Short Answer Questions (SAQ): Dental Caries

Q1. Define dental caries and describe its pathophysiology.

1. Dental pellicle (salivary glycoproteins) forms on tooth surface
2. Early colonization by streptococci and Actinomyces species
3. Plaque biofilm matures (300-400 bacterial species)
4. Bacteria (especially S. mutans) metabolize dietary carbohydrates - plaque pH drops below critical threshold - enamel hydroxyapatite dissolves to soluble calcium and phosphate ions

Cariogenesis - from pellicle formation to acid attack on enamel (Sherris & Ryan's Medical Microbiology)

Q2. What are the stages of dental caries progression?

1. Initial enamel lesion - acid permeates along enamel prism sheaths causing localized dissolution. No cavitation, no dentine involvement. This stage is reversible.
2. Established enamel caries - lesion progresses toward the enamel-dentine junction
3. Dentine caries - acid dissolution, proteolysis, and bacterial invasion of dentinal tubules
4. Pulp involvement - infection and inflammation of dental pulp (pulpitis)
5. Periapical spread - through root canals to periapical area: periapical abscess (acute), periapical granuloma (chronic non-suppurating), or sinus tract/cyst (chronic suppurating)
6. Systemic spread - osteomyelitis of alveolar bone, fascial cellulitis of head and neck, or septic thrombophlebitis

Q3. What is the role of Streptococcus mutans in dental caries?

• Efficient sucrose metabolism - metabolizes sucrose more efficiently than other oral bacteria
• Acid production - rapidly ferments dietary carbohydrates, dropping plaque pH to levels sufficient to demineralize hydroxyapatite
• Extracellular polyglycan synthesis - uses transferase enzymes to produce dextrans and levans from sucrose, promoting bacterial aggregation and adherence to tooth surface
• Intracellular glycogen storage - stores carbohydrate intracellularly, prolonging acidogenesis beyond oral clearance time of the dietary substrate
• Acid tolerance - survives long periods of sugar starvation and persists in low-pH environments

Q4. What is the demineralization-remineralization cycle?

• After carbohydrate intake, plaque bacteria produce acid rapidly - plaque pH drops, causing enamel demineralization
• As the substrate is exhausted, acid production stops and pH slowly returns to neutral
• Saliva provides calcium, phosphate and fluoride ions to remineralize the enamel surface
• With repeated snacking between meals, plaque pH may never return to normal - demineralization dominates and caries develops
• Foods high in sucrose that adhere to teeth (long oral clearance time) are more cariogenic than sugar-containing liquids

Q5. What are the risk factors for dental caries?

• Newly erupted teeth (most susceptible before posteruptive maturation)
• Xerostomia (dry mouth) - loss of saliva's protective functions
• Narrow fissures, pits, poor interdental contact points
• Inadequate dental restoration margins

• Colonization by S. mutans and other acidogenic/aciduric organisms
• Mature plaque biofilm formation

• High intake of free/refined sugars (especially sucrose)
• Frequent snacking - repeated acid challenges
• Sticky, adherent foods with prolonged oral clearance time

• Reduced salivary flow (drugs, Sjogren's, radiation)
• Reduced buffering capacity

Q6. What is the role of fluoride in prevention of dental caries?

1. Systemic fluoride - during tooth formation, fluoride ions replace hydroxyl ions in hydroxyapatite → forms fluorapatite, a more acid-resistant mineral phase
2. Topical fluoride - surface dissolution of hydroxyapatite followed by recrystallization incorporating fluoride → more acid-resistant surface
3. Inhibition of demineralization and promotion of remineralization of incipient carious lesions by fluoride ions in oral fluid - now considered the most important mechanism

Q7. Outline the clinical diagnosis and management of dental caries.

• Visual and tactile inspection using blunt dental probes
• Dental radiographic examination
• Stages classified by surfaces involved: Class I (pits/fissures), Class II (interproximal), Class III/IV (anterior), Class V (cervical)

• Oral hygiene - toothbrushing, flossing, removal of plaque biofilm
• Dietary modification - reduce free sugar intake and snacking frequency
• Fluoride - water fluoridation, fluoride toothpaste, topical fluoride
• Fissure sealants for susceptible pits and fissures
• Regular dental review

Q8. What are the complications of untreated dental caries?

• Pulpitis (reversible → irreversible)
• Pulp necrosis
• Periapical abscess
• Periapical granuloma
• Dental/periapical cyst (from epithelial rests of Malassez in periodontal ligament)

• Osteomyelitis of alveolar bone
• Facial cellulitis (fascial space infections of head and neck)
• Septic thrombophlebitis (via venous channels)
• Ludwig's angina (bilateral submandibular space infection)

Key Points Summary

• Dental caries = dynamic, multifactorial, bacterial disease driven by the plaque-acid-demineralization cycle
• Four factors: plaque, dental tissue, saliva, substrate
• Key organism: Streptococcus mutans (acidogenic, aciduric, adherent via glucans, prolongs acidogenesis via glycogen stores)
• Critical concept: demineralization-remineralization balance - tip it repeatedly toward demineralization = caries
• Reversible only at the enamel stage - once dentine is involved, operative treatment is required
• Fluoride is the most effective preventive measure
• Sucrose is the most cariogenic substrate