Etiology of Dental Caries

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 • Susceptible Tooth Surface • Micro-organism • Diet (Sucrose) • 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 hydroxyapetitecrystals.

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.

22. Thank you