Periodontitis (Gum Disease)

Periodontitis is what gum inflammation becomes when it stops being confined to the gums and starts destroying the bone and fibres that hold the teeth in the jaw. It affects roughly four to five in ten adults over 30, it is the leading cause of tooth loss in adults, and, unlike gingivitis, the damage it does is permanent. Treatment is often highly successful — but it arrests the disease, it does not rewind it.

Table of Contents

1. What Periodontitis Is
2. The Line That Matters: Irreversible
3. Causes and Risk Factors
4. Symptoms
5. Diagnosis: Staging and Grading
6. Treatment
7. Prevention and Lifelong Maintenance
8. Systemic Links — What the Evidence Actually Shows
9. Complications
10. When to See a Dentist
11. Key Research Papers
12. Connections
13. Featured Videos

What Periodontitis Is

Periodontitis is a chronic inflammatory disease in which the immune response to a dysbiotic bacterial biofilm destroys the periodontium — the apparatus that holds each tooth in place. That apparatus has four parts: the gingiva, the periodontal ligament, the cementum covering the root, and the alveolar bone of the jaw. Periodontitis eats into the last three.

The sequence is worth understanding because it explains why the disease is so quiet for so long:

1. Plaque accumulates at the gum margin and matures into a biofilm.
2. The gum becomes inflamed — gingivitis. This is reversible. Nothing is lost yet.
3. In a susceptible person, the biofilm shifts in character. The community becomes dominated by anaerobic, Gram-negative organisms — the classic “red complex” of Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola described by Socransky. This is dysbiosis: not an invasion by an outside pathogen, but a resident community tipping out of balance.
4. The junctional epithelium — the seal where gum meets tooth — detaches and migrates down the root. A periodontal pocket forms.
5. The pocket is anaerobic, protected, and impossible to clean with a toothbrush. The bacteria there are now sheltered from both hygiene and the immune system, so the inflammation becomes self-sustaining.
6. The host inflammatory response — not the bacteria directly — does most of the actual damage. Matrix metalloproteinases degrade collagen; RANKL-driven osteoclast activity resorbs alveolar bone. The tooth is being unscrewed from the inside.
7. With enough bone gone, the tooth loosens, drifts, and is eventually lost.

This host-mediated destruction is the central insight of modern periodontology, articulated in Hajishengallis’s work: periodontitis is best understood not as an infection to be sterilised but as a disruption of host–microbe homeostasis in which the immune response is subverted and turned destructive. It is why antibiotics alone do not cure it, and why two people with identical plaque can have completely different outcomes.

Not everyone is susceptible. Löe’s 15-year study of Sri Lankan tea labourers who had never received dental care found that around 8% were rapid progressors who lost teeth young, roughly 81% progressed moderately, and about 11% had essentially no attachment loss despite heavy lifelong plaque. Plaque is necessary; it is not sufficient. The host decides.

The Line That Matters: Irreversible

If you read nothing else, read this.

• Gingivitis is reversible. The gum is inflamed. The attachment and bone are intact. Remove the plaque and the tissue heals completely, usually within one to two weeks. Nothing has been lost.
• Periodontitis is not reversible. Clinical attachment has been lost and alveolar bone has been resorbed. Treatment stops further loss — and it does that very well — but the bone that has gone does not spontaneously regrow, and the gum does not climb back up the root.

The one genuine exception is regenerative surgery, and its limits should be stated plainly. In specific, favourable defect shapes — deep, narrow, contained intrabony defects and certain furcation lesions — grafts, barrier membranes, and biologics such as enamel matrix derivative can regenerate a meaningful amount of bone and attachment. In the far more common pattern of broad, flat, horizontal bone loss, they cannot. Most bone lost to periodontitis is gone for good.

The practical consequence: the goal of treatment is to stop the disease where it is. A patient diagnosed at Stage I with 2 mm of attachment loss and a patient diagnosed at Stage III with 6 mm can both be stabilised for life — but one of them keeps far more bone. Catching this early is worth more than any treatment technique. Which is why bleeding gums, the free warning, matter so much.

Causes and Risk Factors

The Necessary Cause

A dysbiotic subgingival biofilm. No plaque, no periodontitis. But plaque alone does not explain who gets it or how badly, which is where the risk factors come in.

