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THE ROLE OF ACQUIRED IMMUNITY AND PERIODONTAL DISEASE PROGRESSION

^* Division of Periodontics, School of Dentistry, and Department of Microbiology & Immunology, Faculty of Medicine & Dentistry, the University of Western Ontario, London, Ontario N6A 5C1, Canada; Lawson Health Research Institute, London Health Sciences Centre, London, Ontario N6A 4G5; and Division of Periodontics, Eastman Dental Clinic, Center for Oral Biology, and Dept. of Microbiology and Immunology, School of Medicine & Dentistry, University of Rochester, NY, USA 14620-2989;

^* addresses for correspondence, yateng{at}uwo.ca and andy_teng{at}urmc.rochester.edu

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.

Abbreviations used in the paper are as follows: Antibody, Ab; antigen, Ag; antigen-presenting cells, APC; Actinobacillus actinomycetemcomitans, A. actinomycetemcomitans or Aa; ß₂-microglobulin, ß₂m; cytotoxic CD8⁺ ß T-lymphocytes, CTL; dendritic cells, DC; delayed-type hypersensitivity, DTH; immunoglobulin, Ig; Fc receptor, Fc-R; interferon-, IFN-; receptor activator of NF-B ligand, RANK-L; molecular weight, MW; Porphyromonas gingivalis, P. gingivalis or Pg; localized juvenile periodontitis, LJP; lipopolysaccharide, LPS; mouse mammalian tumor virus, MMTV; non-obese diabetic and severe combined immunodeficiency mice, NOD/SCID mice; osteoclast, OC; T-helper cells, Th; superantigen, SAg; transforming growth factor-ß, TGF-ß; secretory-IgA, s-IgA; T-cell receptor, TCR; T cytotoxic-1 cells, Tc1; and T cytotoxic-2 cells, Tc2.

Key words. Human periodontitis, acquired immunity, CD4⁺ T-cell immune repertoire, type-1 vs type-2 cytokines, osteoclastogenesis, RANK-L