Editing Periodontal disease (section)

== Causes ==
Periodontitis is an inflammation of the [[periodontium]], i.e., the tissues that support the teeth. The periodontium consists of four tissues:
* [[gingiva]], or gum tissue,
* [[cementum]], or outer layer of the roots of teeth,
* [[dental alveolus|alveolar bone]], or the bony sockets into which the teeth are anchored, and
* [[periodontal ligament]]s (PDLs), which are the [[connective tissue]] fibers that run between the cementum and the alveolar bone.

[[File:Periodontalboneloss.JPG|thumb|right|This [[radiograph|X-ray film]] displays two lone-standing [[Human mandible|mandibular]] teeth, the lower left first premolar and canine, exhibiting severe bone loss of 30–50%. Widening of the [[periodontal ligament]] surrounding the [[premolar]] is due to [[occlusal trauma|secondary occlusal trauma]].]]

The primary cause of gingivitis is poor or ineffective [[oral hygiene]],<ref name=Mayo-2017>{{cite web |author=<!--staff writers, no byline--> |title=Gingivitis |date=4 August 2017 |url=https://www.mayoclinic.org/diseases-conditions/gingivitis/symptoms-causes/syc-20354453 |website=Mayo Clinic |publisher=[[MFMER]] |location=Rochester, Minnesota |access-date=10 May 2018}}</ref> which leads to the accumulation of a [[mycosis|mycotic]]<ref>{{cite journal | vauthors = Crich A | journal = Canadian Medical Association Journal | volume = 26 | issue = 6 | pages = 662–5 | date = June 1932 | pmid = 20318753 | pmc = 402380 | title = Blastomycosis of the Gingiva and Jaw }}</ref><ref>{{cite journal | vauthors = Urzúa B, Hermosilla G, Gamonal J, Morales-Bozo I, Canals M, Barahona S, Cóccola C, Cifuentes V | title = Yeast diversity in the oral microbiota of subjects with periodontitis: Candida albicans and Candida dubliniensis colonize the periodontal pockets | journal = Medical Mycology | volume = 46 | issue = 8 | pages = 783–93 | date = December 2008 | pmid = 18608938 | doi = 10.1080/13693780802060899 }}</ref><ref>{{cite journal | vauthors = Matsuo T, Nakagawa H, Matsuo N | title = Endogenous Aspergillus endophthalmitis associated with periodontitis | journal = Ophthalmologica. Journal International d'Ophtalmologie. International Journal of Ophthalmology. Zeitschrift für Augenheilkunde | volume = 209 | issue = 2 | pages = 109–11 | year = 1995 | pmid = 7746643 | doi = 10.1159/000310592 }}</ref><ref>{{cite journal | vauthors = Migliari DA, Sugaya NN, Mimura MA, Cucé LC | title = Periodontal aspects of the juvenile form of paracoccidioidomycosis | journal = Revista do Instituto de Medicina Tropical de Sao Paulo | volume = 40 | issue = 1 | pages = 15–8 | year = 1998 | pmid = 9713132 | doi = 10.1590/S0036-46651998000100004 | doi-access = free }}</ref> and bacterial matrix at the gum line, called [[dental plaque]]. Other contributors are poor nutrition and underlying medical issues such as [[diabetes]].<ref>{{cite journal | vauthors = Lalla E, Cheng B, Lal S, Kaplan S, Softness B, Greenberg E, Goland RS, Lamster IB | title = Diabetes mellitus promotes periodontal destruction in children | journal = Journal of Clinical Periodontology | volume = 34 | issue = 4 | pages = 294–8 | date = April 2007 | pmid = 17378885 | doi = 10.1111/j.1600-051X.2007.01054.x }}</ref> Diabetics must be meticulous with their homecare to control periodontal disease.<ref>{{cite web |url=https://www.webmd.com/diabetes/periodontal-disease#1 |title=Diabetes and Periodontal Disease |author=<!--Not stated--> |website=WebMD }}</ref> New finger prick tests have been approved by the [[Food and Drug Administration]] in the US, and are being used in dental offices to identify and screen people for possible contributory causes of gum disease, such as diabetes.