Smoking — the biggest modifiable risk factor

Smoking is far and away the most important modifiable driver. Analysis of the US NHANES III data by Tomar and Asma found current smokers had roughly four times the odds of periodontitis compared with people who had never smoked, and estimated that about 42% of periodontitis cases in US adults were attributable to current smoking, with another ~11% attributable to former smoking — i.e. more than half of adult periodontitis in that population was linked to tobacco.

Smoking makes it worse in several ways at once: it impairs neutrophil function and wound healing, it reduces the gingival blood supply, it worsens response to treatment, and it masks the warning sign — vasoconstriction means smokers’ gums bleed less, so the disease advances silently. Quitting improves the response to periodontal treatment; the risk falls toward that of never-smokers over years of abstinence.

Diabetes

Poorly controlled diabetes (type 1 or type 2) substantially increases both the risk and the severity of periodontitis. Hyperglycaemia drives the formation of advanced glycation end-products, amplifies the inflammatory response, and impairs healing. Well-controlled diabetes carries much less excess risk. This relationship runs in both directions — see the systemic links section.

Other Risk Factors

• Poor oral hygiene and irregular dental care.
• Genetics and family history — susceptibility is substantially heritable. Periodontitis in a parent or sibling, particularly early-onset, matters.
• Age — prevalence rises steeply with age. This is cumulative exposure, not an inevitability of getting older.
• Male sex — consistently higher prevalence in men.
• Socioeconomic disadvantage and poor access to dental care — among the strongest predictors globally, and largely why this is a public-health problem rather than a personal failing.
• Obesity and metabolic syndrome.
• Stress — plausibly via cortisol and immune effects, and via the hygiene and smoking habits that go with it.
• Immunosuppression, including HIV infection and immunosuppressant drugs.
• Dry mouth from medication or from conditions such as Sjögren’s syndrome.
• Rare genetic conditions — Papillon-Lefèvre syndrome, leukocyte adhesion deficiency, Down syndrome, and others cause severe, early, aggressive disease.
• Poor nutrition, particularly severe vitamin C deficiency.
• Bruxism (tooth grinding) — it does not cause periodontitis, but occlusal trauma on a periodontally weakened tooth accelerates its loosening.

Symptoms

The defining problem with periodontitis is that in its early and moderate stages it is usually painless. People routinely present only when a tooth becomes loose — by which point a great deal of bone is already gone. Do not wait for pain. Pain is a late symptom in this disease.

Early

• Bleeding gums when brushing, flossing, or eating (and remember: smokers may not bleed).
• Red, swollen, or tender gums.
• Persistent bad breath or a persistent bad taste.

Established

• Gum recession — teeth looking “longer,” and exposed, darker root surfaces.
• Sensitivity to cold, sweet, or touch on exposed roots.
• Black triangles — gaps opening between the teeth as the interdental papillae are lost.
• Deep pockets — you will not feel these; your dentist measures them.
• Pus at the gum margin, or on pressing the gum.

Advanced

• Loose or mobile teeth.
• Teeth drifting, flaring, or splaying outward; new gaps appearing; a bite that suddenly feels different.
• Pain on chewing; difficulty eating harder foods.
• Periodontal abscess — acute, painful, swollen; this one does hurt.
• Tooth loss.

Diagnosis: Staging and Grading

Diagnosis rests on a full periodontal examination — probing six sites around every tooth — plus radiographs. Three measurements do the work:

1. Probing depth — the depth of the crevice or pocket. Up to 3 mm is normal. 4 mm and above with bleeding is a concern; 6 mm and above is deep and cannot be self-cleaned.
2. Clinical attachment loss (CAL) — measured from the cementoenamel junction, a fixed landmark on the tooth. This is the measurement that distinguishes periodontitis from gingivitis. A swollen gum can create a false pocket; only CAL tells you whether attachment has actually been destroyed.
3. Radiographic bone loss — how far the crest of the alveolar bone has receded down the root, expressed as a percentage of root length.

Bleeding on probing, pus, tooth mobility, and furcation involvement (bone loss between the roots of a multi-rooted tooth) are also recorded.

The 2018 Classification: Stage and Grade

The 2017 World Workshop replaced the old “chronic vs aggressive” labels with a two-axis system borrowed conceptually from oncology. It answers two different questions: how bad is it now? and how fast is it moving?

