期刊
JOURNAL OF ENDODONTICS
卷 49, 期 2, 页码 137-143出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.joen.2022.11.012
关键词
Osteopontin; osteoprotegerin; periapical periodontitis; receptor activator of nuclear factor kappa B ligand; smoking; tumor necrosis factor alpha
This study compared the immunoexpression of biomarkers RANKL, OPG, OPN, and TNF-a in smokers and nonsmokers with chronic apical periodontitis (CAP). The results showed significant differences in the expression of RANKL, OPG, OPN, and TNF-a between smokers and nonsmokers.
Introduction: Smoking can be considered a risk factor for chronic apical periodontitis (CAP). This study compared the immunoexpression of biomarkers receptor activator of nuclear factor kappa B ligand (RANKL), osteoprotegerin (OPG), osteopontin (OPN), and tumor necrosis factor alpha (TNF-a) in CAP in smokers and nonsmokers. Methods: Twelve smokers and 12 nonsmokers diagnosed with CAP and indicated for tooth extraction were selected. Exclusion factors were teeth with a diagnosis of root fracture, previous endodontic treatment, or endoperiodontal injury, in addition to individuals with systemic diseases, under 18 years of age, users of anti-inflammatory and/or antibiotics in the last 3 months, and drug users. Specimens were processed for histopathologic and immunohistochemical analysis. Results: Qualitative analysis of RANKL expression showed 66.66% weak/moderate and 33.33% strong in smokers and 100% weak/moderate in nonsmokers. OPG and OPN expressions were 100% negative to focal in the smoker group and 50% negative to focal and 50% weak/moderate in the nonsmoker group. TNF-a was 25% negative to focal and 75% weak/moderate in the smoker group and 33.33% negative to focal and 66.66% weak/ moderate in the nonsmoker group. Quantitative analysis of the data using the Mann-Whitney U test showed that there was a significant difference in the immunoexpression of RANKL (P < .05), OPG (P < .05), and OPN (P < .05), but there was no statistical difference in the immunoexpression of TNF-a (P . .05) between the 2 groups. Conclusions: These findings suggest that smoking is capable of altering the inflammatory response, influencing the evolution of CAP.
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