View source for Periodontal disease

{{Short description|Disease of the tissues surrounding the teeth (periodontium)}}
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{{Use dmy dates|date=December 2020}}
{{Infobox medical condition (new)
| name            = Periodontal disease
| synonyms        = Gum disease, pyorrhea, periodontitis
| image           = Paro1.JPG
| caption         = [[Radiograph]] showing bone loss between the two roots of a tooth (black region). The spongy bone has receded due to infection under tooth, reducing the bony support for the tooth.
| field           = [[Periodontology]]
| pronounce       = Periodontitis {{IPAc-en|ˌ|p|ɛr|i|oʊ|d|ɒ|n|ˈ|t|aɪ|t|ɪ|s}}, pyorrhea {{IPAc-en|ˌ|p|aɪ|ə|ˈ|r|iː|ə}}
| symptoms        = Red, swollen, painful, bleeding gums, loose teeth, [[bad breath]]<ref name=NIH2018/>
| complications   = [[Tooth loss]], [[gum abscess]]<ref name=NIH2018/><ref>{{cite web|title=Gum Disease Complications|url=https://www.nhs.uk/conditions/gum-disease/complications/|website=nhs.uk|access-date=13 March 2018}}</ref>
| onset           = Getting [[gingivitis]]<ref name="P&S">{{cite journal |last1=Page |first1=RC |last2=Schroeder |first2=HE |title=Pathogenesis of inflammatory periodontal disease. A summary of current work |journal=Laboratory Investigation |volume=34 |issue=3 |pages=235–49 |year=1976 |pmid=765622}}</ref>
| duration        =
| types           =
| causes          = Bacterial [[Dental plaque|plaque]] buildup<ref name=NIH2018/>
| risks           = [[Smoking]],<ref name="J. Periodontol.">{{cite journal |last1=Albandar |first1=Jasim M. |last2=Adensaya |first2=Margo R. |last3=Streckfus |first3=Charles F. |last4=Winn |first4=Deborah M. |date=December 2000 |title=Cigar, Pipe, and Cigarette Smoking as Risk Factors for Periodontal Disease and Tooth Loss |journal=[[Journal of Periodontology]] |publisher=[[American Academy of Periodontology]] |volume=71 |issue=12 |pages=1874–81 |doi=10.1902/jop.2000.71.12.1874 |issn=0022-3492 |pmid=11156044 |s2cid=11598500}}</ref> [[diabetes]], [[HIV/AIDS]], certain medications<ref name=NIH2018/>
| diagnosis       = Dental examination, X-rays<ref name=NIH2018/>
| differential    =
| prevention      =
| treatment       = Good oral hygiene, regular professional cleaning<ref name=CDC2015/>
| medication      =
| prognosis       =
| frequency       = 538 million (2015)<ref name=GBD2015Pre/>
| deaths          =
}}

'''Periodontal disease''', also known as '''gum disease''', is a set of inflammatory conditions affecting the [[Periodontium|tissues surrounding the teeth]].<ref name=CDC2015>{{cite web|title=Periodontal Disease|url=https://www.cdc.gov/oralhealth/conditions/periodontal-disease.html|website=CDC|access-date=3 January 2023|date=10 July 2013}}</ref> In its early stage, called [[gingivitis]], the gums become swollen and red and may bleed.<ref name=CDC2015/> It is considered the main cause of tooth loss for adults worldwide.<ref name=Baelum04>{{cite journal |vauthors=Baelum V, Lopez R |title=Periodontal epidemiology: towards social science or molecular biology? |journal=Community Dent Oral Epidemiol |volume=32 |issue=4 |pages=239–49 |date=August 2004 |pmid=15239775 |doi=10.1111/j.1600-0528.2004.00159.x }}</ref><ref name="Nicchio I 2021">{{cite journal |vauthors=Nicchio IG, Cirelli T, Nepomuceno R, Hidalgo MA, Rossa C, Cirelli JA, Orrico SR, Barros SP, Theodoro LH, Scarel-Caminaga RM |title=Polymorphisms in Genes of Lipid Metabolism Are Associated with Type 2 Diabetes Mellitus and Periodontitis, as Comorbidities, and with the Subjects' Periodontal, Glycemic, and Lipid Profiles |journal=J Diabetes Res |volume=2021 |article-number=1049307 |date=2021 |pmid=34805411 |pmc=8601849 |doi=10.1155/2021/1049307 |doi-access=free}}</ref> In its more serious form, called '''periodontitis''', the gums can pull away from the [[tooth]], bone can be lost, and the teeth may loosen or [[tooth loss|fall out]].<ref name=CDC2015/> [[Bad breath|Halitosis (bad breath)]] may also occur.<ref name=NIH2018>{{cite web|title=Gum Disease|url=https://www.nidcr.nih.gov/health-info/gum-disease|website=National Institute of Dental and Craniofacial Research|access-date=13 March 2018|date=February 2018}}</ref>

Periodontal disease typically arises from the development of [[Dental plaque|plaque]] biofilm, which harbors harmful bacteria such as ''[[Porphyromonas gingivalis]]'' and ''[[Treponema denticola]]''. These bacteria infect the gum tissue surrounding the teeth, leading to inflammation and, if left untreated, progressive damage to the teeth and gum tissue.<ref>{{Cite journal |last1=Visentin |first1=David |last2=Gobin |first2=Ivana |last3=Maglica |first3=Željka |date=July 2023 |title=Periodontal Pathogens and Their Links to Neuroinflammation and Neurodegeneration |journal=Microorganisms |language=en |volume=11 |issue=7 |page=1832 |doi=10.3390/microorganisms11071832 |doi-access=free |issn=2076-2607 |pmc=10385044 |pmid=37513004}}</ref> Recent meta-analysis have shown that the composition of the [[Oral microbiology|oral microbiota]] and its response to periodontal disease differ between [[Man|men]] and [[Woman|women]]. These differences are particularly notable in the advanced stages of periodontitis, suggesting that sex-specific factors may influence susceptibility and progression.<ref>{{Cite journal |last1=Del Pinto |first1=Rita |last2=Ferri |first2=Claudio |last3=Giannoni |first3=Mario |last4=Cominelli |first4=Fabio |last5=Pizarro |first5=Theresa T. |last6=Pietropaoli |first6=Davide |date=2024-09-10 |title=Meta-analysis of oral microbiome reveals sex-based diversity in biofilms during periodontitis |journal=JCI Insight |language=en |volume=9 |issue=17 |article-number=e171311 |doi=10.1172/jci.insight.171311 |issn=2379-3708 |pmc=11385077 |pmid=39253976}}</ref> Factors that increase the risk of disease include [[smoking]],<ref name="J. Periodontol."/> [[diabetes]], [[HIV/AIDS]], family history, high levels of [[homocysteine]] in the blood and certain medications.<ref name=NIH2018/> Diagnosis is by inspecting the [[Gingiva|gum tissue]] around the teeth both visually and with a [[Periodontal probe|probe]] and [[radiograph|X-ray]]s looking for bone loss around the teeth.<ref name=NIH2018/><ref>{{cite journal | vauthors = Savage A, Eaton KA, Moles DR, Needleman I | title = A systematic review of definitions of periodontitis and methods that have been used to identify this disease | journal = Journal of Clinical Periodontology | volume = 36 | issue = 6 | pages = 458–67 | date = June 2009 | pmid = 19508246 | doi = 10.1111/j.1600-051X.2009.01408.x | doi-access = free }}</ref>

