Secretory IgA and other indicators for tooth decay among children with diagnosed pyelonephritis and nephrotic syndrome

Abstract

Investigations ascertain that secretory IgA is characterized with a protective role against tooth decay. People with caries-resistant dentition are with significantly higher levels of salivary IgA compared with caries-active people. Normally secreted salivary IgA antibodies influence the immunological control of tooth decay. Secretory IgA in saliva, acting as the first line of protection of oral mucosa, contributes to inhibition of the colonization of Streptococcus Mutans upon smooth teeth surfaces, as well as to neutralization of microorganisms` metabolic products - enzymes and toxins. In concentrations non-toxic for the human body, nitrites have a considerable effect on the inhibition of acids` production performed not only by S. mutans, but also by other acids-producing representatives of oral microbiota - A. naeslundii and L. casei. The purpose of this study is to establish correlations between the number of carious lesions, the number of areas of de-mineralization and the level of sIgA, PLI, GI, pH and nitrites in samples of non-stimulated saliva in children suffering from pyelonephritis and nephrotic syndrome, parallel to a group of healthy controls. A correlation analysis with registration of the coefficient by Pearson has been applied. Slight negative correlation was calculated between sIgA and number of carious lesions in patients with pyelonephritis and healthy children. Moderate negative correlation was determined between indicators sIgA and PLI, and between indices of sIg A and GI among patients with nephrotic syndrome. These are characterized with significant negative correlation between sIgA and number of areas of de-mineralization. The interpretation of tooth decay as an infectious disease associates the considerable reduction of salivary sIgA with initiation of new and progression of already existing carious lesions and spots of de-mineralization. The decreased level of sIgA maintains favorable conditions for inflammatory reactions of gingival tissue.