Gum Disease (Periodontitis) — Causes, Symptoms & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Periodontal disease encompasses a spectrum of inflammatory conditions affecting the supporting structures of the teeth — the gingiva (gums), periodontal ligament, cementum, and alveolar bone. Gingivitis — the milder, reversible form — refers to gingival inflammation caused by bacterial plaque accumulation, without destruction of the supporting bone or ligament. Periodontitis — the irreversible, progressive form — involves chronic inflammation that destroys the periodontal ligament and alveolar bone, creating periodontal pockets (spaces between the tooth and gum where bacteria accumulate) and, if untreated, eventual tooth loss. Severe periodontitis is the 6th most prevalent condition globally (GBD 2017), affecting approximately 11% of adults (743 million people). Mild-moderate periodontitis affects 45-50% of adults worldwide. Periodontitis is the leading cause of tooth loss in adults over 35. Beyond oral health, extensive evidence links periodontitis to systemic diseases: cardiovascular disease (atherosclerosis — periodontal bacteria and inflammatory mediators translocate to the bloodstream); type 2 diabetes (bidirectional relationship — periodontitis worsens glycaemic control by 0.4-0.5% HbA1c; diabetes impairs gingival healing); adverse pregnancy outcomes (premature birth, low birth weight); respiratory infections; and rheumatoid arthritis. The 2017 World Workshop Classification categorised periodontitis by stage (I-IV — severity) and grade (A-C — risk of progression).

Periodontitis is caused by a dysbiotic (imbalanced) polymicrobial biofilm (dental plaque) on the tooth surface and subgingivally. The principal periodontal pathogens are gram-negative anaerobes: Porphyromonas gingivalis (the 'keystone pathogen' — disrupts host immunity and enables the entire dysbiotic biofilm); Tannerella forsythia; Treponema denticola; Fusobacterium nucleatum; and Prevotella intermedia. These bacteria trigger a host inflammatory response involving IL-1β, TNF-alpha, prostaglandin E2, and matrix metalloproteinases (MMPs) that destroy periodontal ligament and alveolar bone — it is the dysregulated host immune response, not direct bacterial action, that causes tissue destruction. Risk factors for developing and worsening periodontitis: smoking (the most significant modifiable risk factor — smokers have 3-6x higher periodontitis risk; smoking reduces gingival vascularity — masking bleeding signs — and impairs healing; light-to-moderate smokers have 2x the risk); poorly controlled type 2 diabetes (diabetes impairs neutrophil function, increases AGE formation in periodontal tissues, and promotes inflammatory cytokine production — HbA1c above 9% is associated with severe periodontitis); genetic susceptibility (heritability estimated 30-50% — IL-1 gene polymorphisms); stress (elevated cortisol impairs immune function); medications causing gingival overgrowth (phenytoin, calcium channel blockers — amlodipine, nifedipine — cyclosporin); immunosuppression (HIV, chemotherapy); pregnancy (hormonal changes exacerbate gingivitis — 'pregnancy gingivitis' — affecting 35-100% of pregnant women); and poor oral hygiene (insufficient plaque removal).

Gingivitis: red, swollen, and tender gums; bleeding on brushing or flossing (the cardinal sign of gingivitis — healthy gums do not bleed); gums that bleed when eating certain foods; and bad breath (halitosis). Crucially, gingivitis causes no bone destruction and is completely reversible with professional cleaning and improved oral hygiene. Periodontitis (chronic infection causing irreversible bone loss): gum recession (gums appear to 'pull away' from teeth, exposing the root surface — teeth appear longer); loose or drifting teeth (as alveolar bone support is lost); tooth sensitivity to cold or heat (exposed dentine from root exposure); persistent bad breath (halitosis from anaerobic bacteria in periodontal pockets); changes in bite (teeth no longer fitting together normally as teeth drift); and tooth loss (in advanced, untreated disease). Periodontal pockets: deeper than 3mm on probing with a periodontal probe — 4-5mm is mild, 6mm+ is moderate-severe periodontitis. Periodontal abscess: acute, painful swelling of the gum with purulent discharge — a localised acute infection within a periodontal pocket requiring drainage. Important: periodontitis is frequently painless until advanced — many patients are unaware they have it until radiographic bone loss or tooth mobility is detected. Bleeding on gentle probing is the most sensitive clinical sign of active inflammation.

Periodontal diagnosis requires a clinical periodontal examination, usually supplemented by dental radiographs. Basic Periodontal Examination (BPE): the standard screening tool used in UK dental practice — a periodontal probe is inserted into 6 sites around each tooth and the maximum depth recorded per sextant on a colour-coded score 0-4 (0: healthy; 1: bleeding on probing only; 2: calculus or overhanging margins detected; 3: pockets 3.5-5.5mm; 4: pockets 5.5mm or deeper). BPE scores 3-4 trigger detailed full-mouth periodontal charting. Full periodontal chart (six-point pocket depth chart): records probing depth (PD), bleeding on probing (BOP), recession, furcation involvement, and mobility at six sites per tooth — provides a comprehensive 'map' of disease severity. Gingival recession: measured from cementoenamel junction (CEJ) to gingival margin. Furcation involvement: classification (Hamp I-III) indicating bone loss between the roots of multi-rooted teeth. Dental radiographs: periapical and bitewing X-rays assess alveolar bone levels — bone loss pattern (horizontal vs vertical defects), furcation involvement, and tooth prognosis. The 2017 Classification stages periodontitis I-IV by severity (bone loss percentage, pocket depths, tooth loss) and grades A-C by rate of progression risk (grade C if HbA1c above 7% or smoking above 10 cigarettes/day — these patients have rapid-progressing disease).

