Читать книгу Applied Oral Physiology - Robin Wilding - Страница 31

1. How would you account for the hardness of enamel and its resistance to acid attack?

2. What evidence supports the view that enamel caries is a dynamic process, and not simply a progressive demineralization of enamel?

3. Why is there a high concentrated fluoride at the periphery of a carious lesion?

4. Why is it useful to consider the pulp and dentin as one biological unit?

5. What is the clinical significance of the high concentration of dentinal tubules in root dentin?

6. What factors alter the permeability of dentin?

7. What zones of caries have been described in dentin, and how can you account for them?

8. What is the clinical significance of discriminating between infected and affected dentin?

9. How does the pulp–dentin develop a mineral barrier to caries?

10. What is the likely consequence of some bacteria remaining in a sealed cavity?

11. Why does the rate of caries progression in dentin differ from enamel?

12. What is the difference between biomineralization and dissolution/precipitation?