Dentine, unlike enamel, has the ability to react to the progression of caries due to the presence of odontoblasts.

1. PROGRESSION OF ENAMELCARIES
Makerere University
BDSIII

2. Properties of enamel
Physical properties
 hardest substance of human body.
 Very brittle and low tensile strength (like ceramics
 Enamel is translucent and varies in color from light
yellow to whitish.
 thicker over cusps (2.5 mm) to a feather edge at the
cervical line.
 it is partially permeable to some fluids, bacteria and
other products of the oral
 it is totally acellular .
 Unsupported enamel is subject to easily fracture or
cleave along rod boundaries
Chemical and inorganic
composition.
 Highly mineralized crystalline structure, 96%
inorganic materials by weight; hydroxyapatite
(HA), 4% by weight organic content and water.
 The organic matrix ,non-collagenous proteins and
enzymes. Of the enamel proteins 90% are
amelogenins and 10% are non-amelogenins. The
different types of non amelogenins associated with
formation of enamel are ameloblastin, enamelin
and tuftelin. The primary function of the organic
material is to direct the growth of enamel crystals .

3. Structure
Structure and organization
 3 structures
 Rods or prisms( crystallites formed by
,tomes process of the ameloblasts)
 Rod sheath
 Cementing inter rod substance
 Rods are perpendicular to DEJ,wavy course
towards the cusp tip(Gnareled enamel).
Histological features
 Gnarled enamel(sstrenth and resistance to fracture.
 hunter- Schreger bands
 Perikymata
 Enamel cuticle(nasmyth’s membrane
 Enamel pellicle(hinder bacterial attachment)
 Enamel lamellae(planes of tension)
 Enamel spindles (odontoblastic origin)
 Enamel tufts(protein enmelin,anchor dentine to enamel
 Cross striations
 Striae of Retzious
 Neontal line

4. Histologic features
E.spindle

6. PROGRESSION OF ENAMEL CARIES
1. INITIAL (submicroscopic)LESION
2. NONBACTERIAL ENAMEL
CRYSTAL DESTRUCTION
3. CAVITY FORMATION
4. BACTERIAL INVASION
INITIAL STAGE;4 ZONES
 Zone 1: Translucent Zone.
 Zone 2: Dark Zone
 Zone 3: Body of the Lesion.
 Zone 4: Surface Zone.
HAS 4 STAGES

7. 1: THE INITIAL (Submicroscopic) LESION
 Seen as a white opaque spot that forms just adjacent to a
contact point It is conical in shape with its apex towards the
dentine, and a series of four zones of differing translucency
can be discerned. From the deepest, is a translucent zone (1%
pores, only demineralization);
 the second dark zone(2-4% pores, both mineralization and
demineralization);
 the third consists of the body of the lesion (the pore volume
is 5% at the periphery but increases to at least 25% in the
Center) and the fourth consists of the surface zone (1% pore
volume mineralization, radiopaque

8. Conti….
 Cross-section of small carious lesion in enamel examined in quinoline by transmitted light (x 100).
Surface (a) appears to be intact. Body of lesion (b)
shows enhancement of striae of Retzius. Dark zone (c)
surrounds body of lesion while translucent zone (d) is
evident over entire advancing front of lesion. (From
Silverstone LM. In Silverstone LM et al, editors:
Dental caries,London and Basingstoke, 1981,
Macmillan.)

9. Zone 1: Translucent Zone.
 loss of 1% of minerals
demineralization
 In this zone, the pores or voids form along the enamel
prism (rod) boundaries, presumably because of the ease of
hydrogen ion penetration during the carious process.

10. Zone 2: Dark Zone.
 The total pore volume is 2% to 4%.
 the dark zone may be formed by deposition of ions into an area
previously only containing large pores remineralization.
 There is also a loss of crystalline structure in the dark zone,
suggestive of the process of demineralization and remineralization.
 The size of the dark zone is probably an indication of the amount of
remineralization that has recently occurred.

11. Zone 3: Body of the Lesion.
 It has the largest pore volume, varying from 5% at the periphery to 25% at the
center. The striae of Retzius are well marked in the body of the lesion,
indicating preferential mineral dissolution along these areas of relatively higher
porosity.
 The first penetration of caries enters the enamel surface via the striae of Retzius.
 Bacteria may be present in this zone if the pore size is large enough to permit
their entry.
 SEM(scanning electron microscopy )demonstrate the presence of bacteria
invading between the enamel rods (prisms) in the body zone .

12. Zone 4: Surface Zone.
 It has a lower pore volume than the body of the lesion (less than 5%) and a radiopacity
comparable to unaffected adjacent enamel
 The surface of normal enamel is hypermineralized by contact with saliva and has a
greater concentration of fluoride ion than the immediately subjacent enamel.
 it serves as a barrier to bacterial invasion. As the enamel lesion progresses, conical-
shaped defects in the surface zone can be seen by SEM. These are probably the first
sites where bacteria can gain entry into a carious lesion.
 Arresting the caries process at this stage results in a hard surface that may at times be
rough, though cleanable.

13. Cross-section of small carious lesion in enamel examined in quinoline by transmitted light (x 100).
Surface (a) appears to be intact. Body of lesion (b) shows
enhancement of striae of Retzius. Dark zone (c)
surrounds body of lesion while translucent zone (d) is
evident over entire advancing front of lesion. (From
Silverstone LM. In Silverstone LM et al, editors: Dental
caries,London and Basingstoke, 1981, Macmillan.)

14. 2: STAGE OF Nonbacterial ENAMEL CRYSTAL
DESTRUCTION
 Highly mobile hydrogen ions permeate the organic matrix enabling them to
attack the surface of the apatite crystals which become progressively smaller.
 Microdissection of the translucent zone has shown that the apatite crystals
have declined in diameter from the normal of 35-40 nm to 25-30 nm and in
the body of the lesion to 10-30 nm. In the dark zone, by contrast, enamel
crystals appeared to have grown to 50-100 nm and in the surface zone to 35-
40 nm. These findings also suggest that demineralisation and remineralisation
are alternating processes.

15. 3: CAVITY FORMATION
 demineralisation comes to dominate the process.
 prisms disappear - formation of pathways large enough for
bacteria to enter, bacteria reach amelodentinal junction –
spread laterally - enamel undermining.
 pinhole lesion in enamel - large underlying cavity
fragmentation of enamel on the surface – clinically obvious
cavity
 bacterial attack of dentine enabled

16. 4: BACTERIAL INVASION
 Bacteria do not physically penetrate enamel until acid destruction of the
tissue has provided pathways large enough for them to enter
 Defects eventually become large enough to allow bacteria to enter.
 In superficial lesions; streptococcus viridans are predominant.
 In deep lesions; mixed bacterial effect with lactobacilli predominating.

17. Enamel caries
Macroscopically
In case of a superficial caries:
Reversible white spot lesion without macroscopic
destruction
Fissure caries:
Whitish-yellowish or brownish-blackish
discoloration

18. Radiological illustration of progression of caries

19. Thank you for listening.