AmelogensisBy:dr.Nafha Shihab

(Periodontist)

Amelogensis is a two step process when enamel first forms, it mineralizes partially to approximately 30٪. As the organic matrix breaks down and is removed, crystals grow wider and thicker until the full thickness of enamel layer has been formed to attain greater than 96 ٪mineral content. The process of amelogeneis is under cellular control and the associated cells undergo significant morphologic changes throughout amelogensis reflecting their evolving physiologic activity.

Enamel formation begin at early crown stage of tooth development and involves the differentiation of the cells of the inner enamel epithelium first at the tips of cusp and incisal edge. Ameloblasts secrete matrix proteins and are responsible for creating and maintaining an extracellular environment favorable to mineral deposition. This epithelial cell exhibits a unique life cycle characterized by progressive phenotype changes that reflect its primary activity at various times of enamel's formation.

Amelogensis has been divided into :

•Morphogenic phase:- in this phase the inner enamel epithelia, are low columnar or cuboidal, with large centrally located nucleus. IEE close to the undifferentiated mesenchymal cells of dental papilla interact with these cells to determined the shape of the crown (morphodifferentiation). Mitochondria and other cytoplasmic components are scattered throughout the cells.

•Differentiation phase:- in this stage the IEE differentiate into pre ameloblasts, they elongate and their nuclei shift proximally toward the stratum intermedium. The cytoplasmic organells aggregate at the distal side of the cell (secretory end of the cells). During ameloblasts differentiation, proximal and distal junctional complex appear between them. These junctional complex play an important role in amelogenesis by tightly holding together ameloblasts and determining at different times what may, and what may not, pass between them to enter or leave the enamel.

Presecretory stage

Secretory stageWhen the first layer of dentin is formed the preameloblast become ameloblasts. The cell become highly columnar, nucleus at proximal end, cytoplasm fill with synthetic organells like RER, mitochondria, Golgi apparatus, secretory vesicles, and ribosomes. The secretory stage begins with the formation of thin layer of enamel matrix opposite to the dentin (rodless enamel).

The secretory end of ameloblasts becomes pyramidal in shape forming a process called Tomes' process which is responsible for secretion and orientation of enamel rods and their crystals.

At this stage ameloblasts synthesis and secrete enamel matrix which consist of proteins like amelogenin, enamelin, ameloblastin, tuftelin, amelin, these proteins matrix form about 66%. About 25-30% minerals which are hydroxyapatite crystals of enamel matrix which secreted by ameloblasts at the same time. The ameloblasts where secrete enamel matrix, it retard back word toward the enamel organ, and it secret the whole enamel matrix at one time.

Maturation stage•Transitional phase:- after full thickness of immature enamel has formed, ameloblasts undergo significant morphological involving a reduction in height of the ameloblasts and decrease in their volume and organelle content. Ameloblasts undergo programmed cell death (apoptosis). Approximately 25% of the ameloblasts die during transition phase, and another 25% die as enamel maturation proceeds. In this phase the Tomes' process disappear, microvilli or brush borders appear instead.

•Maturation Proper:- massive influx of calcium and phosphates occurs and at the same time there is selective loss of enamel proteins, mainly amelogenin and water. The ameloblasts modulate between two phenotypes depending on the morphology of their distal ends. The ameloblasts either have numerous microvilli forming a rumed border or their distal ends are even (straight), thus forming two morphologically different types, namely Rume-ended ameloblasts ( 80 % of maturation ameloblasts) and Smooth-ended ameloblasts (20 %), respectively. The two morphological types of ameloblasts are grouped into alternating bands during this stage, thus maturation ameloblasts modulate i.e. change their morphology from one type to the other and back.

Protective stage

Ameloblasts lose their differentiation and become short cuboidal cells which together with the remnants of the other layers of the dental organ form a multilayered structure, namely the reduced enamel (dental) epithelium. This structure remains on the surface of fully formed enamel until the tooth erupts. It separates the enamel from the dental sac and thus protect it from being in contact with connective tissue cells in the dental sac. If this contact accidentally happens, either enamel is resorbed resulting in pitting or dental sac cells in the contact area differentiate into cementoblasts and lay down cementum on the enamel surface. Both produce adverse (unsightly) effects on enamel appearance. The reduced dental epithelium and the oral epithelium jointly form the dentogingival junction of the erupting tooth.

Desmolyic stage

The reduce enamel epithelium elaborate the desomolytic enzyme to destroy connective tissue fibers that surround the crown of the tooth to facilitate the eruption of the tooth. After that the reduce enamel epithelia fuse with oral epithelium and form eruptive canal from which the tooth will erupt without any bleeding.

Mineralization pattern of enamel:- Mineralization starts in the oldest enamel (tip of cusp) and proceeds in 2 general

directions: spreading down along the D-E junction and progressing toward the enamel surface. If the tooth is a multicuspid, enamel formation starts at the tip of each cusp, spreads down and fuses at the base of the cusps in the regions of pits and fissures in the occlusal surface of tooth.

Factors affect growth of crystals are:-•Non collagenous protein able to bind to different surface of crystals preventing further growth.•Pyrophosphate inhibit further growth of crystal.•Alkaline phosphatase enzyme is associated with production of any mineralized tissue, it is involved with blood vessels and cell membrane of ameloblasts. Alkaline phosphatase activity breaks down pyrophosphate, thereby permitting crystal growth to proceed.

Defects of amelogensis•Defect in enamel can be caused by febrile disease resulting in distinctive bands of malformed enamel.

•Defects can be formed by tetracycline induced disturbances in teeth. Tetracycline antibiotics are incorporated into mineralizing tissues, in case of enamel, this incorporation may result in a band of brown pigmentation or even total pigmentation, hypoplasia or absences of enamel also may occur.

•Fluoride ions can interfere with amelogensis. chronic ingestion of fluoride ion concentrations in excess of 5ppm (5 times the amount in fluoridated water supplies) interferes sufficiently with ameloblast function to produce mottled enamel, mottled enamel is seen as white patches of hypo mineralized and altered enamel.

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