Aim The purpose of this case–control study was to compare the prevalence of apical periodontitis (AP) in patients affected by autoimmune disorders (AD) (inflammatory bowel disease [IBD], rheumatoid arthritis [RA] and psoriasis [Ps]) with the prevalence of AP in subjects without AD. The prevalences of AP in patients taking biologic medications, conventional medications and no medication were also compared. Methodology Eighty‐nine patients (2145 teeth) with AD were investigated and the control group included 89 patients (2329 teeth) with no systemic diseases. Full dental panoramic tomograms were used to determine the periapical status of the teeth. Additional variables investigated included patient's socio‐demographic characteristics, medications taken by AD patients, the decayed, missing and filled teeth (DMFT) index. The chi‐square test and logistic regression analysis were used to evaluate the correlation between AD and AP. p‐Values lower than .05 were considered to be statistically significant. Results The prevalence of AP was 89.9% in AD patients and 74.2% in control subjects (odds ratio [OR] = 3.75, p = .015). The DMFT score was found to be significantly higher in the AD group (p = .004). Patients with RA had the highest risk of being affected by AP, whereas those with IBD had the lowest risk. Multiple binary logistic regression analysis indicated that the teeth of AD patients who were not taking any medication or were being treated with biologic disease‐modifying anti‐rheumatic drugs (bDMARDs) had a higher risk of being affected by AP than did the teeth of the control subjects (OR = 1.42 and OR = 2.03, respectively; p = .010). The teeth of patients taking conventional DMARDs (cDMARDs) were less affected by AP compared with those of patients taking bDMARDs. Conclusions Patients with AD, whether treated or not with biologic medications, showed a higher prevalence of AP than did those in the control group. The DMFT index score, which was higher in AD patients compared with controls was identified as a significant predictor of AP prevalence.

This study aimed to assess the effect of apical periodontitis and its treatment on the profile of salivary inflammatory markers and to investigate its correlation with serum inflammatory markers. Saliva samples were collected from 115 recruited participants. Patients were reviewed after 1 and 2 years following treatment. Saliva samples were analysed using Multiplex microbead immunoassay for identifying the inflammatory biomarkers’ profile. Biomarker levels were compared against healthy controls at baseline. Longitudinal comparison of those markers was further analysed for the review appointments and correlated with the size of the periapical radiolucency, treatment outcome and serum inflammatory biomarker levels. The salivary cytokines, matrix metalloproteinases (MMPs) and vascular adhesion molecules were higher at the review appointments. Pre-operative salivary levels of high-sensitivity C-reactive protein (hs-CRP) were significantly higher in the treatment group than in the control group (p < 0.001). At 1 year, hs-CRP was decreased than baseline. While, in 2 years, fibroblast growth factor (FGF)-23 was significantly lower compared to baseline levels (p = 0.005). Furthermore, the post-operative size of radiolucency was significantly correlated with the levels of several markers. When correlating the salivary levels of biomarkers with the serum levels, a significant correlation was seen in FGF-23 (p = 0.04) at baseline; in intercellular adhesion molecule (ICAM)-1 (p = 0.02) at 1 year post-treatment; and in TNF-α, ICAM-1 and E-Selectin at 2 years post-treatment (p = 0.046; p = 0.033; p = 0.019, respectively). Therefore, his study suggests that higher salivary cytokines, MMPs and vascular adhesion molecules at the post-treatment reviews are related to periapical bone healing and remodelling, whereas salivary FGF-23 and hs-CRP could be prognostic biomarkers. Correlation of some salivary with serum biomarkers suggests that saliva sampling could be a feasible non-invasive option for the measurement of inflammatory marker levels; however, further longitudinal studies are required.