Dentistry & Family Medicine & Internal Medicine
Gingivitis and periodontitis
Gingivitis and periodontitis are the two major forms of periodontal disease - chronic inflammatory diseases of the tooth's supporting tissues initiated by bacterial plaque. Gingivitis, a reversible inflammation confined to the marginal gingiva, represents the early, treatable stage of periodontal disease. Left untreated, it can progress to periodontitis - destructive inflammation affecting the alveolodental ligament, cementum and alveolar bone, leading to irreversible loss of attachment, the formation of periodontal pockets and, ultimately, tooth loss. With an estimated prevalence of severe periodontitis of 10-15 % of the world's adult population, periodontal disease is the sixth most prevalent chronic disease worldwide. Beyond its impact on oral health, periodontitis has bidirectional relationships with several major systemic diseases - type 2 diabetes, cardiovascular disease, premature pregnancy, respiratory disease - making its management a global health issue that goes beyond the dental sphere.
Pathophysiology, classification, and clinical presentation
- Pathophysiology of periodontal disease—from biofilm to tissue destruction: subgingival biofilm (dental plaque): structured polymicrobial community organized on the tooth surface and under the gum - composition: over 700 bacterial species identified - transition from commensal flora (Gram+, aerobic) to pathogenic flora (Gram-, strict anaerobic) in the absence of oral hygiene - main pathobionts of the red complex (Socransky) : Porphyromonas gingivalis + Tannerella forsythia + Treponema denticola - virulence factors: proteases (gingipains from P. gingivalis) + endotoxins (LPS) + outer membrane vesicles → invasion of gingival epithelium + immune escape; host inflammatory response : bacterial LPS → activation of macrophages and gingival epithelial cells → secretion of pro-inflammatory cytokines (IL-1β + TNF-α + IL-6 + IL-8 + PGE2) → influx of PNN (neutrophils) + T and B lymphocytes → activation of RANKL (receptor activator of NF-κB ligand) on osteoblasts → stimulation of osteoclasts → irreversible alveolar bone resorption - in gingivitis: inflammation limited to the gingiva + no bone destruction + reversible if biofilm is removed - in periodontitis : apical extension of inflammation + destruction of alveolodental ligament + bone resorption + formation of periodontal pockets (space between gum and tooth >3 mm); dental calculus : secondary mineralization of dental plaque (salivary calcium + phosphate) → supragingival calculus (visible - white or yellow - calcified deposits) + subgingival calculus (clinically invisible - brown-black - very adherent - incorporated bacterial toxin + LPS) → shelters pathogenic plaque + protects biofilm from natural defenses + makes hygiene impossible → professional scaling essential
- Classification of periodontal diseases — EFP/AAP consensus 2017: the 2017 revised international classification (European Federation of Periodontology + American Academy of Periodontology) distinguishes three broad categories; periodontal health: absence of inflammation + probing depth ≤3 mm + no loss of attachment + intact alveolar bone; gingivitis: gingival inflammation without loss of attachment or bone destruction - plaque-induced gingivitis: the most common (50-90 % of the adult population at some point in their lives) + non-plaque-induced gingivitis (rarer) : viral infections (HIV + HSV + CMV) + specific bacterial (gonorrhea + tuberculosis) + fungal (candidiasis) + genetic conditions (hereditary gingival fibromatosis) + drug reactions (drug-induced gingival hyperplasia: phenytoin + ciclosporin + nifedipine) + hormonal changes (pregnancy - gravid gingivitis + puberty + menstrual cycle); periodontitis: division into stages (I to IV - severity) and grades (A, B, C - risk of progression): stage I: attachment loss 1-2 mm + probing depth ≤4 mm + no bone loss or <15 % + stage II: loss of attachment 3-4 mm + probing depth ≤5 mm + bone loss 15-33 % + stage III: loss of attachment ≥5 mm + probing depth ≥6 mm + bone loss ≥33 % ± tooth mobility + stage IV : as stage III + collapse of masticatory function (non-functional teeth + occlusal collapse) - grade A (slow progression - no systemic risk factors) + grade B (moderate progression - smoking <10 cigarettes/d - diabetes HbA1c <7 %) + grade C (rapid progression - smoking ≥10/d - diabetes HbA1c ≥7 % - other systemic factors); other periodontal conditions: necrotizing periodontitis (gingivitis/ulceronecrotic periodontitis - GUNA/PUNA): classic triad: necrotic gingival ulcerations + sharp pain + halitosis - context: immunodepression (HIV ++) + stress + smoking + malnutrition + noma (extensive and devastating form in sub-Saharan Africa) + periodontal abscesses + endo-periodontal lesions + gingival recessions
