Editing Tooth decay (section)

===Dentin===
Unlike enamel, the dentin reacts to the progression of dental caries. <!--- It was unclear in the preceding section that enamel '*does not* react to the progression of caries ---> After [[Animal tooth development|tooth formation]], the [[ameloblast]]s, which produce enamel, are destroyed once [[amelogenesis|enamel formation]] is complete and thus cannot later regenerate enamel after its destruction. On the other hand, dentin is [[dentinogenesis|produced]] continuously throughout life by [[odontoblast]]s, which reside at the border between the pulp and dentin. Since odontoblasts are present, a stimulus, such as caries, can trigger a biologic response. These defense mechanisms include the formation of sclerotic and [[tertiary dentin]].<ref>"[http://www.usc.edu/hsc/dental/PTHL312abc/312b/09/Reader/reader_set.html Teeth & Jaws: Caries, Pulp, & Periapical Conditions] {{webarchive|url=https://web.archive.org/web/20070506034332/http://www.usc.edu/hsc/dental/PTHL312abc/312b/09/Reader/reader_set.html |date=2007-05-06 }}," hosted on the [http://www.usc.edu/hsc/dental/ University of Southern California School of Dentistry] {{webarchive|url=https://web.archive.org/web/20051207020003/http://www.usc.edu/hsc/dental/ |date=2005-12-07 }} website. Page accessed June 22, 2007.</ref>

In dentin from the deepest layer to the enamel, the distinct areas affected by caries are the advancing front, the zone of bacterial penetration, and the zone of destruction.<ref name="kidd"/> The advancing front represents a zone of demineralized dentin due to acid and has no bacteria present. The zones of bacterial penetration and destruction are the locations of invading bacteria and ultimately the decomposition of dentin. The zone of destruction has a more mixed bacterial population where proteolytic enzymes have destroyed the organic matrix. The innermost dentin caries has been reversibly attacked because the collagen matrix is not severely damaged, giving it potential for repair.

[[File:Smooth Surface Caries GIF.gif|thumb|150px|left|alt=Animated image showing the shape progression of a caries lesion in the cervical region of a tooth.|The faster spread of caries through dentin creates this triangular appearance in smooth surface caries.]]

====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.

====Tertiary dentin====
{{See also|Tertiary dentin}}
In response to dental caries, there may be production of more dentin toward the direction of the pulp. This new dentin is referred to as tertiary dentin.<ref name="cate152"/> Tertiary dentin is produced to protect the pulp for as long as possible from the advancing bacteria. As more tertiary dentin is produced, the size of the pulp decreases. This type of dentin has been subdivided according to the presence or absence of the original odontoblasts.<ref name="transdentinal">{{cite journal |vauthors=Smith AJ, Murray PE, Sloan AJ, Matthews JB, Zhao S |title=Trans-dentinal stimulation of tertiary dentinogenesis |journal=Advances in Dental Research|volume=15 |pages=51–4 |date=August 2001 |pmid=12640740 |doi=10.1177/08959374010150011301|s2cid=7319363 }}</ref> If the odontoblasts survive long enough to react to the dental caries, then the dentin produced is called "reactionary" dentin. If the odontoblasts are killed, the dentin produced is called "reparative" dentin.

In the case of reparative dentin, other cells are needed to assume the role of the destroyed odontoblasts. [[Growth factor]]s, especially [[TGF beta|TGF-β]],<ref name="transdentinal"/> are thought to initiate the production of reparative dentin by [[fibroblast]]s and [[Mesenchymal stem cell|mesenchymal]] cells of the pulp.<ref name="summit14">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. 14. {{ISBN|0-86715-382-2}}.</ref> Reparative dentin is produced at an average of 1.5&nbsp;μm/day, but can be increased to 3.5&nbsp;μm/day. The resulting dentin contains irregularly shaped dentinal tubules that may not line up with existing dentinal tubules. This diminishes the ability for dental caries to progress within the dentinal tubules.