Stage (I–IV) — severity and complexity

• Stage I — initial periodontitis. Roughly 1–2 mm of interdental CAL at the worst site; bone loss confined to the coronal third (<15%); no teeth lost to periodontitis.
• Stage II — moderate. Around 3–4 mm CAL; bone loss still in the coronal third (15–33%); no teeth lost to periodontitis.
• Stage III — severe, with potential for additional tooth loss. CAL of 5 mm or more; bone loss extending into the middle third of the root or beyond; up to four teeth lost to periodontitis; deep pockets, furcation involvement, vertical defects.
• Stage IV — advanced, with loss of the dentition and a need for complex rehabilitation. Five or more teeth lost to periodontitis, plus problems such as severe bite collapse, drifting and flaring, and severe mobility.

Stage is further described as localised (<30% of teeth) or generalised, or as a molar-incisor pattern.

Grade (A, B, C) — rate of progression

Grade estimates how fast the disease is likely to move, primarily by dividing the percentage of bone loss at the worst site by the patient’s age:

• Grade A — slow progression (bone loss % / age < 0.25).
• Grade B — moderate progression (0.25–1.0).
• Grade C — rapid progression (> 1.0).

The grade is then modified upward by risk factors — smoking (10 or more cigarettes a day pushes toward Grade C) and diabetes (an HbA1c of 7.0% or higher does the same). This is the part patients most often find clarifying: a 30-year-old with 40% bone loss is a very different problem from a 75-year-old with the same 40%, and the classification says so.

Screening

Because full charting takes time, most practices screen with a basic periodontal examination (BPE, or PSR in the US) — a quick sextant-by-sextant score with a ball-ended probe. A high score triggers a full examination. If you have never had a probe run around your gums, you have never been screened for this disease.

Treatment

The European Federation of Periodontology’s S3-level guideline set the modern standard of care as a stepwise protocol, re-evaluating after each step. Treatment is very effective — most patients, including many with severe disease, can be stabilised and keep their teeth for life.

Step 1 — Behaviour and Risk Factors

Before any instrument goes below the gumline: oral hygiene instruction, supragingival plaque and calculus removal, and control of risk factors — smoking cessation and glycaemic control above all. This step is not a formality. A patient who does not change their plaque control will not hold the result of anything done in Steps 2–4.

Step 2 — Subgingival Instrumentation (Scaling and Root Planing)

The core of non-surgical periodontal therapy. Under local anaesthetic, hand and ultrasonic instruments are used to remove plaque and calculus from the root surfaces inside the pockets and to leave those surfaces smooth. Often done in quadrants over several visits, or as a full-mouth disinfection.

This works. Pockets shrink — partly through genuine reattachment, partly because inflamed tissue shrinks back — and inflammation resolves. Non-surgical therapy alone stabilises the great majority of Stage I–II disease and a substantial share of Stage III.

Adjuncts: locally delivered antimicrobials placed into a pocket have modest benefit. Systemic antibiotics are not routine — current guidance explicitly discourages their general use, reserving them for selected cases such as young patients with rapidly progressing Grade C disease, because the benefit in ordinary cases is small and does not justify the adverse effects and resistance cost.

Step 3 — Managing What Did Not Respond

Re-evaluate around 6–12 weeks later. Where deep pockets (typically 6 mm or more) persist and still bleed:

• Repeat subgingival instrumentation.
• Access flap surgery — the gum is lifted so the roots can be cleaned under direct vision.
• Resective surgery — reshaping bone and gum to eliminate the pocket.
• Regenerative surgery — bone grafts, guided tissue regeneration membranes, or enamel matrix derivative, in the favourable defect shapes described above. This is the only route by which any lost bone comes back, and it is available to a minority of defects.

Step 4 — Supportive Periodontal Care (for life)

This is not optional, and it is where treated cases are won or lost. Professional maintenance at intervals of typically three to four months — the interval matters, because the subgingival biofilm re-establishes itself in roughly that window — with re-probing, re-instrumentation of any recurring sites, and reinforcement of hygiene. Patients who attend maintenance keep their teeth at dramatically higher rates than those who complete active treatment and then disappear.

Stage IV

Advanced cases with collapsed bites and missing teeth need the periodontal disease stabilised first, then rehabilitation — orthodontics, splinting, prostheses, or implants. Implants are not an escape from periodontitis: a patient who has lost teeth to periodontitis is at elevated risk of peri-implantitis, the same destructive process around an implant, where it is harder to treat.

