Distinctive characteristics of oral tissues, such as the inability of enamel to remodel and the high cellular turnover rate of oral mucosa, the rates of alveolar bone growth, and the production of saliva, make oral tissues a unique indicator of physiologic perturbations. The oral cavity is a site of symptoms of many chronic diseases including dental caries, periodontal disease, acquired immunodeficiency syndrome (AIDS), nutritional anemias, herpes, salivary gland disorders, osteoporosis, diabetes, and cancer. Congenital anomalies such as cleft lip and palate are birth defects that have a complex genetic and environmental etiology linked to maternal nutrient status, folate in particular.

The linkages between oral disease and systemic health are expanding in depth and breadth with some profound observations. Within the past two decades, clear linkages have been established between periodontal disease and cardiovascular disease, diabetes, stroke, and adverse pregnancy outcomes. For example, periodontal disease is associated with increased risk of cardiovascular disease (1) and preterm delivery (2, 3). The inherent nature of oral infectious d iseases requires an adequately functioning immune and cellular repair system, and unequivocal data link nutrient intake and these host defense mechanisms. The relationships among oral health, systemic health, and nutrition require the careful attention of all health professionals including physicians, dentists, registered dietitians, and nurses (3).

To fully appreciate these complex relationships, it is vital to understand the structure and function of the craniofacial-oral-dental complex. Teeth are specialized structures necessary for the initial processing of food and are composed of three mineralized tissues: enamel, dentin, and cementum, which encase the highly vascular dental pulp or “nerve.” These relationships can be seen in the schematic cross section of a tooth in Figure 73.1. The teeth are retained in their bony sockets by means of a fibrous structure termed the periodontal membrane or ligament. Factors such as bacteria and the inflammatory immune response can affect the integrity of this structure and bone surrounding the socket, resulting in periodontal disease that may progress sufficiently to cause loosening and loss of the teeth (4).

Each tooth develops from a tooth bud or germ located in the jaws. The bud consists of an epithelial component that arises as an invagination from the surface and produces enamel. The mesenchymal component consists of the dental papilla, which produces the tooth pulp and dentin, and the dental follicle, which produces the cementum and periodontal ligament once the tooth has formed. Table 73.1 details the chronology of the formation of the human dentition. The primary teeth begin forming at approximately 6 weeks in utero when cells in the primitive oral cavity differentiate to form the dental lamina, which is the site of tooth bud development. The formation of the crown of the tooth begins with the secretion of a dentin matrix containing collagen fibrils. Mineral ions then enter the matrix to form small crystals on or between the collagen fibrils. Enamel formation begins as soon as the first dentin layer has been laid down. This mineralization process constitutes the maturation of enamel and continues after the matrix is fully formed. As can be seen in Table 73.1, the mineralization process begins as early as 4 months in utero and continues into late adolescence. After the tooth erupts into the oral cavity, it continues to incorporate minerals (including fluoride) into its structure from saliva, food, and drinking fluids (5).

The life history of a tooth may be divided into three main eras: (a) the period during which its crown is forming and mineralizing in the jaw, (b) the period of maturation when the tooth is erupting into the oral cavity and its root or roots are forming, and (c) the maintenance period while it is functioning in the oral cavity (5). During the preeruptive period, the developing enamel and dentin are subject to nutritional deficiencies or imbalances in the same manner as any other developing tissues. Nutrient deficiencies can affect the secretory and the maturation stages of enamel formation. Following eruption into the oral cavity, the enamel is bathed in saliva and is exposed to oral microorganisms and their byproducts as well as food, so nutritional deficiencies or excesses and dietary habits may affect teeth in a local manner (5).

At least three striking differences exist between the mineralized tissues of teeth and other tissues of the body. First, enamel contains no capillary or lymphatic vessels to act as transport systems; however, the intimate relationships between the organic and the inorganic components of enamel suggest that pathways in the enamel exist for diffusion of ions and small molecules from saliva, and possibly from blood. Although the dentin likewise contains no vascular elements, it is more readily permeable to the passage of extracellular fluids from the blood, by way of the dentinal tubules that traverse the dentin. The interchange among elements in the enamel takes place through the bathing of its external surface with saliva. In contrast, the interchange in the dentin occurs by the movement of ions present in the blood supply to the pulp or periodontal membrane (4). Second, because of the
absence of cells, mineralized dental tissues do not have a microscopically or chemically detectable ability to repair improperly formed or mineralized areas, and the tooth does not have the ability to repair itself after a portion has been destroyed by tooth decay or mechanical injury. An exception is the remineralization of slightly demineralized, superficial areas of the enamel where the organic matrix and surface integrity are still intact, commonly referred to as “white spots.” In addition, secondary dentin is formed by the odontoblasts, which persist throughout life on the pulpal surface of the dentin, in response to chemical stimuli from an advancing carious lesion in an effort to mitigate the noxious influence. Lack of ability to repair dental tissues is in direct contrast to bone, with its continual turnover and ability to remodel (4). Third, unlike other tissues, the mineralized tissues of teeth undergo a partial change of environment. When the tooth begins to emerge into the oral cavity, the vascular supply to the enamel organ is severed, and the enamel surface comes in contact with a complex mixture of saliva, microorganisms, food debris, and epithelial remnants. Thus, instead of a pure systemic environment, the erupted tooth has, in addition, an oral or external environment. As a consequence, the enamel and cementum surfaces on which carious lesions are initiated by microbial action are largely outside the influences of humoral immune systems, so immune relationships with the caries process are primarily limited to those in saliva (4).

The development and maintenance of the soft tissues and bone that support the teeth are also subject to nutrient defects. The periodontium, as seen in Figure 73.1, comprises the gingiva; the periodontal ligament ( peridental membrane), which joins the root cementum to the alveolar bone; the root cementum, which is a specialized, mineralized tissue similar to bone that covers the root of the tooth; and the alveolar bone, which forms and supports the sockets of the teeth. The alveolar bone grows in response to dental eruption, is modified by dental changes, and resorbs when teeth are lost. The finite space between the tooth and the gingiva, known as the gingival sulcus, is lined by a nonkeratinized epithelium. In addition, dental plaque, one of the primary agents responsible for the initiation of both dental caries and gingivitis, contains a high concentration of bacteria, which, in the gingival sulcus, are juxtaposed with a “naked” epithelium. Thus, bacteria and their byproducts or antigens can permeate the gingival epithelium and precipitate a classic inflammatory response that denotes periodontal disease. In fact,
an intact immune system, which is highly dependent on nutrient status, is vital to maintain periodontal health. The diversity of hard and soft tissues that comprise the oral structures and the distinctive nutritional needs of each contribute to the uniqueness of the mouth as an external reflection of past and present nutritional problems (3, 6).