The role of acquired immunity and periodontal disease progression

• Published in: Critical reviews in oral biology and medicine Vol. 14; no. 4; pp. 237 - 252
• Main Author: Teng, Yen-Tung A
• Format: Journal Article
• Language: English
• Published: United States 2003
• Subjects: Aggregatibacter actinomycetemcomitans - immunology; Alveolar Bone Loss - immunology; Animals; Carrier Proteins - immunology; CD4-Positive T-Lymphocytes - immunology; CD8-Positive T-Lymphocytes - immunology; Dentistry; Disease Progression; Humans; Membrane Glycoproteins - immunology; Mice; Periodontitis - immunology; Periodontitis - microbiology; RANK Ligand; Receptor Activator of Nuclear Factor-kappa B
• ISSN: 1544-1113
• DOI: 10.1177/154411130301400402

Our understanding of the pathogenesis in human periodontal diseases is limited by the lack of specific and sensitive tools or models to study the complex microbial challenges and their interactions with the host's immune system. Recent advances in cellular and molecular biology research have demonstrated the importance of the acquired immune system not only in fighting the virulent periodontal pathogens but also in protecting the host from developing further devastating conditions in periodontal infections. The use of genetic knockout and immunodeficient mouse strains has shown that the acquired immune response-in particular, CD4+ T-cells-plays a pivotal role in controlling the ongoing infection, the immune/inflammatory responses, and the subsequent host's tissue destruction. In particular, studies of the pathogen-specific CD4+ T-cell-mediated immunity have clarified the roles of: (i) the relative diverse immune repertoire involved in periodontal pathogenesis, (ii) the contribution of pathogen-associated Th1-Th2 cytokine expressions in periodontal disease progression, and (iii) micro-organism-triggered periodontal CD4+ T-cell-mediated osteoclastogenic factor, 'RANK-L', which is linked to the induction of alveolar bone destruction in situ. The present review will focus on some recent advances in the acquired immune responses involving B-cells, CD8+ T-cells, and CD4+ T-cells in the context of periodontal disease progression. New approaches will further facilitate our understanding of their underlying molecular mechanisms that may lead to the development of new treatment modalities for periodontal diseases and their associated complications.