Abstract
This pilot study aimed to evaluate the influence of smoking on clinical and microbiological parameters after nonsurgical periodontal therapy. Forty-eight subjects were grouped into smokers (SM, n = 24) and nonsmokers (NS, n = 24) and paired according to gender, age, ethnicity, and periodontal status. Both groups received oral hygiene education and scaling and root planing. Clinical evaluation was performed using plaque index (PI), bleeding on probing (BOP), pocket probing depth (PPD), gingival recession (GR), and clinical attachment level (CAL) before instrumentation (baseline) and at 3 and 6 months. The prevalence of Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythia, Candida albicans, Candida glabrata, Candida tropicalis, and Candida dubliniensis in subgingival biofilm was determined by polymerase chain reaction. The data were statistically analyzed considering p < 0.05. Clinical conditions improved between baseline and 3 months after periodontal treatment. However, NS had a better clinical response, presenting greater PPD reduction and CAL increase in comparison to SM. Periodontal treatment reduced the levels of P. gingivalis, A. actinomycetemcomitans, and T. forsythia individually after 3 months for the NS group and after 6 months for both groups. The prevalence of Candida species was markedly higher in SM than in NS at all time points evaluated. Periodontopathogens associated or not with C. albicans or C. dubliniensis were more prevalent in SM than in NS at baseline and after 3 months. It was concluded that smoking impairs clinical and microbiological responses to periodontal therapy. Periodontopathogens combined or not with some Candida species are resistant to short-term periodontal therapy in SM.
Highlights
Several countries have been investing in numerous initiatives and in government policies to control tobacco consumption; cigarette smoking still remains prevalent in the world, with more than 1 billion smokers, and more than 8 million deaths from one or more diseases related to tobacco use will have occurred every year by 2030.1 In addition to systemic damages, such as increased risk for the development of chronic obstructive pulmonary disease, cardiovascular complications, Braz
Several studies all around the world have pointed out a strong association between tobacco use/smoking habit and periodontal disease, evidenced by greater clinical attachment loss, gingival recession, and tooth loss,[3,4,5] as well as by reduced bone height and density.[6,7,8]
The presence of cigarette components could alter the oral environment and trigger the colonization of periodontal sites by uncommon pathogens, as shown by Kamma et al.,[16] who compared the microbial profile of smokers and nonsmokers in a group of patients with early-onset periodontitis and found significant levels of E. coli, C. albicans, S. aureus, and other exogenous pathogens in smokers’ microbiota
Summary
Several countries have been investing in numerous initiatives and in government policies to control tobacco consumption; cigarette smoking still remains prevalent in the world, with more than 1 billion smokers, and more than 8 million deaths from one or more diseases related to tobacco use will have occurred every year by 2030.1 In addition to systemic damages, such as increased risk for the development of chronic obstructive pulmonary disease, cardiovascular complications, Braz. Several studies all around the world have pointed out a strong association between tobacco use/smoking habit and periodontal disease, evidenced by greater clinical attachment loss, gingival recession, and tooth loss,[3,4,5] as well as by reduced bone height and density.[6,7,8] The harmful effects of smoking on periodontal tissues are caused by cytotoxic and vasoactive substances present in tobacco, including nicotine, carbon monoxide, and reactive oxygen species These substances cause oxidative stress and alter immunoinflammatory responses, reducing the functional activity of leukocytes, macrophages, lymphocytes, and other immune cells, and impairing wound healing and microbial identification.[9]. Some authors have reported a high number of pathogens belonging to the red and orange complexes at periodontal sites in smokers[10,11,12] while others have not found any differences between smokers and nonsmokers.[13,14,15] The presence of cigarette components could alter the oral environment and trigger the colonization of periodontal sites by uncommon pathogens, as shown by Kamma et al.,[16] who compared the microbial profile of smokers and nonsmokers in a group of patients with early-onset periodontitis and found significant levels of E. coli, C. albicans, S. aureus, and other exogenous pathogens in smokers’ microbiota
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