Treatment involves good [[oral hygiene]] and regular professional [[teeth cleaning]].<ref name=CDC2015/> Recommended oral hygiene include daily [[tooth brushing|brushing]] and [[flossing]].<ref name=CDC2015/> In certain cases [[antibiotics]] or [[dental surgery]] may be recommended.<ref name=NHS2018>{{cite web|title=Gum Disease Treatment|url=https://www.nhs.uk/conditions/gum-disease/treatment/|website=nhs.uk|access-date=13 March 2018}}</ref> Clinical investigations demonstrate that quitting smoking and making dietary changes enhance periodontal health.<ref name=":3">{{cite journal |last1=Sáenz-Ravello |first1=Gustavo |last2=Matamala |first2=Loreto |last3=dos Santos |first3=Nidia Castro |last4=Cisternas |first4=Patricia |last5=Gamonal |first5=Jorge |last6=Fernandez |first6=Alejandra |last7=Bello-Escamilla |first7=Natalia |last8=Hernandez |first8=Marcela |last9=Baeza |first9=Mauricio |title=Healthy Dietary Patterns on Clinical Periodontal Parameters: A GRADE Compliant Systematic Review and Meta-analysis |journal=Current Oral Health Reports |date=1 June 2022 |volume=9 |issue=2 |pages=32–55 |doi=10.1007/s40496-022-00307-y |s2cid=246752560 |language=en |issn=2196-3002}}</ref><ref name="JCPguideline2020">{{cite journal |title=Treatment of stage I–III periodontitis—The EFP S3 level clinical practice guideline |journal=Journal of Clinical Periodontology |date=2020 |doi=10.1111/jcpe.13290 |last1=Sanz |first1=Mariano |last2=Herrera |first2=David |last3=Kebschull |first3=Moritz |last4=Chapple |first4=Iain |last5=Jepsen |first5=Søren |last6=Berglundh |first6=Tord |last7=Sculean |first7=Anton |last8=Tonetti |first8=Maurizio S. |last9=Merete Aass |first9=Anne |last10=Aimetti |first10=Mario |last11=Kuru |first11=Bahar Eren |last12=Belibasakis |first12=Georgios |last13=Blanco |first13=Juan |last14=Bol-Van Den Hil |first14=Ellen |last15=Bostanci |first15=Nagihan |last16=Bozic |first16=Darko |last17=Bouchard |first17=Philippe |last18=Buduneli |first18=Nurcan |last19=Cairo |first19=Francesco |last20=Calciolari |first20=Elena |last21=Carra |first21=Maria Clotilde |last22=Cortellini |first22=Pierpaolo |last23=Cosyn |first23=Jan |last24=d'Aiuto |first24=Francesco |last25=Dannewitz |first25=Bettina |last26=Danser |first26=Monique |last27=Demirel |first27=Korkud |last28=Derks |first28=Jan |last29=Sanctis |first29=Massimo |last30=Dietrich |first30=Thomas |volume=47 |issue=Suppl 22 |pages=4–60 |pmid=32383274 |pmc=7891343 |display-authors=1 }}</ref> Globally, 538 million people were estimated to be affected in 2015 and has been known to affect 10–15% of the population generally.<ref name=Baelum04/><ref name="Nicchio I 2021"/><ref name=GBD2015Pre>{{cite journal | author = ((GBD 2015 Disease and Injury Incidence and Prevalence Collaborators)) | title = Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990–2015: a systematic analysis for the Global Burden of Disease Study 2015 | journal = Lancet | volume = 388 | issue = 10053 | pages = 1545–1602 | date = October 2016 | pmid = 27733282 | pmc = 5055577 | doi = 10.1016/S0140-6736(16)31678-6 }}</ref> In the United States, nearly half of those over the age of 30 are affected to some degree and about 70% of those over 65 have the condition.<ref name=CDC2015/> Males are affected more often than females.<ref name=CDC2015/>
[[File:En.Wikipedia-VideoWiki-Periodontal disease.webm|thumb|thumbtime=0:32|upright=1.3|Video summary ([[Wikipedia:VideoWiki/Periodontitis|script]])]]
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==Signs and symptoms==
[[File:Periodontal terms diagram gingival recession.png|thumb|right|'''1''': Total loss of attachment (clinical attachment loss, CAL) is the sum of '''2''': Gingival recession, and '''3''': Probing depth]]
In the early stages, periodontitis has very few symptoms, and in many individuals, the disease has progressed significantly before they seek treatment.

Symptoms may include:
* Redness or bleeding of gums while brushing [[tooth|teeth]], using [[dental floss]] or biting into hard food (e.g., apples) (though this may also occur in [[gingivitis]], where there is no attachment loss or gum disease)
* Gum swelling that recurs
* Spitting out blood after brushing teeth
* [[Halitosis]], or bad breath, and a persistent metallic taste in the mouth
* Gingival recession, resulting in apparent lengthening of teeth (this may also be caused by heavy-handed brushing or brushing with a stiff toothbrush)
* Deep pockets between the teeth and the gums ([[gingival and periodontal pockets|pockets]] are sites where the attachment has been gradually destroyed by [[collagen]]-destroying enzymes, known as [[collagenases]])
* Loose teeth, in the later stages (though this may occur for other [[occlusal trauma|reasons]], as well)

Gingival inflammation and bone destruction are largely painless. Hence, people may wrongly assume painless bleeding after teeth cleaning is insignificant, although this may be a symptom of progressing periodontitis in that person. 
[[File:Periodontal_Disease.png|thumb|Periodontal disease]]

