Talk:Tooth decay

"Signs and Symptoms" update, "Cause: Introductory paragraph" edit

Thanks Lesion! I updated the signs and symptoms section per your request and I have edited the Cause section. Changes made in the cause section were the following:

1. I thought that a simplified statement on tooth breakdown (demineralization and remineralization) was sufficient for this introduction. The pathophysiology included in this section I've moved to its proper section.

2. Specific bacterial species, I think should be listed in the bacteria section of cause.

3. I've added a source to substantiate the 80% of cavities occuring in pit an fissure surfaces.

4. I stated that severe complications happen in UNTREATED cases of spreading infection.

5. Clarified the bad breath associated with caries derives from debris accumulation.

6. I took the pH of 5.5 out because numerous reputable sources indicate that other factors such as calcium and phosphate in the saliva cause that number to vary substantially.

7. I moved the discussion on Sjogrens and radiation to the other factors section of Cause.

8. The sentence on dental caries not occurring on teeth within bone does not belong in this section and I took it out.

9. The names in parenthesis are reviews I think are needed to substantiate important points. After finding out which review articles will go into the page, I will add the citations. The ones I've added are a review from the New England Journal of Medicine from JH Shaw called Causes and control of dental caries with 108 refs, written in 1987. I added Non-Carious cervical tooth surface loss: A literature review by Ian Wood in the Journal of dentistry 2008. The source on pit and fissure caries (Brown) is from the JADA selected findings from the Third National Health and Nutrition Examination.

Here are my revisions:

Signs and Symptoms

A person experiencing caries may not be aware of the disease.[3] The earliest sign of a new carious lesion is the appearance of a chalky white spot on the surface of the tooth, indicating an area of demineralization of enamel. This is referred to as a white spot lesion, an incipient carious lesion or a "microcavity".[4] As the enamel and dentin are destroyed, the cavity becomes more noticeable. It can turn brown but will eventually turn into a cavitation ("cavity"). Before the cavity forms, the process is reversible, but once a cavity forms, the lost tooth structure cannot be regenerated. A tooth weakened by extensive internal decay can sometimes suddenly fracture under normal chewing forces. A lesion that appears dark brown and shiny suggests dental caries were once present but the demineralization process has stopped, leaving a stain. Active decay is lighter in color and dull in appearance.[5] The affected areas of the tooth change color and become soft to the touch.

Once the caries progress through enamel it can interact with the dentinal tubules, which are passageways to the nerve of the tooth. As these tubules become exposed, pain can results. It may be transient, temporarily worsening with exposure to heat, cold, or sweet foods and drinks.[1] When the decay has progressed enough to allow the bacteria to overwhelm the pulp tissue in the center of the tooth, Death of the pulp tissue (pulp necrosis) and infection are common consequences spontaneous, aching pain and even pain from biting or pressure can often occur, signaling that the caries are now affecting the apex of the tooth.. In these cases, the tooth will no longer be sensitive to hot or cold, but can be very tender to pressure.

Dental caries can also harbor food and bacterial debris that cause bad breath and if the caries have draining abscesses, foul tastes result.[6] In highly progressed cases, infection can spread from the tooth to the surrounding soft tissues. In cases where infection is untreated, complications such as cavernous sinus thrombosis and Ludwig angina can be life-threatening.[7][8][9]

Cause

There are four main criteria required for caries formation: a tooth surface (enamel or dentin), caries-causing bacteria, fermentable carbohydrates (such as sucrose), and time.[10] Bacteria on teeth deposit acid as a byproduct of carbohydrate fermentation. Overtime this leads to breakdown of tooth structure ^(Shaw). However, it is also known that these four criteria are not always enough to cause the disease. A sheltered environment promoting development of a cariogenic biofilm is often required. The caries process does not have an inevitable outcome, and different individuals will be susceptible to different degrees depending on the shape of their teeth, oral hygiene habits, the buffering capacity of their saliva and other factors.[11]

Tooth decay disease is caused by specific types of bacteria that produce acid in the presence of fermentable carbohydrates such as sucrose, fructose, and glucose.[13][14][15]

Acid demineralization occurs where bacterial plaque is left on teeth. Because most plaque-retentive areas are between teeth and inside pits and fissures on chewing surfaces where plaque is more difficult to remove, over 80% of cavities occur here.^(Brown) In contrast, areas of teeth where plaque is more easily removed, such as the front and back surfaces (facial and lingual), develop fewer cavities.

Dental caries is not the only pathology that destroys tooth structure. It should be noted that some acidic foods and drinks can result in tooth demineralization in the absence of bacteria. This is known as erosion, rather than caries, because the acid is not bacterial in origin. Attack by acid from systemic complications such as vomiting can also cause tooth erosion. Other non-carious tooth lesions include abfraction (from occlusal force), attrition (tooth wear) and abrasion (wear from foreign objects like toothbrushes). Many of these conditions occur in the area of teeth nearest the gums and can be grouped into a category called non-carious dental lesions ^(Wood).

Thanks!

