LAUSR

AIM To evaluate the effects of cigarette smoke inhalation (CSI) on inflammation, proinflammatory mediators and haematological parameters in rats with induced apical periodontitis (AP). METHODOLOGY Thirty-two 3-month-old male Wistar rats were divided into four experimental groups (n=8): C - Control; S - rats with CSI; AP - rats with AP; and SAP - rats with CSI + AP. Animals in groups S and SAP inhaled cigarette smoke by remaining inside a smoking chamber for 8 minutes, 3 times daily, for 50 days. After 20 days of smoke inhalation, animals in AP and SAP groups had the pulps of the lower right first molar exposed to oral environment for 30 days to induce AP. In these subsequent 30 days, animals in group S and SAP continued with CSI. On day 50th, animals were euthanized and mandibles were histologically processed to assess inflammatory infiltrate, immunohistochemical interleukins (IL-1β, IL-6 and TNF-α), and blood sample collected for laboratory analysis. The Mann-Whitney test was performed for nonparametric data and the pairwise analyses of Student's t-test for parametric data, with a significance level of P<0.050. RESULTS Inflammatory infiltrate was moderate in AP group and more severe in the SAP (P=0.010). The interleukins IL-6, IL-1β and TNF-α were higher in SAP group (P<0.001) when compared with the AP group. A greater number of red blood cells (P=0.010), haemoglobin (P=0.007), and neutrophils (P=0.014) were observed in the SAP group in comparison with the AP group. CONCLUSION Cigarette smoke inhalation induced a more severe inflammatory infiltrate, with increased levels of proinflammatory cytokines and changes in haematological parameters in rats with induced AP. Thus, cigarette smoke inhalation aggravated AP, exacerbating the inflammatory response.