===Associated conditions===
Periodontitis has been linked to increased [[inflammation]] in the body, such as indicated by raised levels of [[C-reactive protein]] and [[interleukin-6]].<ref>{{cite journal | vauthors = D'Aiuto F, Parkar M, Andreou G, Suvan J, Brett PM, Ready D, Tonetti MS | title = Periodontitis and systemic inflammation: control of the local infection is associated with a reduction in serum inflammatory markers | journal = Journal of Dental Research | volume = 83 | issue = 2 | pages = 156–60 | date = February 2004 | pmid = 14742655 | doi = 10.1177/154405910408300214 | s2cid = 34329326 }}</ref><ref>{{cite journal | vauthors = Nibali L, D'Aiuto F, Griffiths G, Patel K, Suvan J, Tonetti MS | title = Severe periodontitis is associated with systemic inflammation and a dysmetabolic status: a case-control study | journal = Journal of Clinical Periodontology | volume = 34 | issue = 11 | pages = 931–7 | date = November 2007 | pmid = 17877746 | doi = 10.1111/j.1600-051X.2007.01133.x }}</ref><ref>{{cite journal | vauthors = Paraskevas S, Huizinga JD, Loos BG | title = A systematic review and meta-analyses on C-reactive protein in relation to periodontitis | journal = Journal of Clinical Periodontology | volume = 35 | issue = 4 | pages = 277–90 | date = April 2008 | pmid = 18294231 | doi = 10.1111/j.1600-051X.2007.01173.x }}</ref><ref>{{cite journal | vauthors = D'Aiuto F, Ready D, Tonetti MS | title = Periodontal disease and C-reactive protein-associated cardiovascular risk | journal = Journal of Periodontal Research | volume = 39 | issue = 4 | pages = 236–41 | date = August 2004 | pmid = 15206916 | doi = 10.1111/j.1600-0765.2004.00731.x }}</ref> It is associated with an increased risk of stroke,<ref>{{cite journal | vauthors = Pussinen PJ, Alfthan G, Jousilahti P, Paju S, Tuomilehto J | title = Systemic exposure to Porphyromonas gingivalis predicts incident stroke | journal = Atherosclerosis | volume = 193 | issue = 1 | pages = 222–8 | date = July 2007 | pmid = 16872615 | doi = 10.1016/j.atherosclerosis.2006.06.027 }}</ref><ref>{{cite journal | vauthors = Pussinen PJ, Alfthan G, Rissanen H, Reunanen A, Asikainen S, Knekt P | title = Antibodies to periodontal pathogens and stroke risk | journal = Stroke | volume = 35 | issue = 9 | pages = 2020–3 | date = September 2004 | pmid = 15232116 | doi = 10.1161/01.STR.0000136148.29490.fe | doi-access = free }}</ref> [[myocardial infarction]],<ref>{{cite journal | vauthors = Pussinen PJ, Alfthan G, Tuomilehto J, Asikainen S, Jousilahti P | title = High serum antibody levels to Porphyromonas gingivalis predict myocardial infarction | journal = European Journal of Cardiovascular Prevention and Rehabilitation | volume = 11 | issue = 5 | pages = 408–11 | date = October 2004 | pmid = 15616414 | doi = 10.1097/01.hjr.0000129745.38217.39 | s2cid = 34400631 }}</ref> [[atherosclerosis]]<ref>{{cite journal | vauthors = Ford PJ, Gemmell E, Timms P, Chan A, Preston FM, Seymour GJ | title = Anti-P. gingivalis response correlates with atherosclerosis | journal = Journal of Dental Research | volume = 86 | issue = 1 | pages = 35–40 | date = January 2007 | pmid = 17189460 | doi = 10.1177/154405910708600105 | s2cid = 5567995 }}</ref><ref>{{cite journal | vauthors = Beck JD, Eke P, Heiss G, Madianos P, Couper D, Lin D, Moss K, Elter J, Offenbacher S | title = Periodontal disease and coronary heart disease: a reappraisal of the exposure | journal = Circulation | volume = 112 | issue = 1 | pages = 19–24 | date = July 2005 | pmid = 15983248 | doi = 10.1161/CIRCULATIONAHA.104.511998 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Scannapieco FA, Bush RB, Paju S | title = Associations between periodontal disease and risk for atherosclerosis, cardiovascular disease, and stroke. A systematic review | journal = Annals of Periodontology | volume = 8 | issue = 1 | pages = 38–53 | date = December 2003 | pmid = 14971247 | doi = 10.1902/annals.2003.8.1.38 }}</ref><ref>{{cite journal | vauthors = Wu T, Trevisan M, Genco RJ, Dorn JP, Falkner KL, Sempos CT | title = Periodontal disease and risk of cerebrovascular disease: the first national health and nutrition examination survey and its follow-up study | journal = Archives of Internal Medicine | volume = 160 | issue = 18 | pages = 2749–55 | date = October 2000 | pmid = 11025784 | doi = 10.1001/archinte.160.18.2749 }}</ref><ref>{{cite journal | vauthors = Beck JD, Elter JR, Heiss G, Couper D, Mauriello SM, Offenbacher S | title = Relationship of periodontal disease to carotid artery intima-media wall thickness: the atherosclerosis risk in communities (ARIC) study | journal = Arteriosclerosis, Thrombosis, and Vascular Biology | volume = 21 | issue = 11 | pages = 1816–22 | date = November 2001 | pmid = 11701471 | doi = 10.1161/hq1101.097803 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Elter JR, Champagne CM, Offenbacher S, Beck JD | title = Relationship of periodontal disease and tooth loss to prevalence of coronary heart disease | journal = Journal of Periodontology | volume = 75 | issue = 6 | pages = 782–90 | date = June 2004 | pmid = 15295942 | doi = 10.1902/jop.2004.75.6.782 }}</ref><ref>{{cite journal | vauthors = Humphrey LL, Fu R, Buckley DI, Freeman M, Helfand M | title = Periodontal disease and coronary heart disease incidence: a systematic review and meta-analysis | journal = Journal of General Internal Medicine | volume = 23 | issue = 12 | pages = 2079–86 | date = December 2008 | pmid = 18807098 | pmc = 2596495 | doi = 10.1007/s11606-008-0787-6 }}</ref> and [[hypertension]].<ref>{{cite journal | vauthors = Martin-Cabezas R, Seelam N, Petit C, Agossa K, Gaertner S, Tenenbaum H, Davideau JL, Huck O | title = Association between periodontitis and arterial hypertension: A systematic review and meta-analysis | journal = American Heart Journal | volume = 180 | pages = 98–112 | date = October 2016 | pmid = 27659888 | doi = 10.1016/j.ahj.2016.07.018 }}</ref> It is also linked in those over 60 years of age to impairments in delayed memory and calculation abilities.<ref>{{cite journal | vauthors = Noble JM, Borrell LN, Papapanou PN, Elkind MS, Scarmeas N, Wright CB | title = Periodontitis is associated with cognitive impairment among older adults: analysis of NHANES-III | journal = Journal of Neurology, Neurosurgery, and Psychiatry | volume = 80 | issue = 11 | pages = 1206–11 | date = November 2009 | pmid = 19419981 | pmc = 3073380 | doi = 10.1136/jnnp.2009.174029 }}</ref><ref>{{cite journal | vauthors = Kaye EK, Valencia A, Baba N, Spiro A, Dietrich T, Garcia RI | title = Tooth loss and periodontal disease predict poor cognitive function in older men | journal = Journal of the American Geriatrics Society | volume = 58 | issue = 4 | pages = 713–8 | date = April 2010 | pmid = 20398152 | pmc = 3649065 | doi = 10.1111/j.1532-5415.2010.02788.x }}</ref> Individuals with [[impaired fasting glucose]] and [[diabetes mellitus]] have a higher degrees of periodontal inflammation and often have difficulties with balancing their blood [[glucose]] level, owing to the constant systemic inflammatory state caused by the periodontal inflammation.<ref name="glucose">{{cite journal | vauthors = Zadik Y, Bechor R, Galor S, Levin L | title = Periodontal disease might be associated even with impaired fasting glucose | journal = British Dental Journal | volume = 208 | issue = 10 | pages = E20 | date = May 2010 | pmid = 20339371 | doi = 10.1038/sj.bdj.2010.291 | doi-access = free }}</ref><ref name="DM">{{cite journal | vauthors = Soskolne WA, Klinger A | title = The relationship between periodontal diseases and diabetes: an overview | journal = Annals of Periodontology | volume = 6 | issue = 1 | pages = 91–8 | date = December 2001 | pmid = 11887477 | doi = 10.1902/annals.2001.6.1.91 }}</ref> Although no causal association was proven, there is an association between chronic periodontitis and [[erectile dysfunction]],<ref name="ED">{{cite journal | vauthors = Zadik Y, Bechor R, Galor S, Justo D, Heruti RJ | title = Erectile dysfunction might be associated with chronic periodontal disease: two ends of the cardiovascular spectrum | journal = The Journal of Sexual Medicine | volume = 6 | issue = 4 | pages = 1111–6 | date = April 2009 | pmid = 19170861 | doi = 10.1111/j.1743-6109.2008.01141.x | s2cid = 3421903 }}</ref> [[inflammatory bowel disease]],<ref>{{Cite journal|last1=Poyato-Borrego|first1=M.|last2=Segura-Egea|first2=J.-J.|last3=Martín-González|first3=J.|last4=Jiménez-Sánchez|first4=M.-C.|last5=Cabanillas-Balsera|first5=D.|last6=Areal-Quecuty|first6=V.|last7=Segura-Sampedro|first7=J.-J.|date=27 August 2020|title=Prevalence of endodontic infection in patients with Crohn´s disease and ulcerative colitis|journal=Medicina Oral, Patologia Oral y Cirugia Bucal|volume=26|issue=2|pages=e208–e215|doi=10.4317/medoral.24135 |pmid=32851982|pmc=7980298|doi-access=free}}</ref> and heart disease.<ref>{{cite journal |last1=Perk |first1=J. |last2=De Backer |first2=G. |last3=Gohlke |first3=H. |last4=Graham |first4=I. |last5=Reiner |first5=Z. |last6=Verschuren |first6=M. |title=European Guidelines on cardiovascular disease prevention in clinical practice (version 2012): The Fifth Joint Task Force of the European Society of Cardiology and Other Societies on Cardiovascular Disease Prevention in Clinical Practice (constituted by representatives of nine societies and by invited experts) Developed with the special contribution of the European Association for Cardiovascular Prevention & Rehabilitation (EACPR) |journal=European Heart Journal |date=3 May 2012 |volume=33 |issue=13 |pages=1635–1701 |doi=10.1093/eurheartj/ehs092 |pmid=22555213 |doi-access=free }}</ref>
==== Diabetes and periodontal disease ====
A positive correlation between raised levels of glucose within the blood and the onset or progression of periodontal disease has been shown in the current literature.

Data has also shown that there is a significant increase in the incidence or progression of periodontitis in patients with uncontrolled diabetes compared to those who do not have diabetes or have well-controlled diabetes. In uncontrolled diabetes, the formation of [[reactive oxygen species]] can damage cells such as those in the connective tissue of the periodontal ligament, resulting in cell [[necrosis]] or [[apoptosis]]. Furthermore, individuals with uncontrolled diabetes mellitus who have frequent exposure to periodontal pathogens have a greater immune response to these bacteria. This can subsequently cause and/or accelerate periodontal tissue destruction, leading to periodontal disease.<ref>{{Cite journal |last1=Nascimento |first1=Gustavo G. |last2=Leite |first2=Fábio R. M. |last3=Vestergaard |first3=Peter |last4=Scheutz |first4=Flemming |last5=López |first5=Rodrigo |date=July 2018 |title=Does diabetes increase the risk of periodontitis? A systematic review and meta-regression analysis of longitudinal prospective studies |journal=Acta Diabetologica |volume=55 |issue=7 |pages=653–667 |doi=10.1007/s00592-018-1120-4 |issn=1432-5233 |pmid=29502214|s2cid=3689420 }}</ref>

===Oral cancer and periodontal disease===

Current literature suggests a link between periodontal disease and oral cancer. Studies have confirmed an increase in systemic inflammation markers such as [[C-reactive protein|C-Reactive Protein]] and [[Interleukin 6|Interleukin-6]] to be found in patients with advanced periodontal disease. The link between systemic inflammation and oral cancer has also been well established.

Both periodontal disease and cancer risk are associated with genetic susceptibility, and there may be a positive association due to a shared genetic susceptibility in the two diseases.

