Influence of cigarette smoking on synthesis of eicosanoids, isoprostanes and lipoxygenase metabolites in apical periodontitis

Arachidonic acid (AA) is metabolized to eicosanoids and isoprostanes (IPs) via different pathways. The presence of granuloma in apical periodontitis (AP) is linked with inflammation and the synthesis of metabolites of AA. ive estigated the conversion rate of 14C labelled arachidonic acid (14C-AA), the lipoxygenases (LOX) products and the endogenous synthesis of eicosanoids and IPs in extracted granuloma. Furthermore, we assessed if there are markers for bone destruction and the influence of cigarette smoking. ts and methods patients with symptoms and corresponding radiological signs of AP, teeth were extracted including the periapical granuloma. The endogenous synthesis of eicosanoids and IPs, the conversion rate of 14C-AA and LOX products in extracted granuloma were analyzed. s nd that smoking increases significantly the synthesis of IPs and LOX-metabolites in granuloma. Furthermore, smoking may have contributed to significant differences in qualitative and quantitative profile of eicosanoids, IPs and the conversion rate of 14C-AA independent of the size of the granuloma. sions ta demonstrate that in smokers with granuloma due to AP products of lipid peroxidation as 8-iso-PGF2α and products of the LOX-pathway are increased at the expense of cyclooxygenase products. The size of granuloma did not influence the amount of synthesized eicosanoids, IPs or LOX-metabolites out of 14C-AA whereas cigarette smoking was a significantly influencing and modifiable risk factor.