Tooth Decay (Dental Caries) — Causes, Fluoride, Fillings & Prevention Guide — Symptoms, Causes & Treatment | MyMedicPlus

Dental caries (tooth decay) is a multifactorial infectious disease caused by the interaction of cariogenic bacteria, fermentable carbohydrates, a susceptible tooth surface, and time. It is the world's most prevalent non-communicable disease, affecting an estimated 3.5 billion people globally — more than any other condition. Caries results from bacterial acid demineralisation of the tooth hard tissues (enamel, dentine, and, in severe cases, pulp). The process is cyclical: after sugar consumption, oral bacteria (primarily Streptococcus mutans and Lactobacillus species) produce organic acids (mainly lactic acid) that dissolve mineral (hydroxyapatite) from the enamel surface. If this demineralisation is not reversed by remineralisation from saliva and fluoride, the lesion progresses through white spot (initial), cavitation (frank caries), dentine involvement, pulpitis (pulp inflammation), and finally pulp necrosis. Early lesions are entirely reversible; cavitated lesions require operative intervention. Globally, untreated caries is the most common oral disease — 34% of adults have untreated caries in permanent teeth and 40-50% of 5-year-olds in low-income settings have early childhood caries.

The aetiology of dental caries follows Keyes' triad: susceptible host (tooth), cariogenic microflora, and dietary fermentable carbohydrates — with time as the fourth determinant (Newbrun's modification). Cariogenic bacteria: Streptococcus mutans is the principal cariogenic organism — it adheres to tooth surfaces, ferments sucrose to produce lactic acid, and produces glucan (dextran) that forms the extracellular matrix of dental plaque. Lactobacillus species are important in advancing established caries into dentine. Dietary sugars: free sugars (sucrose, glucose, fructose, and lactose — from milk) are fermented by oral bacteria to produce acid. The COMA Report (UK) and WHO both recommend reducing free sugars to below 5% of total energy intake. Frequency of sugar exposure is more important than total sugar quantity — each sugar exposure triggers an acid attack lasting 20-40 minutes ('Stephan curve'). Risk factors: poor oral hygiene (insufficient plaque removal); low fluoride exposure; reduced salivary flow (xerostomia — from Sjogren's syndrome, head and neck radiotherapy, and over 500 medications including antidepressants, antihypertensives, antihistamines, and diuretics); gastro-oesophageal reflux disease and eating disorders (acid erosion synergises with caries); age (infants — early childhood caries from prolonged bottle feeding; elderly — root caries from gingival recession); socioeconomic deprivation; and lack of access to dental care.

Early caries (enamel-only): typically asymptomatic — white spot lesions (initial demineralisation appearing as chalky white opacities on drying) are often detected only at dental examination; no cavitation at this stage; entirely reversible with fluoride remineralisation. Cavitated enamel caries: visible brown or black cavity or discolouration; localised tooth sensitivity to sweet foods; still no pain at rest. Dentine caries: pain or sensitivity to cold, hot, or sweet stimuli (thermal sensitivity from dentinal tubule fluid movement); spontaneous pain (toothache) is not typically present until the pulp is involved. Pulpitis (pulp inflammation): Reversible pulpitis — sharp, brief pain to thermal stimuli that resolves within 30 seconds; Irreversible pulpitis — intense, spontaneous, lingering pain often waking the patient at night; pain may be poorly localised. Pulp necrosis: paradoxically, pain may diminish as the pulp becomes necrotic — replaced by periapical abscess formation. Dental abscess: severe, constant, throbbing toothache; swelling, redness and tenderness of overlying gum or face; fever and malaise; difficulty opening the mouth (trismus) if spreading infection; and difficulty swallowing if it spreads to the neck (Ludwig's angina — a life-threatening deep space infection).

Clinical examination: dental mirror and probe examination of all tooth surfaces; caries detection probing identifies cavitated lesions; visual-tactile examination is the primary diagnostic method. ICDAS (International Caries Detection and Assessment System): a standardised scoring system (0-6) used in research and increasingly in clinical practice — grades lesion severity from initial enamel changes (1-2) through frank cavitation (3-4) to pulpal involvement (5-6). Radiographic diagnosis: bitewing radiographs (BW) are essential for detecting interproximal (between-teeth) caries invisible to direct vision — the most important diagnostic tool for posterior caries; periapical radiographs for suspected pulpitis, abscess, or root caries. Transillumination (FOTI — fibreoptic transillumination): useful for detecting early interproximal caries without radiation — shadowing indicates demineralisation. Laser fluorescence (DIAGNOdent): quantifies laser fluorescence from carious lesion — useful for occlusal caries detection. Clinical signs of pulp involvement: percussion sensitivity (periapical abscess), heat sensitivity (irreversible pulpitis), and electric pulp testing (EPT) — assesses pulp vitality; cold testing with Endo-Ice or ethyl chloride. Swabs and culture only for severe spreading odontogenic infection.

