Etiology of Dental Caries

Dr.Rai Tariq Masood

Early Theories

• Worm Theory• Humour Theory• Parasitic Theory• Vital Theory• Chemical Theory• Chemo-parasitic Theory• Proteolytic Theory• Proteolysis-Chelation Theory

Current Concepts of Caries Etiology

Keyes Circles• Caries is multi-factorial disease comprising of

four factors1. Susceptible Tooth Surface2. Micro-organism3. Diet (Sucrose)4. Appropriate time

Each one of them is of equal importance in aetiology of caries

Classification Based on Morphology

• Occlusal Caries ( Pit & Fissure Caries)• Smooth Surface Caries

Buccal & Lingual CariesProximal Caries

Classification Based on Severity & Progression

• Rampant Caries• Early Childhood Caries ( Baby Bottle Tooth

Decay)• Radiation Caries

Classification Based on Part of Tooth Involved

• Enamel Caries• Dentinal Caries• Cemental Caries

Classification Based on Activity

• Primary Caries• Secondary Caries• Residual Caries• Arrested Caries

Clinical Manifestations of Caries Process

1- Early Changes• First time demineralization of enamel when

PH falls below 5.2 – 5.5• Demineralization can not be detected clinically

2- White Spot Lesion

• First visible clinical presentation• Caused by sub-surface enamel

demineralization• Surface is intact• It may or may not progress to frank cavitation

3- Hidden or Occult Caries

• Calcium and Phosphate moves from subsurface to the surface.

• Calcium and Phosphate along with fluoride from saliva precipitate on effected surface enamel.

• It will occlude the pores that limits demineralization of surface enamel.

• Hence intact surface enamel and caries in subsurface level.

• Not clinically visible.

4- Frank Cavitation

• Sub-surface carious lesion increases in dimensions.

• Collapse of surface layer• Cavitation• More plaque accumulation so rapid tooth

destruction.• It takes 18 (+- 6 months) to progress from

white lesion to cavitation.

5- Arrested Caries

• Carious lesion can become arrested at any stage.

• If the causal factors are changed or protective factors are increased.

• Example :Proximal Carious lesion and if adjacent tooth is lost then it becomes self cleansing.

Micro-Biology of Dental Caries

Streptococcus Mutans• Ability to stick to tooth surfaces• Ability to produce lactic acid• Resist the acidogenic environment• Produce intracellular polysaccharide

Streptococcus SobrinusLactobacillus

Formation of Plaque

• Adherence of bacteria to pellicle or enamel surface.

• Adhesion between bacteria by polysaccharide chains

• Subsequent growth of bacteria

Risk Factors/Protective Factors

• Total oral Bacterial population• Tooth Morphology• Salivary secretion rate• Intake of carbohydrates• Oral Hygiene Habits• Use of Fluorides

Role of Saliva in Caries• Also called Liquid Enamel because of high mineral

content• Cleansing Action• Buffering Capacity• Antibacterial Action by

Lysozyme,Lactoperoxidase,hemoprotein enzyme (Prevents bacterial colonization)

• Saturated with Calcium and Phosphate• Most prominent antibody in saliva IGA.• Proteins like statherin protects hydroxyapetite crystals.

• Flow rate: Role of saliva, with respect to caries, is in the removal of bacterial and debris. Average un-stimulated flow rate is 0.3 ml/minute and amount prior to swallowing 0.9-1.2 ml

• Quantity: Normal is 700-800 ml/day. Less leads to rampant caries as seen in Xerostomia.

• Viscosity: Thick saliva associated with high caries but not confirmed.

• pH: Depends on bicarbonate content.Saliva may be slightly acidic as it is secreted at unstimulated flow rates but may reach PH of 7.8 at high flow rates.

Buffering Action

• Bicarbonates are most important buffers• It reacts with acid and release weak carbonic

acid.• Carbonic acid is rapidly decomposed into

water and carbon dioxide.• So acid is completely removed.• When there is excess sucrose intake,intense

acid production will breakdown the buffers.

Thank you