In some people, gingivitis progresses to periodontitis — with the destruction of the [[gingival fibers]], the gum tissues separate from the tooth and deepened sulcus, called a [[periodontal pocket]]. Subgingival microorganisms (those that exist under the gum line) colonize the periodontal pockets and cause further inflammation in the gum tissues and progressive bone loss. Examples of secondary causes are those things that, by definition, cause microbic plaque accumulation, such as restoration overhangs and root proximity.
[[File:Overhangs.jpg|275px|thumb|left|The excess restorative material that exceeds the natural contours of restored teeth, such as these, are termed "overhangs", and serve to trap microbic plaque, potentially leading to localized periodontitis.]]

[[Health effects of tobacco|Smoking]] is another factor that increases the occurrence of periodontitis, directly or indirectly,<ref>{{cite journal | vauthors = Obeid P, Bercy P | title = Effects of smoking on periodontal health: a review | journal = Advances in Therapy | volume = 17 | issue = 5 | pages = 230–7 | year = 2000 | pmid = 11186143 | doi = 10.1007/BF02853162 | s2cid = 2227017 }}</ref><ref>{{cite journal | vauthors = Tomar SL, Asma S | title = Smoking-attributable periodontitis in the United States: findings from NHANES III. National Health and Nutrition Examination Survey | journal = Journal of Periodontology | volume = 71 | issue = 5 | pages = 743–51 | date = May 2000 | pmid = 10872955 | doi = 10.1902/jop.2000.71.5.743 }}</ref><ref>{{cite journal | vauthors = Ryder MI | title = The influence of smoking on host responses in periodontal infections | journal = Periodontology 2000 | volume = 43 | issue = 1 | pages = 267–77 | year = 2007 | pmid = 17214844 | doi = 10.1111/j.1600-0757.2006.00163.x | doi-access = free }}</ref> and may interfere with or adversely affect its treatment.<ref>{{cite journal | vauthors = Pauletto NC, Liede K, Nieminen A, Larjava H, Uitto VJ | title = Effect of cigarette smoking on oral elastase activity in adult periodontitis patients | journal = Journal of Periodontology | volume = 71 | issue = 1 | pages = 58–62 | date = January 2000 | pmid = 10695939 | doi = 10.1902/jop.2000.71.1.58 }}</ref><ref>{{cite journal | vauthors = Persson L, Bergström J, Gustafsson A | title = Effect of tobacco smoking on neutrophil activity following periodontal surgery | journal = Journal of Periodontology | volume = 74 | issue = 10 | pages = 1475–82 | date = October 2003 | pmid = 14653394 | doi = 10.1902/jop.2003.74.10.1475 }}</ref><ref>{{cite journal | vauthors = Bergström J, Boström L | title = Tobacco smoking and periodontal hemorrhagic responsiveness | journal = Journal of Clinical Periodontology | volume = 28 | issue = 7 | pages = 680–5 | date = July 2001 | pmid = 11422590 | doi = 10.1034/j.1600-051x.2001.028007680.x | doi-access = free }}</ref> It is arguably the most important environmental risk factor for periodontitis. Research has shown that smokers have more bone loss, attachment loss and tooth loss compared to non-smokers.<ref name=Preshaw04>{{cite journal |vauthors=Preshaw PM, Seymour RA, Heasman PA |title=Current concepts in periodontal pathogenesis |journal=Dent Update |volume=31 |issue=10 |pages=570–2, 574–8 |date=December 2004 |pmid=15656071 |doi=10.12968/denu.2004.31.10.570  |url=https://www.dental-update.co.uk/issuesThreeArticle.asp?aKey=421|url-access=subscription}}</ref> This is likely due to several effects of smoking on the immune response including decreased wound healing, suppression of [[antibody]] production, and the reduction of [[phagocytosis]] by [[neutrophil]]s<ref name=Preshaw04/>

[[Ehlers–Danlos syndrome]] and [[Papillon–Lefèvre syndrome]] (also known as palmoplantar keratoderma) are also risk factors for periodontitis.

If left undisturbed, microbial plaque calcifies to form [[dental calculus|calculus]], which is commonly called tartar. Calculus above and below the gum line must be removed completely by the dental hygienist or dentist to treat gingivitis and periodontitis. Although the primary cause of both gingivitis and periodontitis is the microbial plaque that adheres to the tooth surfaces, there are many other modifying factors. A very strong risk factor is one's genetic susceptibility. Several conditions and diseases, including [[Down syndrome]], diabetes, and other diseases that affect one's resistance to infection, also increase susceptibility to periodontitis.

