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

Dental caries (tooth decay) is a biofilm-mediated, diet-modulated, multifactorial, non-communicable disease resulting in localised destruction of susceptible dental hard tissues — enamel, dentine, and cementum. It is the most prevalent chronic disease globally, affecting an estimated 2.5 billion people with untreated caries in permanent teeth and 520 million children with caries in primary (baby) teeth. The caries process is a dynamic interplay between acidogenic bacteria (predominantly Streptococcus mutans and Lactobacillus species) in dental biofilm (plaque), fermentable carbohydrates (particularly sucrose), and the susceptibility of tooth surfaces. These bacteria metabolise dietary sugars into organic acids (lactic acid, acetic acid) that dissolve the hydroxyapatite mineral in dental hard tissues — a process of demineralisation. Saliva acts as the primary natural defence by buffering acid and providing calcium and phosphate ions for remineralisation. Early caries (white spot lesions) can be reversed; advanced cavitation requires operative intervention.

The caries process requires four essential interacting factors (Keyes diagram): susceptible tooth surface, cariogenic bacteria (Streptococcus mutans — produces lactic acid and glucan polymers promoting plaque adhesion), fermentable carbohydrates (sucrose most cariogenic — substrate for acid production), and time (frequency and duration of acid exposure). Streptococcus mutans is transmissible — mothers with high oral bacterial load transmit cariogenic bacteria to infants via saliva (kissing, sharing utensils). Risk factors: high-frequency sugar consumption (sticky, slow-dissolving sweets, carbonated drinks, fruit juices), poor oral hygiene (inadequate plaque removal), low fluoride exposure (non-fluoridated water, no fluoride toothpaste), xerostomia (dry mouth from medications — antihistamines, antidepressants, anticholinergics — or radiotherapy or Sjogren's syndrome — saliva is the primary natural caries defence), visible plaque accumulation, active caries in a caregiver, socioeconomic deprivation, acid reflux (GORD — exposes teeth to stomach acid), bulimia nervosa (frequent vomiting erodes enamel), and mouth breathing.

Early-stage caries (enamel demineralisation): no pain or visible cavity — a chalky white spot (white spot lesion) on the enamel surface is the earliest detectable sign, visible on dental inspection. Progressing caries: tooth sensitivity to sweet foods and temperature (cold, sometimes hot) — mild, transient, relieved quickly. Visible cavity or hole in the tooth: usually brown or black discolouration and a palpable cavity. Dentinal caries: more pronounced sensitivity to temperature and sweet stimuli as the caries penetrates through enamel into dentine. Pulpitis (infection reaching the pulp): severe toothache — initially a sharp pain triggered by hot, cold, or sweets lasting more than 30 seconds (irreversible pulpitis); progresses to spontaneous, throbbing, constant pain, often worse at night (tooth abscess forming). Periapical abscess: severe constant pain, swelling of the gum or face, fever, lymph node enlargement — bacteria have spread beyond the tooth root apex. Complications: dental abscess, spreading infection (cellulitis, Ludwig's angina — life-threatening floor-of-mouth infection), loss of tooth, and in children, impact on speech development, nutrition, and school attendance.

Clinical dental examination: visual inspection with dental mirror and probe — detects cavitation (ICDAS classification — International Caries Detection and Assessment System — grades caries from 0–6: 0=sound, 1–2=initial or moderate lesions, 3–6=cavitation). Bitewing radiographs (X-rays): the standard method for detecting interproximal (between teeth) caries not visible clinically — particularly important in patients with tight contacts between teeth; detect caries in the dentine layer before it becomes clinically cavitated. Periapical radiographs: for assessing root canals, periapical pathology (abscess — periapical radiolucency), and bone loss. Digital radiography reduces radiation dose by 70% compared to conventional film. Transillumination (FOTI/DIFOTI): light passed through the tooth; caries scatters light, appearing darker. Laser fluorescence (DIAGNOdent): measures bacterial porphyrin fluorescence in carious lesions. Caries risk assessment: CAMBRA (Caries Management by Risk Assessment) framework evaluates biological risk factors (oral hygiene, diet, saliva flow, cariogenic bacteria levels) and protective factors (fluoride, sealants, saliva) to stratify patient risk and guide prevention intensity.

