The role of smoking as a risk factor for Periodontitis was assessed separately in diabetic and nondiabetic study groups. Subject listings stratified for age (19 to 40 years) and sex were obtained for subjects with insulin-dependent diabetes mellitus (IDDM) and nondiabetic subjects. For both the IDDM group (n = 132) and the nondiabetic group (n = 95), age and sex stratified samples were constructed by random selection of subjects from each subject listing. Patients were recruited by phone, examined, and their medical and dental histories obtained. Among nondiabetic subjects, the prevalence of Periodontitis was markedly higher among current smokers compared with never smokers (P < 0.005) in both the 19 to 30 year-old (46% vs. 12%) and 31 to 40 year-old groups (88% vs. 33%). The subject mean percent of sites with gingival pocket depth >4 mm was higher among current smokers than never smokers (P = 0.001) in the 19 to 30 (8.2% vs. 3.4%) and 31 to 40 (14.3% vs. 4.3%) age groups. The effects of smoking among IDDM subjects were similar to that observed in the nondiabetic population. There were no differences between current and never smokers in the proportion of sites positive for plaque. Attributable risk percents from prevalence data suggest that among nondiabetic subjects, a large proportion, perhaps as much as 51% of the Periodontitis in the 19 to 30 year old group and 32% of the Periodontitis in the 31 to 40 year old group, is associated with smoking. These findings suggest that smokers are a high risk group for Periodontitis, and that smoking may be the single most important environmental risk factor for Periodontitis. / Periodontol 1993; 64:16-23.
A selective medium, malachite green bacitracin agar, was developed for the isolation of Actinobacillus actinomycetemcomitans from subgingival plaque of periodontally diseased patients. The medium consisted of Trypticase soy agar 40 gm/liter, bacitracin 128 micrograms/ml, malachite green 8 micrograms/ml and 5% defibrinated sheep blood. The medium, when incubated in an atmosphere of air plus 10% CO2 for 5 days, permitted greater than 80% recovery of pure cultures of A. actinomycetemcomitans when compared with a nonselective medium. The most frequent contaminant in plaque samples from different clinical conditions was Haemophilus aphrophilus. Decomposition of H2O2 was useful in differentiating these two species. Clinical studies employing the malachite green bacitracin medium revealed a significant association between the presence of the organism, A. actinomycetemcomitans and juvenile periodontitis.
Eight juvenile periodontitis (JP) patients with progressing disease were evaluated for clinical, immunologic, and microbiologic features. Clinically, bleeding on probing, pocket depth, and attachment level were unrelated to progressing disease. Only Actinobacillus actinomycetemcomitans was related to a marked increase in attachment loss when examined on both a site and patient basis. Eikenella corrodens was significantly elevated in progressing sites with A. actinomycetemcomitans as opposed to non-progressing sites harboring A. actinomycetemcomitans. Eikenella corrodens may function synergistically with A. actinomycetemcomitans to enhance disease in JP patients. Darkfield microscopy was of no value in distinguishing disease activity. All patients screened had elevated serum IgG levels to the same serotype of A. actinomycetemcomitans as that isolated from the subgingival flora. Other elevated serum IgG responses were noted to various organisms including F. nucleatum. B. intermedius, B. gracilus, B. gingivalis and E. corrodens.
Three treatment regimens including local tetracycline delivery, systemic doxycycline and surgery plus systemic doxycycline were investigated in a localized juvenile periodontitis (LJP) population. Of the investigated treatments only surgery plus systemic doxycycline for 14 days was effective in eliminating or suppressing Actinobacillus actinomycetemcomitans, an organism strongly associated with LJP lesions. While surgery plus antibiotics was the superior treatment, it appears that the possibility of reinfection or incomplete elimination of the organism exists. Careful long‐term follow‐up, including clinical and microbiological monitoring, is highly recommended in this periodontal population.
Longitudinal clinical and microbiological monitoring of subjects with localized juvenile periodontitis indicated that Actinobacillus actinomycetemcomitans and Eikenella corrodens were significantly associated (P < 0.05) with active tissue destruction.Localized juvenile periodontitis (LJP) is a distinct clinical form of periodontal disease. In its classic form, it is a disease of adolescents in which individuals between 12 and 20 years of age demonstrate a rapid loss of supporting alveolar bone around the first permanent molars and incisors (1,8). The classic condition exhibits apparent minimal clinical inflammation, bacterial plaque, calculus, or pain. It is a particularly intriguing condition in that a hereditary component has been hypothesized (4,38). In a study of LJP patients, Newman et al. (35) described two numerically dominant groups of microorganisms, groups III and IV, which were later shown to include strains of Actinobacillus actinomycetemcomitans (46).A cross-sectional study of 42 patients by Slots et al. (39) revealed a carrier rate of A. actinomycetemcomitans in 20% of normal juveniles, 36% of normal adults, and 50 and 90% of adult periodontitis and LJP patients, respectively. Zambon et al. (53) examined 403 patients for the incidence of A. actinomycetemcomitans and found 95% of juvenile periodontitis patients harbored the organism, whereas only 15% of his other population groups did. In a recent study, Mandell and Socransky (31) examined the subgingival flora of deep pockets displaying radiographic bone loss. They found a significant association between A. actinomycetemcomitans and LJP but not with gingivitis or adult periodontitis.The purpose of this investigation was to longitudinally follow sites in an LJP population and their siblings. Utilizing the running median technique (11), periodontal pockets undergoing active destruction would be identified and cultured for a group of organisms, including Bacteroides intermedius, Actinomyces spp., Fusobacterium nucleatum, Capnocytophaga spp., Streptococcus spp., A. actinomycetemcomitans, and Eikenella corrodens. These groups were sought because prior reports (34,40,42) related each of these organisms with health or disease.Eight patients aged 10 to 18 years were selected for study. Longitudinal attachment measurements were performed (11) on days 1, 7, 30, and 37 after entry into the study by the patients. Active disease was defined as a loss of connective tissue attachment of .2 mm. A total of 168 sites per patient (6 sites per tooth) were followed, so that over 1,200 total sites were studied. Of these sites or pockets, eight displayed active disease. An additional 16 sites were selected as controls. Pocket depths averaged 8.4 mm (range 5 to 10 mm) in the diseased sites versus 4.8 mm (range 3 to 7 mm) in the 778 control sites. The sampled sites were either molars or incisors, because these areas are most frequently affected in LJP (20). Subgingival plaque samples were taken from the base of the periodontal pockets with a sterile Morse (00) scaler inser...
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