Periodontology & Dentistry & Family Medicine
Periodontitis
Periodontitis is a chronic infectious and inflammatory disease of the periodontium - the set of tooth-supporting structures comprising the gingiva, alveolar-dental ligament (desmodont), root cementum and alveolar bone - caused by subgingival bacterial biofilms that trigger a host immuno-inflammatory response leading to irreversible destruction of periodontal tissues, notably the alveolar bone. It is the leading cause of tooth loss in adults over 35 worldwide, and represents a major public health problem: according to the World Health Organization, severe periodontitis affects around 19 % of the world's adult population, or over one billion people. In Canada and Quebec, some 30 to 40 % of adults suffer from some form of periodontal disease, including 10 to 15 % in a severe form with significant bone destruction. The distinction between gingivitis - reversible inflammation limited to the marginal gingiva without bone destruction or loss of attachment - and periodontitis - inflammation extending to deeper structures with irreversible destruction of the connective tissue of attachment and alveolar bone - is fundamental, as only periodontitis involves permanent lesions. Periodontitis is not just a local disease of the oral cavity: increasingly strong evidence points to bidirectional links between severe periodontitis and several chronic systemic diseases, including type 2 diabetes (periodontitis worsens glycemic control and diabetes worsens periodontitis), cardiovascular disease (atherosclerosis + infarction + stroke), pregnancy complications (prematurity + low birth weight), chronic kidney disease and certain forms of aspiration pneumonia - making periodontitis a condition of general medical interest beyond its strictly dental setting.
Pathophysiology and microbial etiology
- Subgingival biofilm — primary etiological factor : The bacterial biofilm (dental plaque) accumulates in the gingival sulcus. In the absence of effective cleaning, a mature subgingival biofilm forms. The major periodontal pathogens form Socransky's red complex: Porphyromonas gingivalis + Tannerella forsythia + Treponema denticola → production of proteases + LPS + toxins → activation of the host's innate immune system → chronic inflammation
- Dysbiosis and the red complex: Periodontitis is not a simple classic bacterial infection but results from dysbiosis—an imbalance of the subgingival bacterial ecosystem → increase in Gram-negative anaerobic pathobionts + decrease in beneficial commensals + P. gingivalis plays a «keystone pathogen» role by modulating the immune response to favor its own development and that of the dysbiotic biofilm
- Host inflammatory response — mechanism of destruction: Bacterial LPS → activation of gingival macrophages and neutrophils → production of pro-inflammatory cytokines (IL-1β + IL-6 + TNF-α + PGE2) → osteoclast activation via the RANK-L/RANK pathway → alveolar bone resorption + destruction of periodontal ligament collagen by matrix metalloproteinases (MMPs) + bone destruction is therefore mainly mediated by the host's immuno-inflammatory response rather than directly by bacteria
- Modifiable risk factors: smoking (most powerful risk factor — multiplies risk of severe periodontitis by 5 to 7 + masks clinical signs of inflammation due to vasoconstriction) + type 2 diabetes (high HbA1c → protein matrix glycosylation + alteration of PMNs + hyperscretion of inflammatory mediators) + genetics (IL-1β + TNF-α polymorphisms) + immunosuppression (HIV + chemotherapy) + medications (nifedipine + phenytoin + cyclosporine → gingival hyperplasia) + stress + alcoholism + obesity
Classification of periodontitis (2018 - Global Workshop)
| Stadium | Severity (loss of clinical attachment) | Complexity and associated signs |
|---|---|---|
| Stage I - Initial periodontitis | Clinical attachment loss (CAL) interproximal of 1 to 2 mm + probing depth ≤ 4 mm + no or slight bone loss (≤ 15 % of root length) | Few complexity factors + no advanced furcation class + no increased tooth mobility + predominance in the coronal third |
| Stage II — Moderate Periodontitis | Interproximal contact of 3 to 4 mm + probing depth ≤ 5 mm + radiographic bone loss 15–33 % of root length | Moderate complexity factors + possible furcation class I or II + slight tooth mobility + vertical bone defects < 3 mm |
| Stage III - Severe periodontitis | Interproximal bone loss ≥ 5 mm + probing depth ≥ 6 mm + bone loss ≥ 33% % or reaching the apical third of the root | Significant complexity factors: furcation class II or III, dental mobility ≥ class 2, vertical bone defects ≥ 3 mm, possible tooth loss (≤ 4 teeth lost for periodontal reasons) |
| Stage IV — Very severe periodontitis | Stage III idem + periodontal tooth loss of 5 or more teeth + compromised occlusion | Maximum complexity + occlusal collapse + tooth drift + severe malocclusion + mastication problem + necessity for complex multidisciplinary rehabilitation |
Progression Speed Grade (Grades A, B, C)
- Grade A - slow progression No documented bone loss over 5 years + few or no risk factors + patient not a smoker + normal blood sugar
- Grade B - moderate progression : bone loss < 2 mm in 5 years + smoking < 10 cigarettes/day + diabetes with HbA1c < 7 %
- Grade C — rapid progression: bone loss ≥ 2 mm in 5 years + smoking ≥ 10 cigarettes/day + diabetes with HbA1c ≥ 7 % + other aggravating systemic factors
Clinical signs and periodontal diagnosis
- Gingival signs: gums red + swollen + bleeding easily when brushed or probed (bleeding on probing) + halitosis (chronic bad breath) + suppuration of the gingival sulcus (pus) + in advanced forms: gingival recession (gums that descend → teeth that «lengthen») → dentinal sensitivity
- Deep periodontal signs: periodontal pockets (probing depth > 3 mm on periodontal probing with a graduated probe) + loss of clinical attachment measured from the amelo-cementary junction + exposed furcation + increased tooth mobility + tooth migration or drift (teeth moving or pulling apart)
- Panoramic and periapical radiograph visualizes horizontal (most frequent) or vertical (angular — associated with funnel-shaped bone defects) alveolar bone loss + evaluates the level of the alveolar crest relative to the cemento-enamel junction + essential for the diagnosis and monitoring of periodontal treatment
ℹ️
The bidirectional link between periodontitis and diabetes is one of the best-documented among periodontitis-systemic disease associations. Nonsurgical periodontal treatment (scaling and root planing) reduces HbA1c by an average of 0.4–0.5% % in diabetic patients— an effect comparable to adding a second-line oral hypoglycemic agent. All diabetic patients should receive an annual periodontal assessment, and all patients with unexplained severe periodontitis should be screened for type 2 diabetes.
