Editing Tooth decay (section)

==Pathophysiology==
[[File:Dental carries anaerobic fermentation.tiff|thumb|443x443px|Microbe communities attach to tooth surface and create a biofilm. As the biofilm grows an anaerobic environment forms from the oxygen being used. Microbes use sucrose and other dietary sugars as a food source. The dietary sugars go through anaerobic fermentation pathways producing lactate. The lactate is excreted from the cell onto the tooth enamel then ionizes. The lactate ions demineralize the hydroxyapatite crystals causing the tooth to degrade.]]
[[File:Pit-and-Fissure-Caries-GIF.gif|thumb|150px|alt=Animated image showing the shape progression of a caries lesion in the fissure of a tooth.|The progression of pit and fissure caries resembles two triangles with their bases meeting along the junction of enamel and dentin.]]

Teeth are bathed in saliva and have a coating of bacteria on them ([[biofilm]]) that continually forms. The development of biofilm begins with [[Dental pellicle|pellicle]] formation. Pellicle is an acellular proteinaceous film which covers the teeth. Bacteria colonize on the teeth by adhering to the pellicle-coated surface. Over time, a mature biofilm is formed, creating a cariogenic environment on the tooth surface.<ref>{{Cite book|title=Dental caries : the disease and its clinical management|url=https://archive.org/details/dentalcariesdise00ofej|url-access=limited|publisher=Blackwell Munksgaard|others=Fejerskov, Ole., Kidd, Edwina A. M.|year=2008|isbn=978-1-4051-3889-5|edition=2nd|location=Oxford|pages=[https://archive.org/details/dentalcariesdise00ofej/page/n190 166]–169|oclc=136316302}}</ref><ref>{{Cite book|title=Pickard's manual of operative dentistry|last=Banerjee, Avijit.|others=Watson, Timothy F.|year=2011|isbn=978-0-19-100304-2|edition=Ninth|location=Oxford|pages=2|oclc=867050322}}</ref> The minerals in the hard tissues of the teeth {{ndash}} enamel, dentin and cementum {{ndash}} are constantly undergoing demineralization and remineralization. Dental caries result when the demineralization rate is faster than the remineralization, producing net mineral loss, which occurs when there is an ecologic shift within the dental biofilm from a balanced population of microorganisms to a population that produces acids and can survive in an acid environment.<ref>Fejerskov O, Nyvad B, Kidd EA (2008) "Pathology of dental caries", pp 20–48 in Fejerskov O, Kidd EAM (eds) ''Dental caries: The disease and its clinical management''. Oxford, Blackwell Munksgaard, Vol. 2. {{ISBN|1444309285}}.</ref>

===Enamel===
Tooth enamel is a highly mineralized acellular tissue, and caries act upon it through a chemical process brought on by the acidic environment produced by bacteria. As the bacteria consume the sugar and use it for their own energy, they produce lactic acid. The effects of this process include the demineralization of crystals in the enamel, caused by acids, over time until the bacteria physically penetrate the dentin. [[Enamel rod]]s, which are the basic unit of the enamel structure, run perpendicularly from the surface of the tooth to the dentin. Since demineralization of enamel by caries follows the direction of the enamel rods, the different triangular patterns between pit and fissure and smooth-surface caries develop in the enamel because the orientation of enamel rods are different in the two areas of the tooth.<ref name="kidd">{{cite journal |vauthors=Kidd EA, Fejerskov O |title=What constitutes dental caries? Histopathology of carious enamel and dentin related to the action of cariogenic biofilms |journal=Journal of Dental Research|volume=83 Spec No C |pages=C35–8 |year=2004 |pmid=15286119 |doi=10.1177/154405910408301S07|s2cid=12240610 }}</ref>
<!--- The preceding sentence is unclear to the uninitiated reader --->

As the enamel loses minerals, <!--- Is this an acceptable way to put it? ---> and dental caries progresses, the enamel develops several distinct zones, visible under a light microscope. From the deepest layer of the enamel to the enamel surface, the identified areas are the: translucent zone, dark zones, body of the lesion, and surface zone.<ref>{{cite journal |author=Darling AI |title=Resistance of the enamel to dental caries |journal=Journal of Dental Research|volume=42 |issue=1 Pt2 |pages=488–96 |year=1963 |pmid=14041429 |doi=10.1177/00220345630420015601|s2cid=71450112 }}</ref> The translucent zone is the first visible sign of caries and coincides with a one to two percent loss of minerals.<ref>{{cite journal |vauthors=Robinson C, Shore RC, Brookes SJ, Strafford S, Wood SR, Kirkham J |title=The chemistry of enamel caries |journal=Critical Reviews in Oral Biology & Medicine|volume=11 |issue=4 |pages=481–95 |year=2000 |pmid=11132767 |doi=10.1177/10454411000110040601}}</ref> A slight remineralization of enamel occurs in the dark zone, which serves as an example of how the development of dental caries is an active process with alternating changes.<ref>[[#Nanci|Nanci]], p. 121</ref> The area of greatest demineralization and destruction is in the body of the lesion itself. The surface zone remains relatively mineralized and is present until the loss of tooth structure results in a cavitation.

===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.

===Cementum===
The incidence of cemental caries increases in older adults as gingival recession occurs from either trauma or periodontal disease. It is a chronic condition that forms a large, shallow lesion and slowly invades first the root's cementum and then dentin to cause a chronic infection of the pulp (see further discussion under classification by affected hard tissue). Because dental pain is a late finding, many lesions are not detected early, resulting in restorative challenges and increased tooth loss.<ref>Fehrenbach, MJ and Popowics, T (2026). ''Illustrated Dental Embryology, Histology, and Anatomy'', 6th edition. Elsevier, p. 194.</ref>