dental papilla, leaving behind a cytoplasmic extension called the odontoblastic process. The odontoblastic process is embedded in mineralized dentin tissues, and the tubular character of dentin is established. Dentin formation proceeds toward the inside of the dental papilla and odontoblastic process and results in the secretion of hydroxyapatite crystals and mineralization of the matrix (see Fig 2-11).
Amelogenesis. Although dentin must be present for enamel formation, within the enamel organ the preameloblasts differentiate before the odontoblasts and have an inductive influence on the odontoblasts, sending a message that causes them to differentiate and secrete dentin. Ameloblasts also require the signal of dentin formation to initiate their secretory activities. A message is sent from the newly differentiated odontoblasts to the inner enamel epithelium, causing further cell differentiation and activating secretory ameloblasts to form enamel tissue. This prerequisite is an example of the biologic concept termed reciprocal induction.
Enamel formation generally occurs in two stages: (1) the secretory stage and (2) the maturation stage. In the first stage of amelogenesis, the function of the ameloblasts is to secrete and release enamel proteins into the surrounding area and produce an organic matrix against the newly formed dentin surface. Ameloblasts immediately become mineralized by alkaline phosphatase enzymes and form the first layer of enamel tissue, causing a separation of the ameloblastic cells from the dentin and leaving enamel tissue behind (see Fig 2-6).
Initial mineralization of enamel matrix takes place almost simultaneously with organic matrix production; an unmineralized organic matrix cannot be found.
In the maturation stage, ameloblasts change their function from enamel matrix production to mineralization. Mineralization takes place by transferring substances used in the formation of enamel. In this stage, most of the materials transported by ameloblasts are proteins used to complete mineralization.
Mineralization of dental hard tissues (calcification
are initially secreted by ameloblasts and odontoblasts as a nonvital extracellular secretion in the form of a tissue matrix. The tissue matrix is deposited layer by layer along the future dentinoenamel and dentinocemental junctions. The organic matrix for enamel tissue is not collagenous, but the organic matrix for dentin, cementum, and bone is collagenous. The organic matrix for enamel comprises mainly unique proteins (mostly amelogenin), reflecting the tissue’s epithelial origin. The organic matrix in dentin forms a substantial part of the mineralized tissue.
The organic matrix of enamel is removed during the final stage of mineralization and leaves less than 1% of the weight of organic matrix. Matured enamel organic matrix is replaced with hydroxyapatite. Thus, enamel is physically different from dentin and cementum because it is formed from a noncollagenous matrix (mostly amelogenin) that is almost completely removed after mineralization.
As already mentioned, the formation of dentin always precedes enamel formation and marks the onset of the crown stage of tooth development. At this stage, the dental lamina is disintegrating, so the tooth germ now continues its development separated from the oral epithelium. The crown pattern of the tooth is established by folding of the internal dental epithelium. This folding reduces the amount of stellate reticulum over the future cusp tip. Dentin and enamel have begun to form at the crest of the folded internal dental epithelium. This stage is associated with the formation of the dental hard tissues, commencing at about the 18th week (Fig 2-14).
Fig 2-14 Crown stage. A shows the enamel space that has been lost during slide preparation. B—
dentin; C—dental papilla.
Calcification
The second stage of dental hard tissue formation, like other hard tissues, is calcification or mineralization. This process takes place following the matrix deposition by precipitation of inorganic calcium salts (primarily in the form of calcium hydroxyapatite crystals) within the deposited matrix.
The mechanism involved in mineralization is not completely understood, especially in the first step, the formation of first crystals. According to Berkovitz et al,4 any tissue could calcify after crystal formation because blood plasma is supersaturated with calcium and phosphate ions, meaning that mineralization is not limited by the supply of basic ions. An example of this phenomenon is the pathologic calcification that can occur in soft tissues (eg, muscle and tendon).
The structural unit of calcified tissues is the crystal or crystallite, which has a basic shape in all four calcified tissues (enamel, dentin, cementum, and bone). The sizes of the crystals within these tissues are all different.
Calcification of cartilage, which is controlled by the cells, is another mechanism that seems to be occurring in the initial formation of dentin and bone. These cells form small matrix vesicles that contain calcium and phosphate ions, alkaline phosphatase, and calcium-binding lipids. These vesicles separate from the cells, and conditions within the vesicles permit formation of hydroxyapatite crystals.
Precipitation of small niduses of crystals continues with precipitation of further niduses (calcospherites) spreading around the original nidus and increasing its size by the addition of concentric lamination. Finally, through approximation and fusion, these individual calcospherites transform into a homogenously mineralized layer of tissue matrix.
After the secretory phase of amelogenesis is completed and the ameloblasts enter the maturation stage, they perform a functional and structural task, removing proteins and water from the maturing enamel and allowing them to achieve complete mineralization. Once the enamel is completely mineralized, the ameloblasts shrink from columnar to cubical or flattened cells but remain a part of the reduced enamel epithelium that forms a more or less continuous lining over the completed enamel.
Figure 2-14 shows the crown stage of tooth development at a point when hard tissue formation is well advanced.
Developing abnormalities at the mineralization stage
Any systemic disturbance or local trauma that injures the ameloblastic cells during enamel formation can interrupt or arrest matrix apposition, resulting in enamel hypoplasia. These disturbances include tetracycline deposition, which causes yellow to brown hypoplastic enamel, and dental fluorosis, which results when an individual receives too much fluoride during tooth development.
Dentin hypoplasia is less common than enamel hypoplasia and occurs only after severe systemic disturbances. If the calcification process is disturbed, there is a lack
of fusion of the calcospherites. These deficiencies are not readily identified in enamel, but they are evident microscopically in dentin and are referred to as interglobular dentin.