Periodontal Inflammation as a Modifiable Contributor to Low-Grade Systemic Inflammation: A narrative review

Abstract

The biologically active component of periodontitis, a chronic inflammatory disease, is periodontal inflammation, which is caused by an abnormal subgingival biofilm and influenced by the body's immune system. Clinically, the disease affects the gums (loss of attachment), pockets around teeth (periodontal pocketing), and bone around teeth (alveolar bone loss) and can cause tooth loss.

The present narrative review critically assesses the association between periodontitis and systemic inflammation. This narrative review synthesizes mechanistic, clinical, and epidemiological evidence from periodontal-systemic literature. The review did not present the oral-systemic connection as a single biological pathway but instead assessed biologically plausible mechanisms, significant biomarkers, and clinical outcomes that support the oral-systemic mechanism. Key biologically plausible mechanisms include transient bacteremia, dissemination of microbial products and inflammatory mediators, and endothelial activation—pathways supported by human studies.

The strongest evidence shows an association between periodontitis and increased systemic inflammatory markers, including C-reactive protein, and a rapid decline in C-reactive protein post-treatment for periodontal disease. In addition, cardiovascular disease is associated with diabetes, but the evidence is heterogeneous. The biological plausibility of the cardiovascular disease association is supported by observational studies, microbial studies, animal models, and endothelial function trials. Diabetes and periodontal disease have a bidirectional relationship. The treatment effects of glycated hemoglobin are significant but vary among clinical trials and meta-analyses. In conclusion, periodontal inflammation is a modifiable contributor to the overall systemic inflammatory burden, but causal relationships should not be overstated based on hard clinical endpoints.