lec.2 Dr.

Abdulkareem AlMezouri 2018

Caries of Enamel

Features and structure of the enamel:

Enamel covers the anatomic crown of the tooth and varies in thickness in different
areas. It is thicker at the incisal and occlusal areas of a tooth and becomes progressively
thinner until it terminates at the cementoenamel junction (CEJ). The thickness also varies
from one class of tooth to another, averaging 2 mm at the incisal ridges of incisors, and
2.5 to 3 mm at the cusps of molars. The normal color of enamel varies from light yellow
to grayish (bluish) white. Enamel is a rigid structure that is both strong and brittle (high
elastic modulus, high compressive strength, and low tensile strength) and requires a
dentin support to withstand masticatory forces. Surface enamel is harder, denser, and less
porous than subsurface enamel.
Enamel composed of mineral (96% by weight) in the form of hydroxyapatite
Ca10 (Po4) (OH)2. The remaining non-mineral content is water (about 3%) and 1%
organic material. Enamel does not contain collagen, as found in other hard tissues such as
dentin and bone, but it does contain two unique classes
of proteins: amelogenins and enamelins. Enamel is formed by ameloblast cells, and is
incapable of repairing itself once destroyed because the ameloblast cells degenerates after
formation of enamel. Enamel is avascular and has no nerve supply within it and is not
renewed, however, it is not a static tissue as it can undergo mineralization changes.
Structurally, enamel is composed of millions of enamel rods or prisms, which are
the largest structural components, rod sheaths, and a cementing inter-rod substance in
some areas. The structural components of the enamel prism are millions of small,
elongated apatite crystallites that vary in size and shape. The crystallites are tightly
packed in a distinct pattern of orientation that gives strength and structural identity to the
enamel prisms.. Although crystal packing is very tight, each crystal is actually separated
from its neighbor by tiny intercrystalline space or pores. These spaces are filled with
water and organic material. When enamel is exposed to acid attack, mineral is removed
from the surface of the crystal which shrinks in size, and hence the intercrystalline spaces
enlarge and the tissue becomes more porous. This increased porosity can be clinically
seen as a white spot.
 lec.2 Dr. Abdulkareem AlMezouri 2018

Noncavitated enamel caries lesion:

On clean, dry teeth, the earliest evidence of caries on the smooth enamel surface
of a crown is a white spot, these lesions are usually observed on the facial and lingual
surfaces of the teeth.

White spots are chalky white, opaque areas that are revealed only when the tooth
surface is dried, and are termed noncavitated enamel caries lesion. These areas of
enamel lose their translucency because of the extensive subsurface porosity caused by
demineralization. Care must be exercised to distinguish white spots of noncavitated caries
from developmental white spot hypocalcifications of enamel. Noncavitated (white spot)
caries will partially or totally disappear visually when the enamel is hydrated (wet), while
hypocalcified enamel is relatively unaffected by drying and wetting.
 lec.2 Dr. Abdulkareem AlMezouri 2018
Hypocalcified enamel does not represent a clinical problem except when its
appearance is objectionable esthetically. The surface texture of a noncavitated lesion is
unaltered and is undetectable by tactile examination with an explorer. A more advanced
lesion develops a rough surface that is softer than the unaffected, normal enamel. It also
should be noted that careless use of an explorer tip can cause actual cavitation for a
previously noncavitated area, thus requiring, in most cases, restorative intervention.
Similar noncavitated lesions occur on the proximal smooth surfaces but usually are
undetectable by visual or tactile (explorer) examination. Noncavitated enamel lesions
sometimes can be seen on radiographs as a faint radiolucency, limited to the superficial
enamel. When a proximal lesion is clearly visible radiographically, the lesion may have
advanced significantly and histological alteration of the underlying dentin probably has
already occurred, whether the lesion is cavitated or not.