Periodontal treatment
| Treatment phase | Interventions | Objectives and expected results |
|---|---|---|
| Phase I - Cause-related therapy | Oral hygiene education and motivation + brushing instruction (Bass technique) + dental floss and interdental brush use + supra- and subgingival scaling + root planing (mechanical debridement of root surfaces with curettes or sonic/ultrasonic instruments) + removal of plaque-retentive factors (overhanging fillings + ill-fitting dentures) + smoking cessation + glycemic control in diabetics | Reduction of probing depths by 1–2 mm + reduction of bleeding on probing by 50–70% % + cessation of periodontal destruction in 70–80% % of stage I–II cases + mandatory re-evaluation 6–8 weeks after initial therapy |
| Phase II — Surgical Corrective Treatment | Reconstructive periodontal surgery (flap elevation + osteoplasty) to access inaccessible areas + regenerative surgery (bone graft + guided tissue regeneration membranes + enamel matrix proteins - Emdogain®) for vertical bone defects + crown lengthening for residual inaccessible pockets after phase I + extraction of non-restorable teeth | Stages III–IV resistant to phase I → further reduction of residual pockets + possible bone regeneration in vertical defects + improved access for post-surgical home care |
| Phase III – Supportive Periodontal Therapy (Maintenance) | Professional periodontal maintenance visits every 3 to 6 months based on periodontal risk + maintenance scaling and root planing + hygiene reinforcement + periodontal stability assessment (probing + radiographs) + treatment of localized recurrences | Maintenance is essential for life — without regular professional maintenance, 80–90 % of patients relapse within 5 years + maintenance reduces the risk of further tooth loss by 50–70 % + frequency adapted to the individual risk profile |
Periodontitis and systemic complications
- Type 2 Diabetes: The most documented bidirectional relationship: severe periodontitis worsens insulin resistance and HbA1c + periodontal treatment reduces HbA1c by 0.4–0.5 % on average + diabetes screening recommended in the presence of unexplained severe periodontitis + glycemic control is essential for the response to periodontal treatment
- Cardiovascular diseases : Epidemiological associations between severe periodontitis and atherosclerosis, coronary heart disease, stroke. Hypothetical mechanism: repeated bacteremias, systemic release of inflammatory mediators (IL-6, CRP), direct passage of P. gingivalis in atherosclerotic lesions (viral DNA found in plaques) + meta-analyses: 10-15% % reduction in cardiovascular risk associated with periodontal treatment
- Pregnancy: Maternal periodontitis associated with an increased risk of premature birth (before 37 weeks) and low birth weight (< 2,500 g) due to bacteremia and systemic inflammation + mechanism: periodontal cytokines (IL-6 + PGE2) can cross the placenta and trigger premature contractions + periodontal assessment recommended preconceptionally and in early pregnancy
- Respiratory diseases: oral pathobiont aspiration → bacterial aspiration pneumonias (especially in the elderly in long-term care facilities + ventilated individuals) + periodontitis associated with increased COPD risk + good oral hygiene reduces the incidence of hospital-acquired pneumonia in intensive care units
Situations Requiring a Prompt Dental Consultation
Consult a dentist or periodontist quickly if gums bleed regularly during brushing for more than 2 weeks, if teeth appear to be lengthening or spaces are appearing between teeth, if a tooth becomes loose or pus appears around a tooth, or if there is persistent bad breath despite good hygiene. These signs indicate active periodontitis requiring professional periodontal intervention—bone loss is irreversible and periodontitis does not heal without treatment.
For the screening of periodontitis in diabetic or cardiovascular patients, or those presenting with suggestive signs, and for referrals to a dentist or periodontist, Clinique Omicron offers medical consultations at its service points in Quebec and via telemedicine. To make an appointment, visit cliniqueomicron.ca.
Consult at Clinique Omicron
Clinique Omicron's physicians and nurse practitioners (NPs) educate their patients about the links between periodontitis and systemic diseases (diabetes, cardiovascular disease, pregnancy), screen for signs of periodontitis during routine clinical examinations, prescribe glycemic testing (HbA1c) for unexplained severe periodontitis, and systematically refer patients to dentists or periodontists for periodontal evaluation and treatment. Consultations are available at several service locations across Quebec and via telemedicine. To book an appointment, visit cliniqueomicron.ca.
The content of this page is provided for informational purposes only and does not substitute the advice of a dentist or periodontist. The diagnosis and treatment of periodontitis require a comprehensive periodontal examination with probing and radiographs, performed by a qualified dental health professional.
Omicron Clinic
Need to consult a doctor?
Treatment within 24-48 hours. In-clinic or telemedicine, anywhere in Quebec.
Insurance receipts. 7j/7. No family doctor required.