- Clinical presentation and clinical signs: gingivitis - clinical signs: gingival bleeding on brushing or spontaneously (first clinical sign - due to inflammation and neovascularization) + red (erythema) or edematous (shiny + smooth appearance) gums → healthy gums: pinkish + pitted (orange peel appearance) + firm + inflamed gums: red + swollen + shiny + halitosis (bad breath - products of anaerobic bacterial metabolism: volatile sulfur compounds - VSCs) + absence of pain in the majority of cases (painless gingivitis → underestimation by patients) + no tooth loosening + reversible with good oral hygiene and scaling; periodontitis - additional clinical signs: periodontal pockets (periodontal probing ≥4 mm - measured by millimetric periodontal probe) + bleeding on probing (BoP - bleeding on probing - marker of active inflammation) + gingival recession (descending gingiva exposing the root - sensitivity to cold + heat) + tooth mobility (grade I to III depending on amplitude) + gingival suppuration (pus on probing) + displacement or spacing of teeth (recent diasthenes) + tooth loss (advanced stage) + variable pain (often absent - silent periodontitis + sometimes very painful acute periodontal abscess) + modifiable risk factors : smoking (× 2-7 risk of severe periodontitis - reduced gingival immune response - masks bleeding = false security) + poorly controlled diabetes (HbA1c >7 % - bidirectional relationship) + psychological stress + obesity + pregnancy + medications (immunosuppressants + antiepileptics + calcium channel blockers)
Diagnosis, treatment, and associated systemic diseases
| Clinical aspect | Diagnosis and assessment | Treatment and follow-up |
|---|---|---|
| Periodontal assessment and diagnosis Survey — X-rays — classification |
Diagnosis of periodontal disease is based on comprehensive periodontal clinical examination and imaging; periodontal clinical examination - parameters measured by millimetric periodontal probe: probing depth (PS): distance from free gingival margin to pocket bottom - measured at 6 sites per tooth (mesiovestibular + vestibular + distovestibular + mesiolingual + lingual + distolingual) - normal value: ≤3 mm + clinical attachment level (NAC): distance from amelocecal junction to pocket floor → independent of gingival position → best indicator of past destruction + bleeding on probing (BoP): marker of inflammatory activity → expressed as percentage of positive sites (BoP >10 % = active inflammation) + suppuration + tooth mobility (grade 0-3) + gingival recession + furcations (Hamp's classification: grades I-III); periodontal chart (periodontogram): systematic recording of all these parameters on a complete dental diagram → basic reference for longitudinal follow-up → repeated at each periodontal reassessment (6-8 weeks post-treatment); periodontal imaging: retroalveolar radiographs (RA): gold standard for assessing alveolar bone loss - level of bone crest (normal: 1-2 mm below the ameloceolar junction) + angulation of bone defects (horizontal or vertical) - limitations: 2D assessment only - CBCT (cone beam computed tomography): 3D imaging - indicated for complex bone defects + furcation lesions + pre-implant surgery - higher radiation exposure → targeted use; rapid periodontal screening in general practice - CPI (Community Periodontal Index) or BPE (Basic Periodontal Examination): screening tool in 6 sextants - score 0 (healthy) to 4 (pocket ≥6 mm) - recommended by WHO + UFSBD - usable in family medicine to refer to dentist; microbiological and genetic tests: periodontal culture + pathobiont PCR (red complex - P. gingivalis + T. forsythia + T. denticola) → useful in refractory or rapidly progressing periodontitis (grade C) + IL-1 genotyping (IL-1A/IL-1B polymorphism - associated with genetic susceptibility to severe periodontitis) → specialist use | Therapeutic objectives of periodontal treatment: elimination of bacterial infection + control of inflammation + arrest of disease progression + treatment of residual bone defects + long-term maintenance through a periodontal booster program; phase 1 - non-surgical etiological treatment (all periodontitis) : personalized oral hygiene instructions: brushing 2 min × 2/d (soft toothbrush + modified Bass technique) + use of dental floss or interdental brushes (BoP reduction of 30-40 % vs brushing alone) + tongue scraper if halitosis + scaling-root resurfacing (DSR): supragingival scaling (visible calculus) + subgingival root planing (curettage of pocket walls - removal of subgingival calculus + biofilm + infected cementum layers) → performed per sector under local anesthesia → periodontal reassessment at 6-8 weeks (PS + BoP + NAC) → expected pocket reduction of 1-2 mm + BoP reduction of 40-60 %; adjuvant systemic antibiotics to DSR: indicated as an adjunct to DSR (not as a replacement) in severe stage III-IV grade C periodontitis + refractory periodontitis + necrotizing periodontitis: metronidazole 400 mg × 3/d × 7 days + amoxicillin 500 mg × 3/d × 7 days (in combination - EFP 2020 recommendation - proven efficacy in reducing deep pockets + red complex bacteria) → azithromycin 500 mg/d × 3 days : alternative - low-dose doxycycline (Periostat - 20 mg × 2/d × 3-9 months): anti-MMP (matrix metalloproteinase inhibition) + anti-inflammatory activity - no antibiotic activity at this dose → FDA-approved as adjuvant treatment for chronic periodontitis |
| Periodontal surgical treatment Resective surgery — regenerative — graft |
Periodontal surgery is indicated when non-surgical etiological treatment alone is insufficient to control the disease; indications for periodontal surgery: residual pockets ≥6 mm after post-DSR reassessment + deep vertical bone defects accessible to regeneration + grade II-III furcation lesions + aesthetic needs (gingival corrections) + reconstruction before implants + recurrent periodontal abscess; types of resective periodontal surgery: open flap debridement (OFD): debridement of a mucoperiosteal flap + surgical access to roots and bone + bone curettage + osteoplasty (bone remodeling) + flap repositioning - objective: eliminate deep residual pockets + improve access to hygiene - results: reduction of pockets by 2-4 mm + gingivectomy: excision of excess gingival tissue - indicated in drug-induced gingival hyperplasia (phenytoin + cyclosporine + nifedipine) + chronic hyperplastic gingivitis; regenerative periodontal surgery: objective: reconstitution of destroyed tissues (cementum + ligament + alveolar bone) - indicated for intraosseous (vertical) bone defects and grade II furcations - guided tissue regeneration (GTR): resorbable (collagen) or non-resorbable (e-PTFE) membrane interposed between flap and bone defect → guides ligament cell repopulation (periodontal ligament cells with regenerative potential) → results: 2-3 mm attachment gain + bone gain + enamel matrix proteins (EMD - Emdogain - amelogenin matrix derivative) : application to prepared root surface → stimulates differentiation of periodontal ligament cells → attachment gain comparable to RTG + simpler to use - EMD + bone graft combination → superior results in deep defects; bone grafts: autogenous bone (gold standard - taken from the patient) + allogenic bone (bone bank - DFDBA - demineralized freeze-dried bone allograft) + synthetic bone substitutes (β-TCP - beta-tricalcium phosphate - hydroxyapatite) → gradually resorbable and replaced by neoformed bone | Gingival grafts and mucogingival surgery: gingival recessions (Cairo classification 2011 - RT1 to RT3): main indication for gingival grafting - objectives: root coverage + increase in keratinized tissue + prevention of sensitivity and progression of recession; subepithelial connective tissue grafting (GTCS - gold standard): harvesting of a connective graft from the palate + insertion under a coronally positioned flap (CPF) → root coverage in 70-95 % of Cairo class RT1 and RT2 recessions + free gingival graft (GGL): harvesting of a palatal epithelio-conjunctive graft → increase in keratinized tissue + less aesthetic coverage + coronally