Bacterial biofilm-driven destruction of tooth (caries) and supporting structures (gingivitis/periodontitis) — most prevalent infectious diseases globally.
Also known as: dental caries, tooth decay, cavities, gingivitis, periodontitis, periodontal disease
Overview
Dental caries is a multifactorial disease in which acid produced by cariogenic bacterial biofilm demineralizes tooth enamel and dentin, producing cavities. Gingivitis is reversible inflammation of the gingiva from plaque biofilm. Periodontitis is irreversible inflammatory destruction of the periodontal ligament and alveolar bone, characterized by clinical attachment loss and periodontal pocketing — the leading cause of adult tooth loss.
Epidemiology
Dental caries and periodontal disease are the most prevalent chronic infectious diseases globally. >90% of US adults have a history of caries; ~25% have untreated decay. Severe periodontitis affects ~10-15% of adults and rises with age. Disparities are marked by income, race/ethnicity, and access to fluoride/dental care.
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Bottle-feeding with sugary liquids at bedtime (early childhood caries)
Genetic susceptibility; immunocompromise; HIV
Pathophysiology
Caries: acidogenic bacteria (Streptococcus mutans, Lactobacillus) ferment dietary carbohydrates to produce acid that demineralizes hydroxyapatite below a critical pH (~5.5). Repeated acid attacks overwhelm salivary remineralization, leading to enamel cavitation and progression into dentin and pulp. Periodontal disease: dental plaque biofilm matures from gram-positive aerobes to anaerobes (Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola — the 'red complex'). Host inflammatory response generates cytokines (IL-1, IL-6, TNF-α) and matrix metalloproteinases that destroy the periodontal ligament and alveolar bone. Risk factors such as diabetes and smoking impair host immunity and amplify destruction.
Clinical presentation
Symptoms
Caries: tooth sensitivity to cold/sweet, localized pain with chewing, visible discoloration or cavitation; may be asymptomatic until pulp involvement
Pulpitis: spontaneous throbbing pain, prolonged pain with hot, often poorly localized
Periapical abscess: localized swelling, severe pain, percussion tenderness, possible fever
Gingivitis: bleeding gums with brushing/flossing, red swollen gingiva, halitosis
Periodontitis: receding gums, loose teeth, malodor, occasionally exudate from sulcus; usually painless until advanced
Signs / physical exam
Visible caries (chalky white spot lesion → brown discoloration → cavitation)
Plaque and calculus (tartar) at gingival margin
Gingival erythema, edema, and bleeding on probing
Periodontal pocketing >3 mm with attachment loss on probing
Tooth mobility, drifting, exposed root surfaces
Tenderness to percussion (apical inflammation/abscess)
Facial or submandibular swelling, lymphadenopathy in odontogenic infection
Chalky white spot lesion progressing to brown cavitation = caries; bleeding gingiva on probing with pockets >3 mm and attachment loss = periodontitis.
Differential diagnosis
Reversible vs irreversible pulpitis — Pulpitis with lingering pain, spontaneous pain, or hot sensitivity → irreversible; needs root canal or extraction
Periapical abscess — Tooth pain with swelling, sensitivity to percussion, possible facial cellulitis; antibiotics + dental drainage
Pericoronitis (around partially erupted molar) — Pain and swelling around erupting third molar; warm saline rinses, dental referral
Aphthous ulcers — Painful round white lesions with red halo on non-keratinized mucosa; self-limited
Oral candidiasis — White plaques scraping off; immunocompromise; topical nystatin/clotrimazole or oral fluconazole
Sinusitis (referred pain) — Maxillary tooth pain that worsens with bending; no carious lesion; CT sinuses
TMJ disorder — Jaw pain, clicking, pain with chewing; no caries; bite splint
Trigeminal neuralgia — Lancinating pain in V2/V3 distribution triggered by light touch; carbamazepine
Diagnostic workup
Diagnostic criteria
AAP/EFP 2017 classification — Stage I-IV periodontitis by clinical attachment loss and radiographic bone loss; Grade A-C by rate of progression and risk factors (smoking, diabetes).
