1. Etiology of Dental Caries Dr.Rai Tariq Masood

2. Early Theories Worm Theory Humour Theory Parasitic Theory Vital Theory Chemical Theory Chemo-parasitic Theory Proteolytic Theory Proteolysis-Chelation Theory

3. 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

4. Classification Based on Morphology Occlusal Caries ( Pit & Fissure Caries) Smooth Surface Caries Buccal & Lingual Caries Proximal Caries

6. Classification Based on Severity & Progression Rampant Caries Early Childhood Caries ( Baby Bottle Tooth Decay) Radiation Caries

7. Classification Based on Part of Tooth Involved Enamel Caries Dentinal Caries Cemental Caries

8. Classification Based on Activity Primary Caries Secondary Caries Residual Caries Arrested Caries

10. 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

11. 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

13. 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.

14. 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.

15. 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.

16. 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

17. Formation of Plaque Adherence of bacteria to pellicle or enamel surface. Adhesion between bacteria by polysaccharide chains Subsequent growth of bacteria

18. Risk Factors/Protective Factors Total oral Bacterial population Tooth Morphology Salivary secretion rate Intake of carbohydrates Oral Hygiene Habits Use of Fluorides

19. 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.

20. 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.

21. 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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