Gclive (talk) 14:26, 10 April 2014 (UTC)

"signs and symptoms" edit

As I am editing sections of this page, I'll post them here before definitively editing the page. Here are my first edits to the signs and symptoms. They are not too different from the original and are mostly done to make it more succinct. Here goes:

“ A person experiencing caries may not be aware of the disease.[3] The earliest sign of a new carious lesion is the appearance of a chalky white spot on the surface of the tooth, indicating an area of demineralization of enamel. This is referred to as a white spot lesion, an incipient carious lesion or a "microcavity".[4] As the enamel and dentin are destroyed, the cavity becomes more noticeable. It can turn brown but will eventually turn into a cavitation ("cavity"). Before the cavity forms, the process is reversible, but once a cavity forms, the lost tooth structure cannot be regenerated. A tooth weakened by extensive internal decay can sometimes suddenly fracture under normal chewing forces. A lesion that appears dark brown and shiny suggests dental caries were once present but the demineralization process has stopped, leaving a stain. Active decay is lighter in color and dull in appearance.[5] As the enamel and dentin are destroyed, the cavity becomes more noticeable.

Once the caries progress through enamel, it can interact with the dentinal tubules, which are passageways to the nerve of the tooth. As these tubules become exposed pain can results. It may be transient, temporarily worsening with exposure to heat, cold, or sweet foods and drinks.[1] When the decay has progressed enough to allow the bacteria to overwhelm the pulp tissue in the center of the tooth, a toothache can result and the pain will become more constant. Death of the pulp tissue (pulp necrosis) and infection are common consequences. In these cases, the tooth will no longer be sensitive to hot or cold, but can be very tender to pressure.

Dental caries can also cause bad breath and associated abscesses can cause foul tastes.[6] In highly progressed cases, infection can spread from the tooth to the surrounding soft tissues. Very rare complications such as cavernous sinus thrombosis and Ludwig's angina can be life-threatening.[7][8][9]

”

If you have any concerns or changes, feel free to post.

Geoff — Preceding unsigned comment added by Gclive (talk • contribs) 13:15, 8 April 2014 (UTC)

Sounds good. In the last paragraph, I would switch the order of the sentences because abscesses naturally leads after the comment about spread from the tooth to the surrouning tissues. More detail about bad breath: Halitosis is not caused by caries itself, but rather by stagnation of food debris within large cavities and the activity of bacteria on this debris which releases volatile sulfur compounds. Dental caries doesn't normally cause any odor otherwise. The term Pulpitis should be mentioned imo. Lesion 13:23, 8 April 2014 (UTC)

It is also worth stressing that people do not often die of dental caries anymore. Maybe before antibiotics were discovered this happened more. Lesion 13:24, 8 April 2014 (UTC)

Overall Disorganized

I was disappointed to find this article disorganized and lacking information. I have been reviewing it and made the following points: 1. The introduction of the cause section describes several times the demineralization. A more effective, single paragraph on the issue would suffice in the pathophysiology section. 2. No mention of Non-Carious cervical lesions was made, which are often confused with caries.

3. Toxicities of lead and other ions is interesting, but it might be mentioned, that this is mostly academic, not clinical.

4. Pathophysiology section had an enamel section and three dentin sections. I would recommend consolidating into enamel, dentin, dentinal response, cementum, and then adding the following two, pulp and periodontium/periapex.

4. the diagnosis section didn't mention patient subjective pain being a diagnostic factor. It also didn't discuss vitality testing effectively.

5. The classification section had a picture of GV black's classification, but no mention of Class I, Class II was made in the caption or text.

6. Prevention, I would place dietary modification before oral hygiene if it in fact is the larger impact on caries. I don't recall much being discussed about mouthwash, gum or fluoridated water.

I'm still working my way to treatment, epidemiology and history. But that's what I've found for now. I'm making edits on my laptop and if you have anything else you'd like to discuss with me, please post. Thanks! — Preceding unsigned comment added by Gclive (talk • contribs) 02:53, 27 March 2014 (UTC)

Gclive, hello and welcome. Thanks for offering to work on this article. All Wikipedia articles are a work-in-progress, so there is always room for improvement and scientific knowledge gets updated. For references, please try to use textbooks or review papers for reference, we tend to avoid original research studies, case reports etc. For more info, please see WP:MEDRS. If you require any assistance, just post here. Regards, Lesion (talk) 11:56, 27 March 2014 (UTC)

Epidemiology Section Unclear

It states that caries affect baby teeth in approximately 620 million people. Then it says this is 9% of the population. That's true, but a small percentage of the world population actually has baby teeth since they are usually all lost by age 12. If we add a percentage of BABY teeth that are affected, or a percentage of CHILDREN, it would make the section much more informative.

