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Calculus (dental)

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This article is about the dental problem. For other uses, see Calculus (disambiguation).
Heavy staining and calculus deposits exhibited on the lingual surface of the mandibular anterior teeth, along the gumline.
Calculus deposit on x-ray image

In dentistry, calculus or tartar is a form of hardened dental plaque. It is caused by precipitation of minerals from saliva and gingival crevicular fluid (GCF) in plaque on the teeth. This process of precipitation kills the bacterial cells within dental plaque, but the rough and hardened surface that is formed provides an ideal surface for further plaque formation. This leads to calculus buildup, which compromises the health of the gingiva (gums). Calculus can form both along the gumline, where it is referred to as supragingival ("above the gum"), and within the narrow sulcus that exists between the teeth and the gingiva, where it is referred to as subgingival ("below the gum").

Calculus formation is associated with a number of clinical manifestations, including bad breath, receding gums and chronically inflamed gingiva. Brushing and flossing can remove plaque from which calculus forms; however, once formed, it is too hard and firmly attached to be removed with a toothbrush. Calculus buildup can be removed with ultrasonic tools or dental hand instruments (such as a periodontal scaler).

Etymology

Calcis, in Greek, was a term used for various kinds of stones, coming from the term for limestone. This spun off many modern words, including "calculate" (use stones for mathematical purposes), and "calculus", which came to be used, in the 18th century, for accidental or incidental mineral buildups in human and animal bodies, like kidney stones and minerals on teeth.[1]

Tartar, on the other hand, originates in Greek as well, but as the term for the white encrustation inside casks, aka potassium bitartrate commonly known as cream of tartar. This came to be a term used for calcium phosphate on teeth in the early 19th century.[2]

Calculus composition

Calculus is composed of both inorganic (mineral) and organic (cellular and extracellular matrix) components. The mineral proportion of calculus ranges from approximately 40–60%, depending on its location in the dentition,[3] and consists primarily of calcium phosphate crystals organized into four principal mineral phases: octacalcium phosphate, hydroxyapatite, whitlockite, and brushite. The organic component of calculus is approximately 85% cellular and 15% extracellular matrix.[3] Cell density within dental plaque and calculus is very high, consisting of an estimated 200,000,000 cells per milligram.[4][5] The cells within calculus are primarily bacterial, but also include at least one species of archaea (Methanobrevibacter oralis) and several species of yeast (e.g., Candida albicans). The organic extracellular matrix in calculus consists primarily of proteins and lipids (fatty acids, triglycerides, glycolipids, and phospholipids),[3] as well as extracellular DNA.[4][6] Trace amounts of host, dietary, and environmental microdebris are also found within calculus, including salivary proteins,[7] plant DNA,[8] milk proteins,[9] starch granules,[10] textile fibers,[11] and smoke particles.[12]

Calculus formation

The processes of calculus formation from dental plaque are not well understood. Supragingival calculus formation is most abundant on the buccal (cheek) surfaces of the maxillary molars and on the lingual (tongue) surfaces of the mandibular incisors.[13] These areas experience high salivary flow because of their proximity to the parotid and sublingual salivary glands. Subgingival calculus forms below the gumline and is typically darkened in color by the presence of black-pigmented bacteria,[13] whose cells are coated in a layer of iron obtained from heme during gingival bleeding.[14] Dental calculus typically forms in incremental layers[15] that are easily visible using both electron microscopy and light microscopy.[7] These layers form during periodic calcification events of the dental plaque,[13] but the timing and triggers of these events are poorly understood. The formation of calculus varies widely among individuals and at different locations within the mouth. Many variables have been identified that influence the formation of dental calculus, including age, gender, ethnic background, diet, location in the oral cavity, oral hygiene, bacterial plaque composition, host genetics, access to professional dental care, physical disabilities, systemic diseases, tobacco use, and drugs and medications.[13]

Clinical significance

Plaque accumulation causes the gingiva to become irritated and inflamed, and this is referred to as gingivitis. When the gingiva become so irritated that there is a loss of the connective tissue fibers that attach the gums to the teeth and bone that surrounds the tooth, this is known as periodontitis. Dental plaque is not the sole cause of periodontitis, however it is many times referred to as a primary aetiology. Plaque that remains in the oral cavity long enough will eventually calcify and become calculus.[13] Calculus is detrimental to gingival health because it serves as a trap for increased plaque formation and retention; thus, calculus, along with other factors that cause a localized build-up of plaque, is referred to as a secondary aetiology of periodontitis.