Due to the low incidence rate of oral cancer, studies have not been able to conduct quality studies to prove the association between the two; however, future larger studies may aid in the identification of individuals at a higher risk.<ref>{{Cite journal |last1=Michaud |first1=Dominique S. |last2=Fu |first2=Zhuxuan |last3=Shi |first3=Jian |last4=Chung |first4=Mei |date=January 2017 |title=Periodontal Disease, Tooth Loss, and Cancer Risk |journal=Epidemiologic Reviews |volume=39 |issue=1 |pages=49–58 |doi=10.1093/epirev/mxx006 |pmc=5868279 |pmid=28449041}}</ref>

===Blood Pressure===
A Cochrane review assessed whether periodontal treatment lowers [[Blood pressure|blood pressure]] in people with periodontitis, including those with [[Hypertension|hypertension]]. Overall, the evidence showed no consistent difference in blood pressure between people who received periodontal treatment and those who did not. In comparison with no treatment or with limited cleaning (supra-gingival scaling), no meaningful changes in blood pressure were observed. Only one study among people with diagnosed hypertension showed a short-term reduction in blood pressure following treatment, but this was not sustained or replicated. The review concluded that there is insufficient evidence to support the use of periodontal treatment for controlling blood pressure.<ref>{{Cite journal |last1=Luo |first1=Y |last2=Huilin |first2=Y |last3= Liu |first3=W |last4= Lv |first4=Zongkai |last5=Jia |first5=Y |last6=Li |first6=C |last7=Zhang |first7=Y |date=December 2021 |title= Effect of periodontal treatments on blood pressure |journal=Cochrane Database of Systematic Reviews |volume=2021 |issue=12 |article-number=CD009409 |doi= 10.1002/14651858.CD009409.pub2|pmid=34897644 |pmc=8666138 }}</ref>

===Systemic implications===

Periodontal disease (PD) can be described as an inflammatory condition affecting the supporting structures of the teeth. Studies have shown that PD is associated with higher levels of systemic inflammatory markers such as Interleukin-6 (IL-6), C-Reactive Protein (CRP), and Tumor Necrosis Factor (TNF). To compare, elevated levels of these inflammatory markers are also associated with cardiovascular disease and cerebrovascular events such as ischemic strokes.<ref>{{Cite journal |last1=Gomes-Filho |first1=Isaac Suzart |last2=Freitas Coelho |first2=Julita Maria |last3=da Cruz |first3=Simone Seixas |last4=Passos |first4=Johelle Santana |last5=Teixeira de Freitas |first5=Camila Oliveira |last6=Aragão Farias |first6=Naiara Silva |last7=Amorim da Silva |first7=Ruany |last8=Silva Pereira |first8=Milena Novais |last9=Lima |first9=Thiago Lopes |last10=Barreto |first10=Maurício Lima |date=July 2011 |title=Chronic periodontitis and C-reactive protein levels |journal=Journal of Periodontology |volume=82 |issue=7 |pages=969–978 |doi=10.1902/jop.2010.100511 |issn=1943-3670 |pmid=21189085}}</ref>

The presence of a wide spectrum of inflammatory oral diseases can increase the risk of an episode of stroke in an acute or chronic phase. Inflammatory markers, CRP and IL-6, are known risk factors for stroke. Both inflammatory markers are also biomarkers of PD and found to be an increased level after daily activities, such as mastication or toothbrushing, are performed. Bacteria from the periodontal pockets will enter the bloodstream during these activities and the current literature suggests that this may be a possible triggering of the aggravation of the stroke process.<ref>{{Cite journal |last=Loos |first=Bruno G. |date=November 2005 |title=Systemic markers of inflammation in periodontitis |journal=Journal of Periodontology |volume=76 |issue=11 Suppl |pages=2106–15 |doi=10.1902/jop.2005.76.11-S.2106 |issn=0022-3492 |pmid=16277583}}</ref>

Other mechanisms have been suggested; PD is a known chronic infection. It can aid in the promotion of atherosclerosis by the deposition of cholesterol, cholesterol esters, and calcium within the subendothelial layer of vessel walls.<ref>{{Cite journal |last1=Libby |first1=Peter |last2=Ridker |first2=Paul M. |last3=Hansson |first3=Göran K. |last4=Leducq Transatlantic Network on Atherothrombosis |date=2009-12-01 |title=Inflammation in atherosclerosis: from pathophysiology to practice |journal=Journal of the American College of Cardiology |volume=54 |issue=23 |pages=2129–38 |doi=10.1016/j.jacc.2009.09.009 |issn=1558-3597 |pmc=2834169 |pmid=19942084}}</ref> Unstable atherosclerotic plaque may rupture and release debris and thrombi that may travel to different parts of the circulatory system, causing embolization and therefore, an ischemic stroke. Therefore, PD has been suggested as an independent risk factor for stroke.

A variety of cardiovascular diseases can also be associated with periodontal disease. Patients with higher levels of inflammatory markers such as TNF, IL-1, IL-6 and IL-8 can lead to progression of atherosclerosis and the development and perpetuation of atrial fibrillation,<ref>{{Cite journal |last1=Harada |first1=Masahide |last2=Van Wagoner |first2=David R. |last3=Nattel |first3=Stanley |date=2015 |title=Role of Inflammation in Atrial Fibrillation Pathophysiology and Management |journal=Circulation Journal |volume=79 |issue=3 |pages=495–502 |doi=10.1253/circj.cj-15-0138 |pmid=25746525 |pmc=4457364 |issn=1346-9843}}</ref> as it is associated with platelet and coagulation cascade activations, leading to thrombosis and thrombotic complications.

Experimental animal studies have shown a link between periodontal disease, oxidative stress, and cardiac stress. Oxidative stress favours the development and progression of heart failure as it causes cellular dysfunction, oxidation of proteins and lipids, and damage to the deoxyribonucleic acid (DNA), stimulating fibroblast proliferation and metalloproteinases activation, favoring cardiac remodelling.<ref>{{Cite journal |last1=Tsutsui |first1=Hiroyuki |last2=Kinugawa |first2=Shintaro |last3=Matsushima |first3=Shouji |date=December 2011 |title=Oxidative stress and heart failure |journal=American Journal of Physiology. Heart and Circulatory Physiology |volume=301 |issue=6 |pages=H2181–90 |doi=10.1152/ajpheart.00554.2011 |issn=1522-1539 |pmid=21949114|s2cid=25334639 }}</ref>

During SARS Covid 19 pandemic, Periodontitis was significantly associated with a higher risk of complications from COVID‐19, including ICU admission, need for assisted ventilation, and death, and increased blood levels of markers such as D‐dimer, WBC, and CRP, which are linked with worse disease outcome.<ref>{{cite journal |last1=Marouf |first1=Nadya |title=Association between periodontitis and severity of COVID-19 infection: A case–control study |journal=Journal of Clinical Periodontology |date=2021 |volume=48 |issue=4 |pages=483–491 |doi=10.1111/jcpe.13435 |pmid=33527378|pmc=8014679 }}</ref>

== Clinical significance ==
{{Cleanup rewrite|date=April 2024|it focuses on a single aspect of the disease while ignoring other clinical consequences.|section=yes}}

=== Inadequate nutrition and periodontal disease ===
Periodontal disease is multifactorial, and nutrition can significantly affect its prognosis. Studies have shown that a healthy and well-balanced diet is crucial to maintaining periodontal health.<ref name=":3" /> Nutritional deficiencies can lead to oral manifestations such as those in scurvy and rickets disease. 
Different vitamins will play different roles in periodontal health:
* Vitamin C: Deficiencies may lead to gingival inflammation and bleeding, subsequently advancing periodontal disease
* Vitamin D: Deficiencies may lead to delayed post-surgical healing
* Vitamin E: Deficiencies may lead to impaired gingival wound healing
* Vitamin K: Deficiencies may lead to gingival bleeding
Nutritional supplements of vitamins have also been shown to positively affect healing after periodontal surgery and many of these vitamins can be found in a variety of food that we eat within a regular healthy diet.<ref name=":3" /> 
Therefore, vitamin intakes (particularly vitamin C) and dietary supplements not only play a role in improving periodontal health, but also influence the rate of bone formation and periodontal regeneration. However, studies supporting the correlation between nutrition and periodontal health are limited, and more long-term research is required to confirm this.<ref>{{cite journal |last1=Najeeb |first1=Shariq |last2=Zafar |first2=Muhammad Sohail |last3=Khurshid |first3=Zohaib |last4=Zohaib |first4=Sana |last5=Almas |first5=Khalid |title=The Role of Nutrition in Periodontal Health: An Update |journal=Nutrients |page=530 |doi=10.3390/nu8090530 |date=30 August 2016|volume=8 |issue=9 |pmid=27589794 |pmc=5037517 |doi-access=free }}</ref>

== 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 home care 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 a 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, is termed "overhangs", and serves 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 in 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]] appears to play a role in determining the risk for periodontitis. It is believed that genetics could explain why some people with good plaque control have advanced periodontitis, while others with poor oral hygiene are free from the disease. Genetic factors that 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 | article-number = 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.

