Objectives
This study aimed to identify disease-related markers in persistent apical periodontitis (PAP) biopsies and examine whether these were associated with comorbidities like rheumatoid arthritis (RA) and cardiovascular diseases (CVD).
Materials and method
The levels of the cytokines/chemokines GM-CSF, IFN-γ, IL-2, IL-6, IL-9, IL-10, IL-13, IL-15, IL-17E/IL-25, IL-21, IL-23, IL-27, IL-28A/IFN -λ2, IL-33, MIP-3α/CCL20, and TNF-α were determined in lesions from patients with PAP (n = 20) and compared to healthy bone samples (n = 20).
Results
We identified eleven cytokines to be differently expressed, and among them, IL-2, IL-6, IL-17E, IL-21, and IL-27 appeared to drive the discrepancy between the disease and healthy groups. The levels of T follicular helper (Tfh) cell promoting cytokines (IL-21, IL-6, IL-27) were enhanced while T helper (Th) 1 cell promoting cytokine (IL-2), Th2 cell promoting cytokine (IL-13), and Th17 cell promoting cytokine (IL-17E) were reduced in the PAP group. The data also indicate that Tfh cell differentiation (IL-21), along with Th1 (GM-CSF, IFNγ), Th2 (IL-13), and Th17 (GM-CSF) cell differentiation, might be increased in the subpopulation of patients suffering from RA, whereas no differences were found in patients with CVD.
Conclusions
Levels of cytokines/chemokines in PAP were identified, and cluster analyzes indicated that these markers may be associated with the differentiation of different T cell populations. Patients with PAP and RA comorbidities showed elevated levels of markers reinforcing this association.
Clinical relevance
Molecular analyses of PAP may result in identification of prognostic markers.