Apical periodontitis (AP) is the outcome of host-microbiome interaction at the root-apex. The effect of this interaction on the immune system, translated in concentration of circulatory inflammatory mediators, has been investigated in the past, but some methodological flaws in terms of study design and treatment have been identified. A systematic review and meta-analysis, that we previously conducted,  revealed that t AP adds on to systemic inflammation by elevating C-reactive protein, interleukin 6, asymmetric dimethylarginine, and C3 levels. These effects on inflammatory mediators were observed in individuals with several or big lesions (moderate/severe PAI). Additionally, great heterogeneity between the studies was observed.

Taking the information from the systematic review into consideration we designed a prospective case-control intervention study, to study the impact of the minimum burden (1 AP). The aim of the study was: To explore he influence of apical periodontitis (AP) in inflammatory markers in blood of otherwise healthy individuals and to depict the inflammatory profile of the healing after dental extraction. The cohort consisted of healthy human volunteers with one tooth with a root-tip inflammation and matched healthy controls. Peripheral blood was drawn at 6 time points, 3 before and 3 after the extraction of the tooth with AP. The teeth were pulverised, DNA extraction and sequencing were performed.

The results revealed that AP has an effect on the immune fitness of the individuals. The immunologic profile of chronic apical periodontitis in one tooth and its healing profile reveals a systemic low-grade inflammation through compensatory immunosuppression. A larger lesion or multiple lesions could disrupt the balance that the system is trying to maintain, resulting in loss of homeostasis (health). The analysis of the microbiome of the teeth with AP, revealed a difference between symptomatic and asymptomatic infections and also between primary and secondary AP. The immunologic profile of the patients with asymptomatic infections revealed a difference in the concentration of some inflammatory markers compared to symptomatic. Finally, an association between member of the microbiome of the endodontic infection and blood mediators has been found, and this correlation was different depending on the presence or absence of pain.

In conclusion, there is now evidence that AP, even when asymptomatic, is a health risk and should not be left untreated.

Dr. Athina C. Georgiou
a.c.georgiou@acta.nl

ACTA - Amsterdam - Netherlands