==Mechanism==
As dental plaque or biofilm accumulates on the teeth near and below the gums there is some [[dysbiosis]] of the normal [[oral microbiome]].<ref name=Kinane2017rev>{{cite journal | vauthors = Kinane DF, Stathopoulou PG, Papapanou PN | title = Periodontal diseases | journal = Nature Reviews. Disease Primers | volume = 3 | article-number = 17038 | date = June 2017 | pmid = 28805207 | doi = 10.1038/nrdp.2017.38 | s2cid = 28018694 }}</ref> As of 2017 it was not certain what species were most responsible for causing harm, but [[gram-negative]] anaerobic bacteria, spirochetes, and viruses have been suggested; in individual people it is sometimes clear that one or more species is driving the disease.<ref name=Kinane2017rev/> Research in 2004 indicated three gram negative anaerobic species: ''[[Aggregatibacter actinomycetemcomitans]]'', ''[[Porphyromonas gingivalis]]'', ''[[Bacteroides forsythus]]'' and ''[[Eikenella corrodens]]''.<ref name=Preshaw04/>

Plaque may be soft and uncalcified, hard and calcified, or both; for plaques that are on teeth, the calcium comes from saliva; for plaques below the gumline, it comes from blood via [[Transudate|oozing]] of inflamed gums.<ref name=Kinane2017rev/>

The damage to teeth and gums comes from the immune system as it attempts to destroy the microbes that are disrupting the normal symbiosis between the oral tissues and the oral microbe community. As in other tissues, [[Langerhans cells]] in the [[epithelium]] take up [[antigens]] from the microbes, and present them to the immune system, leading to movement of [[white blood cell]]s into the affected tissues. This process in turn activates [[osteoclasts]], which begin to destroy bone, and it activates [[matrix metalloproteinases]] that destroy ligaments.<ref name=Kinane2017rev/> So, in summary, it is bacteria that initiate the disease, but key destructive events are brought about by the exaggerated response from the host's immune system.<ref name=Preshaw04/>

==Classification==
[[File:Depiction of a Periodontitis patient.png|thumb|upright=1.3|Person with periodontitis]]
{{See also|List of periodontal diseases}}
There were several attempts to introduce an agreed-upon classification system for periodontal diseases: in 1989, 1993, 1999,<ref name=armitage1999/> and 2017.

=== 1999 classification ===
The 1999 classification system for periodontal diseases and conditions listed seven major categories of periodontal diseases,<ref name="armitage1999">{{cite journal | vauthors = Armitage GC | title = Development of a classification system for periodontal diseases and conditions | journal = Annals of Periodontology | volume = 4 | issue = 1 | pages = 1–6 | date = December 1999 | pmid = 10863370 | doi = 10.1902/annals.1999.4.1.1 | s2cid = 24243752 | doi-access = free }}</ref> of which 2–6 are termed ''destructive'' periodontal disease, because the damage is essentially irreversible. The seven categories are as follows:

* [[Gingivitis]]
* [[Chronic periodontitis]]
* [[Aggressive periodontitis]]
* [[Periodontitis as a manifestation of systemic disease]]
* [[Necrotizing periodontal diseases|Necrotizing ulcerative gingivitis/periodontitis]]
* [[Abscesses of the periodontium]]
* [[Combined periodontic-endodontic lesions]]

Moreover, terminology expressing both the extent and severity of periodontal diseases are appended to the terms above to denote the specific diagnosis of a particular person or group of people.

====Severity====

The "severity" of disease refers to the amount of [[periodontal ligament]] fibers that have been lost, termed "clinical attachment loss". According to the 1999 classification, the severity of chronic periodontitis is graded as follows:<ref>{{cite web|url=http://www.cda-adc.ca/jcda/vol-66/issue-11/594.html|title=The Periodontal Disease Classification System of the American Academy of Periodontology — An Update|website=American Academy of Periodontology}}</ref>
* Slight: {{convert|1|–|2|mm|abbr=on}} of attachment loss
* Moderate: {{convert|3|–|4|mm|abbr=on}} of attachment loss
* Severe: ≥ {{convert|5|mm|abbr=on}} of attachment loss

====Extent====
The "extent" of disease refers to the proportion of the dentition affected by the disease in terms of percentage of sites.<ref>{{Citation |last1=Gasner |first1=Noah S. |title=Periodontal Disease |date=2025 |work=StatPearls |url=http://www.ncbi.nlm.nih.gov/books/NBK554590/ |access-date=2025-10-07 |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=32119477 |last2=Schure |first2=Ryan S.}}</ref> Sites are defined as the positions at which probing measurements are taken around each tooth, and, generally, six probing sites around each tooth are recorded, as follows: mesiobuccal, mid-buccal, and distobuccal; mesiolingual, mid-lingual, and distolingual.<ref>{{Cite journal |last1=Mittal |first1=Swati |last2=Komiyama |first2=Maki |last3=Ozaki |first3=Yuka |last4=Yamakage |first4=Hajime |last5=Satoh-Asahara |first5=Noriko |last6=Yasoda |first6=Akihiro |last7=Wada |first7=Hiromichi |last8=Funamoto |first8=Masafumi |last9=Shimizu |first9=Kana |last10=Miyazaki |first10=Yusuke |last11=Katanasaka |first11=Yasufumi |last12=Sunagawa |first12=Yoichi |last13=Morimoto |first13=Tatsuya |last14=Takahashi |first14=Yuko |last15=Nakayama |first15=Takeo |date=2022-05-19 |title=Gingival bleeding and pocket depth among smokers and the related changes after short-term smoking cessation |journal=Acta Odontologica Scandinavica |volume=80 |issue=4 |pages=258–263 |doi=10.1080/00016357.2021.1995040 |issn=0001-6357 |pmid=34893003|doi-access=free }}</ref>

If up to 30% of sites in the mouth are affected, the manifestation is classified as "localized"; for more than 30%, the term "generalized" is used.<ref>{{Cite web |title=Chapter 5: periodontal diseases |url=https://www.gov.uk/government/publications/delivering-better-oral-health-an-evidence-based-toolkit-for-prevention/chapter-5-periodontal-diseases |access-date=2025-10-07 |website=GOV.UK |language=en}}</ref>

=== 2017 classification ===
The 2017 classification of periodontal diseases is as follows:<ref>{{cite journal | vauthors = Jepsen S, Caton JG, Albandar JM, Bissada NF, Bouchard P, Cortellini P, Demirel K, de Sanctis M, Ercoli C, Fan J, Geurs NC, Hughes FJ, Jin L, Kantarci A, Lalla E, Madianos PN, Matthews D, McGuire MK, Mills MP, Preshaw PM, Reynolds MA, Sculean A, Susin C, West NX, Yamazaki K | title = Periodontal manifestations of systemic diseases and developmental and acquired conditions: Consensus report of workgroup 3 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions | journal = Journal of Clinical Periodontology | volume = 45 | pages = S219–S229 | date = June 2018 | issue = Suppl 20 | pmid = 29926500 | doi = 10.1111/jcpe.12951 | url = https://research-information.bristol.ac.uk/files/161189168/R2corr_Workgroup3_Consensus_Report.pdf | doi-access = free }}</ref><ref>{{cite journal | vauthors = Berglundh T, Armitage G, Araujo MG, Avila-Ortiz G, Blanco J, Camargo PM, Chen S, Cochran D, Derks J, Figuero E, Hämmerle CH, Heitz-Mayfield LJ, Huynh-Ba G, Iacono V, Koo KT, Lambert F, McCauley L, Quirynen M, Renvert S, Salvi GE, Schwarz F, Tarnow D, Tomasi C, Wang HL, Zitzmann N | title = Peri-implant diseases and conditions: Consensus report of workgroup 4 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions | journal = Journal of Clinical Periodontology | volume = 45 | pages = S286–S291 | date = June 2018 | issue = Suppl 20 | pmid = 29926491 | doi = 10.1111/jcpe.12957 | doi-access = free | hdl = 2027.42/144618 | hdl-access = free }}</ref><ref name=":2" />

Periodontal health, [[Gums|gingival]] disease and conditions

* Periodontal health and [[Gums|gingival]] health
** Clinical gingival health on an intact periodontium
** Clinical gingival health on an intact periodontium
*** Stable periodontitis
*** Non-periodontitis person
*[[Gingivitis]] — Dental [[biofilm]] induced
**Associated with the dental biofilm alone
**Mediated by systemic and local risk factors
**Drug-induced gingival enlargement.
*[[Gingival disease]]s — Non dental [[biofilm]] induced
**Genetic/developmental disorders
**Specific infections
**Inflammatory and immune conditions
**Reactive processes
**Neoplasms
**Endocrine, nutritional, and metabolic
**Traumatic lesions
**Gingival pigmentation.

