Periodontal disease immunology: 'double indemnity' in protecting the host

Jeffrey L. Ebersole, Dolphus R. Dawson, Lorri A. Morford, Rebecca Peyyala, Craig S. Miller, Octavio A. Gonzaléz
2013 Periodontology 2000  
The immunobiology of periodontal disease continues to evolve, resulting in a number of foundational changes to the view of this disease across scientific disciplines. The first level of this evolution was fundamentally based upon the extraordinary microbiologic studies that provided a solid framework for understanding the basic stimuli for the disease (48), as seen in its recent incarnation of the Human Microbiome Project (292). The second evolving level was directly linked to the continued
more » ... ress in parsing out the complexity of the human inflammatory, innate and adaptive immune responses that paralleled these microbiological findings. This molecular knowledge has created a schematic of the host-bacterial interactions that likely occur in the periodontium, as the host responds to the resident microbiota, both commensals and pathogens, with the outcomes being a maintenance of homeostasis or select individuals succumbing to a disease process. These findings were interpreted to indicate that the disease process in the periodontium was 'collateral damage' from the normal host response repertoire attempting to manage the chronic septic environment and resulting challenge to host tissues. This review attempts to enlighten the interdisciplinary research community that is documenting the complexity of periodontal disease on the historical evolution of the field of periodontal immunology, and the ongoing research emphasis that is 'drilling down' ever more deeply into the molecular workings of the cells and tissues to explain the variation in disease initiation, progression, and resolution across the population. 'The Way We Were' Taking the community back about 40 years in the field of periodontology, our view of the biology of the disease was focused on two primary issues: (i) the identification and study of selected bacteria that had been cultured from the oral cavity and seemed to increase in periodontal lesions, albeit with a recognition by the 'bacteriologists' that the majority of species in the subgingival plaque were unculturable; and (ii) the incorporation of the rapidly emerging findings describing the complexity of the host response to infection, including molecular studies of inflammatory cells and biomolecules, emerging concepts of innate immunity and a more detailed description of the molecular processes needed for adaptive immunity, including the recently delineated mucosal (secretory) immune system. Resistance to infection Based on the hypothesis that accumulation and emergence of bacterial species in the gingival sulcus could act as a trigger for periodontal disease, studies were conducted that attempted to delineate how the host could resist the direct deleterious effects of this NIH Public Access
doi:10.1111/prd.12005 pmid:23574466 pmcid:PMC4131201 fatcat:rkbdfes7uvbvrab36bzqnlkrym