Would have to give a range of percentages from different countries. I think the proportion of children affected varies from district to district and from country to country. — Preceding unsigned comment added by 212.183.140.5 (talk) 20:51, 27 September 2013 (UTC)

Signs and Symptoms

I elaborated on the Signs and Symptoms section, but perhaps the information could be merged in with the Patho-physiology section.LFlagg (talk) 00:38, 18 June 2013 (UTC)

Not doing this right

Im probably not doing this right, but on this part: Medicinal plants in the treatment of dental caries it lists a bunch of medicinal plants. Why is this listed? Wikipedia should not be giving medical advice. —Preceding unsigned comment added by 69.171.161.105 (talk) 19:51, 26 February 2011 (UTC)

Other Main Factors

It seems to me that there should be a source and quote for users of medical cannabis that also develop dry mouth and decreased saliva production. —Preceding unsigned comment added by Deftdrummer (talk • contribs) 07:16, 12 October 2007 (UTC)

on the subject of cannabis, is it accepted that specifically THC is responsible for reduced saliva? as there are other cannabinols that are associated with the narcotic effects and surely many more compounds that aren't, is there the evidence to suggest that this particular substance is responsible? also the link bewtween cannabis consumption and diets prone to elevated risk of caries should be seen to be anecdotal. even if studies have shown higher risks of caries, this doesn't support this link as other groups surely show both tendenciesDubfeather (talk) 15:17, 14 July 2010 (UTC)

Regarding THC causing reduced saliva and this causing caries, these assertions should be sourced. Preferably, the source will show a strong correlation between THC use and frequency of caries. The amount and duration of decreased saliva caused by THC may be insignificant. 174.252.240.195 (talk) 12:55, 5 July 2011 (UTC)

I think the term "Xerostomia" should be featured in this section. This section lists the many possible causes of Xerostomia (dry mouth) quite well, but maybe could be organized a little better. I think that radiation induced xerostomia should be placed ahead of marijuana induced xerostomia. I believe there is a good deal of literature showing increased caries after radiation induced exerostomia, but little or no scientific literature on increased caries after marijuana induced xerostomia.

As a practicing dentist, I have a strong clinical impression that marijuana use is indeed associated higher levels of tooth decay and the most logical explaination is transient dry mouth, (probably associated with "the munchies"--the tendency to eat snacky foods while under the influence). But we need to primarily focus on factors supported by the literature.

Practicing dentists have many valuable insights worth sharing, but clinical impressions are not a good enough basis for inclusion in Wikipedia unless associated with a scientific article. — Preceding unsigned comment added by LFlagg (talk • contribs) 19:10, 7 January 2012 (UTC)

GA Reassessment

This discussion is transcluded from Talk:Dental caries/GA1. The edit link for this section can be used to add comments to the reassessment.

GA Sweeps: On hold

As part of the WikiProject Good Articles, we're doing Sweeps to determine if the article should remain a Good article. I believe the article currently meets the majority of the criteria and should remain listed as a GA. However, in reviewing the article, I have found there are several issues that need to be addressed.

Citations

1. The "Other general descriptions", "Rate of progression", and "Affected hard tissue" sections are unsourced.
2. In the "Etiology" section, a Dr. Miller is mentioned for the first time. It would be beneficial to indicate the full name as well as cite the quote and three factors.
3. "Before the cavity forms, the process is reversible, but once a cavity forms, the lost tooth structure cannot be regenerated." This statement has been tagged since last month with needing a citation.
4. "The progression and loss of mineralization on the root surface is 2.5 times faster than caries in enamel."
5. "Intrauterine and neonatal lead exposure promote tooth decay." This statement is followed by seven citations. I don't think the statement is controversial, so a few of those could be removed (maybe for sourcing other material or for expanding on the topic).
6. "Occlusal caries accounts for between 80 and 90 percent of caries in children (Weintraub, 2001)" This should be converted to an inline citation similar to the style currently used for the majority of the article.
7. "Older people may also benefit from the use of tooth sealants, but their dental history and likelihood of caries formation are usually taken into consideration." This could use a cite to avoid OR.

Other issues

1. Although it is not required by GA criteria (so it will not be a requirement for the review), it would be beneficial to add alt text to the images. See WP:ALT for assistance.
2. There are multiple dead links that need to be fixed. The Internet Archive may be able to help.
3. There are a few dabs that need to be fixed.
4. "Moreover, sixty-three percent of the most commonly prescribed medications in the United States list dry mouth as a known side effect." Include a year here when this statistic was announced as medication likely changes from year to year.
5. "As of 2004, such a vaccine has been successfully tested on animals,[81] and is in clinical trials for humans as of May 2006." Has there been any updates for this?
6. I don't know if there are guidelines that recommend keeping the history section at the end of the article (if there are, ignore this), but it would probably be beneficial to include it towards the beginning of the article to provide the reader a better understanding of how long caries have around for.
7. The history section also ends around 1920. It would be beneficial to include breakthroughs in treating and understanding caries to be mentioned that have occurred within the last 90 years.

