Systemic Immunologic Consequences of Chronic Periodontitis

Abstract

Chronic periodontitis (ChP) is a prevalent inflammatory disease affecting 46% of the US population. ChP produces a profound local inflammatory response to dysbiotic oral microbiota that leads to destruction of alveolar bone and tooth loss. ChP is also associated with systemic illnesses, including cardiovascular diseases, malignancies, and adverse pregnancy outcomes. However, the mechanisms underlying these adverse health outcomes are poorly understood. In this prospective cohort study, we used a highly multiplex mass cytometry immunoassay to perform an in-depth analysis of the systemic consequences of ChP in patients before ( n = 28) and after ( n = 16) periodontal treatment. A high-dimensional analysis of intracellular signaling networks revealed immune system–wide dysfunctions differentiating patients with ChP from healthy controls. Notably, we observed exaggerated proinflammatory responses to Porphyromonas gingivalis–derived lipopolysaccharide in circulating neutrophils and monocytes from patients with ChP. Simultaneously, natural killer cell responses to inflammatory cytokines were attenuated. Importantly, the immune alterations associated with ChP were no longer detectable 3 wk after periodontal treatment. Our findings demarcate systemic and cell-specific immune dysfunctions in patients with ChP, which can be temporarily reversed by the local treatment of ChP. Future studies in larger cohorts are needed to test the boundaries of generalizability of our results.

Treatment of periodontitis reduces systemic inflammation in type 2 diabetes

“…Intriguingly, the differences lie with innate immune signalling and responses rather than in the proportions of cellular elements; this endorses the value of candidate studies of key inflammatory mediators in investigating the influence of oral inflammation on systemic health. Significantly, systemic parameters of inflammation reverted to values more closely associated with periodontal health after periodontal treatment, providing strong evidence that systemic immune processes are indeed influenced by oral inflammation (Gaudilliere et al, 2019). It will be interesting to apply these novel analytical and bioinformatic approaches to studies of diabetes and periodontitis.…”

“…Recently, comprehensive and high‐resolution studies of systemic inflammation in periodontitis using mass cytometry immunoassays have revealed substantial “immune system dysfunctions” in patients with periodontitis as compared to periodontally healthy individuals (Gaudilliere et al, 2019). Intriguingly, the differences lie with innate immune signalling and responses rather than in the proportions of cellular elements; this endorses the value of candidate studies of key inflammatory mediators in investigating the influence of oral inflammation on systemic health.…”

Immunomodulatory Properties of Stem Cells in Periodontitis: Current Status and Future Prospective

“…For example, these bacteria escape neutrophil-mediated assault and protect themselves from complement. As a result, periodontal tissue breakdown is increased by neutrophil-mediated responses due to the inability of the neutrophil to control the dysbiotic microbial attack [ 20 ].…”

Proteome Analysis of Molecular Events in Oral Pathogenesis and Virus: A Review with a Particular Focus on Periodontitis

“…Periodontal disease originates in the gingiva and involves the periodontal tissues, the cementum, periodontal ligament, and alveolar bone, and the progression of gingivitis to periodontal disease is caused by irritation from the plaque lasting for a long period of time [ 9 , 10 , 11 ]. Worldwide research on periodontal and systemic diseases has resulted in a number of reports on the effects of general condition on periodontal tissues [ 12 , 13 , 14 ]. Both diabetes mellitus and periodontal disease are representative lifestyle habit illnesses and diet and smoking are associated lifestyle habit factors, with diabetes mellitus along with smoking said to be two big risk factors for periodontal disease [ 15 , 16 , 17 , 18 ].…”