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Chronic Adult Periodontitis (chronic + adult_periodontitis)
Selected AbstractsHHV-6, HHV-7, HHV-8 in gingival biopsies from chronic adult periodontitis patientsJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 3 2003A case, control study Abstract Background: Recent reports have suggested that various herpesviruses may be involved in the occurrence and progression of different forms of periodontal disease. Objective: The objective of the present study was to investigate the presence of the novel herpesviruses HHV-6, HHV-7 and HHV-8 in gingival biopsies from patients affected by chronic adult periodontitis. As control, gingival biopsies from periodontally healthy subjects were analysed. Materials and methods: Gingival biopsies were harvested from 23 volunteers: 13 patients affected by chronic adult periodontitis (CAP) and 10 periodontally healthy subjects. Each CAP patient contributed two biopsies involving the epithelium and connective tissue facing the sulcus/periodontal pockets: one biopsy from a site having a probing pocket depth (PPD) 5 mm and presenting with bleeding upon probing (affected site) at the time of biopsy collection, and the other biopsy from a site with PPD3 mm and without bleeding on probing (nonaffected site). After DNA extraction, nested PCR was used in herpesvirus identification. Results: HHV-6 DNA sequences were detected in one non-affected site (8%) and no affected sites (0%) of CAP patients. One biopsy (10%) in healthy subjects revealed HHV-6 positivity. Tissue specimens in 10/13 CAP patients (77%) and 7/10 healthy subjects (70%) contained HHV-7 DNA. HHV-7 prevalence in affected and nonaffected sites of CAP patients was 77% and 54%, respectively. HHV-8 was detected in 7.7% of CAP patients and 0% of healthy subjects. Conclusions: Gingival tissue may act as a reservoir for HHV-7. A high prevalence of HHV-7 was detected in both periodontally diseased and healthy individuals. The prevalence of HHV-6 and -8 was similarly low in both groups. Our data do not support an association of investigated herpesvirus species with destructive periodontal disease. Zusammenfassung Hintergrund: Kürzliche Studien haben angedeutet, dass verschiedene Herpesviren bei der Entstehung und Progression verschiedener Formen der parodontalen Erkrankungen involviert sein könnten. Ziel: Das Ziel der vorliegenden Studie war die Untersuchung einer Präsenz von neuen Herpesviren HHV-6, HHV-7 und HHV-8 in gingivalen Biopsien von Patienten mit chronischer Erwachsenen-Parodontitis. Als Kontrollen dienten gingivale Biopsien von parodontal gesunden Personen. Material und Methoden: Gingivale Biopsien wurden von 23 Freiwilligen, 13 Patienten mit chronischer Erwachsenen-Parodontitis (CAP) und 10 parodontal gesunden Personen gesammelt. Von jedem CAP Patient wurden zwei Biopsien mit Epithel und Bindegewebe von der parodontalen Tasche genommen: eine Biopsie von einer Fläche mit einer Sondierungstiefe (PPD) , 5 mm und positiver Provokationsblutung (geschädigte Fläche) zur Zeit der Biopsieentnahme, die andere Biopsie von einer Fläche mit einer PPD , 3 mm und ohne Provokationsblutung (nicht geschädigte Fläche). Nach der DNA-Extraktion wurde die PCR zur Virusidentifikation benutzt. Ergebnisse: HHV-6 DNA-Sequenzen wurden in einer nicht geschädigten Fläche gefunden (8 %) und bei keiner geschädigten Fläche (0 %) von CAP-Patienten. Eine Biopsie (10 %) bei gesunden Personen war HHV-6 positiv. Gewebeproben von 10/13 CAP Patienten (77 %) und von 7/10 gesunden Personen (70 %) enthielten HHV-7 DNA. Die HHV-7 Prävalenz in geschädigten und nicht geschädigten Flächen von CAP Patienten war 77 % und 54 %. HHV-8 wurde in 7,7 % der CAP Patienten und bei 0 % der gesunden Personen gefunden. Zusammenfassung: Gingivales Gewebe kann als Reservoir für HHV-7 dienen. Eine hohe Prävalenz von HHV-7 wurde sowohl bei parodontal erkrankten als auch bei gesunden Personen gefunden. Das Vorkommen von HHV-6 und HHV-8 war in beiden Gruppen ähnlich. Unsere Daten unterstützen eine Beziehung der untersuchten Herpesviren mit destruierenden parodontalen Erkrankungen nicht. Résumé Des rapports récents ont suggéré que différents virus de l'herpès pouvaient être associés à l'apparition et la progression de différentes formes de la maladie parodontale. Le but de l'étude présente a été d'analyser la présence des virus herpétiques HHV-6, HHV-7 et HHV-8 dans des biopsies gingivales provenant de patients