Periodontitis

*[[Necrotizing periodontal diseases]]
**[[Acute necrotizing ulcerative gingivitis|Necrotizing Gingivitis]]
**Necrotizing periodontitis
**Necrotizing stomatitis
* [[Periodontitis as a manifestation of systemic disease]]
* Periodontitis

Other conditions affecting the [[periodontium]]

(Periodontal Manifestations of Systemic Diseases and Developmental and Acquired Conditions)

* Systemic disease of conditions affecting the [[periodontal]] support tissues
* Other Periodontal Conditions
** Periodontal [[abscess]]es
** [[Endodontics|Endodontic-]] periodontal [[lesion]]s
*[[Mucogingival junction|Mucogingival]] deformities and conditions
**Gingival Phenotype
**Gingival/Soft Tissue Recession
**Lack of Gingiva
**Decreased Vestibular Depth
**Aberrant Frenum/muscle position
**Gingival Excess
**Abnormal Color
**Condition of the exposed root surface
*[[Occlusal trauma|Traumatic occlusal forces]]
**Primary Occlusal Trauma
**Secondary Occlusal Trauma
* Tooth and [[Dental prosthesis|prosthesis]] related factors
** Localized tooth-related factors
** Localized dental prostheses-related factors

Peri-implant diseases and conditions

* Peri-implant health
*[[Peri-implant mucositis]]
*[[Peri-implantitis]]
* Peri-implant soft and hard tissue deficiencies

==== Staging ====
The goals of staging periodontitis are to classify the severity of damage and assess specific factors that may affect management.<ref name=":2" />

According to the 2017 classification, periodontitis is divided into four stages, after considering a few factors such as:

* Amount and percentage of bone loss radiographically
* Clinical attachment loss, probing depth
* Presence of furcation
* Vertical bony defects
* History of tooth loss related to periodontitis
* Tooth hypermobility due to secondary occlusal trauma<ref name=":2">{{cite journal | vauthors = Caton JG, Armitage G, Berglundh T, Chapple IL, Jepsen S, Kornman KS, Mealey BL, Papapanou PN, Sanz M, Tonetti MS | title = A new classification scheme for periodontal and peri-implant diseases and conditions — Introduction and key changes from the 1999 classification | journal = Journal of Periodontology | volume = 89 | pages = S1–S8 | date = June 2018 | issue = Suppl 1 | pmid = 29926946 | doi = 10.1002/jper.18-0157 | s2cid = 49353912 | url = http://pure-oai.bham.ac.uk/ws/files/50172936/Caton_et_al_Version_3.0_NO_TABLES_PNP_amendments_1_ILC.pdf | doi-access = free }}</ref>

==== Grading ====
According to the 2017 classification, the grading system for periodontitis consists of three grades:<ref name=sgp2017>{{Cite web|url=http://perio.org/sites/default/files/files/Staging%20and%20Grading%20Periodontitis.pdf|title=Staging and Grading Periodontitis }}</ref>

*Grade A: Slow progression of disease; no evidence of bone loss over the last five years
*Grade B: Moderate progression; < 2mm of bone loss over the last five years
*Grade C: Rapid progression or future progression at high risk; ≥ 2mm bone loss over five years

Risk factors affecting which grade a person is classified into include:<ref name=sgp2017/>

*Smoking
* Diabetes

=== Periodontal probing ===
{{Unreferenced section|date=April 2024}}
Dentists and dental hygienists measure periodontal disease using a device called a [[periodontal probe]]. This thin "measuring stick" is gently placed into the space between the gums and the teeth, and slipped below the gumline. If the probe can slip more than {{convert|3|mm|abbr=on}} below the gumline, the person is said to have a gingival pocket if no migration of the epithelial attachment has occurred or a periodontal pocket if apical migration has occurred. This is somewhat of a misnomer, as any depth is, in essence, a pocket, which in turn is defined by its depth, i.e., a 2-mm pocket or a 6-mm pocket. However, pockets are generally accepted as self-cleansable (at home, by the person, with a toothbrush) if they are 3&nbsp;mm or less in depth. This is important because if a pocket is deeper than 3&nbsp;mm around the tooth, at-home care will not be sufficient to cleanse the pocket, and professional care should be sought. When the pocket depths reach {{convert|6|to|7|mm|abbr=on}} in depth, the hand instruments and ultrasonic scalers used by the dental professionals may not reach deeply enough into the pocket to clean out the microbial plaque that causes gingival inflammation. In such a situation, the bone or the gums around that tooth should be surgically altered, or it will always have inflammation, which will likely result in more bone loss around that tooth. An additional way to stop the inflammation would be for the person to receive subgingival antibiotics (such as [[minocycline]]) or undergo some form of gingival surgery to access the depths of the pockets and perhaps even change the pocket depths so they become 3&nbsp;mm or less in depth and can once again be properly cleaned by the person at home with his or her toothbrush.

== Prevention ==
Daily [[oral hygiene]] measures to prevent periodontal disease include:
*[[toothbrush|Brushing]] properly regularly (at least twice daily), with the person attempting to direct the toothbrush bristles underneath the gumline, helps disrupt the bacterial-mycotic growth and formation of subgingival plaque.{{citation needed|date=May 2018}}
*[[Flossing]] daily and using interdental brushes (if the space between teeth is large enough), as well as cleaning behind the last tooth, the third molar, in each quarter.{{citation needed|date=May 2018}}
*Using an antiseptic [[mouthwash]]: [[Chlorhexidine gluconate]]-based mouthwash in combination with careful oral hygiene may cure gingivitis, although they cannot reverse any attachment loss due to periodontitis.{{citation needed|date=May 2018}}
*Regular dental check-ups and professional teeth cleaning as required: Dental check-ups serve to monitor the person's oral hygiene methods and levels of attachment around teeth, identify any early signs of periodontitis, and monitor response to treatment.

Typically, dental hygienists (or dentists) use special instruments to clean (debride) teeth below the gumline and disrupt any plaque growing below the gumline. This is a standard treatment to prevent any further progression of established periodontitis. Studies show that after such a professional cleaning (periodontal debridement), microbial plaque tends to regrow to precleaning levels after about three to four months. Nonetheless, the continued stabilization of a person's periodontal state depends largely, if not primarily, on the person's oral hygiene at home, as well as on the go. Without daily [[oral hygiene]], periodontal disease will not be overcome, especially if the person has a history of extensive periodontal disease.{{citation needed|date=June 2016}}

==Management==
[[File:Generalized perio -touched up.jpg|thumb|right|This section from a panoramic [[radiograph|X-ray film]] depicts the teeth of the lower left quadrant, exhibiting generalized severe bone loss of 30–80%. The ''red line'' depicts the existing bone level, whereas the ''yellow line'' depicts where the gingiva was located originally (1–2 mm above the bone), before the person developed periodontal disease. The ''pink arrow'', on the right, points to a [[Furcation defect|furcation involvement]], or the loss of enough bone to reveal the location at which the individual roots of a molar begin to branch from the single root trunk; this is a sign of advanced periodontal disease. The ''blue arrow'', in the middle, shows up to 80% bone loss on tooth No. 21, and clinically, this tooth exhibited gross mobility. Finally, the ''peach oval'', to the left, highlights the aggressive nature with which periodontal disease generally affects mandibular incisors. Because their roots are generally situated very close to each other, with minimal [[Commonly used terms of relationship and comparison in dentistry|interproximal]] bone, and because of their location in the mouth, where plaque and calculus accumulation is greatest because of the pooling of [[saliva]],{{Citation needed|date=December 2011}} mandibular anteriors are affected excessively. The ''split in the red line'' depicts varying densities of bone that contribute to a vague region of definitive bone height.]]

The cornerstone of successful periodontal treatment starts with establishing excellent [[oral hygiene]]. This includes twice-daily [[toothbrush|brushing]] with daily [[flossing]]. Also, the use of an [[interdental brush]] is helpful if the space between the teeth allows. For smaller spaces, products such as narrow picks with soft rubber bristles provide excellent manual cleaning. Persons with dexterity problems, such as with [[arthritis]], may find oral hygiene to be difficult and may require more frequent professional care and/or the use of a powered toothbrush. Persons with periodontitis must realize it is a chronic inflammatory disease and a life-long regimen of excellent hygiene and professional maintenance care with a dentist/hygienist or [[periodontist]] is required to maintain affected teeth.

===Initial therapy===
Removal of microbial plaque and calculus is necessary to establish periodontal health. The first step in the treatment of periodontitis involves nonsurgical cleaning below the gum line with a procedure called "root surface instrumentation" or "RSI", which causes a mechanical disturbance to the bacterial biofilm below the gum line.<ref name=Preshaw04/> This procedure involves the use of specialized curettes to mechanically remove plaque and calculus from below the gumline, and may require multiple visits and [[local anesthesia]] to adequately complete. In addition to initial RSI, it may also be necessary to adjust the occlusion (bite) to prevent excessive force on teeth that have reduced bone support. Also, it may be necessary to complete any other dental needs, such as replacement of rough, plaque-retentive restorations, closure of open contacts between teeth, and any other requirements diagnosed at the initial evaluation. It is important to note that RSI is different from [[scaling and root planing]]: RSI only removes the [[Calculus (dental)|calculus]], while scaling and root planing removes the calculus as well as diseased cementum, which leaves behind a smooth and glassy surface, which is not a requisite for periodontal healing. Therefore, RSI is now advocated over root planing.<ref name=Preshaw04/>

===Reevaluation===
Nonsurgical [[scaling and root planing]] are usually successful if the periodontal pockets are shallower than {{convert|4|–|5|mm|abbr=on}}.<ref>{{cite journal | vauthors = Stambaugh RV, Dragoo M, Smith DM, Carasali L | title = The limits of subgingival scaling | journal = The International Journal of Periodontics & Restorative Dentistry | volume = 1 | issue = 5 | pages = 30–41 | year = 1981 | pmid = 7047434 }}</ref><ref>{{cite journal | vauthors = Waerhaug J | title = Healing of the dento-epithelial junction following subgingival plaque control. I. As observed in human biopsy material | journal = Journal of Periodontology | volume = 49 | issue = 1 | pages = 1–8 | date = January 1978 | pmid = 340634 | doi = 10.1902/jop.1978.49.1.1 }}</ref><ref>{{cite journal | vauthors = Waerhaug J | title = Healing of the dento-epithelial junction following subgingival plaque control. II: As observed on extracted teeth | journal = Journal of Periodontology | volume = 49 | issue = 3 | pages = 119–34 | date = March 1978 | pmid = 288899 | doi = 10.1902/jop.1978.49.3.119 }}</ref> The dentist or hygienist must perform a re-evaluation four to six weeks after the initial scaling and root planing, to determine if the person's oral hygiene has improved and inflammation has regressed. Probing should be avoided then, and an analysis by the gingival index should determine the presence or absence of inflammation. The monthly reevaluation of periodontal therapy should involve periodontal charting as a better indication of the success of treatment, and to see if other courses of treatment can be identified. Pocket depths of greater than {{convert|5|–|6|mm|abbr=on}} which remain after initial therapy, with bleeding upon probing, indicate continued active disease and will very likely lead to further bone loss over time. This is especially true in [[molar (tooth)|molar]] tooth sites where [[Furcation defect|furcations]] (areas between the roots) have been exposed.

