Prevalence of Porphyromonas Gingivalis Fimbrial Subunit Genotype in Smokers and Nonsmokers After Periodontal Therapy

Prevalence of Porphyromonas Gingivalis Fimbrial Subunit Genotype in Smokers and Nonsmokers After Periodontal Therapy

The aims of the present study will be identify 5 types of fimbrial subunit genotype strains in smokers and nonsmokers with periodontitis, before and after periodontal therapy. Third two periodontitis patients will be selected to these study, 16 nonsmokers and 16 smokers. Clinical and microbiological parameters were evaluated at baseline and 3 months after periodontal treatment: Plaque Index, Bleeding On Probe, Probing Depth, Gingival Recession and Clinical Attachment Level. The prevalence of P. gingivalis and fimbrial subunit gene strains will be determined by Polymerase Chain Reaction.

Porphyromonas gingivalis is one of the most prevalent periodontopathogens present in red complex that is considered to be infectious agent causing several types of periodontal diseases. P. gingivalis has ability to invade gingival epithelial cells and can survive for extended periods of time. Fimbriae have been characterized to be key factors in adhesion, invasion, and colonization. Fimbriae are also responsible for invasion of membrane vesicles into host cells. Long fimbriae (FimA), also known as major fimbriae, are long, peritrichous, filamentous components. They have a role in initial attachment and organization of biofilms, as they act as adhesins that mediate invasion and colonization of host cells contributing to P. gingivalis virulence.

Fimbrillin (FimA; structural subunit protein of fimbriae) is classified into 5 variants (types I to V) based on their nucleotide sequences. P. gingivalis strains possessing type II fimA are correlated with P. gingivalis-positive patients, and its occurrence was significantly increased with the more severe forms of periodontitis. Previous studies evaluated the differences among the prevalence of fimA genotypes and periodontal health status in adults. P. gingivalis was detected in 36.8% of the healthy subjects and in 87.1% periodontitis patients. Among the P. gingivalis-positive healthy adults, the most prevalent fimA type was type I (76.1%), followed by type V (29.7%). In contrast, a majority of the periodontitis patients carried type II fimA organisms (66.1%), followed by type IV (28.9%). These findings indicate that there are both disease-associated and non-disease-associated strains of P. gingivalis, and that their infectious traits influencing periodontal health status could be differentiated based on the clonal variation of fimA genes.

Tobacco consumption is a risk factor for periodontal disease. Several studies have been reported that smoker habit is associated with greater clinical attachment loss, recession and tooth loss and reduced bone height and density. However, controversial report has been discussed about the differences between smokers and non-smokers periodontopathogens. P. gingivalis have been report 52.2% prevalence in non-smokers and 66.7% in smokers (pocket depth 3-5 mm) , and are associated with high levels in sites with periodontitis.

The mechanism that tobacco affects the periodontal tissue is related with nicotine that has been associated with various cellular changes that may contribute to the initiation and subsequent progression of periodontal disease. It is promote local effect like the reduction of the gingival blood flow, what can be due to long-term effects on the inflammatory lesions, higher incidence of gingival recession and others clinical parameters in smokers is correlated with cytotoxic and vasoactive substances present in tobacco, including nicotine, carbon monoxide and reactive oxidant substances and systemic effect is that smoking is responsible for 90% of cases of lung cancer, type deadliest cancer for men and women smokers, as well as being associated with various lung diseases. Furthermore, they promote oxidative stress and alterations in the immunoinflammatory responses, reducing functional activity of leucocytes, macrophages, lymphocytes and other immune cells, impaired wound healing and microbial recognition.

Nonsurgical therapy using scaling and root planning is the most usual periodontal therapy, well-recognized by the improvement in clinical and microbiological parameters. Fewer studies evaluated longitudinal clinical and microbiological status of smokers undergoing periodontal maintenance therapy and controversial results were found with absence of difference in disease progression in comparison with nonsmokers. P. gingivalis has been reduced after periodontal treatment. Previous report related reduction of 93 % to P.gingivalis for non-smokers and 88 % for smokers after periodontal treatment.

Inclusion Criteria:

Clinical diagnosis of chronic periodontitis Consumption of 10 or more cigarettes/day.

Exclusion Criteria:

Diabetes mellitus Osteoporosis Pregnant and lactating females Immune suppressive medication Phenytoin Cyclosporine Calcium channel blockers Immunotherapy or diagnosed as HIV+