Etiology of Dental Caries Dr Rai Tariq Masood

Etiology of Dental Caries Dr. Rai Tariq Masood

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

Current Concepts of Caries Etiology Keyes Circles • Caries is multi-factorial disease comprising of four factors 1. Susceptible Tooth Surface 2. Micro-organism 3. 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 Caries Proximal 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 Sobrinus Lactobacillus

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. • p. H: 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.

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