Abstract

ObjectiveTo investigate the effect of smoking on the expression levels of matrix metalloproteinase (MMP)-1, MMP-9, tissue inhibitor of metalloproteinase-1 (TIMP-1), and the concentrations of TNF-α and IL-10 in patients with chronic periodontitis (ChP). MethodsThis is an ex-vivo study. Our study consisted of 78 cases, all of which were diagnosed with ChP and were selected according to the inclusion and exclusion criteria. Among these 78 cases, 38 patients were classified into the smoking group (S-ChP group), and 40 patients in the non-smoking group (NS-ChP group). The clinical periodontal parameters of all patients were recorded, including the plaque index (PLI), probing depth (PD), loss of attachment (LA) and sulcus bleeding index (SBI). Serum was collected from forearm blood to establish a Porphyromonas gingivalis (Pg) internalizing KB cell model. Enzyme-linked immunosorbent assay (ELISA) was used to determine the concentrations of MMP-1, MMP-9 and TIMP-1 in the KB cell lysis solution as well as IL-10 and TNF-α in the gingival crevicular fluid (GCF). ResultsFewer Pg internalizing KB cell colonies were observed in the NS-ChP group than in the S-ChP group (P<0.01). When 400μL serum was added, there were remarkable differences in the concentrations of MMP-1 and TIMP-1 secreted from the KB cells between the S-ChP and NS-ChP groups (MMP-1: t=−21.71, P<0.01; TIMP-1: t=64.35, P<0.001). Additionally, when 800μL serum was added, there were significant differences in the concentrations of MMP-1, MMP-9 and TIMP-1 in the KB cells between the S-ChP and NS-ChP groups (MMP-1: t=−81.89, P<0.001; MMP-9: t=−15.67, P<0.001; TIMP-1: t=109.4, P<0.001). The TNF-α levels were higher, but the IL-10 levels were lower in the GCF from the ChP patients in the S-ChP group than those in the NS-ChP group (both P<0.001). ConclusionThe serum of S-ChP patients can enhance the concentrations of MMP-1 and MMP-9, but reduce TIMP-1 secreted from Pg internalizing KB cells. However, the concentration of TNF-α was increased and IL-10 was decreased. Abnormal concentrations of ChP-associated biomarkers may be conducive to the development and progression of ChP.

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