Periodontal treatment aims to eliminate infection, halt bone destruction, and establish conditions for long-term periodontal stability. Step 1 — Cause-related therapy: professional scaling (supragingival and subgingival calculus removal using ultrasonic and hand instruments — scalers and curettes); oral hygiene instruction (OHI) — twice-daily brushing with a soft toothbrush (2 minutes each time) + interdental cleaning (floss or interdental brushes — critical for plaque removal from interproximal surfaces where periodontitis initiates). For gingivitis: professional cleaning alone with improved home care achieves complete resolution — the response to Step 1 is 100% reversible. Subgingival scaling and root planing (SRP — debridement): for periodontitis — thorough mechanical disruption and removal of subgingival biofilm and calculus from root surfaces under local anaesthesia (using full-mouth disinfection or quadrant-by-quadrant approach); effectively reduces probing depths, bleeding, and bacterial load; achieves closure of 4-5mm pockets in most cases. Systemic adjunctive antibiotics: systemic azithromycin or metronidazole/amoxicillin may be indicated as adjuncts to SRP in generalised severe periodontitis (stage III-IV, grade C) in non-smoking patients. Local antibiotics: subgingival doxycycline (Atridox) or chlorhexidine chips in persistent deep pockets. Step 2 — Reassessment (8-12 weeks after SRP): probe depths, BOP, radiographic assessment — identify sites requiring surgical intervention. Periodontal surgery (for residual pockets above 5-6mm after SRP, unfavourable anatomy, furcation involvement): resective surgery (osseous surgery — pocket elimination by bone reshaping); regenerative surgery (guided tissue regeneration — GTR — with barrier membranes and bone grafts to regenerate lost periodontal attachment — particularly effective for vertical bone defects); and flap surgery for access. Step 3 — Supportive Periodontal Therapy (SPT): regular 3-6 monthly periodontal maintenance appointments for life — periodontal disease is a chronic condition that cannot be 'cured' but can be controlled with ongoing professional maintenance and meticulous home care.

Gum disease (periodontal disease) causes serious complications that extend well beyond the mouth when inadequately treated. Tooth loss: the most direct dental complication — periodontitis is the leading cause of tooth loss in adults over 35; alveolar bone loss progresses with each cycle of infection and inflammation, eventually leaving teeth with insufficient bone support; edentulism (total tooth loss) causes severe functional impairment in chewing and speech, and significant psychological distress. Cardiovascular disease: strong epidemiological and mechanistic evidence links severe periodontitis with increased cardiovascular risk — periodontal bacteria (Porphyromonas gingivalis) enter the bloodstream during chewing and dental procedures, contributing to atherosclerosis, endothelial inflammation, and increased fibrinogen; systematic reviews report 24-35% increased coronary artery disease risk in severe periodontitis. Infective endocarditis: periodontal bacteria can cause endocarditis in patients with structural cardiac defects or prosthetic valves — antibiotic prophylaxis is required before dental procedures in high-risk cardiac patients. Diabetes bidirectional relationship: periodontitis worsens glycaemic control in T2DM by increasing systemic inflammation and insulin resistance; conversely, diabetes impairs periodontal healing; periodontal treatment improves HbA1c by 0.3-0.4%. Adverse pregnancy outcomes: severe periodontitis in pregnancy is associated with premature birth, low birth weight, and pre-eclampsia. Cognitive decline: recent studies associate P. gingivalis infection with Alzheimer's disease pathology — gingipain enzymes found in AD brain tissue.

Periodontal disease is largely preventable with consistent oral hygiene and professional care. Brush teeth twice daily with a fluoride toothpaste (minimum 1,000 ppm fluoride; 1,450 ppm for adults) using a soft-bristled toothbrush or oscillating-rotating electric toothbrush (electric toothbrushes are more effective at plaque removal) — brush for at least 2 minutes. Interdental cleaning: use interdental brushes (the most effective interdental cleaning method for adults with existing periodontitis — select the largest brush that fits the space comfortably) or dental floss daily — for patients without existing significant periodontitis who cannot use interdental brushes. Smoking cessation: the single most important modifiable risk factor — periodontal treatment response is markedly better in non-smokers. Diabetes management: achieving good glycaemic control (HbA1c below 7%) dramatically improves periodontal treatment outcomes. Regular dental check-ups and professional cleaning every 6 months (annually for low-risk individuals; every 3-4 months for those with history of periodontitis or risk factors). Chlorhexidine mouthwash (0.2% — short-term use only — 2-4 weeks): effective adjunct to mechanical cleaning, not a substitute. Xylitol-containing products (gum, mints) reduce Mutans streptococci and may have adjunctive periodontal benefits.

See a dentist promptly for: gums that bleed when brushing or eating — bleeding on brushing is never normal and always indicates gum inflammation requiring assessment; persistent bad breath that does not resolve with regular brushing (possible periodontitis with subgingival infection); gum recession causing tooth sensitivity or teeth that appear longer than before; loose or drifting teeth in an adult (significant bone loss); a painful swelling of the gum with pus (periodontal abscess — requires drainage and antibiotics urgently); and any changes in your bite. Do not wait until teeth are loose or painful — periodontitis is mostly painless and causes irreversible bone loss long before symptoms appear. Adults should have a periodontal examination at every routine dental check-up. Patients with systemic conditions linked to periodontitis (diabetes, cardiovascular disease, rheumatoid arthritis, those planning pregnancy) should prioritise periodontal assessment and regular SPT — periodontal treatment in diabetic patients reduces HbA1c by 0.4-0.5%.