Non-operative (remineralising) treatment for early caries (white spot lesions, initial enamel caries — ICDAS 1–2): high-concentration fluoride application (5% sodium fluoride varnish — applied by dentist 2–4 times/year; reduces caries incidence by 40% in children; promotes remineralisation); 10% casein phosphopeptide-amorphous calcium phosphate (CPP-ACP — Tooth Mousse); silver diamine fluoride (SDF) 38% solution — arrests caries progression, particularly in children and elderly; intensive oral hygiene instruction; dietary counselling to reduce sugar frequency. Operative restorative treatment (cavitated caries requiring fillings — ICDAS 3–6): composite resin (tooth-coloured filling — preferred aesthetic material for anterior teeth and most posterior teeth); glass ionomer cement (GIC — releases fluoride, adhesive to tooth — used for root caries, paediatric dentistry, and areas with difficult moisture control); dental amalgam (silver alloy — durable for high-load posterior restorations, now restricted in the EU from 2025 due to mercury environmental concerns). Pulpitis and abscess: root canal therapy (endodontic treatment — removal of infected pulp tissue, cleaning and shaping of root canals, filling with gutta-percha — preserves the tooth); dental extraction if the tooth is non-restorable or patient preference. Antibiotics (amoxicillin 500 mg TDS or metronidazole 400 mg TDS for 5 days): only for spreading dental infection with cellulitis or systemic signs (fever above 38°C, trismus) — antibiotics alone do not resolve dental infection without drainage, root canal, or extraction. Fissure sealants (dental sealants): resin placed in occlusal pits and fissures of molar teeth — reduce caries incidence by 70% in children.

Untreated dental caries (tooth decay) progresses through a series of complications that escalate in severity and can have serious systemic consequences. Pulpitis and toothache: as caries advances through enamel and dentine to reach the dental pulp, pulpal inflammation (pulpitis) causes severe, spontaneous pain — initially reversible (responds to cold and settles), then irreversible (spontaneous throbbing pain, worse at night); untreated irreversible pulpitis progresses to pulp necrosis. Dental abscess: infection of the necrotic pulp extends periapically through the root apex into the alveolar bone — periapical abscess causes intense localised pain, gum swelling, and systemic fever; dental abscesses are one of the commonest causes of emergency dental presentations. Dental sepsis and cellulitis: spread of dental infection through fascial spaces of the head and neck causes cellulitis — presenting with facial swelling, trismus, dysphagia; in severe cases, Ludwig's angina (bilateral cellulitis of the floor of the mouth) is a life-threatening emergency causing airway compromise. Deep space neck infections require emergency surgical drainage. Tooth loss: untreated caries leading to non-restorable tooth destruction requires extraction — multiple missing teeth impair chewing efficiency, cause bone loss, alter speech, and allow adjacent teeth to drift, causing further dental problems. Nutritional deficiency: severe dental pain or tooth loss impairs the ability to eat a nutritionally adequate diet — contributing to malnutrition. Infective endocarditis: dental bacteraemia during procedures in patients with structural cardiac defects.

Brush twice daily with fluoride toothpaste (1,000–1,450 ppm fluoride for adults; 1,000 ppm for children) — brushing last thing at night and at least one other time is the most important caries prevention measure. Spit, do not rinse after brushing — rinsing washes away protective fluoride. Floss or use interdental brushes daily — removes plaque from between teeth where toothbrush cannot reach. Reduce sugar frequency (not just quantity) — the number of times per day the mouth is exposed to fermentable carbohydrates determines acid attack episodes; limit sugary snacks and drinks to mealtimes. Drink fluoridated tap water — community water fluoridation reduces caries prevalence by 20–40%. Avoid frequent consumption of acidic drinks (carbonated drinks, fruit juices, sports drinks). Use fluoride mouthwash if at high caries risk (0.05% NaF daily or 0.2% weekly). Six-monthly dental check-ups — dentists detect caries at early, non-cavitated stages when remineralisation is possible without drilling. Fissure sealants in all first and second molar teeth of children at caries risk.

Go to hospital immediately if dental infection causes: swelling spreading to the neck or floor of the mouth (Ludwig's angina — life-threatening), difficulty breathing or swallowing, high fever above 38.5°C, trismus (inability to open the mouth), or facial swelling rapidly spreading — these require emergency surgical drainage and IV antibiotics. See a dentist urgently (same day or next day) for: severe toothache that is spontaneous, constant, or disturbs sleep; visible facial swelling from a dental abscess; a tooth knocked out (reimplant within 1 hour — keep in milk or saliva). Book a routine dental appointment within 2 weeks for: tooth sensitivity to temperature or sweet foods, visible brown or black spot or cavity, or bleeding gums. Regular six-monthly check-ups are the cornerstone of dental caries prevention — do not wait until you are in pain.