DNA probe detection of periodontopathogens in advanced periodontitis

Abstract

Species‐specific DNA probes were used to determine the presence of Actinobacillus actinomycetemcomitans (A.a.), Porphyromonas (Bacteroides) gingivalis, Prevotella intermedia, Treponema denticola. Eikenella corrodens, Fusobacterium nucleatum, and Wolinella recta in subgingival plaque from deep pockets/sites of patients with advanced periodontitis. The subjects were 20 patients with severe adult periodontitis, 13 men and 7 women (mean age 45.6 ± 6.7 yr). For each subject, 9–10 subgingival sites with the deepest probing depths from each quadrant were sampled by the paper point method, a total of 198 sites, with mean probing depth 7.2 ± 1.6 mm and clinical attachment level 9.5 ± 2.7 mm. A.a. was present in at least one site in 75% of the subjects; P. gingivalis was found in 95%; P. intermedia and W. recta were found in 90%, respectively; and T. denticola, E. corrodens, and F. nucleatum were found in all subjects. In the 198 samples, A.a. was detected in 25.8%, P. gingivalis in 51.5%, P. intermedia in 64.1%, T. denticola in 60.6%, E. corrodens in 72.9%, F. nucleatum in 74.7%, and W. recta in 65.7%. The predominant combination was the simultaneous presence of P. intermedia, T. denticola, E. corrodens, F. nucleatum, and W. recta in 89.5% of the subjects and 46.8% of the sites. Of these sites, 51.1% showed the combined presence of P. gingivalis and 28.4% that of both A.a. and P. gingivalis. None of the seven bacteria could be detected in 14.4% of the total sites sampled. The present study indicates that severe destructive adult periodontitis is a multibacterial infection and that certain combinations of periodontopathogens seein to be important in the pathogenesis of the disease.

Signaling Cascades Triggered by Bacterial Metabolic End Products during Reactivation of Kaposi's Sarcoma-Associated Herpesvirus

“…gingivalis and F. nucleatum, two common oral pathogens associated with human periodontitis (44) and potent activators of viral reactivation, release the short-chain fatty acid (butyrate) as one of the major by-products into the microenvironment (19), along with other volatile fatty acids (25). Moreover, histone hyperacetylation in T cells has been reported following the exposure of T cells to culture supernatants of P. gingivalis (22).…”

Butyric acid retention in gingival tissue induces oxidative stress in jugular blood mitochondria

“…Periodontopathic bacterial pathogens, such as Porphyromonas gingivalis and Fusobacterium nucleatum, play a significant role in producing a variety of virulence factors, like BA, which in high amounts lead to the development of periodontal diseases (Socransky and Haffajee 1991;Soder et al 1993;Teng et al 2002). Previous published works related to our group have shown that BA induces apoptosis in inflamed fibroblasts (Kurita-Ochiai et al 2008), Jurkat T cells (Kurita-Ochiai et al 1997;KuritaOchiai and Ochiai 2010), human peripheral blood mononuclear cells (Kurita-Ochiai et al 1999), WEHI 231 and RAJI B-lymphoma cells (Kurita-Ochiai et al 1998), splenic T cells and B cells (Kurita-Ochiai et al 1997, and murine thymocytes (Kurita-Ochiai et al 1997).…”

Cellular Events Involved in Butyric Acid-Induced T Cell Apoptosis

“…Severe destructive adult periodontitis is caused by a mixed infection and the combination of certain periodontopathogens, for example, Porphyromonas, Prevotella, and Fusobacterium spp. are important in pathogenesis (2). These bacteria produce a variety of virulence factors, such as proteases, LPS, fimbriae, and butyric acid.…”