Immunopathogenesis of chronic inflammatory periodontal disease: cellular and molecular mechanisms

Abstract

Recent studies of the cellular mechanisms involved in chronic inflammatory periodontal disease (CIPD) have contributed significantly to our understanding of the pathogenesis of the disease process. Functional studies have demonstrated polymorphonuclear neutrophil (PMN) chemotactic defects in some 70% of subjects with localized juvenile periodontitis while chemiluminescence data have suggested that peripheral blood PMNs from young subjects with adult periodontitis (AP) may be in a metabolically active state. Further studies have shown that stimulation of PMNs with a number of periodontopathic bacteria resulted in the production of an IL-1 inhibitor suggesting a possible regulatory role for PMNs in CIPD in addition to their established protective role. Most work on the immunoregulation of CIPD has, however, concentrated on T-cells. Recent limit dilution analysis has demonstrated the presence of periodontopathic bacteria-specific T cells in peripheral blood and the involvement and homing of these cells to the local lesions of CIPD is currently the focus of many studies. In animal studies, Actinobacillus actinomycetemcomitans (Aa)-specific T-cell clones home to the gingival tissues where they may exert a protective role. Homing and retention of lymphocytes to and in specific sites is dependent upon the expression of adhesion molecules. Recent data indicate however, that while there are increasing levels of ICAM-1, LECAM-1 and PECAM-1 expression with increasing degrees of inflammation, there are no differences between gingivitis and periodontitis lesions. Cytokine profiles may be related to the role of T-cell clones homing to the gingiva in CIPD.(ABSTRACT TRUNCATED AT 250 WORDS)

IgG and IgA subclass mRNA-bearing plasma cells in periodontitis gingival tissue and immunoglobulin levels in the gingival crevicular fluid

“…Therefore the distribution of IgA1-and IgA2-producing cells in inflamed gingiva may reflect a difference in the predominant type and nature of antigens involved in the induction of the local humoral immune response in periodontium. The observed preponderance of IgA1 or IgA2 cells in gingival tissues may be due to differences in the original precursors of IgA plasma cells destined for the gingival tissue, selective homing of specific B cells and/or the local expansion of specific B cell clones by various antigens that induce preferential IgA1 or IgA2 responses [52,53].…”

Human dendritic cells respond to Porphyromonas gingivalis LPS by promoting a Th2 effector response in vitro

“…It is extremely important, however, to establish whether P. gingivalis LPS induces a Th2-effector response in the human system, in which the disease chronic periodontitis (CP) occurs. CP patients have elevated local levels of both Th2-and Th1-biasing cytokines (reviewed in [13,14]) and increased local numbers of DC subpopulations [15][16][17][18][19], CD4 + T cells [13][14][15][16] and B cells / plasma cells [14,20]. Many reports cite the induction of a strong humoral immune response towards P. gingivalis in adult periodontitis subjects (reviewed in [21]), including evidence for induction of high IgG antibodies to P. gingivalis LPS [22], with elevated IgG4 [23,24].…”

Effects of miR-223 on expression of IL-1β and IL-6 in human gingival fibroblasts

“…It affects the periodontal tissues, and when advanced can result in tissue destruction, occasional pain, alveolar bone resorption, and eventual tooth loss (1)(2)(3). The response to periodontal pathogens is determined by the nature and control of both adaptive and innate immune responses (4). Cytokines are central regulators of the immune responses that are produced by various cell types including fibroblasts, epithelial cells, macrophages, dendritic cells and T-helper cells in response to microbial contact (5).…”