Saliva and Dental Caries

Caries is a unique multifactorial infectious disease. Our understanding of etiological factors, the progress of the disease, and the effectiveness of prophylactic procedures have led us to believe that we understand the disease. However, we still have too few answers to many questions: "Why can we not predict who will get the disease?" "Why do we not become immunized?" "How much saliva is enough?" or "Which salivary components are protective?" and "Which salivary components predispose for caries?" It is generally accepted, however, that saliva secretion and salivary components secreted in saliva are important for dental health. The final result, "caries to be or not to be", is a complex phenomenon involving internal defense factors, such as saliva, tooth surface morphology, general health, and nutritional and hormonal status, and a number of external factors-for example, diet, the microbial flora colonizing the teeth, oral hygiene, and fluoride availability. In this article, our aim is to focus on the effects of saliva and salivary constituents on cariogenic bacteria and the subsequent development of dental caries. Human saliva not only lubricates the oral tissues, making oral functions such as speaking, eating, and swallowing possible, but also protects teeth and oral _ mucosal surfaces in different ways. The lubricating and antimicrobial functions of saliva are maintained mainly by resting saliva. Stimulation of saliva results in a flushing effect and the clearance of oral debris and noxious agents. However, the protective functions of saliva are not limited to the above-mentioned functions. Recent studies have revealed a large number of functions, mediated by both the inorganic and organic components of saliva, that should be considered in assessments of the effects of human saliva on dental caries. Some of these studies have introduced a new approach to dental caries from being a bacterially induced multifactorial disease to a disease which may also be influenced by inherited salivary factors. Such genetically regulated salivary components may influence both the colonization and the clearance of micro-organisms from the oral cavity. Caries-Who, When, and Where? The notion that dental caries in animals is an infectious, transmissible disease was first demonstrated by Keyes (1960). Since then, a group of phenotypically similar bacteria, collectively known as mutans streptococci, has been implicated as the principal bacterial component responsible for the initiation and the development of dental caries (Loesche, 1986). The tooth surface is unique among all body surfaces in two ways. First, it is a non-shedding hard surface, and, second, this surface is introduced into the human mouth during the first years of life. The earliest point at which the cariogenic mutans streptococci may become established is when the first teeth erupt. Solid surfaces are required for both streptococcal colonization and multiplication (Loesche, 1986). The relationship between the establishment of mutans streptococci and the initiation of dental caries in young children has been extensively studied. Several studies have shown that children who experience colonization by mutans streptococci early in life are at greater risk of developing dental caries than those who are colonized later (Alaluusua and Renkonen, 1983; Caufield et al., 1993). The extent of colonization of mutans streptococci and also, to some degree, subsequent caries activity experience are often correlated with the mother's salivary levels of mutans streptococci (Li and Caufield, 1995). Once mutans streptococci become established, they are considered difficult to eliminate, and the caries process is made possible. The current concepts of dental caries focus on the fermentation of carbohydrates by cariogenic-bacteriaproducing organic acids. Plaque bacteria produce a variety of end-products that may differ depending on the diet. When fermentable carbohydrates are present, the main organic acids produced are lactic, formic, and acetic acids (Geddes, 1975, 1981). These acids coincide with a pH drop in plaque, resulting in demineralization of the tooth (Loesche, 1986; Nyvad and Fejerskov, 1996) and creating an environment which is advantageous for further growth of Streptococcus mutans (Bradshaw et al., 1989; Dashper and Reynolds, 2000). In addition to acid production, mutans streptococci express a wide range of virulence factors that are responsible for the cariogenicity of the dental plaque. However, saliva provides the main host defense systems against these virulence factors, and the balance between deand remineralization is continuously affected by the interaction of bacterial virulence factors and host defense. The final result, "caries to be or not to be", is a complex phenomenon (Fig. 1) involving internal defense factors, such as saliva, tooth surface morphology, general health, and nutritional and hormonal status, and a number of external factors-for example, diet, the microbial flora colonizing the teeth, oral hygiene, and fluoride availability. In this article, our aim is to focus on the effects of saliva and salivary constituents on cariogenic bacteria and the subsequent development of dental caries. Salivary Flow Rate, Buffer Effect, and Dental Caries Probably the most important caries-preventive functions of saliva are the flushing and neutralizing effects, commonly referred to as "salivary clearance" or "oral clearance capacity" (Lagerlof and Oliveby, 1994). In general, the higher the flow rate, the faster the clearance (Miura et al., 1991) and the higher the buffer capacity (Birkhed and Heintze, 1989). Reduced salivary flow rate and the concomitant reduction of oral defense systems may cause severe caries and mucosal inflammations (Daniels et al., 1975; Van der Reijden et ah, 1996). Dental caries is probably the most common consequence of hyposalivation (Brown et al, 1978; Scully, 1986). Caries lesions develop rapidly and also on tooth surfaces that are