Treatment is determined by lesion severity and stage. Active non-cavitated lesions (white spots): remineralisation — 2.26% fluoride varnish applied professionally every 3-6 months (Duraphat); 1000-1500 ppm fluoride toothpaste (twice daily for adults; 1000 ppm for children aged 3-6); Casein Phosphopeptide-Amorphous Calcium Phosphate (CPP-ACP) pastes (GC Tooth Mousse) applied after brushing; dietary advice (reduce free sugar frequency). Cavitated enamel or dentine caries (restorable): composite resin fillings: tooth-coloured, bonded directly to tooth structure — the preferred modern restorative material for most teeth (anterior and posterior); glass ionomer cement (GIC): alternative for primary teeth and root caries — releases fluoride and chemically bonds to dentine; dental amalgam: highly durable silver-coloured material for posterior teeth — declining in use due to mercury concerns (EU phased restriction from 2025); Hall technique for primary molars: stainless steel crown placed over carious molar with minimal preparation — highly effective, evidence-based, and well-tolerated by children. Deep caries (approaching pulp): indirect pulp capping (calcium hydroxide or MTA over near-exposure); direct pulp cap for vital pulp exposure. Irreversible pulpitis or pulp necrosis: root canal treatment (RCT) — pulp chamber and root canals cleaned, shaped, and obturated with gutta-percha; followed by permanent restoration (crown for posterior teeth). Dental abscess: incision and drainage (I&D) of fluctuant abscess; oral amoxicillin 500 mg TDS or metronidazole 400 mg TDS for spreading infection; extraction or RCT of offending tooth. Spreading space infection (Ludwig's angina): hospital admission, IV antibiotics (amoxicillin-clavulanate plus metronidazole), airway protection, and surgical drainage.

Dental pain is the most immediate complication — severe irreversible pulpitis causing intense, spontaneous, sleep-disrupting toothache is among the most severe acute pain experiences, significantly impairing work, school attendance, nutrition, and wellbeing. Dental abscess: periapical or periodontal abscess from pulp necrosis — swelling, fever, and risk of spreading to adjacent deep spaces. Ludwig's angina: a life-threatening bilateral cellulitis of the submandibular, sublingual, and submental spaces — causes airway obstruction and requires emergency intubation, IV antibiotics, and surgical drainage; carries approximately 8% mortality in severe cases. Cavernous sinus thrombosis: rare but life-threatening intracranial spread of dental infection — presenting with fever, chemosis (conjunctival oedema), proptosis, and cranial nerve palsies. Early childhood caries: in young children, pain causes feeding difficulties, weight loss, developmental impact, and impaired quality of life; severely decayed primary teeth require general anaesthetic (GA) for extraction — one of the most common reasons for GA in children in the UK. Untreated caries causing tooth loss impairs chewing, speech, and aesthetics, affecting social function and mental health.

Fluoride is the single most effective caries-preventive agent: twice-daily brushing with fluoride toothpaste (1000-1500 ppm for adults and children aged 7+; 1000 ppm for children aged 3-6; smear of 1000 ppm for children under 3); spit, do not rinse after brushing to maintain fluoride concentration; professional fluoride varnish (2.26%) applied 2-4 times annually in high-caries-risk patients. Reduce free sugar: WHO recommends less than 5% of total energy from free sugars; limit frequency to a maximum 4 times daily including meals; substitute sugar-containing snacks with sugar-free alternatives; choose sugar-free medications (liquid medicines frequently contain sucrose). Fissure sealants: resin or glass ionomer sealants applied to vulnerable occlusal (biting surface) pits and fissures of permanent first molars at eruption (age 6-7) and second molars (age 12-13) — reduces caries by 70-80% in high-risk children. Regular dental check-ups: 6-monthly for children and high-risk adults; annually for low-risk adults — enables early lesion detection and remineralisation before cavitation. Water fluoridation: community water fluoridation at 0.7-1.0 ppm fluoride reduces caries prevalence by 20-40% — a safe, cost-effective public health measure. Xylitol: a sugar alcohol that is non-fermentable by Streptococcus mutans — chewing gum with xylitol after meals reduces caries incidence; some evidence for mother-to-child transmission reduction.

See a dentist for a routine check-up every 6-12 months — many cavities and early lesions are detectable and reversible at dental examination before causing any symptoms. See a dentist within 1-2 days for: persistent toothache or sensitivity to hot and cold that lasts more than 30 seconds after the stimulus is removed (possible irreversible pulpitis requiring root canal treatment); visible hole or cavity in a tooth. Attend A&E or call 999 immediately for: facial swelling extending to the neck or below the jaw (possible Ludwig's angina — a life-threatening spreading infection requiring emergency management); difficulty breathing, swallowing, or opening the mouth with facial swelling (airway compromise from spreading dental infection — call 999); and dental abscess with high fever and malaise in a patient who is immunocompromised (diabetes, chemotherapy, organ transplant). Children with dental pain causing feeding difficulties or significant distress require prompt dental or GP review, as severe early childhood caries causing acute pain requires urgent dental treatment, sometimes under general anaesthesia.