Periodontitis is considered a non-communicable chronic disease caused by a dysbiotic microbiota, which generates a low-grade systemic inflammation that chronically damages the organism. Several studies have associated periodontitis with other chronic non-communicable diseases, such as cardiovascular or neurodegenerative diseases. Besides, the oral bacteria considered a keystone pathogen, Porphyromonas gingivalis, has been detected in the hippocampus and brain cortex. Likewise, gut microbiota dysbiosis triggers a low-grade systemic inflammation, which also favors the risk for both cardiovascular and neurodegenerative diseases. Recently, the existence of an axis of Oral-Gut communication has been proposed, whose possible involvement in the development of neurodegenerative diseases has not been uncovered yet. The present review aims to compile evidence that the dysbiosis of the oral microbiota triggers changes in the gut microbiota, which creates a higher predisposition for the development of neuroinflammatory or neurodegenerative diseases.The Oral-Gut-Brain axis could be defined based on anatomical communications, where the mouth and the intestine are in constant communication. The oral-brain axis is mainly established from the trigeminal nerve and the gut-brain axis from the vagus nerve. The oral-gut communication is defined from an anatomical relation and the constant swallowing of oral bacteria. The gut-brain communication is more complex and due to bacteria-cells, immune and nervous system interactions. Thus, the gut-brain and oral-brain axis are in a bi-directional relationship. Through the qualitative analysis of the selected papers, we conclude that experimental periodontitis could produce both neurodegenerative pathologies and intestinal dysbiosis, and that periodontitis is likely to induce both conditions simultaneously. The severity of the neurodegenerative disease could depend, at least in part, on the effects of periodontitis in the gut microbiota, which could strengthen the immune response and create an injurious inflammatory and dysbiotic cycle. Thus, dementias would have their onset in dysbiotic phenomena that affect the oral cavity or the intestine. The selected studies allow us to speculate that oral-gut-brain communication exists, and bacteria probably get to the brain via trigeminal and vagus nerves.

Periodontitis is a chronic non-communicable disease caused by dysbiotic changes that affect the subgingival microbiota. During periodontitis, neutrophils play a central role in the initial recognition of bacteria, and their number increases with the appearance of the first signs of periodontal inflammation. Recent evidence has led to the proposition that neutrophils can also functionally polarize, determining selective activity patterns related to different diseases. Two well-defined neutrophil phenotypes have been described, the pro-inflammatory N1 subset and the suppressor N2 subset. To date, it has not been established whether these different neutrophil subtypes play a role in the pathogenesis of periodontitis. Thus, this scoping review aimed to determine whether there was evidence to suggest that the neutrophils present in periodontal tissues can be associated with certain phenotypes. The research question, population, concept, and context sought to identify original articles, in humans, that detected the presence of neutrophils in the periodontal tissues of people affected by periodontitis. Based on the search strategy, we found 3658 studies. After removing the papers with abstracts not related to the outcome measures and eligibility criteria, 16 articles were included for qualitative analysis. Several studies identified the presence of different neutrophil subsets, specifically, the naive, pro- and para-inflammatory, hyper-reactive and hyper-active, and high- and low-responder phenotypes. The existing evidence demonstrates the presence of pro-inflammatory, hyper-reactive and high-responder neutrophils in periodontal tissues affected with periodontitis. There is no evidence demonstrating the presence of the N1 or N2 phenotypes in periodontal tissues during periodontitis. However, the existence of pro-inflammatory phenotypes, which increase NETosis and degranulation, and increase the production of pro-inflammatory cytokines, could be suggestive of the N1 phenotypes.

RESUMENEl propósito del presente estudio fue cuantificar la presencia de la quimiocina CCL5 (RANTES) en Líquido Crevicular Gingival (LCG) de pacientes con Periodontitis Crónica (PC) y/o Diabetes Mellitus tipo 2 (DM2). Se realizó un estudio comparativo, transversal en 40 pacientes. Se tomó LCG de bolsas periodontales y surcos gingivales de 4 grupos de pacientes (10 por grupo de estudio), se excluyó a los pacientes que recibieron tratamiento periodontal, antibiótico y antiinflamatorio 6 meses anteriores al estudio o cursaron con alguna enfermedad sistémica distinta a DM2. Las concentraciones de CCL5 se determinaron mediante ensayos LUMINEX de selección magnética. Se realizó estadística descriptiva, prueba ANOVA de una vía, T de student y correlación de Pearson. La cuantificación de CCL5 fue mayor en los pacientes que presentaron ambas enfermedades, seguidos del grupo con solo PC, los sanos y el grupo con solo DM2. No se encontró diferencia significativa entre los grupos y no hubo correlación entre las cuantificaciones y los indicadores glicémicos. A pesar de que las diferencias no fueron significativas, el grupo de pacientes con ambas enfermedades presentó la mayor cuantificación de CCL5. La expresión de CCL5 en LGC debe considerarse un potencial inductor de destrucción periodontal, su determinación podría ser útil para monitoreo de la salud/enfermedad de los tejidos periodontales. SANSORES L., CARRILLO A., SAURI E., GUZMÁN E., HERNÁNDEZ M., POZOS A., MARTÍNEZ V., 2017: Cuantificación de la quimiocina CCL5 en pacientes con diabetes mellitus tipo 2 y/o periodontitis cronica: Estudio preliminar.-ODOVTOS-Int.