1. Dental Cariology II
Dr. Khalid AL-Tubaigy

2. Early Stages of Plaque Succession
Pellicle
is formed primarily from the selective precipitation of various components of saliva.
Functions of the pellicle are believed to be:
(1) protect the enamel,
(2) reduce friction between the teeth
(3) possibly provide a matrix for remineralization.
Pellicle is formed from salivary proteins that have apparently involved for this function.
These proteins have many basic groups and consequently adsorb to the phosphate ions while other acidic proteins adsorb to calcium ions.

3. Pellicle formation
Microorganisms do not attach themselves directly to the mineralized tooth surface and the teeth are always covered by an a cellular proteinaceous film.
The pellicle forms on the “naked” tooth surface within minutes to hours

5. Major constituents of Pellicle
Salivary glycoprotein
Carbohydrates
Lipid
a lesser extent components from the gingival crevicular fluid

6. Dental plaque
Definition: A gelatinous mass of bacteria (soft, translucent, and tenaciously adherent material) accumulating on the surface of teeth.

7. Mechanisms of plaque formation
Attachment, growth and reattachment of bacteria to the tooth surface is a continuous and dynamic process.

9. Formation and development of dental plaque
Formation of acquired pellicle and primary aggregation
Bacteria growth and development
The mature of dental plaque

10. Composition of Dental plaque
bacteria which form 50-70% of dental plaque
glycoprotein together with extracellular polysaccharides form the plaque matrix
Muco-poly-saccharides such as glucans and fructans
Inorganic components
calcium
phosphorus
fluorides .

11. Classification of Dental plaque
Supra gingival plaque
-----dental caries
Sub gingival plaque
-----periodontal diseases

12. Structure of Dental Plaque
1. Plaque on smooth surface Plaque adhere to dental surface Middle layer condensed microbial layer (body of plaque) 2. Plaque in pit and fissure

13. Micro-organism and caries
Advanced lesions often have a high proportion of lactobacilli
dentinal lesions have a diverse micro-flora with many Gram positive(+), Gram negative(-) bacteria.
Root surface caries was originally associated with Actinomyces, but recent studies suggest a similar etiology to enamel caries
Rampant caries and early childhood caries can occur in xerostomic patients and infants fed with high levels of sugar in pacifiers (nursing bottle caries) the plaque contains high levels of mutans streptococci and lactobacilli.

14. Clinical sites for caries initiation

15. Clinical sites for caries initiation
Pits and Fissures:
Large numbers of MS gram-positive cocci especially S. sanguis are found in the pits and fissures of newly erupted teeth.
In cross-section, the gross appearance of pit & fissure lesion is an
inverted V with narrow entrance and a progressively wider area of involvement closer to the DEJ .

16. Pit & Fissure Caries

17. Clinical sites for caries initiation
Smooth Enamel Surfaces: Less favorable site for plaque attachment. Plaque develops near the gingival area or under proximal contacts. Lesions have broad area of origin and a conical or pointed extension toward the DEJ. Path of ingress of the lesion is roughly parallel to long axes of enamel rods in the region. Cross-section of enamel of the lesion shows V shape with a wide area of origin and the apex of the V directed toward the DEJ.

18. Smooth Enamel Surfaces

19. Smooth Enamel Surfaces

20. Clinical sites for caries initiation
Root Surface:
Cementum is extremely thin and provides little resistance to caries
attack.
Lesions have less well defined margins tend to be U-shaped in
cross-section and progress more rapidly.
In recent years, Prevalence of root caries has significantly increased
because of the increasing number of older persons who retain more
teeth experience gingival recession and usually have cariogenic
plaque on the exposed root surfaces.

21. Progression of carious lesion

22. Progression of carious lesion
The time for progression from incipient caries to cavitations on
smooth surfaces is estimated to be 18 ± 6 months.
Peak rates for the incidence of new lesions occurs 3 years after eruption of the tooth.
Both poor oral hygiene and frequent exposures to sucrose containing
food can produce incipient (white spot).