Labs
Routinely none; consider HbA1c if uncontrolled diabetes suspected (bidirectional with periodontitis)
HIV testing when atypical/aggressive periodontal disease in a young patient
Salivary flow assessment for xerostomia
Imaging
Periapical and bitewing radiographs to detect interproximal caries, periapical lucencies, and alveolar bone loss
Panoramic radiograph for general dentition and odontogenic infections
CT for deep neck space involvement (Ludwig angina, parapharyngeal abscess)
Diagnostic algorithm
Condition
Key Finding
First-Line Management
Antibiotic Indication
Dental caries (non-cavitated)
White spot lesion
Fluoride varnish, sealants, diet/hygiene
No
Dental caries (cavitated)
Visible cavitation, brown discoloration
Restorative dentistry
No
Reversible pulpitis
Brief cold sensitivity
Restoration; remove caries
No
Irreversible pulpitis / periapical abscess
Spontaneous or lingering pain, percussion tenderness, swelling
Pulpectomy, root canal, or extraction; drainage
Yes if systemic signs / spreading cellulitis (amoxicillin ± metronidazole; clindamycin if PCN allergy)
Gingivitis
Bleeding red gingiva, plaque/calculus
Improved hygiene + dental prophylaxis
No
Periodontitis
Pockets >3 mm, attachment loss, mobility
Scaling and root planing; smoking cessation; glycemic control
Dental caries and periodontal disease — diagnosis-specific management and antibiotic indications.
Treatment
First-line
Mechanical plaque control — brushing twice daily with fluoride toothpaste, daily flossing
Reduce frequency of fermentable carbohydrate intake; substitute water for sweetened beverages
Topical fluoride — community water fluoridation, fluoridated toothpaste, professional fluoride varnish (children every 3-6 months — USPSTF recommends fluoride varnish in primary care for children up to age 5)
Sealants on posterior teeth in children/adolescents
Routine dental examinations and prophylaxis every 6-12 months (more frequent if high risk)
Restorative dentistry for cavitated caries — fillings; crowns or extraction for advanced lesions
Scaling and root planing for periodontitis (deep cleaning)
Second-line / adjunct
Chlorhexidine gluconate 0.12% mouth rinse — short-term for gingivitis, perioperative use; staining and taste alteration with prolonged use
Silver diamine fluoride — arrests dentinal caries, especially in pediatric and special-needs patients
Periapical abscess / odontogenic infection — drainage by dentistry plus oral antibiotic when systemic signs, spreading cellulitis, or immunocompromise:
• Amoxicillin 500 mg TID first-line
• Amoxicillin-clavulanate if anaerobic concern or treatment failure
• Clindamycin 300-450 mg QID for penicillin allergy
• Add metronidazole 500 mg TID for severe anaerobic infections
Ludwig angina or deep space infection — IV antibiotics (ampicillin-sulbactam or clindamycin), airway monitoring, surgical drainage
Endocarditis prophylaxis (amoxicillin 2 g 30-60 min before procedure) only for HIGH-risk patients per AHA: prosthetic valves/material, prior IE, certain congenital heart disease, cardiac transplant with valvulopathy
Complications
Tooth loss (leading cause in adults is periodontitis)
Periapical abscess, cellulitis, Ludwig angina, deep neck space infections, brain abscess
Bacteremia and infective endocarditis in susceptible hosts
Worsened glycemic control in diabetes (bidirectional)
Association with adverse pregnancy outcomes (preterm birth/low birth weight)
Aspiration pneumonia in elderly with poor oral hygiene
Bisphosphonate- or antiresorptive-related osteonecrosis of the jaw — dental clearance before initiation in oncology dosing
Pain, malnutrition, social and economic burden
PANCE pearls
Brushing twice daily with fluoride toothpaste plus regular dental care is the single highest-yield intervention for caries and periodontal disease.
Frequency of carbohydrate intake — not just amount — drives caries; sip-all-day sweetened beverages are particularly harmful.
Xerostomia from radiation, Sjögren, methamphetamine, or anticholinergic medications causes rapidly progressive 'rampant' caries (cervical/cuspal pattern).
Diabetes and periodontitis are bidirectional — treating periodontitis modestly improves A1c; uncontrolled diabetes worsens periodontitis.
Antibiotics do NOT replace drainage in an odontogenic abscess — definitive treatment is dental.
Endocarditis prophylaxis is reserved for the highest-risk cardiac patients per the AHA — most patients with valvular disease no longer require it.
USPSTF recommends primary care application of fluoride varnish for all children from primary tooth eruption to age 5, and oral fluoride supplementation in children whose water supply is fluoride deficient.
References
USPSTF 2021 — US Preventive Services Task Force. Screening and Interventions to Prevent Dental Caries in Children Younger Than 5 Years. JAMA 2021;326(21):2172-2178
AAP/EFP 2018 — Caton JG et al. A new classification scheme for periodontal and peri-implant diseases and conditions — Introduction and key changes from the 1999 classification. J Periodontol 2018;89(Suppl 1):S1-S8
AHA 2021 — Wilson WR et al. Prevention of Viridans Group Streptococcal Infective Endocarditis: A Scientific Statement From the AHA. Circulation 2021;143(20):e963-e978
ADA 2019 — American Dental Association. Evidence-Based Clinical Practice Guideline on the Nonrestorative Treatment of Carious Lesions. J Am Dent Assoc 2019;150(3):177-189
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