Periodontitis may be associated with higher stress.<ref>{{cite journal | vauthors = Peruzzo DC, Benatti BB, Ambrosano GM, Nogueira-Filho GR, Sallum EA, Casati MZ, Nociti FH | title = A systematic review of stress and psychological factors as possible risk factors for periodontal disease | journal = Journal of Periodontology | volume = 78 | issue = 8 | pages = 1491–504 | date = August 2007 | pmid = 17668968 | doi = 10.1902/jop.2007.060371 }}</ref> Periodontitis occurs more often in people in the lower classes than people in the upper classes.<ref name="Watt">{{cite book |editor1-last=Watt |editor1-first=RG |editor2-last=Listl |editor2-first=S |editor3-last=Peres |editor3-first=MA |editor4-last=Heilmann |editor4-first=A |title=Social inequalities in oral health: from evidence to action |date=2015 |publisher=UCL |location=London |url=http://media.news.health.ufl.edu/misc/cod-oralhealth/docs/posts_frontpage/SocialInequalities.pdf}}</ref>

[[Genetics]] appear to play a role in determining the risk for periodontitis. It is believed genetics could explain why some people with good plaque control have advanced periodontitis, while some others with poor oral hygiene are free from the disease. Genetic factors which could modify the risk of a person developing periodontitis include:
* Defects of [[phagocytosis]]: person may have hypo-responsive [[phagocyte]]s.
* Hyper-production of [[interleukin]]s, [[prostaglandin]]s and [[cytokine]]s, resulting in an exaggerated [[Immune system|immune response]]. 
* [[Interleukin-1 family|Interleukin 1]] (IL-1) gene polymorphism: people with this polymorphism produce more IL-1, and subsequently are more at risk of developing chronic periodontitis.<ref name=Preshaw04/>
Diabetes appears to exacerbate the onset, progression, and severity of periodontitis.<ref name=Teeuw17>{{cite journal | vauthors = Teeuw WJ, Kosho MX, Poland DC, Gerdes VE, Loos BG | title = Periodontitis as a possible early sign of diabetes mellitus | journal = BMJ Open Diabetes Research & Care | volume = 5 | issue = 1 | pages = e000326 | date = 1 January 2017 | pmid = 28316794 | pmc = 5337701 | doi = 10.1136/bmjdrc-2016-000326 }}</ref> Although the majority of research has focused on [[Diabetes mellitus type 2|type 2 diabetes]], [[Diabetes mellitus type 1|type 1 diabetes]] appears to have an identical effect on the risk for periodontitis.<ref name=Casanova14>{{cite journal | vauthors = Casanova L, Hughes FJ, Preshaw PM | title = Diabetes and periodontal disease: a two-way relationship | journal = British Dental Journal | volume = 217 | issue = 8 | pages = 433–7 | date = October 2014 | pmid = 25342350 | doi = 10.1038/sj.bdj.2014.907 | doi-access = free }}</ref> The extent of the increased risk of periodontitis is dependent on the level of [[Glycemic control|glycaemic control]]. Therefore, in well managed diabetes there seems to be a small effect of diabetes on the risk for periodontitis. However, the risk increases exponentially as glycaemic control worsens.<ref name=Casanova14 /> Overall, the increased risk of periodontitis in diabetics is estimated to be between two and three times higher.<ref name=Teeuw17 /> So far, the mechanisms underlying the link are not fully understood, but it is known to involve aspects of inflammation, immune functioning, neutrophil activity, and cytokine biology.<ref name=Casanova14 /><ref>{{cite journal | vauthors = Taylor JJ, Preshaw PM, Lalla E | title = A review of the evidence for pathogenic mechanisms that may link periodontitis and diabetes | journal = Journal of Clinical Periodontology | volume = 40 | pages = S113–34 | date = April 2013 | issue = Suppl 14 | pmid = 23627323 | doi = 10.1111/jcpe.12059 }}</ref>

Hormonal fluctuations can also play a significant role in the development and progression of gingivitis and periodontitis. Changes in hormone levels, particularly during puberty, menstruation, pregnancy, and menopause, can lead to increased sensitivity and inflammatory responses in the gums. For example, elevated estrogen and progesterone during pregnancy can heighten the inflammatory response to dental plaque, making pregnant individuals more susceptible to gingival disease.