positioned flap alone (CPF) + EMD: effective for multiple recessions + results comparable to GTCS in certain indications - tissue substitutes (Mucograft - porcine collagen): alternative to palatal harvesting → less post-operative morbidity → results slightly inferior to autogenous graft; long-term periodontal follow-up (periodontal support therapy - PST): essential to maintain the results obtained - frequency: every 3-6 months depending on individual periodontal risk - content of PST: reassessment of periodontal parameters + reinforcement of hygiene + professional scaling-polishing + surfacing of residual active sites → longitudinal studies (Axelsson + Lindhe): patients followed up regularly over 30 years → maintenance of teeth + virtual absence of progression vs. patients with no follow-up → PST is the most decisive factor in long-term prognosis |
| Periodontitis and diabetes Bidirectional relationship — HbA1c — glycemic control |
The relationship between periodontitis and diabetes is the best documented of periodontal-systemic associations - it is bidirectional and causal; diabetes → aggravation of periodontitis : chronic hyperglycemia → advanced protein glycation (AGEs - advanced glycation end-products) → binding to RAGE receptors → amplification of inflammatory response + reduced collagen synthesis + impaired gingival vascularization + PNN dysfunction (reduced chemotaxis + phagocytosis) → gingival pathogenic flora thrives in this environment - result: more severe periodontitis + faster progression + less favorable response to periodontal treatment in poorly controlled diabetics (HbA1c >7 %); periodontitis → worsening diabetes : pro-inflammatory cytokines of periodontal origin (TNF-α + IL-6 + IL-1β) → systemic circulation → induction of insulin resistance → elevation of blood glucose + HbA1c - meta-analyses (Engebretson 2013 - JAMA + Simpson 2015 - Cochrane): periodontal therapy (DSR) → reduction in HbA1c by 0.3-0.5 % at 3 months vs. control - modest but clinically significant effect (comparable to adding a 2nd oral antidiabetic) → the IDF (International Diabetes Federation) has officially recommended periodontal management in diabetics since 2009; systematic periodontal assessment in diabetics: annual periodontal examination recommended in all diabetic patients → screening by the family doctor (BPE score) + referral to the dentist if BPE ≥2 + inform the patient of the bidirectional relationship; confounding factors: smoking (common risk factor for periodontitis + type 2 diabetes) + obesity (insulin resistance + chronic inflammation + periodontitis) + stress → comprehensive management of risk factors | Periodontal management in diabetics: periodontal treatment: full DSR + reinforced hygiene → aims to reduce BoP + residual pockets → control periodontal infection → reduce systemic inflammatory load → potential improvement in glycemic control - HbA1c target: HbA1c target 8 %) → prefer non-surgical treatment in initial phase + postpone surgery until glycemic improvement - increased infectious risk → close post-DSR monitoring (4-6 weeks) + periodontal support program every 3 months (vs. 6 months in non-diabetics) ; Diabète-Bouche Santé program (Ordre des dentistes du Québec + Diabète Québec): Quebec initiative to raise awareness of the periodontitis-diabetes relationship → information tools for patients and professionals available on the ODQ and Diabète Québec websites |
| Periodontitis and cardiovascular disease Atherosclerosis — endocarditis — pregnancy |
Periodontal disease is associated with an increased cardiovascular risk — the mechanism is multifactorial and involves common inflammatory and microbial pathways; mechanisms of periodontitis-cardiovascular disease association: periodontal bacteremia: dental procedures (but also daily brushing in periodontal patients) release bacteria into the bloodstream → periodontal bacteria (P. gingivalis ++) detected in atherosclerotic plaques and heart valves - systemic inflammation: periodontal cytokines (TNF-α + IL-6 + IL-1β + CRP) → induction of vascular inflammation + endothelial dysfunction + foam cell formation → accelerated atherogenesis - biological markers: periodontal patients → high sensitivity CRP + high fibrinogen + high IL-6 → independent cardiovascular risk markers; epidemiological data: meta-analyses (Blaizot 2009 + Bahekar 2007): periodontitis associated with 19-44 % increased risk of CHD (OR 1.19-1.44) + 29 % increased risk of stroke (OR 1.29) - current data insufficient to prove causality (association ≠ causality - common risk factors: tobacco + diabetes + obesity) - the EFP and ESC (European Society of Cardiology) recognize the association and recommend periodontal screening and treatment in patients at high cardiovascular risk; infective endocarditis and bacteremia of oral origin: Streptococcus viridans (oral flora) and Enterococcus faecalis are frequent agents of endocarditis → bacteremia induced by dental care (extractions + scaling) + daily bacteremia by brushing and chewing in periodontal patients + pre-dental antibiotic prophylaxis (amoxicillin 2 g PO 1h before) → recommended by AHA 2007 + ESC 2023 in patients at high risk of endocarditis: prosthetic valve + history of endocarditis + unrepaired cyanogenic congenital heart disease | Periodontitis and pregnancy: association between periodontitis and obstetric complications documented - mechanism: periodontal pro-inflammatory cytokines (PGE2 + TNF-α) → systemic diffusion → stimulation of uterine contractions → risk of prematurity + low birth weight - meta-analyses (Vergnes 2007 + Chambrone 2011): periodontitis associated with increased risk of preterm birth (OR 1.5-2.8) and low birth weight (OR 1.8-2.0) - data on the benefit of periodontal treatment during pregnancy: heterogeneous - some studies show a reduced risk of prematurity after DSR (Michalowicz 2006) others not; recommendations for dental care during pregnancy: 2nd trimester = optimal period for dental care (1st trimester = sensitive organogenesis + 3rd trimester = discomfort + risk of cave compression) → DSR under local anesthesia (lidocaine with or without epinephrine - safe during pregnancy) → radiographs: avoid if possible (if essential: lead apron + colimatage) + physiological gingival changes in pregnancy: more sensitive gums + increased bleeding (effect of progesterones + estrogens on gingival microcirculation) → gravidic epulis (pyogenic granuloma on gingiva - spontaneous postpartum regression) → intensified hygiene care + gentle scaling recommended from 1st trimester (without deep surfacing if possible); drug-induced gingivitis and gingival hyperplasia: phenytoin (Dilantin) + cyclosporine + calcium antagonists (nifedipine + amlodipine) → inflammatory + fibrous gingival hyperplasia → treatment: plaque control + DSR (often insufficient alone) + surgical gingivectomy (resection of hyperplastic tissue) + drug switch if possible (substitution of nifedipine by another antihypertensive) |
| Oral hygiene and prevention Brushing — flossing — fluoride — tobacco |
Primary prevention of periodontal disease is based on daily control of plaque and elimination of modifiable risk factors; recommended oral hygiene techniques: tooth brushing: 2 times a day × 2 minutes minimum - modified Bass technique: brush at 45° to the dento-gingival junction + vibrating movements + sweeping from gum to crown - soft or medium toothbrush (hard = risk of abrasion + gingival recession) - oscillating-rotating (Oral-B) or sonic (Sonicare) electric toothbrush : superior to manual brush for plaque + bleeding reduction (Cochrane 2014 meta-analysis) - fluoride toothpaste (1,000-1,500 ppm F - adult): anticariogenic protection + mild antibacterial activity + interdental cleaning: dental floss or interdental brushes : interdental brushes (size adapted to each space - Curaprox + TePe + Oral-B Interdental) are more effective than dental floss in reducing plaque and interdental bleeding (recommended as a priority if interdental spaces allow) + dental jet (Waterpik) : useful adjuvant - does not replace floss or brushes + tongue scraper or brush: reduces halitosis (CSV) + oral bacterial load; adjuvant chemical agents: chlorhexidine mouthwash (Peridex + Perio-Aid + generics): 0.12-0.20 % - gold standard oral antimicrobial - proven efficacy in reducing plaque and bleeding - recommended uses: post periodontal surgery (2-3 weeks) + initial phase of DSR + impossibility of mechanical hygiene - prolonged use not recommended (>3-4 weeks): staining of teeth + dysgeusia + imbalance of oral microbiome + essential oil (Listerine) : less effective than