Cytokines and chemokines have a fundamental role in the maintenance of inflammation and bone response, which culminate in the development of chronic periapical lesions. Regulatory (Treg) and Th17 cytokines play a key role in regulating the immune response involved in this process. The aim of this study was to investigate the role of Treg and Th17 cells in chronic inflammatory periapical disease, by comparing the expression of the immunoregulatory mediators TGF-β, IL-10, CCL4, and the proinflammatory IL-17 and CCL20 in the periapical tissue of teeth with pulp necrosis, with and without associated chronic lesions. Eighty-six periapical tissue samples were obtained from human teeth. The samples were divided into three groups: pulp necrosis with a periapical lesion (n=26); pulp necrosis without a periapical lesion (n=30), and control (n=30). All samples were submitted to histopathological analysis and cytokine and chemokine measurement through ELISA. Statistical analyses were done with Kruskal-Wallis and Mann-Whitney tests and Spearman correlation. The group with pulp necrosis and a periapical lesion showed a higher expression of CCL4 and TGF-β in comparison with pulp necrosis without a lesion. CCL20 was higher in the group with a periapical lesion when compared to the control. In all groups there was a weak positive correlation between IL-17/CCL20, IL-10/CCL4, and IL-17/TGF-β. Both types of cytokines, pro-inflammatory and immunoregulatory, occur simultaneously in periapical tissue. However, a rise in immunosuppressive cytokines and chemokines (CCL4 and TGF-β) in periapical lesions suggests a role of these cytokines in stable periapical disease.

Recent studies have pointed towards a role of tumour-infiltrating neutrophils in cancer biology. Investigations on oral squamous cell carcinoma have indicated a possible association with clinical characteristics. This study aimed to evaluate neutrophil infiltration and the neutrophil/lymphocyte ratio in the central areas and invasive front of oral squamous cell carcinomas at different T stages, and their association with clinicopathological features and patient outcome. Clinical information was retrieved from the charts of patients who had undergone surgical treatment. Samples of the excised tumours were subjected to immunohistochemical analysis for CD66b and CD3. Semi-quantitative analysis was performed in the intratumoural region and in the invasive front. Appropriate statistical tests were used for evaluating the data, including Kaplan–Meier survival analysis and the log-rank test. A p value of less than 0.05 was considered significant. T3–T4 tumours presented higher CD66b infiltration in the intratumoural region and higher CD66b/CD3 ratios in the invasive front than T1–T2 lesions (p < 0.05). There was a strong inverse correlation between CD66b and CD3 in the invasive front of T3–T4 tumours (r = −0.712, p < 0.05). Comparisons of CD66b and the CD66b/CD3 ratio according to N status, tumour location, recurrence, inflammation grade, and histological grade did not reach statistical significance. Survival analysis also did not show any significant differences. The present study showed different degrees of neutrophil infiltration between T1–T2 and T3–T4 oral cancers, with higher indexes in the advanced lesions. However, there was no association with clinicopathological features or with time to recurrence.