Periodontal disease immunology: ‘double indemnity’ in protecting the host

Abstract

During the last two to three decades our understanding of the immunobiology of periodontal disease has increased exponentially, both with respect to the microbial agents triggering the disease process and the molecular mechanisms of the host engagement maintaining homeostasis or leading to collateral tissue damage. These foundational scientific findings have laid the groundwork for translating cell phenotype, receptor engagement, intracellular signaling pathways and effector functions into a ‘picture’ of the periodontium as the host responds to the ‘danger signals’ of the microbial ecology to maintain homeostasis or succumb to a disease process. These findings implicate the chronicity of the local response in attempting to manage the microbial challenge, creating a ‘Double Indemnity’ in some patients that does not ‘insure’ health for the periodontium. As importantly, in reflecting the title of this volume of Periodontology 2000, this review attempts to inform the community of how the science of periodontal immunology gestated, how continual probing of the biology of the disease has led to an evolution in our knowledge base and how more recent studies in the postgenomic era are revolutionizing our understanding of disease initiation, progression and resolution. Thus, there has been substantial progress in our understanding of the molecular mechanisms of host–bacteria interactions that result in the clinical presentation and outcomes of destructive periodontitis. The science has embarked from observations of variations in responses related to disease expression with a focus for utilization of the responses in diagnosis and therapeutic outcomes, to current investigations using cutting‐edge fundamental biological processes to attempt to model the initiation and progression of soft‐ and hard‐tissue destruction of the periodontium. As importantly, the next era in the immunobiology of periodontal disease will need to engage more sophisticated experimental designs for clinical studies to enable robust translation of basic biologic processes that are in action early in the transition from health to disease, those which stimulate microenvironmental changes that select for a more pathogenic microbial ecology and those that represent a rebalancing of the complex host responses and a resolution of inflammatory tissue destruction.

Familial periodontal disease in the cayo santiago rhesus macaques

“…The net outcome of periodontal disease extent and severity appears dependent upon the characteristics of the oral microbial ecology. These include colonization/emergence of some opportunistic pathogens that appear to alter the local environment affecting the overall microbiome attributes and burden, and act in concert with host responses that are regulated by genetics and modified by the environment in humans [Kinane and Bartold, 2007; Hajishengallis et al, 2012; Armitage, 2013; Ebersole et al, 2013; Wade, 2013; Kornman and Polverini, 2014; Duran-Pinedo et al, 2014]. Since descendants of each of these matrilines still exist within the population and preliminary data suggests an increased risk of demonstrating periodontitis in living animals within the 065 matriline.…”

Differential Gene Expression Profiles Reflecting Macrophage Polarization in Aging and Periodontitis Gingival Tissues

“…As the lesion progresses, increasing numbers of mononuclear cells emigrate into the affected tissues and into the subgingival sulcus, consistent with a more chronic inflammatory lesion (Smith, Seymour and Cullinan, 2010). The cellular profiles of these apparent established lesions include various phenotypes of T cells, B cells and plasmacytes producing antibody (Ebersole, Dawson, Morford, Peyyala, Miller and Gonzalez, 2013), and antigen-presenting cells including macrophages (Hajishengallis, 2010, Bartold, Cantley and Haynes, 2010, Merry, Belfield, McArdle, McLennan, Crean and Foey, 2012) and dendritic cells [DC, (Anjana, Joseph and Suresh, 2012, Cutler and Teng, 2007). …”

The intestinal microbiome and skeletal fitness: Connecting bugs and bones

“…This topic has been reviewed elsewhere [14,15]. Recent data suggests that oral commensals in the absence of periodontal disease regulate the amount of alveolar bone, the maxillary and mandibular ridge in which teeth reside.…”