Periodontal Health and Blood Disorders

The hematopoietic tissue is highly susceptible to stimuli, and inflammation is a major modulator. One particular source for this inflammatory burden is periodontitis. We revisit how periodontal infection may modulate the activity of the bone marrow, the fate of hematopoietic stem cells, and its systemic consequences. We also examine periodontal manifestations of particular blood disorders. Herein, we provide a glimpse of the available knowledge and discuss gaps that may be explored in the future. Recent studies have demonstrated that Porphyromonas gingivalis governs osteoclastogenic differentiation by regulating nuclear factor-kappa B ligand and inhibiting noncommitted osteoclasts precursors. This governed cell population exhibits an antigen-specific T cell immune-suppressive activity benefiting the persistence of periodontal infection and compromising the host immune response. The persistence of this low-grade inflammation together with this particular cell population enhances osteoclastogenic precursors from myeloid-derived suppressor cells, increasing the age-associated bone loss in mice. Periodontitis patients exhibit serum biomarkers of anemia, attributed to a state of anemia of inflammation. In other words, the production of hepcidin through the action of cytokines results in higher iron trapping inside macrophages and liver cells ant his may shorten erythrocyte survival. Another possible hypothesis to explain this link is the inflammatory suppression of erythropoietic activity, through the levels of erythropoietin. Periodontal therapy is effective in reducing leukocytosis, but evidence is to scarce regarding red and platelet lineages. Furthermore, periodontitis patients suffering from white blood cells disorders seem more prone to severe periodontal destruction given the pathophysiology of periodontitis and the immune role of leukocyte cells. The systemic inflammatory burden of periodontitis modulates the fate of differentiation of particular bone marrow and interferes with the erythropoietic activity. The impact of periodontal therapy on leukocytosis is robust and based on high quality evidence-based estimates, though its influence on erythrocytic and platelet levels is still limited. The existence of a greater predisposition to periodontal disease in blood disorders is not consensual.