When plaque is supragingival, the bacterial content contains a great proportion of aerobic bacteria and yeast,[16] or those bacteria which utilize and can survive in an environment containing oxygen. Subgingival plaque contains a higher proportion of anaerobic bacteria, or those bacteria which cannot exist in an environment containing oxygen. Several anaerobic plaque bacteria, such as Porphyromonas gingivalis,[17] secrete antigenic proteins that trigger a strong inflammatory response in the periodontium, the specialized tissues that surround and support the teeth. Prolonged inflammation of the periodontium leads to bone loss and weakening of the gingival fibers that attach the teeth to the gums, two major hallmarks of periodontitis. Supragingival calculus formation is nearly ubiquitous in humans,[18][19][20] but to differing degrees. Almost all individuals with periodontitis exhibit considerable subgingival calculus deposits.[13] Dental plaque bacteria have been linked to cardiovascular disease[21] and mothers giving birth to pre-term low weight infants,[22] but there is no conclusive evidence yet that periodontitis is a significant risk factor for either of these two conditions.[23]

Prevention

One effective way to prevent[citation needed] the buildup of calculus is through twice[citation needed] daily toothbrushing and flossing (which removes dental plaque) and regular cleaning visits[citation needed] based on a schedule recommended by the dental health care provider. Calculus accumulates more easily in some individuals, requiring more frequent brushing and dental visits. There are also external factors that facilitate the accumulation of calculus, including smoking and diabetes. While toothpaste with an additive ingredient of zinc citrate has been shown to produce a statistically significant reduction in plaque accumulation, it is of such a small degree that its clinical importance is questionable.[24] Some calculus may form even without plaque deposits, by direct mineralisation of the pellicle.

Calculus in animals

Calculus formation in animals is less well studied than in humans, but it is known to form in a wide range of species. Domestic pets, such as dogs and cats, frequently accumulate large calculus deposits.[25] Animals with highly abrasive diets, such as ruminants and equids, rarely form thick deposits and instead tend to form thin calculus deposits that often have a metallic or opalescent sheen.[26] In animals, calculus should not be confused with crown cementum,[27] a layer of calcified dental tissue that encases the enamel crown and is gradually worn away through abrasion.

Archaeological significance

Dental calculus has been shown to contain well preserved DNA and protein in archaeological samples.[28]

Sub-gingival calculus formation and chemical dissolution

Sub-gingival calculus (tartar) is composed almost entirely of two components: fossilized anaerobic bacteria whose biologic composition has been replaced by calcium phosphate salts, and calcium phosphate salts that have joined the fossilized bacteria in calculus formations. The initial attachment mechanism and the development of mature calculus formations are based on electrical charge. Unlike calcium phosphate, the primary component of teeth, calcium phosphate salts exist as electrically unstable ions. The following minerals are detectable in calculus by X-ray diffraction: brushite (Template:Chemical formula), octacalcium phosphate (Ca8H2(PO4)6.5H2O), magnesium-containing whitlockite (Ca9(MgFe)(PO4)6PO3OH), and carbonate-containing hydroxyapatite (approximately Ca5(PO4)3(OH) but containing some carbonate).[29]

The reason fossilized bacteria are initially attracted to one part of the subgingival tooth surface over another is not fully understood; once the first layer is attached, ionized calculus components are naturally attracted to the same places due to electrical charge. The fossilized bacteria pile on top of one another, in a rather haphazard manner. All the while, free-floating ionic components fill in the gaps left by the fossilized bacteria. The resultant hardened structure can be compared to concrete; with the fossilized bacteria playing the role of aggregate, and the smaller calcium phosphate salts being the cement. The once purely electrical association of fossilized bacteria then becomes mechanical, with the introduction of free-floating calcium phosphate salts. The "hardened" calculus formations are at the heart of periodontal disease and treatment.

See also

Wikimedia Commons has media related to Dental calculus.