===Surgery===
If nonsurgical therapy is found to have been unsuccessful in managing signs of disease activity, periodontal surgery may be needed to stop progressive bone loss and regenerate lost bone where possible. Many surgical approaches are used in the treatment of advanced periodontitis, including open flap debridement and osseous surgery, as well as guided tissue regeneration and bone grafting. The goal of periodontal surgery is access for definitive calculus removal and surgical management of bony irregularities that have resulted from the disease process to reduce pockets as much as possible. Long-term studies have shown that in moderate to advanced periodontitis, surgically treated cases often have less further breakdown over time and, when coupled with a regular post-treatment maintenance regimen, are successful in nearly halting tooth loss in nearly 85% of diagnosed people.<ref>{{cite journal | vauthors = Kaldahl WB, Kalkwarf KL, Patil KD, Molvar MP, Dyer JK | title = Long-term evaluation of periodontal therapy: II. Incidence of sites breaking down | journal = Journal of Periodontology | volume = 67 | issue = 2 | pages = 103–8 | date = February 1996 | pmid = 8667129 | doi = 10.1902/jop.1996.67.2.103 }}</ref><ref>{{cite journal | vauthors = Hirschfeld L, Wasserman B | title = A long-term survey of tooth loss in 600 treated periodontal patients | journal = Journal of Periodontology | volume = 49 | issue = 5 | pages = 225–37 | date = May 1978 | pmid = 277674 | doi = 10.1902/jop.1978.49.5.225 }}</ref>

===Local drug delivery===
Local drug deliveries in periodontology have gained acceptance and popularity compared to systemic drugs due to decreased risk of the development of resistant flora and other side effects.<ref>{{cite journal | vauthors = Kalsi R, Vandana KL, Prakash S | title = Effect of local drug delivery in chronic periodontitis patients: A meta-analysis | journal = Journal of Indian Society of Periodontology | volume = 15 | issue = 4 | pages = 304–9 | date = October 2011 | pmid = 22368351 | pmc = 3283924 | doi = 10.4103/0972-124X.92559 | doi-access = free }}</ref> A meta analysis of local tetracycline found improvement.<ref name="pmid29238136">{{cite journal | vauthors = Nadig PS, Shah MA | title = Tetracycline as local drug delivery in treatment of chronic periodontitis: A systematic review and meta-analysis | journal = Journal of Indian Society of Periodontology | volume = 20 | issue = 6 | pages = 576–583 | year = 2016 | pmid = 29238136 | pmc = 5713079 | doi = 10.4103/jisp.jisp_97_17 | doi-access = free }}</ref> Local application of [[statin]] may be useful.<ref>{{cite journal | vauthors = Bertl K, Parllaku A, Pandis N, Buhlin K, Klinge B, Stavropoulos A | title = The effect of local and systemic statin use as an adjunct to non-surgical and surgical periodontal therapy-A systematic review and meta-analysis | journal = Journal of Dentistry | volume = 67 | pages = 18–28 | date = December 2017 | pmid = 28855141 | doi = 10.1016/j.jdent.2017.08.011 | hdl = 2043/23307 | url = http://urn.kb.se/resolve?urn=urn:nbn:se:mau:diva-16218 | hdl-access = free }}</ref>

===Systemic drug delivery===
Systemic drug delivery in conjunction with non-surgical therapy may be used as a means to reduce the percentage of the bacterial plaque load in the mouth. Many different antibiotics and also combinations of them have been tested; however, there is still very low-certainty evidence of any significant difference in the short and long term compared to non-surgical therapy alone. It may be beneficial to limit the use of systemic drugs, since bacteria can develop antimicrobial resistance and some specific antibiotics might induce temporary mild adverse effects, such as nausea, diarrhoea and gastrointestinal disturbances.<ref name=Khattri20>{{cite journal | vauthors = Khattri S, Kumbargere Nagraj S, Arora A, Eachempati P, Kusum CK, Bhat KG, Johnson TM, Lodi G | title = Adjunctive systemic antimicrobials for the non-surgical treatment of periodontitis. | journal = Cochrane Database of Systematic Reviews | issue = 11 | pages = 1465–1858 | year = 2020 | volume = 2020 | id = CD012568 | doi = 10.1002/14651858.CD012568.pub2| pmid = 33197289 | pmc = 9166531 | s2cid = 226990528 }}</ref>

=== Adjunctive systemic antimicrobial treatment ===
There is currently low-quality evidence suggesting that adjunctive systemic antimicrobials are beneficial for the non-surgical treatment of periodontitis.<ref name=Khattri20/> It is not sure whether some antibiotics are better than others when used alongside scaling and root planing).

===Maintenance===
Once successful periodontal treatment has been completed, with or without surgery, an ongoing regimen of "periodontal maintenance" is required. This involves regular checkups and detailed cleanings every three months to prevent repopulation of periodontitis-causing microorganisms, and to closely monitor affected teeth so early treatment can be rendered if the disease recurs. Usually, periodontal disease exists due to poor plaque control resulting from inappropriate brushing. Therefore, if the brushing techniques are not modified, a periodontal recurrence is probable.

=== Other ===
Most alternative "at-home" gum disease treatments involve injecting antimicrobial solutions, such as [[hydrogen peroxide]], into periodontal pockets via slender applicators or oral irrigators. This process disrupts anaerobic microorganism colonies and is effective at reducing infections and inflammation when used daily. A number of other products, functionally equivalent to hydrogen peroxide, are commercially available, but at substantially higher cost. However, such treatments do not address calculus formations, and so are short-lived, as anaerobic microbial colonies quickly regenerate in and around calculus.

[[Doxycycline]] may be given [[Adjuvant therapy|alongside the primary therapy]] of scaling (see [[#Initial therapy|§ initial therapy]]).<ref name="caton2011">{{cite journal | vauthors = Caton J, Ryan ME | title = Clinical studies on the management of periodontal diseases utilizing subantimicrobial dose doxycycline (SDD) | journal = Pharmacological Research | volume = 63 | issue = 2 | pages = 114–20 | date = February 2011 | pmid = 21182947 | doi = 10.1016/j.phrs.2010.12.003 }}</ref> Doxycycline has been shown to improve indicators of disease progression (namely probing depth and attachment level).<ref name="caton2011" /> Its mechanism of action involves inhibition of matrix metalloproteinases (such as collagenase), which degrade the teeth's supporting tissues ([[periodontium]]) under inflammatory conditions.<ref name="caton2011" /> To avoid killing beneficial [[Oral microbiology|oral microbes]], only small doses of doxycycline (20&nbsp;mg) are used.<ref name="caton2011" />

[[Phage therapy]] may be a new therapeutic alternative.<ref>{{cite journal |vauthors=Steier L, de Oliveira SD, de Figueiredo JA |title=Bacteriophages in Dentistry-State of the Art and Perspectives |journal=Dent J |volume=7 |issue=1 |page=6 |date=January 2019 |pmid=30634460 |pmc=6473837 |doi=10.3390/dj7010006 |doi-access=free}}</ref>

==Prognosis==
If people have 7-mm or deeper pockets around their teeth, as measured by a [[periodontal probe]], then they would likely risk eventual tooth loss over the years.{{Citation needed|date=April 2024}} If this periodontal condition is not identified and people remain unaware of the progressive nature of the disease, then years later, they may be surprised that some teeth will gradually become loose and may need to be extracted, sometimes due to a severe infection or even pain.{{Citation needed|date=April 2024}}

