Premium
Microbial comparison of smoker and non‐smoker adult and early‐onset periodontitis patients by polymerase chain reaction
Author(s) -
Darby I. B.,
Hodge P. J.,
Riggio M. P.,
Kinane D. F.
Publication year - 2000
Publication title -
journal of clinical periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.456
H-Index - 151
eISSN - 1600-051X
pISSN - 0303-6979
DOI - 10.1034/j.1600-051x.2000.027006417.x
Subject(s) - treponema denticola , prevotella intermedia , porphyromonas gingivalis , actinobacillus , periodontitis , medicine , bacteroides , microbiology and biotechnology , bacteroidaceae , etiology , gingival and periodontal pocket , dentistry , biology , bacteria , genetics
A number of bacterial species are involved in the aetiology of periodontitis and include Actinobacillus actinomycetemcomitans , Porphyromonas gingivalis , Prevotella intermedia , Bacteroides forsythus and Treponema denticola. Several studies have shown differences in the microflora between the various forms of periodontal disease. It is recognised that smoking is a risk factor for periodontal disease, but there are conflicting reports on whether or not smoking has an effect on the periodontal microflora. We utilised the polymerase chain reaction to determine the presence of A. actinomycetemcomitans , P. gingivalis , P. intermedia , B. forsythus and T. denticola in subgingival plaque samples in 33 adult periodontitis (AP) patients and 24 generalized early‐onset periodontitis (GEOP) patients prior to treatment. When GEOP and AP patients were compared there were significant differences in the number of positive patients and sites for both A. actinomycetemcomitans and B. forsythus ( p =0.0023 and 0.00001, respectively). No statistically significant differences in the prevalence of these organisms were found between smoker and non‐smoker groups. These results confirm that AP and GEOP sites harbour varied microflora, but show that B. forsythus and A. actinomycetemcomitans were detected to a significantly greater extent in this group of GEOP than in the AP patients investigated. Our findings do not support the hypothesis that smokers have significant differences in the prevalence of periodontal pathogens from non‐smokers.