1. Damion Francis TMRI-ERU
Dental Caries
Damion Francis
TMRI-ERU

2. Eruption Mechanisms of tooth eruption are complex
Teeth eventually appear in mouth through a combination of growth of supporting bone
Elongation of tooth root and growth of pulp

4. Nutrition and Teeth Prenatal nutrition and developing teeth
Prenatal nutrition has very little effect on the developing tooth
Primary teeth begin to calcify in utero
Relatively protected from lack of calcium
Mother provides calcium needed during pregnancy
Ingestion of tetracyclines and high flouride levels by mother causes discoloration in utero

5. Postnatal nutrition and developing teeth
Adequate calcium in a balanced diet is important to tooth development
1950’s vit D was postulated to be important to enamel quality but evidence are lacking to support this in modern research
Osteoporosis as no effect on teeth

6. Nutrition and Dental Caries
Direct cause-and-effect relationship between nutritional status and dental caries
Malnutrition is associated with retarded exfoliation of primary teeth
However unclear if cause by the process itself or the longer time before exfoliation
Permanent teeth eruption seem to be unaffected but have higher rates of caries

7. Enamel Integrity
Tooth enamel structure may be damaged by trauma or acid demineralization
Loss of the tooth mineral structure begins when enamel surface pH is below 5.7 to 5.5
Normal Neutral pH of the oral cavity is around 6

8. Dynamic process of demineralization and remineralization is guided by several factors:
Oral bacteria, salivary flow and composition, presence of fluoride, tooth integrity and dietary habits
Equilibrium shifting of these factors towards demineralization results in enamel dissolution and hence caries formation
Calcium and phosphate ( pH) as well as fluoride, can help remineralize affected areas if the process has not reached the cementoenamel junction

9. Tooth integrity exists when these processes occur without net loss of tooth mass
Carious lesions results when the rate of demineralization exceeds the rate of remineralization over an extended time

10. Diet and Enamel Decalcification
Dental erosion is the loss of dental hard tissues (typically the enamel) caused by local effect of acid on the teeth
Acid may come from sources such as citrus fruits, acidogenic sport drinks, snacks, carbonated beverages etc.
Excessive acidic food or beverages over time may cause enamel dissolution

11. Further facilitated by xerostomia xerostomia as the natural protection by saliva is absent
Important to differentiate this type of erosion from the caries process
Acid produced from plaque bacteria causes the enamel demineralization

12. Caries Process Dental caries is a multifactorial disease
Involves demineralization of the enamel and dentin
Bacteria in dental plaque metabolize fermentable carbohydrates into organic acids
Below the critical pH proteolytic enzymes break down the organic component

13. Caries
Individual Susceptibility

14. The length of exposure is influenced by a food’s inherent retention in the mouth
Eg. Liquids are cleared from the mouth more rapidly than solids; and foods that stimulate salivary flow though their consistency or chemical composition are cleared more rapidly than bland foods.
Proteins from saliva adsorb to the cleaned tooth and form the acquired enamel pellicle

15. Proteinacious coating allows certain bacteria to start to colonize the tooth
protein interactions between bacterial cell wall and pellicle
Mature and thickened plaque contains many species of oral bacteria in extracellular matrix material
More than 500 species of bacteria present in mouth

17. Small proportion of these are acidogenic bacteria that use dietary sugars as an energy source
They produce acids and are associated with the caries development (not all acidogenic bacteria are cariogenic)
In humans the two species of interest are Streptococcus mutans and Streptococcus sobrinus

18. S. mutans is the major pathogenic bacterial species involved in the caries process
Studies show that 93% of children with detectable caries were positive for S. mutans
The physiologic characteristics of the S. mutans that make them prime etiological agent in caries include their ability to:

19. S. mutans Adhere to tooth surface
Produce abundant insoluble extracellular polysaccharides from sucrose
Rapidly produce lactic acid from a number of sugar substrates
Be tolerant to acid
Produce intracellular polysaccharide stores

20. Cariogenic bacteria metabolize sugars to produce energy required for their growth and reproduction
The energy source may be exogenous or endogenous
Metabolism of mono or di saccharides
Once within the cell, glucose enters the Embden-Meyerhof glycolitic pathway

21. End result is production of Lactic acid and or other organic acids
Presence of these acids in dental plaque fluid lowers its optimal pH
The interface between tooth and plaque is no longer saturated with calcium and phosphate ions
Demineralization starts taking place which may go beyond the dentinoenamel junction

22. Stephan Curve after 10% sucrose rinse and 24-h-old dental plaque

23. Acid decalcification progress Bacterial invasion of organic matrix
Degradation by the process of proteolysis
Carious lesions can occur where plaque can sufficiently colonize such as:
Pit and fissure caries (found mainly on the occlusal surfaces of posterior teeth, and in lingual pits of maxillary incisors)

24. Secondary or recurrent caries
Smooth surface caries
Arise on intact enamel surfaces other than pit fissure
Can be divided into smooth surface caries (i.e., caries affecting the buccal and lingual tooth surfaces)
Approximal caries, affecting the contact area of adjoining tooth surface
Root surface caries
Secondary or recurrent caries

25. Earliest clinically detectable stage of caries in the enamel is the incipient lesion
Characterized by an opaque, white appearance
At this stage the process is amenable to remineralization
Further mineral loss result in enamel degradation and frank cavitation
Only treatment option in most cases is the placement of restoration