It's great to see the large amount of sourcing and so many free images within the article. I will leave the article on hold for seven days, but if progress is being made and an extension is needed, one may be given. If no progress is made, the article may be delisted, which can then later be renominated at WP:GAN. I'll contact all of the main contributors and related WikiProjects so the workload can be shared. If you have any questions, let me know on my talk page and I'll get back to you as soon as I can. --Happy editing! Nehrams2020 (talk • contrib) 03:27, 7 February 2010 (UTC)

GA Sweeps: Delisted

The article has been on hold for a week and the issues were not addressed. As a result I have delisted the article as it still has a way to go before meeting the GA criteria. Continue to improve the article, addressing the issues above. Once they are addressed, please renominate the article at WP:GAN. I look forward to seeing the further improvement of the article, and don't hesitate to contact me if you need assistance with any of these. If you disagree with this review, a community consensus can be reached at WP:GAR. If you have any questions, let me know on my talk page and I'll get back to you as soon as I can. --Happy editing! Nehrams2020 (talk • contrib) 00:01, 15 February 2010 (UTC)

Genetics

I thought that having cavities was mainly due to genetics. Is this true? I have never had cavities and neither has my entire family, yet I can't say I am the most orally hygienic. — Preceding unsigned comment added by 192.112.54.2 (talk) 20:50, 12 July 2012 (UTC)

List of primary sources added to talk page with no suggestion as to how the article might be improved.

The following papers explain that some caries are due to high lead levels and fluoride doesn't help in these cases.

"Enamel biopsies taken from school children in a community where exposure to lead was a health hazard were analyzed for lead and fluoride. The children with high enamel lead had significantly higher caries scores than the children with low enamel lead, in spite of the fact that the high lead group also was higher in enamel fluoride. There was no increase in enamel lead with age. The lead in saliva was only a fraction of that in blood. Infants with lead poisoning showed higher saliva lead than a normal infant."

•"Lead in Enamel and Saliva, Dental Caries and the Use of Enamel Biopsies for Measuring Past Exposure to Lead" http://jdr.sagepub.com/content/56/10/1165.abstract The fluoride in their teeth did not prevent the caries.

Lead is passed on from mother to child. The child doesn't necessarily have to ingest the lead. It can be transferred by the mother to her offspring, just like fluoride.

See "Association of Dental Caries and Blood Lead Levels" in JAMA. http://jama.jamanetwork.com/article.aspx?articleid=190537

See "Blood lead level and dental caries in school-age children" http://www.ncbi.nlm.nih.gov/pubmed/12361944

"Mean blood lead level was significantly greater among the urban subgroup, as was the mean number of carious tooth surfaces. Blood lead level was positively associated with number of caries among urban children, even with adjustment for demographic and maternal factors and child dental practices."

This study suggests that the fluoridation of water can lead to higher lead levels:

•"Association of silicofluoride treated water with elevated blood lead" PMID: 11233755 http://www.ncbi.nlm.nih.gov/pubmed/11233755

Chronic, low-level dosage of silicofluoride (SiF) has never been adequately tested for health effects in humans. We report here on a statistical study of 151,225 venous blood lead (VBL) tests taken from children ages 0-6 inclusive, living in 105 communities of populations from 15,000 to 75,000. For every age/race group, there was a consistently significant association of SiF treated community water and elevated blood lead. The highest likelihood of children having VBL> 10 microg/dL occurs when they are exposed to SiF treated water and subject to another risk factor known to be associated with high blood lead (e.g., old housing).

"Abstract: Lead, a toxin that lowers dopamine function, has been associated with violent behavior as well as learning deficits. Hydrofluosilicic acid and sodium silicofluoride, which were substituted for sodium fluoride without testing as chemicals for public water treatment, increase absorption of lead from the environment and are associated with violent behavior. Given the costs of incarcerating violent criminals, these side-effects justify a moratorium on using silicofluorides for water treatment until they are shown to be safe."

http://oehha.ca.gov/prop65/public_meetings/052909coms/fluoride/RMasters.pdf — Preceding unsigned comment added by 99.61.178.14 (talk) 01:25, 27 December 2012 (UTC)

• Comment: we need to use reliable secondary sources for medical content WP:MEDRS. Talk pages are for discussion about how to improve the article. Lesion (talk) 00:42, 18 June 2013 (UTC)

Radiation

One sentence reads: "Lasers for detecting caries allow detection without radiation" but lasers, like every other kind of light, are a form of radiation, so it is more appropriate to write: "Lasers for detecting caries allow detection without ionizing radiation" when a comparison with x-rays is made. — Preceding unsigned comment added by 93.146.172.146 (talk) 16:21, 12 August 2012 (UTC)

Good point, I will change this as you suggest. Lesion (talk) 18:05, 6 April 2013 (UTC)

Odontogenic infection redirects here?

Is that really appropriate? If you define an infection as invasion of micrioorganisms into tissues (enamel and dentin etc are tissues) then dental caries could be called an infection (sort of), but odontogenic specifies that it is an infection coming from a tooth. Ideally we need a separate article for odontogenic infection, but for now I feel it would be better to point the odontogenic infection page to dental abscess. Lesion (talk) 18:04, 6 April 2013 (UTC)

I agree. The term odontogenic infection is generally used to refer to a dental abcess, an infection originating from the tooth. Dental caries is not generally referred to as an odontogenic infection. Odontogenic infection should redirect to dental abcess.LFlagg (talk) 23:13, 17 June 2013 (UTC)

I started a new article called odontogenic infection after writing that, but it could do with significant expansion. Alternative is to forget having a separate article and just redirect the page to dental abscess. Lesion (talk) 00:48, 18 June 2013 (UTC)

How is this an evolutionary consideration?

