Systemic and immunologic factors
Of the chronic systemic diseases, by far the most important risk factor and prognostic risk factor for dental caries is Sjogren’s syndrome, because of its extremely depressive effect on both the salivary secretion rate and the quality of the saliva. Indirectly, reduced SSR is associated with other chronic diseases in which medical management involves regular use of drugs with side effects on the salivary system. Some other general chronic diseases, such as leukemia, acquired immunodeficiency syndrome, diabetes mellitus, and Down’s syndrome, impair the immune system generally or specifically.
Several studies have shown that dental caries does not lead to acquired immunity.
However, the soft and hard tissues of the oral cavity are protected by both nonspecific and specific immune factors. The nonspecific immune factors present in saliva include lysozyme, the lactoperoxidase system, lactoferrin, various little-known antibacterial compounds, high-molecular weight glycoproteins, and other salivary components that may act as bacterial agglutinins. Even phagocytozing polymorphonuclear neutrophil leukocyte cells derived from the gingival crevice represent the nonspecific immune system in the oral cavity. In whole saliva, the following specific immune factors are present: secretory IgA, IgG, IgM, and serum IgA. In both secretory and serum IgA two subclasses¾IgA1 and IgA2¾have been identified.
Because mutans streptococci, the most cariogenic bacteria, do not colonize the mouths of infants and toddlers until after significant maturation and expansion of the host immune networks, such colonization should be vulnerable to specific (and innate) host immune mechanisms. If there is delayed development of one or more of these mechanisms, then the child is at increased risk for early colonization by mutans streptococci.
Although definitive immune predictors of caries risk are incompletely defined, the absence of a functioning secretory immune system appears to be a primary indicator of increased risk. Because placental transfer of IgG antibody may regulate the early immune responses of the offspring, elevated maternal levels of serum IgG antibody (especially IgG1) to critical colonization antigens may indicate decreased risk for dental caries in the primary dentition. Similarly, the passive transfer of similar secretory IgA antibody specificities during breast-feeding, if continued during the
period of early challenges by cariogenic streptococci, may delay colonization and thus decrease future caries risk.
Theoretically, a vigorous set of immune responses, active during the period of initial colonization of newly erupted tooth surfaces, should influence selection of the colonizing bacteria. A lag in the expansion of lymphocytes of a particular IgA subclass may delay the synthesis of antibody to certain types of important oral antigens. Because of poor oral hygiene in 1 to 3 year olds, a flora rich in organisms secreting IgA1 proteases (S sanguis and S mitis) could decrease the protective potential of this IgA subclass. Both phenomena might create an increased risk of
disease.
The importance of the role of infective dose in early immune stimulation is still
unclear, but it is likely that artificial triggering of the secretory or systemic antibody
compartment to synthesize appropriate antibody prior to infection would significantly
modify the caries experience of the child. Many questions remain unanswered in the
understanding of initial colonization and the participation of the host in modulating
this process:
1. What are the antigenic components of the oral streptococci critical for effective
immune responses?
2. To what extent are these components immunogenic and do they favor the formation
of antibody of a particular subclass?
3. What is the nature of the interplay between specific serum and salivary immune
components and innate host factors in these processes?
Answers to these questions may allow us not only to assess risk more clearly but also
to accelerate the processes resulting in caries prevention.