chlorhexidine but without chromogenic effects → option for daily maintenance + tin fluoride (SnF2 - Colgate Total + Crest Pro-Health): anti-plaque activity + gingival anti-inflammatory effects - interesting alternative for daily maintenance | Modifiable risk factors and systemic prevention: smoking: major risk factor for periodontitis (× 2-7 risk) + impairs periodontal healing + masks gingival bleeding (vasoconstriction - false impression of healthy gums) → smoking cessation: significantly improves response to periodontal treatment + reduces progression → systematic minimal smoking cessation advice at every dental consultation (5A method + referral to the J'ARRÊTE - 1 866 JARRETE line in Quebec); diet and periodontitis: diet rich in refined sugars: promotes growth of pathogenic biofilm + Mediterranean diet (rich in omega-3 + antioxidants + fruits and vegetables): anti-inflammatory effects - studies show an inverse association between Mediterranean diet + vitamin D intakes + severe periodontitis + vitamin C deficiency : scurvy → severe periodontal destruction (severe deficiency - rare in developed countries); stress management: chronic stress → immunosuppression + risk behaviors (tobacco + alcohol + poor hygiene) → documented stress-parodontitis association → stress management techniques (MBSR + CBT) → can improve periodontal control; access to dental care in Quebec: RAMQ dental insurance for children aged 0-10 (PAPEM program) + social assistance (General Dental Services Program) + university dental clinics (Université de Montréal + McGill + Laval + Sherbrooke): reduced rates + access to specialized periodontal care + Ordre des dentistes du Québec (ODQ): referral to a periodontist if indication for periodontal surgery + oral health resources available on the Québec health portal and on the ODQ site |
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Periodontitis is silent — act before tooth loss: Unlike tooth decay, periodontitis is usually painless until advanced stages. Bleeding gums when brushing - often trivialized by patients - are the first warning sign of active gingivitis. Healthy gums do not bleed. Any gingival bleeding that persists for more than two weeks despite good oral hygiene should prompt a dental consultation. The family doctor has a key role to play in systematic periodontal screening, particularly for patients who are diabetics, smokers or taking medication at risk of gingival hyperplasia.
Situations requiring urgent medical or dental evaluation
Acute necrotizing ulcerative gingivitis (ANUG): Necrotic gingival ulcers + severe pain + fever + cervical adenopathy + intense halitosis → dental emergency → debridement + metronidazole + chlorhexidine mouthwash + search for immunodepression (HIV) if evocative context.
Acute periodontal abscess: painful fluctuant swelling + deep periodontal pocket + fever + cervical lymphadenopathy → incision-drainage + DSR of site + antibiotics if systemic signs (amoxicillin 500 mg × 3/d × 7 days or metronidazole + amoxicillin).
Cervicofacial cellulitis of dental or periodontal origin: trismus + hard cervical swelling + dysphagia + high fever → hospital emergency → cervico-facial CT scan + IV antibiotic therapy + surgical drainage (risk of mediastinal extension - Ludwig's angina).
Patient with a prosthetic valve or history of endocarditis planning a dental scaling or extraction → mandatory antibiotic prophylaxis (amoxicillin 2 g PO 1h before) according to AHA/ESC recommendations + cardiological opinion if in doubt.
Consult at Clinique Omicron
Clinique Omicron physicians integrate periodontal screening into the follow-up of diabetic patients, pregnant women, and patients taking medications with a risk of gingival hyperplasia. BPE score assessment, referrals to dentists or periodontists, management of dental emergencies (abscesses + cellulitis), and coordination with dental care teams are among the services available at several service points in Quebec and via telemedicine. To book an appointment, visit cliniqueomicron.ca.
The content of this page is for informational purposes only and does not replace the advice of a dentist or periodontist. Any persistent gum bleeding or signs of gum recession should be evaluated by an oral health professional.
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