Evolutionary Considerations

Humans are susceptible to dental caries for a variety of reasons, from poor oral hygiene, to lower socio-economic status, to diet. However, these are proximate explanations, and looking at the ultimate cause of caries can offer a different perspective. Tooth decay has been present throughout human history, from early hominids millions of years ago, to modern humans . The prevalence of caries increased dramatically in the 19th century, as the Industrial Revolution made certain items, such as cane sugar and refined flour, readily available. The diet of the “newly industrialized English working class” then became centered on bread, jam, and sweetened tea, greatly increasing both sugar consumption and caries. The ultimate evolutionary explanation for why we are vulnerable to caries is that tooth enamel destroyed by decay cannot be regenerated. Humans, as well as other primates, are diphyodont , or develop only two sets of teeth in their lifetime. This evolutionary legacy is what makes us vulnerable to decay in a modern, sugar-laden diet.

Comments

That peoples diet have changes is not evolution and this aspect is better dealt with in other sections of the article (where it is already). Doc James (talk · contribs · email) (if I write on your page reply on mine) 02:38, 20 November 2013 (UTC)

I think the gist of this addition was that evolution has not caught up with changing diet patterns, same as concept in obesity. Lesion (talk) 10:54, 20 November 2013 (UTC)

Or that we have involved a brain so that as individually we can brush our teeth and as a society we can put together programs of dental coverage such that mortality from dental caries is low in much of the world.

We are not now going to involve more resistant teeth as people do not typically die from caries before reproductive age. Doc James (talk · contribs · email) (if I write on your page reply on mine) 10:58, 20 November 2013 (UTC)

Good point. Teeth were only ever meant to make us survive into reproductive age. Yes loss of teeth may have once meant you risked starvation, but this is not likely anymore. The only thing I might argue would be that people with decayed looking teeth might be less attractive to the opposite sex and therefore less likely to reproduce, but this theory would hinge on people not visiting a dentist and fixing their teeth.

I don't have a huge problem with this section, but if you think it is unsuitable happy for it to be removed. Lesion (talk) 11:19, 20 November 2013 (UTC)

The issues around diet are better dealt with in other section IMO. Doc James (talk · contribs · email) (if I write on your page reply on mine) 12:06, 20 November 2013 (UTC)

User:CzechmateVV who added this is in user:Sanetti's Darwinian medicine class. CzechmateVV, could you respond to the above criticism? There is feedback that you have not mentioned anything about evolution, but you put this content into an evolution section, and that the content you added to some people seems better suited for integration into other parts of this article. Thanks for your attention. Blue Rasberry (talk) 14:28, 20 November 2013 (UTC)

Thank you for your feedback. I was focusing on the evolution of human vulnerability to dental caries, namely that diet changes influenced their prevalence. Where would you suggest I move this to instead? CzechmateVV (talk) 02:48, 21 November 2013 (UTC)

How about here [1] Doc James (talk · contribs · email) (if I write on your page reply on mine) 03:36, 21 November 2013 (UTC)

Because you talk about the industrial revolution, putting it in Dental_caries#History would be appropriate. There is no discussion of evolution in the text added. Blue Rasberry (talk) 14:33, 21 November 2013 (UTC)

I think James might be right when you think about it. The vulnerability of the dental hard tissues to demineralization in acidic mileau has not changed. Environmental factors such as fluoridated water supply and toothpastes on the one hand, and the high "cariogenic diet" on the other are what has changed. It is not the diet in and of itself that is cariogenic, because you could eat such a diet every day through a nasogastric tube and never get any tooth decay. Although instinctive attraction to such a diet is the result of evolution, this is not evolution in the Darwinian sense since it has not lead to any genetic change. Rather, this is changing disease prevalence due to (modifiable) environmental factors. Lesion (talk) 12:29, 21 November 2013 (UTC) Edited. CzechmateVV (talk) 04:42, 24 November 2013 (UTC)

Diagrams

I added the classic circle diagram.

Suggest also need a Stephan Curve

Perhaps also a chemical reaction diagram to show transfer of the various ions from saliva into dental hard tissues above critical pH and from hard tissues to saliva below critical pH. Lesion (talk) 16:16, 28 March 2014 (UTC)

Caries risk

I think a section about caries risk assessment should be included in this page. Sa2lehmann (talk) 01:00, 10 April 2014 (UTC)

Sa2lehmann, this would be good. Are you interested in writing it? Lesion 08:15, 10 April 2014 (UTC)

Related Links

E.g. dental carries vaccines page on Wikipedia — Preceding unsigned comment added by 24.10.208.192 (talk) 04:00, 4 June 2014 (UTC)

Update: Cause:Teeth,bacteria, fermentable carbohydrates, exposure, other factors

Here is my revision to the sections above. Changes I made were adding an introduction to the teeth section, describing the demineralization of teeth in the teeth section, adding species of bacteria and a couple citations by Lang (from oral microbiology and immunology 2007) and Kianoush on pH gradient and distribution of strep species. I also deleted a controversial sentence on THC causing xerostomia and added a reference on poverty and caries.