References

  1. ^ "Online Etymology Dictionary". etymonline.com.
  2. ^ "Online Etymology Dictionary". etymonline.com.
  3. ^ a b c "Supragingival calculus: formation and control". Critical Reviews in Oral Biology and Medicine. 13 (5): 426–441. 2002. doi:10.1177/154411130201300506. PMID 12393761.
  4. ^ a b "Dental biofilms: difficult therapeutic targets". Periodontology 2000. 28 (1): 12–55. 2002. doi:10.1034/j.1600-0757.2002.280102.x. PMID 12013340.
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  7. ^ a b "Pathogens and host immunity in the ancient human oral cavity". Nature Genetics. 46 (4): 336–344. 2014. doi:10.1038/ng.2906. PMC 3969750. PMID 24562188.
  8. ^ "The human oral microbiome". Journal of Bacteriology. 192 (19): 5002–5017. 2010. doi:10.1128/JB.00542-10. PMC 2944498. PMID 20656903.
  9. ^ "Direct evidence of milk consumption from ancient human dental calculus". Scientific Reports. 4: 7104. 2014. doi:10.1038/srep07104. PMC 4245811. PMID 25429530.
  10. ^ "Starch granules, dental calculus and new perspectives on ancient diet". Journal of Archaeological Science. 36 (2): 248–255. 2009. doi:10.1016/j.jas.2008.09.015.
  11. ^ "Dirty teeth and ancient trade: evidence of cotton fibres in human dental calculus from Late Woodland, Ohio". International Journal of Osteoarchaeology. 21 (6): 669–678. 2011. doi:10.1002/oa.1173.
  12. ^ "Neanderthal medics? Evidence for food, cooking, and medicinal plants entrapped in dental calculus". Naturwissenschaften. 99 (8): 617–626. 2012. doi:10.1007/s00114-012-0942-0. PMID 22806252.
  13. ^ a b c d e f "Calculus removal and the prevention of its formation". Periodontology 2000. 55 (1): 167–188. 2011. doi:10.1111/j.1600-0757.2010.00382.x. PMID 21134234.
  14. ^ "Phototargeting oral black-pigmented bacteria". Antimicrobial Agents and Chemotherapy. 49 (4): 1391–1396. 2005. doi:10.1128/aac.49.4.1391-1396.2005. PMC 1068628. PMID 15793117.
  15. ^ Schroeder HE (1969). Formation and Inhibition of Dental Calculus. Hans Huber Publishers. ISBN 9783456002354.
  16. ^ Clayton YM, Fox EC., YM; Fox, EC (1973). "Investigations into the mycology of dental calculus in town-dwellers, agricultural workers and grazing animals". J Periodontol. 44 (5): 281–285. doi:10.1902/jop.1973.44.5.281. PMID 4572515.
  17. ^ "Complete genome sequence of the oral pathogenic bacterium Porphyromonas gingivalis strain W83". Journal of Bacteriology. 185 (18): 5591–5601. 2003. doi:10.1128/jb.185.18.5591-5601.2003. PMC 193775. PMID 12949112.
  18. ^ "Diet and the aetiology of dental calculus". Int. J. Osteoarchaeol. 9 (4): 219–232. 1999. doi:10.1002/(SICI)1099-1212(199907/08)9:4<219::AID-OA475>3.0.CO;2-V.
  19. ^ "Processes contributing to the formation of dental calculus". Biofouling. 4 (1–3): 209–218. 1991. doi:10.1080/08927019109378211.
  20. ^ "Dental calculus: recent insights into occurrence, formation, prevention, removal and oral health effects of supragingival and subgingival deposits". Eur J Oral Sci. 105 (5): 508–522. 1997. doi:10.1111/j.1600-0722.1997.tb00238.x. PMID 9395117.
  21. ^ "Detection of oral bacteria in cardiovascular specimens". Oral Microbiology and Immunology. 24 (1): 64–68. 2009. doi:10.1111/j.1399-302x.2008.00479.x. PMID 19121072.
  22. ^ "Periodontal disease—the emergence of a risk for systemic conditions: pre-term low birth weight". Ann Acad Med Singap. 34 (1): 111–116. 2005. PMID 15726229.
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  25. ^ http://jn.nutrition.org/content/128/12/2712S.full.pdf
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  27. ^ "The developmental biology of cementum". International Journal of Developmental Biology. 45 (5/6): 695–706. 2001. PMID 11669371.
  28. ^ "Ancient human oral plaque preserves a wealth of biological data". Nature Genetics. 46 (4): 321–323. 2014. doi:10.1038/ng.2930. PMID 24675519. Retrieved 2014-11-11.
  29. ^ A. Molokhia and G. S. Nixon, "Studies on the composition of human dental calculus. Determination of some major and trace elements by instrumental neutron activation analysis", Journal Journal of Radioanalytical and Nuclear Chemistry, Volume 83, Number 2, August, 1984, p. 273-281. (abstract)
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