It has been shown experimentally and clinically that noncavitated caries of

enamel can be remineralized. Noncavitated enamel lesions retain most of the original
crystalline framework of the enamel rods and the etched crystallites serve as nucleating
agents for remineralization. Calcium and phosphate ions from saliva can then penetrate
the enamel surface and precipitate on the highly reactive crystalline surfaces in the
enamel lesion. The supersaturation of the saliva with calcium and phosphate ions serves
as the driving force for the remineralization process. Furthermore, the presence of trace
amounts of fluoride ions during this remineralization process greatly enhances the
precipitation of calcium and phosphate, resulting in the remineralized enamel becoming
more resistant to subsequent caries attack because of the incorporation of more acid-
resistant fluorapatite.

Remineralized (arrested) lesions can be observed clinically as intact, but

discolored, usually brown or black spots. The change in color is presumably due to
trapped organic debris and metallic ions within the enamel. These discolored,
remineralized, arrested caries areas are intact and are more resistant to subsequent caries
attack than the adjacent unaffected enamel. They should not be restored unless they are
esthetically objectionable.
 lec.2 Dr. Abdulkareem AlMezouri 2018

Zones of noncavitated enamel lesion:

Four zones can be distinguished in these lesions which are from inside to outside:

Zone 1: Translucent Zone:

Is the deepest zone and represents the advancing front of the enamel lesion. The
name refers to its structureless appearance when treated with quinoline solution and
examined with polarized light. In this zone, the pores or voids form along the enamel
prism (rod) boundaries. When these boundary area voids are filled with quinoline
solution, which has the same refractive index as enamel, the features of the area
disappear. The pore volume of the translucent zone of enamel caries is 1%, 10 times
greater than normal enamel.

Zone 2: Dark Zone:

Is the next deepest zone, it is known as the dark zone because it does not transmit
polarized light. This light blockage is caused by the presence of many tiny pores too
small to absorb quinoline. These smaller air- or vapor-filled pores make the region
opaque. There is theory that the dark zone is not really a stage in the sequence of the
breakdown of enamel; rather, the dark zone may be formed by deposition of ions into an
area previously only containing large pores. It must be remembered that caries is an
episodic disease with alternating phases of demineralization and remineralization.
Experimental remineralization has demonstrated increases in the size of the dark zone at
the expense of the body of the lesion. 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.

Zone 3: Body of the Lesion:

The body of the lesion is the largest portion of the white spot lesion while in a
demineralizing phase. It has the largest pore volume, varying from 5% at the periphery to
 lec.2 Dr. Abdulkareem AlMezouri 2018
25% at the center. The first penetration of caries enters the enamel surface in sequence
via the striae of Retzius, the interprismatic areas and the rod (prism) cores, which are then
preferentially attacked. Bacteria may be present in this zone if the pore size is large
enough to permit their entry

Zone 4: Surface Zone:

The surface zone is relatively unaffected by the caries attack. 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 has been hypothesized that hypermineralization and increased fluoride content
of the superficial enamel are responsible for the relative immunity of the enamel surface.
However, removal of the hypermineralized surface by polishing fails to prevent the
reformation of a typical, well-mineralized surface over the carious lesion.
 lec.2 Dr. Abdulkareem AlMezouri 2018

Cavity formation: 

Once bacteria have penetrated the enamel they reach the dentino-enamel junction
and spread laterally to undermine the enamel. This has three major effects. First, the
enamel loses the support of the dentine and is therefore greatly weakened. Second, it is
attacked from beneath. Third, spread of bacteria along the dentino-enamel junction
allows them to attack the dentine over a wide area. Thus the primary lesion provides the
bridgehead for the attack on enamel, but undermining of the enamel determines the area
of a cavity.

Clinically this is frequently evident when there is no more than a pinhole lesion in
an occlusal pit, but cutting away the surrounding enamel shows it to be widely
undermined. As undermining of the enamel continues, it starts to collapse under the stress
of mastication and to fragment around the edge of the (clinically obvious) cavity. By this
stage, bacteria damage to the dentine is extensive.
lec.2 Dr. Abdulkareem AlMezouri 2018