Variables that may increase caries risk are disorders in tooth formation, exposure of regions of the tooth that are more susceptible to demineralization and the anatomy and location of teeth in the oral cavity.

The mineral content of teeth is sensitive to increases in acidity from the production of lactic acid (a product of carbohydrate fermentation). As the acidity lowers the environmental pH, the tooth will begin to demineralize. To be specific, the hydroxyapatite mineral in a tooth is in equilibrium with the surrounding saliva. However, when the pH of saliva or bacterial products drops to below 5.5 (Although this number may be higher or lower depending on the calcium and phosphate concentrations in saliva), the hard crystalline structure of the tooth dissolves, because the demineralization is occurring faster than the remineralization; a net decrease in mineralization. This is called bacterial acid demineralization.

There are certain diseases and disorders affecting teeth that may leave an individual at a greater risk for cavities. Amelogenesis imperfecta, which occurs between 1 in 718 and 1 in 14,000 individuals, is a disease in which the enamel does not fully form or forms in insufficient amounts and can fall off a tooth.[16] In both cases, teeth may be left more vulnerable to decay because the enamel, which is more structurally sound and resistant to acid demineralization than dentin, is not able to protect the tooth.[17]

In most people, disorders or diseases affecting teeth are not the primary cause of dental caries. Approximately 96% of tooth enamel is composed of minerals.[18] These minerals, especially hydroxyapatite, will become soluble when exposed to acidic environments. Enamel begins to demineralize at a pH of 5.5.[19] Dentin and cementum are more susceptible to caries than enamel because they have lower mineral content.[20] As a result, dentin and cementum can demineralize at a less acidic pH than enamel. Thus, when root surfaces of teeth are exposed from gingival recession or periodontal disease, caries can develop more readily. Even in a healthy oral environment, however, the tooth is susceptible to dental caries.

The evidence for linking malocclusion and/or crowding to the dental caries is weak;[21][22] however, the anatomy of teeth may affect the likelihood of caries formation. Where the deep developmental grooves of teeth are more numerous and exaggerated, pit and fissure caries are more likely to develop (see next section). Also, caries are more likely to develop when food is trapped between teeth.

Bacteria

The mouth contains a wide variety of oral bacteria, but only a few specific species of bacteria are believed to cause dental caries: Streptococcus mutans, streotococcus sobrinus and Lactobacilli species (Lang). These organisms can produce high levels of lactic acid following fermentation of dietary sugars, and are resistant to the adverse effects of low pH, properties essential for cariogenic bacteria.[13][15] It is thought that as the caries initiates with streptococcus species, but as the caries process progresses the bacterial populations shift more toward lactobacillus due to their resilience to very low pH (Kianoush). As the cementum of root surfaces is more easily demineralized than enamel surfaces, a wider variety of bacteria can cause root caries including Lactobacillus acidophilus, Actinomyces spp., Nocardia spp., and Streptococcus mutans.

S. mutans produces a sticky, extracellular, dextran-based polysaccharide that allows them to cohere, forming plaque biofilm. S. mutans produces this dextran via the enzyme dextransucrase (a hexosyltransferase) using sucrose as a substrate. Some sites collect plaque more commonly than others, for example sites with a low rate of salivary flow (molar fissures). Grooves on the occlusal surfaces of molar and premolar teeth provide microscopic retention sites for plaque bacteria, as do the interproximal sites. Plaque may also collect above or below the gingiva where it is referred to as supra- or sub-gingival plaque, respectively.

These bacterial strains, most notably S. mutans can be transmitted to a child from a caretaker's kiss or through feeding premasticated food.[23] Once colonized early by streptococcus mutans, children may be predisposed to developing caries lesions thoughout their lives.

Fermentable carbohydrates.

Bacteria in a person's mouth ferment glucose, fructose and, most commonly, sucrose (table sugar) and create acid byproducts such as lactic acid glycolyticfermentation.[14] The impact such sugars have on the progress of dental caries is called cariogenicity. Sucrose, which is formed from glucose and fructose bound together, is more cariogenic than a mixture of equal parts of glucose and fructose. This is due to the bacteria utilizing the energy in the saccharide bond between the glucose and fructose subunits. S.mutans creates the sticky dextran polysaccharide by using sucrose as a substrate.

Exposure

The frequency of which teeth are exposed to cariogenic (acidic) environments affects the likelihood of caries development.[26] After meals or snacks, the bacteria in the mouth metabolize sugar, resulting in an acidic by-product that decreases pH. During every exposure to the acidic environment, portions of the inorganic mineral content at the surface of teeth dissolve and can remain dissolved for two hours.[27] As time progresses, the pH returns to normal due to the buffering capacity of saliva. Due to the lag in return to normal pH, consistent bouts of sugar meals prevent the pH of saliva from returning to normal and further aid bacterial deposition of acid byproducts. Since teeth are vulnerable during acidic periods, the development of dental caries relies heavily on the frequency of acid exposure.

