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.

No abstract

Recent studies have suggested that the dys-regulated progressive immune responses in some inflammatory conditions can lead to significantly increased osteoclasts (OC) frequency and activity associated with active bone destruction; termed inflammation-induced bone loss. Among the inflammatory infiltrates, monocytes/macrophages (Mo/MQ), T and B cells, have been well studied and documented as central players in osteoimmunological interactions (osteoimmunology: is an interdisciplinary field linking the immune and skeletal systems). We and others investigated the role(s) of dendritic cells (DC) during inflammation-induced osteoclastogenesis and bone loss. In addition to their innate effector functions, DC are potent professional antigen-presenting cells (APC) involved in triggering and orchestrating adaptive immunity, thereby implicated as potential osteo-immune players. Herein, bone remodeling and DC's biology including their development and functions are reviewed along with the contribution of DC at the crossroad of the osteo-immune interface during the process of inflammation-induced osteoclastogenesis. Furthermore, we provide a summary of recent progress, and discuss a proposed alternative mechanism underlying inflammation-induced bone loss. Understanding the cellular and molecular mechanisms regulating DC's roles in inflammation-induced osteoclastogenesis and bone loss might benefit future treatment approaches, especially if targeting DC can be translated into therapeutic strategies to ameliorate both tissue inflammation and bone destruction during disease progression associated with inflammatory bone diseases.

Based on the results of recent research in the field and Part 1 of this article (in this issue), the present paper will discuss the protective and destructive aspects of the T-cell-mediated adaptive immunity associated with the bacterial virulent factors or antigenic determinants during periodontal pathogenesis. Attention will be focused on: (i) osteoimmunology and periodontal disease; (ii) some molecular techniques developed and applied to identify critical microbial virulence factors or antigens associated with host immunity (with Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis as the model species); and (iii) summarizing the identified virulence factors/antigens associated with periodontal immunity. Thus, further understanding of the molecular mechanisms of the host's T-cell-mediated immune responses and the critical microbial antigens related to disease pathogenesis will facilitate the development of novel therapeutics or protocols for future periodontal treatments.