Histopathology of carious lesion of enamel
I-Introduction
II-Caries lesion of the enamel
1- initial enamel lesion
a* macroscopic aspect
b* microscopic aspect
1- translucent zone
2- dark area
3- body of the lesion
4- surface layer
c* ultrastructural aspect of the lesion
carious enamel
III-Chemical mechanisms of carious lesion
I/ Introduction:
Carious lesion is a pathological process leading to the destruction of the hard tissues of the dental organ by acid demineralization.
It affects enamel, dentin and cementum to varying degrees, ranging from an
initial mineral loss, clinically undetectable, to the total destruction of these mineralized tissues.
The appearance of these lesions and the speed of their evolution depend on several factors, the main ones being the structure and composition of the tissues involved, the quantity and frequency of carbohydrates in the diet, the presence of bacterial plaque linked to oral hygiene, the quantity and quality of saliva
II/ carious lesion of the enamel:
Enamel is formed from hydroxyapatite crystals giving compact units
called prisms and separated by so-called interprismatic spaces.
Each crystal is separated from its neighbors by intercrystalline spaces filled with water and organic material.
These represent a potential route of entry for bacterial acids and are sometimes called micropores
1- INITIAL ENAMEL DAMAGE
Macroscopic aspects
The first clinically detectable sign is the white spot stage, which is more easily visible after the surface has dried.
This white spot can subsequently turn brown or yellow.
The coloring is iron which can be of exogenous origin (dietary, bacterial or tobacco) as well as repeated bleeding.
In the absence of appropriate therapy, the lesion gradually progresses to the cavitation stage.
It is important to know that, histologically, the dentin is already affected by bacteria.
microscopic aspect:
Whatever the location of the initial carious lesion of the enamel, 4 zones can be distinguished; they are arranged in a triangle whose point is directed towards the dentine; each zone passes from one to the other progressively and not sharply.
1-Translucent zone:
This is the front of progression of the carious lesion, but it is only observed in 50% of cases. The alterations of this zone are reflected by the appearance of spaces or pores at the junctions of the prisms. The mineral loss is 1.2%
2- Dark or opaque area:
It is located between the translucent area and the body of the lesion. Its loss of mineral substance is estimated at 6%. The pores therefore remain filled with water with a different refractive index and making the affected area appear dark.
This area, while increasing in volume, spontaneously remineralized, hence the reduction
of the pore diameter.
3- Body of the lesion:
With a 24% reduction in its mineral composition, this area is characterized by increased evidence of Retzius striations and prismatic structures.
The significant loss of mineral matter is replaced by water and organic material from saliva.
4- Surface layer:
Its thickness varies from 20 to 100 μm depending on the type of lesion. It is thinner in active caries and thicker in the case of arrested caries, since there is then reprecipitation of mineral elements.
2-Ultrastructural aspects of the carious lesion of the enamel
Immature enamel has many surface micro-structural defects, which promote the retention of bacterial plaque and partly explain the predisposition of young subjects to carious lesions.
the initial carious lesion, that is to say before the cavitation stage, can be subject to remineralization, in particular from salivary mineral salts and exogenous fluoride intakes (reversible stage).
in the event of resumption and worsening of cariogenic factors, the lesions will extend on the surface and rapidly progress to the cavitation stage
III/ Chemical mechanisms of carious lesions;
Enamel is composed of long, thin crystals of hydroxyapatite surrounded by an aqueous and organic matrix. It is porous since it contains, in addition to the pure, poorly soluble hydroxyapatite, 2 to 4% carbonate (CO2 2–) and 1% elements such as sodium, magnesium, potassium, chlorine and zinc…
Therefore, the enamel crystal should be considered as a “carbonateapatite” crystal, with a “packaging” of water, proteins and lipids.
The protein-lipid fraction and water constitute preferential diffusion pathways for the chemical constituents playing a role in the phenomena of demineralization and remineralization of enamel.
Hydroxyapatite is soluble in acid and the crystal can be remineralized using various substances, the best known of which are fluorides.
These physicochemical phenomena can remain in balance for a certain time and if the external causes are removed, there can be cavitation but remineralization of the beginning lesion favored by the presence of fluorides.
These observations allow us to better understand the methods used in the prevention of carious lesions:
– removal of dental plaque in order to suppress the formation of acids resulting from bacterial metabolism;
– administration of fluorides (drinking water, toothpaste, mouthwashes, etc.) in order to make the enamel more resistant to acid demineralization and to promote reprecipitation phenomena;
– maintenance of a surface film rich in calcium and phosphate thanks to abundant and well-buffered saliva
Histopathology of carious lesion of enamel
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