According to the Sri Lankan tea laborer study, in the absence of any oral hygiene activity, approximately 10% will experience severe periodontal disease with rapid loss of attachment (>2&nbsp;mm/year). About 80% will experience moderate loss (1–2&nbsp;mm/year), and the remaining 10% will not experience any loss.<ref name="JclinPeriodontol1995-Preus">{{cite journal | vauthors = Preus HR, Anerud A, Boysen H, Dunford RG, Zambon JJ, Löe H | title = The natural history of periodontal disease. The correlation of selected microbiological parameters with disease severity in Sri Lankan tea workers | journal = Journal of Clinical Periodontology | volume = 22 | issue = 9 | pages = 674–8 | date = September 1995 | pmid = 7593696 | doi = 10.1111/j.1600-051X.1995.tb00825.x }}</ref><ref name="ComDentOralEpidemiol1984-Ekanayaka">{{cite journal | vauthors = Ekanayaka A | title = Tooth mortality in plantation workers and residents in Sri Lanka | journal = Community Dentistry and Oral Epidemiology | volume = 12 | issue = 2 | pages = 128–35 | date = April 1984 | pmid = 6584263 | doi = 10.1111/j.1600-0528.1984.tb01425.x }}</ref>

== Epidemiology ==
{{main|Epidemiology of periodontal diseases}}
[[File:Periodontal disease world map - DALY - WHO2004.svg|thumb|upright=1.3|[[Disability-adjusted life year]] for periodontal disease per 100,000&nbsp;inhabitants in 2004:<ref>{{cite web |url=https://www.who.int/entity/healthinfo/statistics/bodgbddeathdalyestimates.xls |title=Mortality and Burden of Disease Estimates for WHO Member States in 2002|format=xls |work=World Health Organization|year=2002 }}</ref>
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Periodontitis is very common, and is widely regarded as the second most common dental disease worldwide, after [[dental decay]], and in the United States has a [[prevalence]] of 30–50% of the population, but only about 10% have severe forms.

Chronic periodontitis affects about 750&nbsp;million people or about 10.8% of the world population as of 2010.<ref>{{cite journal | vauthors = Vos T, Flaxman AD, Naghavi M, Lozano R, Michaud C, Ezzati M, etal | title = Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990–2010: a systematic analysis for the Global Burden of Disease Study 2010 | journal = Lancet | volume = 380 | issue = 9859 | pages = 2163–96 | date = December 2012 | pmid = 23245607 | pmc = 6350784 | doi = 10.1016/S0140-6736(12)61729-2 }}</ref>

Like other conditions intimately related to access to hygiene and basic medical monitoring and care, periodontitis tends to be more common in economically disadvantaged populations or regions. Its occurrence decreases with a higher standard of living. In Israeli populations, individuals of Yemenite, North-African, South Asian, or Mediterranean origin have a higher prevalence of periodontal disease than individuals of European descent.<ref name="pmid18780541">{{cite journal | vauthors = Zadik Y, Bechor R, Shochat Z, Galor S | title = [Ethnic origin and alveolar bone loss in Israeli adults] | language = he | journal = Refu'at Ha-Peh Veha-Shinayim | volume = 25 | issue = 2 | pages = 19–22, 72 | date = April 2008 | pmid = 18780541 }}</ref> Periodontitis is frequently reported to be socially patterned, i.e. people from the lower end of the socioeconomic scale are affected more often than people from the upper end of the socioeconomic scale.<ref name="Watt"/>

==History==
An ancient hominid from 3 million years ago had gum disease.<ref>{{cite journal |last1=Forshaw |first1=R. J. |title=Dental health and disease in ancient Egypt |journal=British Dental Journal |date=April 2009 |volume=206 |issue=8 |pages=421–4 |doi=10.1038/sj.bdj.2009.309 |pmid=19396207 |s2cid=24832214 }}</ref> Records from China and the Middle East, along with archaeological studies, show that mankind has had periodontal disease for at least many thousands of years. In Europe and the Middle East, archaeological research looking at ancient plaque DNA shows that in the ancient hunter-gatherer lifestyle, there was less gum disease, but that it became more common when more cereals were eaten. The [[Otzi Iceman]] was shown to have had severe gum disease.{{citation needed|date=April 2020}} Furthermore, research has shown that in the Roman era in the UK, there was less periodontal disease than in modern times. The researchers suggest that smoking may be a key to this.<ref>{{cite web |title=Roman-Britons had less gum disease than modern Britons |url=https://www.heritagedaily.com/2014/10/roman-britons-had-less-gum-disease-than-modern-britons/105351 |website=HeritageDaily — Archaeology News |access-date=22 April 2020 |date=24 October 2014}}</ref>

==Society and culture==

=== Etymology ===
The word "periodontitis" ([[Greek Language|Greek]]: {{lang|grc|περιοδοντίτις}}) comes from the Greek ''peri'', "around", {{transliteration|grc|odous}} (<small>[[Genitive case|GEN]]</small> {{transliteration|grc|odontos}}), "tooth", and the suffix {{transliteration|grc|-''itis''}}, in medical terminology "[[inflammation]]".<ref>{{OEtymD|periodontitis}} {{OEtymD|periodontal}} {{LSJ|o)dou/s|ὀδούς}}, {{LSJ|o)dw/n|ὀδών|ref}}.</ref> The word ''pyorrhea'' (alternative spelling: ''pyorrhoea'') comes from the Greek {{transliteration|grc|pyorrhoia}} ({{lang|grc|πυόρροια}}), "discharge of matter", itself from {{transliteration|grc|pyon}}, "discharge from a sore", ''rhoē'', "flow", and the suffix -''ia''.<ref>{{LSJ|puo/rroia|πυόρροια}}, {{LSJ|pu/on|πύον|}}, {{LSJ|r(oh/|ῥοή|}}; [[cf.]] {{LSJ|puorroe/w|πυορροέω|shortref}}. {{OEtymD|-ia}}</ref> In English this term can describe, as in Greek, any discharge of [[pus]]; i.e. it is not restricted to these diseases of the teeth.<ref>{{cite encyclopedia|url=http://medical-dictionary.thefreedictionary.com/pyorrhea|title=pyorrhea|dictionary=[[Merriam-Webster]] Online}}</ref>

===Economics===
It is estimated that lost [[productivity]] due to severe periodontitis costs the global economy about US$54&nbsp;billion each year.<ref>{{cite journal | vauthors = Listl S, Galloway J, Mossey PA, Marcenes W | title = Global Economic Impact of Dental Diseases | journal = Journal of Dental Research | volume = 94 | issue = 10 | pages = 1355–61 | date = October 2015 | pmid = 26318590 | doi = 10.1177/0022034515602879 | s2cid = 39147394 }}</ref>

==Other animals==
Periodontal disease is the most common disease found in dogs and affects more than 80% of dogs aged three years or older. Its prevalence in dogs increases with age, but decreases with increasing body weight; i.e., toy and miniature breeds are more severely affected. Recent research undertaken at the [[Waltham Centre for Pet Nutrition]] has established that the bacteria associated with gum disease in dogs are not the same as in humans.<ref name="pmid22558330">{{cite journal | vauthors = Dewhirst FE, Klein EA, Thompson EC, Blanton JM, Chen T, Milella L, Buckley CM, Davis IJ, Bennett ML, Marshall-Jones ZV | title = The canine oral microbiome | journal = PLOS ONE | volume = 7 | issue = 4 | article-number = e36067 | date = 2012 | pmid = 22558330 | pmc = 3338629 | doi = 10.1371/journal.pone.0036067 | bibcode = 2012PLoSO...736067D | doi-access = free }}</ref> Systemic disease may develop because the gums are very vascular (have a good blood supply). The bloodstream carries these anaerobic microorganisms, and they are filtered out by the [[kidney]]s and [[liver]], where they may colonize and create microabscesses. The microorganisms traveling through the blood may also attach to the [[heart]] valves, causing vegetative [[infective endocarditis]] (infected heart valves). Additional diseases that may result from periodontitis include chronic [[bronchitis]] and pulmonary [[fibrosis]].<ref>{{cite web | last = Muller-Esnault | first = Susan | title = Periodontal Disease in the Dog and Cat | date = 2009 | url = http://www.critterology.com/articles/periodontal-disease-dog-and-cat | work = Critterology | publisher = Veterinary Internet Company | access-date = 12 March 2009 | archive-url = https://web.archive.org/web/20140827061236/http://www.critterology.com/articles/periodontal-disease-dog-and-cat | archive-date = 27 August 2014 }}</ref>

== Footnotes ==
{{Reflist}}

{{Medical resources
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|  ICD10          = {{ICD10|K|05|4|k|00}}
|  ICD9           = <!--{{ICD9|xxx}}-->
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|  MedlinePlus    = 001059
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|  MeshID         = D010518
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{{Portal|Medicine}}

{{Periodontology}}
{{Oral pathology}}

{{Authority control}}

[[Category:Inflammations]]
[[Category:Periodontal disorders]]
[[Category:Wikipedia medicine articles ready to translate]]
[[Category:Ötzi]]