Bacterial frequency increased from peri-implant/periodontal health to peri-implantitis/periodontitis but not from mucositis/gingivitis to peri-implantitis/periodontitis. There was a trend towards higher bacterial frequency in teeth than implants.

It is unclear when the initial colonization by periodontal pathogens occurs in the oral cavity. Therefore, we report here the association between specific age groups and the time when the initial colonization by periodontal pathogens occurs in the oral cavity in such groups. Findings are based on an epidemiological analysis of the prevalence of five periodontal pathogens in the oral cavities of a wide range of age populations, from newborn to elderly, who were randomly selected in a geographic region of Brazil. These periodontal pathogens include Campylobacter rectus, Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Prevotella intermedia, and Tannerella forsythia and were analyzed in the bacterial samples isolated from gingival sulcus, the dorsum of the tongue, and cheek mucosa of diverse age groups, using a bacterial DNA-specific PCR method. Results indicated that there are distinct age-related groups where initial colonization by the five periodontal pathogens examined in this study can be detected and that the presence of teeth is a permissive factor for colonization by P. gingivalis, P. intermedia, and T. forsythia. Although it remains unclear exactly how or when target pathogens colonize healthy subjects, an understanding of age-related groups does provide a potentially useful tool in the early detection and prevention of periodontitis in healthy individuals.

Pharmacological and periodontal variables were associated with GO in different immunosuppressive regimens. Integration between the medical and the dental team may be an important approach in the post-transplant maintenance routine.

This longitudinal study evaluated the response to periodontal treatment by subjects infected with either JP2 (n ‫؍‬ 25) or non-JP2 (n ‫؍‬ 25) Aggregatibacter (Actinobacillus) actinomycetemcomitans. Participants were treated during the first 4 months by receiving (i) scaling and root planing, (ii) systemic antibiotic therapy, and (iii) periodontal surgery. Probing depth (PD), clinical attachment level (CAL), and gingival and plaque indices (GI and PI, respectively) were monitored at baseline and at 12 months, along with DNA-PCR-based subgingival detection of JP2 or non-JP2 A. actinomycetemcomitans. At baseline, PD, CAL, and GI scores were statistically higher in the JP2 strain-positive group than the non-JP2-strain-positive group. At 12 months, PD, CAL, and GI scores had decreased significantly for both groups, but the reduction rates of PD and CAL were higher in the non-JP2-strain-positive group. Among JP2-strain-positive patients in the baseline, patients who remained JP2 strain positive at 12 months showed significantly higher GIs than did the patients who had lost the detectable JP2 clone. Patients who remained JP2 strain positive at 12 months appeared to be more resistant to mechanical-chemical therapy than did those who were still non-JP2 strain positive, while the elimination of JP2 A. actinomycetemcomitans remarkably diminished gingival inflammation. Early identification and elimination of the JP2 clone of A. actinomycetemcomitans will enable practitioners to effectively predict the outcome of treatments applied to periodontal patients.Compared to gingivitis, or disease-free periodontium, an increased incidence of Aggregatibacter (Actinobacillus) actinomycetemcomitans has been reported in the lesions of localized aggressive periodontitis (LAP) or severe chronic periodontitis (9,13,16,41,44,45). It is also true that while polymicrobial infection is implicated in the pathogenesis of chronic adult periodontitis, oral colonization by A. actinomycetemcomitans is more directly associated with the pathogenesis of LAP. Such pathogenic outcomes related to A. actinomycetemcomitans infection seem to be partially derived from leukotoxin (LTX) produced by A. actinomycetemcomitans. LTX is a potent virulence factor, which is encoded in an operon consisting of four genes (5) and typically causes cytotoxicity in neutrophils (26) and macrophages (37). Furthermore, in vitro experiments revealed that a specific 530-bp sequence in the LTX promoter region, rather than the LTX operon, impacts the transcription regulation of LTX (5), whereas there are several factors that regulate the expression of LTX from A. actinomycetemcomitans (25). It is also true that there may be highly leukotoxic A. actinomycetemcomitans strains other than just the type with the 530-bp deletion (24). Nonetheless, the deletion of this 530-bp promoter region, which is found in some pathogenic strains of A. actinomycetemcomitans, also called JP2 strains, has critical ramifications. For example, faster expression of the LTX gene with the deletion has been o...

These results suggest that in advanced periodontitis, unstimulated saliva is representative of pooled subgingival plaque samples and its use is appropriate in the oral detection of A. actinomycetemcomitans.