The carious process can begin within days of a tooth's erupting into the mouth if the diet is sufficiently rich in suitable carbohydrates. Evidence suggests that the introduction of fluoride treatments have slowed the process.[28] Proximal caries take an average of four years to pass through enamel in permanent teeth.

Other risk factors

Reduced salivary flow rate is associated with increased caries since the buffering capability of saliva is not present to counterbalance the acidic environment created by certain foods. As a result, medical conditions and medications that reduce the amount of saliva produced by salivary glands, in particular the submandibular gland and parotid gland, are likely cause dry mouth and thus predisposition to widespread tooth decay. Examples include Sjögren's syndrome, diabetes mellitus, diabetes insipidus, and sarcoidosis.[29] Medications, such as antihistamines and antidepressants, can also impair salivary flow. Stimulants, most notoriously methylamphetamine ("meth mouth"), also occlude the flow of saliva to an extreme degree. Moreover, 63% of the most commonly prescribed medications in the United States list dry mouth as a known side-effect.[29] Radiation therapy of the head and neck may also damage the cells in salivary glands, increasing the likelihood of caries formation.[30][31]

The use of tobacco may also increase the risk for caries formation. Some brands of smokeless tobacco contain high sugar content, increasing susceptibility to caries.[32] Tobacco use is a significant risk factor for periodontal disease, which can cause the gingiva to recede.[33] As the gingiva loses attachment to the teeth due to gingival recession, the root surface becomes exposed in the mouth. If this occurs, root caries is a concern since the cementum covering the roots of teeth is more easily demineralized by acids than enamel.[34] Currently, there is not enough evidence to support a causal relationship between smoking and coronal caries, but evidence does suggest a relationship between smoking and root-surface caries.[35]

Intrauterine and neonatal lead exposure promote tooth decay.[36][37][38][39][40][41][42] Besides lead, all atoms with electrical charge and ionic radius similar to bivalent calcium,[43] such as cadmium, mimic the calcium ion and therefore exposure may promote tooth decay.[44] These findings, while scientifically significant, are not routinely screened for clinically.

Poverty is also a significant social determinant for oral health.[45] Dental caries have been linked with lower socio-economic status and can be considered a disease of poverty.[46] This is especially true of children and adolescents. (Reisine)

~~Gclive — Preceding unsigned comment added by Gclive (talk • contribs) 00:32, 29 April 2014 (UTC)

Vertical Transmission and Evolutionary Factors of Streptococcus mutans that increased its cariogenicity

I think providing information on the evolutionary forces that lead to S. mutans’s ability to cause dental caries can enhance this article.

1. One of the characteristics that make S. mutans the primary etiological agents for caries is its ability to adhere to the hard surfaces of teeth through formation of biofilms. It is thought that the bacteria acquired the gene to do this through horizontal gene transfer with other lactic acid producing bacteria, such as Lactobacillus. The gene under study is glucosyltranferase, or gtf.

2. Throughout evolutionary history, S. mutans has also acquired adaptations that have increased its fitness in the oral cavity. These traits include improved carbohydrate metabolism and greater acid tolerance. It is estimated that there are currently 14 genes under selection that contribute to these adaptations.

3. Lastly, I'd like to suggest that more detail be provided regarding vertical transmission of S. mutans, which is most often from mother (or caretaker) to child. This is listed in the article, but I would like to provide research findings that support this form of transmission. For example, it was previous thought that S. mutans isn't found in the oral cavity until young children's teeth erupt. However, studies have shown S. mutans to be present in the grooves of the tongue on pre-dentate infants. This suggests support for vertical transmission from mother to child shortly after birth.

Conkle.30 (talk) 20:33, 30 September 2014 (UTC)

This is probably better on the article about the bacteria itself. Maybe some here to I guess. Doc James (talk · contribs · email) (if I write on your page reply on mine) 20:54, 30 September 2014 (UTC)

@Jmh649 - Thank you for your suggestion. When I add my final material to Wikipedia, I'll add it to the S. mutans page specifically. I can see how the evolutionary history pertains more to the bacteria rather than the disease. Perhaps I'll just add the section about vertical transmission to the dental caries page and the in depth evolutionary information to the S. mutans page. Conkle.30 (talk) 15:59, 8 October 2014 (UTC)

Content

Have moved this to the article about the bacteria " It is believed that Streptococcus mutans acquired the gene that enables it to produce biofilms though horizontal gene transfer with other lactic acid bacterial species, such as Lactobacillus. " Overly specific for here IMO. Doc James (talk · contribs · email) (if I write on your page reply on mine) 22:55, 30 September 2014 (UTC)

@Jmh649 - As I mentioned above, I agree with your edit. Thank you for organizing and moving my post. Conkle.30 (talk) 16:01, 8 October 2014 (UTC)

Cavitated v Non-cavitated lesion

I understand this page is going to translation soon, so I thought I'd post here first. The article is really well done. Under the diagnosis and treatment section, I don't see any reference to a positive stick with the explorer or interproximal caries that extend into dentin on BWs. Both of the these are tradition (and commonly used) criteria for operative treatment. Even if these concepts have given way to newer criteria, I think rewording the 1st paragraph of the treatment section might be worthwhile to better explain what cavitation or non-cavitation is.

