{'fraction_non_alphanumeric': 0.021889400921658985, 'fraction_numerical': 0.00576036866359447, 'mean_word_length': 5.433333333333334, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Evaluation of the effect of nicotine and metabolites on the periodontal status and the mRNA expression of interleukin-1β in smokers with chronic periodontitis

Background and Objective: Smoking is an important environmental risk factor involved in the causation and progression of periodontal disease. Smoking can impair various components of the host immune response and immune system. The virulence factors of periodontal pathogens stimulate inflammatory cytokine expression by mononuclear cells. IL-1b is the key mediator involved in the pathogenesis and disease progression. Therefore, whole gingival biopsy samples are assessed for this increased expression of IL-1. Material and Methods: 29 male subjects′ age and gender matched were divided into three groups based on the periodontal and smoking status (Group A:healthy, Group B: non-smokers suffering from chronic periodontitis, Group C: smokers suffering from chronic periodontitis). Periodontal parameters like plaque index, gingival index, probing pocket depth and clinical attachment level were recorded at baseline and post scaling. The mRNA expression of IL-1b was determined by real time polymerase chain reaction and correlated with the periodontal and smoking status. Results: The improvement in the periodontal parameters was statistically significant in the non- smokers (Group B) and there was a 2 fold increase in the mRNA expression in this group. The smokers (Group C) showed lesser improvement in the periodontal parameters and there was an 8 fold increase in the mRNA expression of IL-1b. Conclusion: Association of smoking status with periodontal destruction can thus be correlated with the increased mRNA expression of IL-1b in chronic periodontitis patients.