Prevention and Lifelong Maintenance

• Treat gingivitis. It is the only proven way to prevent periodontitis, and it is easy.
• Brush twice daily for two minutes with a fluoride toothpaste and a soft brush, angled into the gumline.
• Clean between the teeth every day. Interdental brushes where the space allows; floss only for contacts too tight for a brush.
• Do not smoke. Nothing else on this list comes close.
• Control diabetes. Ask for periodontal screening as part of diabetes care — and tell your dentist your HbA1c, because it changes your grade.
• Get screened. A periodontal probe around your gums at check-ups. Ask for it by name if it is not being done.
• Attend maintenance if you have been treated. Every three to four months, indefinitely. Periodontitis is a controlled chronic disease, not a cured one.

Systemic Links — What the Evidence Actually Shows

Periodontitis is associated with a long list of systemic diseases. This is also the area of dentistry most prone to overstatement, so it is worth being precise about what has and has not been demonstrated. The biological rationale is consistent across all of them: a large, chronically ulcerated pocket epithelium — the total surface area in severe periodontitis is often compared to the palm of a hand — allows bacteria and inflammatory mediators continuous access to the bloodstream, raising systemic inflammatory markers such as CRP and IL-6.

Cardiovascular Disease — a real association, not a proven cause

Periodontitis is consistently associated with atherosclerotic cardiovascular disease across many observational studies, and the association survives adjustment for shared confounders such as smoking, age, and diabetes. Porphyromonas gingivalis DNA has been recovered from atherosclerotic plaques. The mechanism is plausible.

But the American Heart Association examined this question formally and reached a careful conclusion: the evidence supports an association that is independent of known confounders, and it does not support a causal relationship. Critically, interventional studies have not demonstrated that treating periodontal disease prevents cardiovascular events or alters the course of atherosclerotic disease. Periodontal treatment does improve surrogate markers — endothelial function, CRP — but a surrogate marker is not a heart attack prevented.

The joint EFP/World Heart Federation consensus reached the same place: strong association, biological plausibility, no proof of causation, and no evidence that periodontal therapy prevents cardiovascular events.

So, plainly: if someone tells you that a deep cleaning will protect you from a heart attack, they are going beyond the evidence. Treat your periodontitis because it will otherwise take your teeth. That reason is sufficient, and it is proven.

Type 2 Diabetes — genuinely bidirectional

This is the best-supported of the oral–systemic relationships, and it runs in both directions:

• Diabetes → periodontitis. Well established. People with poorly controlled diabetes have a markedly higher risk and severity of periodontitis. Periodontitis is sometimes called the “sixth complication” of diabetes.
• Periodontitis → worse glycaemic control. Also supported. Periodontitis is associated with poorer glycaemic control and with a higher incidence of diabetic complications; there is evidence that it is associated with increased risk of developing type 2 diabetes.

And here the interventional evidence is better than it is for the heart. Cochrane’s review of periodontal treatment for glycaemic control found that treating periodontitis produces a real reduction in HbA1c — on the order of 0.3 to 0.5 percentage points depending on the follow-up point, with moderate certainty at 3–4 months. That is a modest effect, comparable in size to adding a second oral hypoglycaemic agent, achieved by cleaning someone’s teeth properly. It is not a diabetes cure, and it does not replace diabetes medication. But it is a genuine, measurable systemic benefit — and it is why the International Diabetes Federation and the European Federation of Periodontology issued joint guidance recommending that people with diabetes be told about their periodontal risk and screened for it.

If you have type 2 diabetes, get your gums checked. This one is real.

Other Associations

• Adverse pregnancy outcomes — associated with preterm birth, low birth weight, and pre-eclampsia. But treatment trials have not consistently shown that treating periodontitis during pregnancy improves these outcomes. Dental treatment in pregnancy is safe and worth having; the promise of preventing preterm birth is not supported.
• Rheumatoid arthritis — an intriguing association with a specific mechanistic hypothesis (P. gingivalis produces a peptidylarginine deiminase enzyme that citrullinates proteins, and anti-citrullinated protein antibodies are central to RA). Still hypothesis-generating.
• Chronic kidney disease, respiratory infections (aspiration pneumonia in dependent elderly patients — here oral care genuinely does reduce risk), certain cancers, and Alzheimer’s disease (the P. gingivalis hypothesis has received attention but remains unproven and contested).

The Honest Summary

Periodontitis is a chronic inflammatory disease that raises systemic inflammation, and it keeps company with a lot of other chronic inflammatory diseases. Some of that is shared causation — smoking, poor diet, poverty, and diabetes cause both gum disease and heart disease. Some of it may be direct. Only the diabetes link currently has interventional evidence behind it. The best reason to treat periodontitis remains that it destroys your teeth, and that treating it works.