Other minor stuff. The picture of "cavity" and "dental caries" could be higher quality. If it's OK, I'll take some new ones and post. Finally, the 1st paragraph is 5 short sentences and difficult to read. I'm not sure who's active here. I'm happy to take a stab and rewording or if someone else has been polishing the article, it might be worth another look. In the meantime, I'll try to get more info on cavitated v non-cavitated lesions. Ian Furst (talk) 19:59, 31 December 2014 (UTC)

Hey Ian. The plan is to only translate the first 4 paragraphs. For translation short sentences are much prefered over long ones. Have combined two particularly short ones though :-) Would love better pictures. Doc James (talk · contribs · email) 05:25, 1 January 2015 (UTC)

I thought that might have been a factor in the sentence structure. I'll get some more photos Monday or Tuesday and put them up.Ian Furst (talk) 18:52, 1 January 2015 (UTC)

Doc James have you sent it yet? Can I play with the 1st four paragraphs a bit? Ian Furst (talk) 02:36, 6 January 2015 (UTC)

Sure. As the body is not being translated am wanting to keep the lead very well referenced. Also trying to use simpler words and short sentences to make it easier for the translators.

Would love to have your helping improve the leads of other dentistry related articles aswell :-) Doc James (talk · contribs · email) 15:46, 6 January 2015 (UTC)

Formatting

Matthew Ferguson Thank you. I'm happy to edit this page some more but I do find it a bit of a struggle and only do bits at a time! Npt1 I see you are having some difficulty with wikipedia's formatting. Don't worry too much about this, I will tidy it up after you are done editing. Many thanks for your help, Matthew Ferguson (talk) 12:04, 18 July 2015 (UTC)

Choice of 2 Stefan curves. Which is best?

Thoughts? Matthew Ferguson (talk) 17:30, 15 August 2015 (UTC)

Unnecessary mass of references in the lead

We current have this one sentence "Caries are also associated with poverty, poor cleaning of the mouth, and receding gums resulting in exposure of the roots of the teeth." supported by 7 refs when all that was needed was two.

• This is a literature review from 2014

• This is a meta analysis from 2015

We do not need these 5

• Review but we have a newer one

• A systematic review but we have a newer one

• Primary source

• This is a primary source

Doc James (talk · contribs · email) 12:05, 16 August 2015 (UTC)

Remineralization - reversal of dental caries.

In the intro, we currently say: "There is no known method to grow back large amounts of tooth." http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4226000/ however, says "They have developed a patented technology for the regeneration of enamel. The monomers of peptide p11-4 (curodont) forms a matrix [that] enables de novo enamel crystal formation from saliva in constant equilibrium with demineralization [19]. In vivo studies revealed that the peptides were shown to decrease demineralization and show a strong trend toward increasing remineralization [20]." (and mentions other progress on tooth regeneration) So while I doubt we have the MEDRS sources to put "There is a known method to grow back very significant amounts of tooth." in the intro, I do think the intro needs some editing in light of this development.

We should have a bit more data in Dec 2016 and Dec 2017. A very promising clinical safety trial is too preliminary.--Elvey^(t•c) 21:29, 4 December 2015 (UTC)

selective excavation

http://www.ncbi.nlm.nih.gov/pubmed/25511906 suggests selective excavation is best practice, so I think the first sentence of the following needs revision; it conflicts with the second one: "Before a restoration can be placed, all of the decay must be removed otherwise it will continue to progress underneath the filling. Sometimes a small amount of decay can be left if it is entombed and the there is a seal which isolates the bacteria from their substrate."--Elvey^(t•c) 21:29, 4 December 2015 (UTC)

Elvey agree should be mentioned if not already. the technique you refer to is called stepwise caries removal or indirect pulp cap. Pulp_capping#Indirect_pulp_cap (stepwise_caries_removal). Matthew Ferguson (talk) 04:01, 5 December 2015 (UTC)

Other prevention

@Johngorman101: thank you for adding the content about other types of prevention. @Doc James: thank you for adding the page number. I tweaked the reference to include both page 6-7 since the content is covered on both pages. Sydney Poore/FloNight♥♥♥♥ 15:29, 10 March 2016 (UTC)

Ah yes see it. Have adjusted the text to better match. Doc James (talk · contribs · email) 17:43, 10 March 2016 (UTC)

We need to know more about Resin Infiltration for Proximal Caries!

http://www.ncbi.nlm.nih.gov/pubmed/?term=proximal+caries+infiltration

http://www.ncbi.nlm.nih.gov/pubmed/26545080

88.192.242.201 (talk) 12:31, 3 April 2016 (UTC)