23. Clinical Characteristics of Enamel Caries

24. Histology of Enamel

25. Clinical Characteristics of Enamel Caries
Incipient Smooth-Surface Lesion: On clean, dry teeth, the earliest evidence of caries is white spot (chalky white) . Incipient caries will partially or totally disappear visually when the enamel is hydrated (wet) while hypocalcified enamel is relatively unaffected by drying and wetting . Injudicious use of explorer tip can cause actual cavitation for a previously noncavitated incipient area thus requiring in most cases restorative intervention.

26. Clinical Characteristics of Enamel Caries
Zones of Incipient Lesion : (a) Intact surface zone (b) Body of lesion (c) Dark zone (d) Translucent zone

27. Clinical Characteristics of Enamel Caries
Zone 1 Translucent Zone 1. Name refers to its structureless appearance when perfused with quinoline solution and examined with polarized light. 2. The deepest zone. 3. Pore volume is 1%.

28. Clinical Characteristics of Enamel Caries
Zone 2 Dark Zone 1. Does not transmit polarized light. 2. Light blockage is caused by the presence of many tiny pores too small to absorb quinoline. 3. These smaller air or vapor, filled pores make the region opaque. 4.Pore volume is 2% - 4% . 5. Size of dark zone is probably an indication of the amount of remineralization that has recently occurred.

29. Clinical Characteristics of Enamel Caries
Zone 3 Body of the Lesion 1.The largest portion. 2. Has the largest pore volume, varying from 5% at periphery to 25% at the center. 3. Bacteria may be present in this zone if the pore size is large enough to permit their entry.

30. Clinical Characteristics of Enamel Caries
Zone 4 Surface Zone 1. Unaffected by the caries attack. 2. Has lower pore volume than the body of the lesion (< 5%) and radiopacity comparable to unaffected adjacent enamel. 3. Surface of normal enamel is hypermineralized by contact with saliva and has a greater concentration of fluoride ion than the immediately subjacent enamel.

31. Clinical Characteristics of dentinal Caries

32. Clinical Characteristics of dentinal Caries
* Pulp-dentin complex reacts to caries attacks by attempting to initiate remineralization and blocking off the open tubules.
* These reactions result from odontoblastic activity and the physical process of demineralization and remineralization .
* Levels of dentinal reaction to caries :
(1) Reaction to long-term, low-level acid demineralization associated with a slowly advancing lesion.
(2) Reaction to moderate-intensity attack.
(3) Reaction to severe, rapidly advancing caries characterized by very high acid levels.

33. Pulp-dentin complex reacts to caries

34. dentinal Caries

35. Clinical Characteristics of dentinal Caries
Zone 1 Normal Dentin.
1. The deepest area is normal dentin,
2. No bacteria are in the tubules.
3. Stimulation of dentin (e.g., by osmotic gradient [sucrose or salt],
bur, dragging instrument, or desiccation from heat or air), produces sharp pain.
Zone 2 Sub-transparent Dentin.
1. Is a zone of demineralization of the inter-tubular dentin .
2. Damage to odontoblastic process is evident.
3. No bacteria .
4. Stimulation of the dentin produces pain, and the dentin is capable of remineralization.

36. dentinal Caries

37. Clinical Characteristics of dentinal Caries
Zone 3 Transparent Dentin
1. is softer than normal dentin .
2. Stimulation of this region produces pain.
3. No bacteria are present.
4. Dentin is self repaired.
Zone 4 Turbid Dentin
1. filled with bacteria .
2. Collagen in this zone is irreversibly de-natured.
3. Dentin is not self-repaired (not remineralized ) and must be removed before restoration.

38. dentinal Caries

39. Clinical Characteristics of dentinal Caries
Zone 5 Infected Dentin
1. The outermost zone .
2. consists of decomposed dentin that is teeming with bacteria.
3. No recognizable structure to dentin and collagen and mineral seem to be absent.
4. Great numbers of bacteria are dispersed in this granular material.

40. dentinal Caries

41. Why the dentine caries brown ?
The possibilities seem to be:
1. The color is exogenous stain absorbed from the mouth (e.g. from tea, coffee, red wine).
2. comes from pigment-producing bacteria.
3. is the product of a chemical reaction called the Maillard Reaction.
4. A brown color is produced when protein breaks down in the presence of sugar .

42. Thank you for your attention!