Complications

• Tooth loss — periodontitis is the leading cause of tooth loss in adults. Severe periodontitis is among the most prevalent diseases in the world; the Global Burden of Disease analysis estimated it affects around 11% of the global population, roughly 740 million people.
• Periodontal abscess — acute, painful, swollen, sometimes with fever. Needs prompt drainage and debridement.
• Tooth migration and bite collapse — teeth drift, flare, and splay; the bite changes; chewing becomes difficult.
• Gum recession, root sensitivity, and root caries — exposed root surface is softer than enamel and decays more readily.
• Impaired nutrition — people who cannot chew shift to softer, more processed, more calorie-dense food. The dietary consequences of tooth loss are underrated.
• Peri-implantitis — the same destructive process around dental implants, to which people with a periodontitis history are especially prone.
• Quality of life — pain, bad breath, visible tooth loss, and the effect on speech, eating, confidence, and employment. This is not cosmetic; it is one of the more socially disabling chronic diseases.
• Systemic inflammatory burden — as discussed above, with the caveats stated.

When to See a Dentist

Book an assessment now if you have:

• Gums that bleed when you brush or floss.
• Receding gums, or teeth that look longer than they used to.
• Gaps opening between your teeth, or teeth that have shifted or splayed.
• Persistent bad breath or bad taste that survives good hygiene.
• Any looseness in any tooth. This is not normal at any age.
• A family history of early tooth loss from gum disease.
• Diabetes — ask for periodontal screening as a matter of course.
• A smoking history — and do not be reassured by an absence of bleeding.
• Not been screened with a periodontal probe in the last year.

Seek urgent care if you have:

• Pus from the gums, or a painful gum swelling — likely a periodontal abscess.
• Facial swelling with fever. If swelling is spreading, closing the eye, or affecting swallowing or breathing, go to an emergency department — that is a spreading facial infection, not a dental inconvenience.
• A tooth that has become suddenly and markedly mobile.

What to ask for

Ask for a full periodontal charting, your stage and grade, and a written treatment plan with a maintenance interval. If a tooth is being condemned, a second opinion from a periodontist is reasonable — teeth that look hopeless can sometimes be saved, and the specialty exists precisely for this.

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Key Research Papers

Peer-reviewed literature underpinning the classification, treatment, and systemic associations of periodontitis. Each citation links to the full text via DOI.

