Dental canaliculi|dentinal tubules]], which radiate outward from the pulp chamber to the exterior cementum or enamel border.<ref>Ross, Michael H., Kaye, Gordon I. and Pawlina, Wojciech (2003) ''Histology: a text and atlas.'' 4th edition, p. 450. {{ISBN|0-683-30242-6}}.</ref> The diameter of the dentinal tubules is largest near the pulp (about 2.5&nbsp;μm) and smallest (about 900&nbsp;nm) at the junction of dentin and enamel.<ref name="cate152">[[#Nanci|Nanci]], p. 166</ref> The carious process continues through the dentinal tubules, which are responsible for the triangular patterns resulting from the progression of caries deep into the tooth. The tubules also allow caries to progress faster.

In response, the fluid inside the tubules brings [[immunoglobulin]]s from the [[immune system]] to fight the bacterial infection. At the same time, there is an increase of mineralization of the surrounding tubules.<ref name="summit13">Summit, James B., J. William Robbins, and Richard S. Schwartz. ''Fundamentals of Operative Dentistry: A Contemporary Approach'' 2nd edition. Carol Stream, Illinois, Quintessence Publishing Co, Inc, 2001, p. 13. {{ISBN|0-86715-382-2}}.</ref> This results in a constriction of the tubules, which is an attempt to slow the bacterial progression. In addition, as the acid from the bacteria demineralizes the hydroxyapatite crystals, calcium and [[phosphorus]] are released, allowing for the precipitation of more crystals which fall deeper into the dentinal tubule. These crystals form a barrier and slow the advancement of caries. After these protective responses, the dentin is considered sclerotic.

According to [[Hydrodynamic theory (dentistry)|hydrodynamic theory]], fluids within dentinal tubules are believed to be the mechanism by which pain receptors are triggered within the pulp of the tooth.<ref>{{cite journal |vauthors=Dababneh RH, Khouri AT, Addy M |title=Dentine hypersensitivity&nbsp;– an enigma? A review of terminology, mechanisms, aetiology and management |journal=British Dental Journal|volume=187 |issue=11 |pages=606–11; discussion 603 |date=December 1999 |pmid=16163281 |doi=10.1038/sj.bdj.4800345a}}</ref> Since sclerotic dentin prevents the passage of such fluids, pain that would otherwise serve as a warning of the invading bacteria may not develop at first.