Protective and Destructive Immunity in the Periodontium: Part 1—Innate and Humoral Immunity and the Periodontium

Abstract

Based on the results of recent research in the field, the present paper will discuss the protective and destructive aspects of the innate vs. adaptive (humoral and cell-mediated) immunity associated with the bacterial virulent factors or antigenic determinants during periodontal pathogenesis. Attention will be focused on: (i) the Toll-like receptors (TLR), the innate immune repertoire for recognizing the unique molecular patterns of microbial components that trigger innate and adaptive immunity for effective host defenses, in some general non-oral vs. periodontal microbial infections; (ii) T-cell-mediated immunity, Th-cytokines, and osteoclastogenesis in periodontal disease progression; and (iii) some molecular techniques developed and used to identify critical microbial virulence factors or antigens associated with host immunity (using Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis as the model species). Therefore, further understanding of the molecular interactions and mechanisms associated with the host's innate and adaptive immune responses will facilitate the development of new and innovative therapeutics for future periodontal treatments.

Fimbrial Proteins of Porphyromonas gingivalis Mediate In Vivo Virulence and Exploit TLR2 and Complement Receptor 3 to Persist in Macrophages

“…Macrophages play a central role in the innate host response in periodontitis and other chronic infections (26,27), and we previously showed that macrophages readily recognize and respond to P. gingivalis fimbriae (11,12,14). We thus investigated whether the reduction in virulence exhibited by the accessory protein-deficient strains could be attributed, at least in part, to differential interactions with macrophages.…”

Identification of Hop Polyphenolic Components Which Inhibit Prostaglandin E2 Production by Gingival Epithelial Cells Stimulated with Periodontal Pathogen

“…5) The gingival epithelial layer is an innate barrier against bacterial attacks, and plays a proactive role in local immune responses. 6,7) Human gingival epithelial (HGE) cells stimulated with periodontal pathogens produce PGE 2 , which further induces excessive host inflammatory responses and results in disease progression and periodontal destruction. Accumulated evidence indicates that periodontal inflammation may be stabilized by anti-inflammatory reagents such as green tea catechin (epigallocatechin gallate; EGCg).…”

Interleukin-10 Inhibits Gram-Negative-Microbe-Specific Human Receptor Activator of NF-κB Ligand-Positive CD4 + -Th1-Cell- Associated Alveolar Bone Loss In Vivo

“…The study of osteoimmunology has demonstrated that host immune responses, especially T-cell immunity, play a pivotal role in regulating osteoclastogenesis and bone remodeling (26,(32)(33)(34)(35)36). The recently identified tumor necrosis factor (TNF) family molecule receptor activator of NF-B ligand (RANKL), its receptor RANK, and its natural antagonist, osteoprotegerin (OPG), have been shown to be the key regulators of bone remodeling involved in differentiation, activation, and survival of osteoclasts and osteoclast precursors (35).…”