1. Papapanou PN, Sanz M, Buduneli N, et al. Periodontitis: Consensus report of workgroup 2 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. Journal of Clinical Periodontology. 2018;45(Suppl 20):S162–S170.
2. Tonetti MS, Greenwell H, Kornman KS. Staging and grading of periodontitis: Framework and proposal of a new classification and case definition. Journal of Clinical Periodontology. 2018;45(Suppl 20):S149–S161. — The source of the Stage I–IV / Grade A–C system.
3. Caton JG, Armitage G, Berglundh T, et al. A new classification scheme for periodontal and peri-implant diseases and conditions — Introduction and key changes from the 1999 classification. Journal of Clinical Periodontology. 2018;45(Suppl 20):S1–S8.
4. Sanz M, Herrera D, Kebschull M, et al. Treatment of stage I–III periodontitis — The EFP S3 level clinical practice guideline. Journal of Clinical Periodontology. 2020;47(Suppl 22):4–60. — The stepwise treatment protocol.
5. Herrera D, Sanz M, Kebschull M, et al. Treatment of stage IV periodontitis: The EFP S3 level clinical practice guideline. Journal of Clinical Periodontology. 2022;49(Suppl 24):4–71.
6. West N, Chapple I, Claydon N, et al. BSP implementation of European S3-level evidence-based treatment guidelines for stage I–III periodontitis in UK clinical practice. Journal of Dentistry. 2021;106:103562.
7. Lockhart PB, Bolger AF, Papapanou PN, et al. Periodontal Disease and Atherosclerotic Vascular Disease: Does the Evidence Support an Independent Association? A Scientific Statement From the American Heart Association. Circulation. 2012;125(20):2520–2544. — Association yes; causation not established; treatment not shown to prevent cardiovascular events.
8. Sanz M, Marco del Castillo A, Jepsen S, et al. Periodontitis and cardiovascular diseases: Consensus report. Journal of Clinical Periodontology. 2020;47(3):268–288.
9. Tonetti MS, Van Dyke TE. Periodontitis and atherosclerotic cardiovascular disease: consensus report of the Joint EFP/AAP Workshop on Periodontitis and Systemic Diseases. Journal of Clinical Periodontology. 2013;40(Suppl 14):S24–S29.
10. Preshaw PM, Alba AL, Herrera D, et al. Periodontitis and diabetes: a two-way relationship. Diabetologia. 2012;55(1):21–31. — The key statement of bidirectionality.
11. Sanz M, Ceriello A, Buysschaert M, et al. Scientific evidence on the links between periodontal diseases and diabetes: Consensus report and guidelines of the joint workshop on periodontal diseases and diabetes by the International Diabetes Federation and the European Federation of Periodontology. Journal of Clinical Periodontology. 2018;45(2):138–149.
12. Simpson TC, Clarkson JE, Worthington HV, et al. Treatment of periodontitis for glycaemic control in people with diabetes mellitus. Cochrane Database of Systematic Reviews. 2022;4(4):CD004714. — The HbA1c reduction.
13. Chapple ILC, Genco R, et al. Diabetes and periodontal diseases: consensus report of the Joint EFP/AAP Workshop on Periodontitis and Systemic Diseases. Journal of Clinical Periodontology. 2013;40(Suppl 14):S106–S112.
14. Socransky SS, Haffajee AD, Cugini MA, Smith C, Kent RL Jr. Microbial complexes in subgingival plaque. Journal of Clinical Periodontology. 1998;25(2):134–144. — The “red complex.”
15. Hajishengallis G, Lamont RJ. Beyond the red complex and into more complexity: the polymicrobial synergy and dysbiosis (PSD) model of periodontal disease etiology. Molecular Oral Microbiology. 2012;27(6):409–419.
16. Hajishengallis G. Periodontitis: from microbial immune subversion to systemic inflammation. Nature Reviews Immunology. 2015;15(1):30–44.
17. Darveau RP. Periodontitis: a polymicrobial disruption of host homeostasis. Nature Reviews Microbiology. 2010;8(7):481–490.
18. Löe H, Anerud A, Boysen H, Morrison E. Natural history of periodontal disease in man. Rapid, moderate and no loss of attachment in Sri Lankan laborers 14 to 46 years of age. Journal of Clinical Periodontology. 1986;13(5):431–445. — Susceptibility varies; plaque is necessary but not sufficient.
19. Tomar SL, Asma S. Smoking-Attributable Periodontitis in the United States: Findings from NHANES III. Journal of Periodontology. 2000;71(5):743–751.
20. Eke PI, Thornton-Evans GO, Wei L, Borgnakke WS, Dye BA, Genco RJ. Periodontitis in US Adults: National Health and Nutrition Examination Survey 2009–2014. Journal of the American Dental Association. 2018;149(7):576–588.
21. Eke PI, Dye BA, Wei L, Thornton-Evans GO, Genco RJ. Prevalence of Periodontitis in Adults in the United States: 2009 and 2010. Journal of Dental Research. 2012;91(10):914–920.
22. Kassebaum NJ, Bernabé E, Dahiya M, Bhandari B, Murray CJL, Marcenes W. Global Burden of Severe Periodontitis in 1990–2010: A Systematic Review and Meta-regression. Journal of Dental Research. 2014;93(11):1045–1053.
23. Tonetti MS, Jepsen S, Jin L, Otomo-Corgel J. Impact of the global burden of periodontal diseases on health, nutrition and wellbeing of mankind: A call for global action. Journal of Clinical Periodontology. 2017;44(5):456–462.
24. Genco RJ, Sanz M. Clinical and public health implications of periodontal and systemic diseases: An overview. Periodontology 2000. 2020;83(1):7–13.
25. Figuero E, Han YW, Furuichi Y. Periodontal diseases and adverse pregnancy outcomes: Mechanisms. Periodontology 2000. 2020;83(1):175–188.

Live PubMed Searches

1. PubMed: periodontitis staging and grading
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7. PubMed: Porphyromonas gingivalis
8. PubMed: peri-implantitis treatment
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10. PubMed: systemic antibiotics in periodontitis

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Connections

• How Cavities Form — interactive animation
• Dentistry & Oral Health
• All Conditions
• Gingivitis
• Halitosis (Chronic Bad Breath)
• Tooth Decay (Dental Caries)
• Atherosclerosis
• Type 2 Diabetes
• Oral Microbiome
• Myrrh
• Myrrh for Oral Health
• Aloe Vera — Oral and Dental
• Vitamin C
• Vitamin D3
• Calcium

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