CHAPTER 4 Development and Morphology of the Primary Teeth
This chapter presents a brief review of the development of the teeth. An accurate chronology of primary tooth calcification is of clinical significance to the dentist. It is often necessary to explain to parents the time sequence of calcification in utero and during infancy. The common observation of tetracycline pigmentation, developmental enamel defects, and generalized hereditary anomalies can be explained if the calcification schedule is known. A brief discussion of the morphology of the primary teeth is also appropriate before considering restorative procedures for children.
A complete review is available in the reference texts on oral histology, dental anatomy, and developmental anatomy listed at the end of the chapter. Furthermore, contemporary scientists are rapidly gaining knowledge of tooth development at the molecular level. We suggest that readers with a special interest in the molecular events of tooth development study the listed references by Smith1 and by Miletich and Sharpe.2
Evidence of development of the human tooth can be observed as early as the sixth week of embryonic life. Cells in the basal layer of the oral epithelium proliferate at a more rapid rate than do the adjacent cells. The result is an epithelial thickening in the region of the future dental arch that extends along the entire free margin of the jaws. This thickening is called the primordium of the ectodermal portion of the teeth and what results is called the dental lamina. At the same time, 10 round or ovoid swellings occur in each jaw in the position to be occupied by the primary teeth.
Certain cells of the basal layer begin to proliferate at a more rapid rate than do the adjacent cells (Fig. 4-1A). These proliferating cells contain the entire growth potential of the teeth. The permanent molars, like the primary teeth, arise from the dental lamina. The permanent incisors, canines, and premolars develop from the buds of their primary predecessors. The congenital absence of a tooth is the result of a lack of initiation or an arrest in the proliferation of cells. The presence of supernumerary teeth is the result of a continued budding of the enamel organ.
(Adapted from Bath-Balogh M, Fehrenbach MJ: Illustrated dental embryology, histology, and anatomy, ed 2, Philadelphia, 2006, Saunders.)
Proliferation of the cells continues during the cap stage. As a result of unequal growth in the different parts of the bud, a cap is formed (see Fig. 4-1B). A shallow invagination appears on the deep surface of the bud. The peripheral cells of the cap later form the outer and inner enamel epithelium.
As with a deficiency in initiation, a deficiency in proliferation results in failure of the tooth germ to develop and in less than the normal number of teeth. Excessive proliferation of cells may result in epithelial rests. These rests may remain inactive or become activated as a result of an irritation or stimulus. If the cells become partially differentiated or detached from the enamel organ in their partially differentiated state, they assume the secretory functions common to all epithelial cells, and a cyst develops. If the cells become more fully differentiated or detached from the enamel organ, they produce enamel and dentin, which results in an odontoma (see Fig. 7-5) or a supernumerary tooth. The degree of differentiation of the cells determines whether a cyst, an odontoma, or a supernumerary tooth develops (see Fig. 27-56).
The epithelium continues to invaginate and deepen until the enamel organ takes on the shape of a bell (see Fig. 4-1C). It is during this stage that there is a differentiation of the cells of the dental papilla into odontoblasts and of the cells of the inner enamel epithelium into ameloblasts.
Histodifferentiation marks the end of the proliferative stage as the cells lose their capacity to multiply. This stage is the forerunner of appositional activity. Disturbances in the differentiation of the formative cells of the tooth germ result in abnormal structure of the dentin or enamel. One clinical example of the failure of ameloblasts to differentiate properly is amelogenesis imperfecta (see Figs. 7-32 and 7-33). The failure of the odontoblasts to differentiate properly, with the resultant abnormal dentin structure, results in the clinical entity dentinogenesis imperfecta (see Fig. 7-31).
In the morphodifferentiation stage, the formative cells are arranged to outline the form and size of the tooth. This process occurs before matrix deposition. The morphologic pattern of the tooth becomes established when the inner enamel epithelium is arranged so that the boundary between it and the odontoblasts outlines the future dentinoenamel junction. Disturbances and aberrations in morphodifferentiation lead to abnormal forms and sizes of teeth. Resulting conditions include peg teeth, other types of microdontia, and macrodontia.
Appositional growth is the result of a layer-like deposition of a nonvital extracellular secretion in the form of a tissue matrix. This matrix is deposited by the formative cells, ameloblasts, and odontoblasts, which line up along the future dentinoenamel and dentinocemental junction at the stage of morphodifferentiation. These cells deposit the enamel and dentin matrix according to a definite pattern and at a definite rate. The formative cells begin their work at specific sites that are referred to as growth centers as soon as the blueprint, the dentinoenamel junction, is completed (see Fig. 4-1D).
Any systemic disturbance or local trauma that injures the ameloblasts during enamel formation can cause an interruption or an arrest in matrix apposition, which results in enamel hypoplasia (see Fig. 7-16). Hypoplasia of the dentin is less common than enamel hypoplasia and occurs only after severe systemic disturbances (see Fig. 7-15).
Calcification (mineralization) takes place following matrix deposition and involves the precipitation of inorganic calcium salts within the deposited matrix. The process begins with the precipitation of a small nidus about which />