atteints de parodontite chronique de l'adulte. Comme contrôle, des biopsies gingivales de patients sains du point de vue parodontal ont été analysées. Des biopsies gingivales ont été prélevées de 23 volontaires, 13 souffrant de parodontite chronique (CAP) et 10 sains. Chaque patient CAP procuraient deux biopsies comprenant l'épithélium et le tissu conjonctif en face des poches parodontales/sillons : une biopsie provenant d'un site avec une profondeur de poche au sondage (PPD) 5mm et présentant un saignement au sondage (site touché) au moment du prélèvement de la biopsie, l'autre biopsie provenait d'un site avec PPD 3 mm sans saignement au sondage (site sain). Après extraction de l'ADN le PCR a été utilisé pour l'identification des virus herpétiques. Des séquences ADN HHV-6 ont été détectées dans un site sain (8%) mais dans aucun site touché (0%) chez les patients CAP. Une biopsie (10%) chez les sujets sains était HHV-6 positive. Les spécimens tissulaires de dix des treize patients CAP (77%) et sept des dix patients sains (70%) avaient de l'ADNHHV-7. La fréquence globale de HHV-7 dans les sites sains et touchés des patients CAP étaient respectivement de 77 et 54 %. HHV-8 était détecté chez 7,7 % des patients CAP et 0% des patients sains. Le tissu gingival peut servir de réservoir au HHV-7. Une importante fréquence globale de HHV-7 était détectée tant chez les individus sains que chez ceux avec parodontite. La fréquence globale de HHV-6 et HHV-8 était pareillement faible dans les deux groupes. Ces données ne défendent pas la thèse d'une association des virus herpétiques étudiés à la maladie parodontale destructrice. [source] Effects of sub-antimicrobial dose doxycycline therapy on crevicular fluid MMP-8, and gingival tissue MMP-9, TIMP-1 and IL-6 levels in chronic periodontitisJOURNAL OF PERIODONTAL RESEARCH, Issue 1 2004Dong-Hoon Choi Objective:, To investigate whether sub-antimicrobial dose doxycycline (SDD) therapy for 120 d in chronic adult periodontitis patients had significant effects on gingival crevicular fluid (GCF) matrix metalloproteinase-8 (MMP-8) levels, and on gingival tissue MMP-9, tissue inhibitor of matrix metalloproteinases-1 (TIMP-1) and interleukin-6 (IL-6) levels. Background:, Tetracycline can significantly inhibit MMP activity in GCF and in gingival tissue, even in much lower dosage then a traditional antimicrobial dosage used in conventional therapy. Sub-antimicrobial dose doxycycline (SDD) therapy has been shown to reduce periodontal disease activity to control MMP and pro-inflammatory cytokines. Methods:, A total of 32 patients with incipient to moderate (probing pocket depth ,,4,7 mm) chronic adult periodontitis were included in the study. Subjects were randomly assigned to two groups. After scaling and root planning (SRP), the SRP + SDD group received SDD, 20 mg bid, whereas the SRP + placebo group received placebo, 20 mg bid. In the follow-up, efficacy measures included the change in probing pocket depth (PD), clinical attachment level (CAL), bleeding on probing (BOP) and gingival crevicular fluid MMP-8 levels, gingival tissue MMP-9, TIMP-1 and IL-6 levels from baseline to 120 d. Results:, After 120 d, PD and CAL improved significantly in the SRP + SDD group. Initial MMP-8 levels for the SRP + SDD group and the SRP + placebo group were 407.13 ± 114.45 ng/ml and 378.71 ± 189.39 ng/ml, respectively, with no statistical difference between the two groups. MMP-8 levels for the SRP + SDD group and the SRP + placebo group were: 235.35 ± 134.58 ng/ml and 364.04 ± 219.27 ng/ml at 30 d; 157.50 ± 95.95 ng/ml and 236.60 ± 186.16 ng/ml at 60 d; 102.70 ± 67.64 ng/ml and 208.56 ± 124.54 ng/ml at 90 d; and 63.77 ± 53.33 ng/ml and 229.13 ± 168.09 ng/ml at 120 d, respectively. The amount of decrease in MMP-8 levels for the SRP + SDD group was statistically significant compared to that for the SRP + placebo group, especially apparent at 120 d (p < 0.05). TIMP-1 levels in both groups increased from the baseline to 120 d with statistical significance (p -value < 0.05), but there was no significant difference between the two groups. Changes in MMP-9 and IL-6 levels were not statistically significant. Conclusion:, Adjunctive SDD therapy can improve the clinical parameters and this clinical improvement is reflected by controlled level of MMP-8 in chronic adult periodontitis after the therapy. [source] The RprY response regulator of Porphyromonas gingivalisMOLECULAR MICROBIOLOGY, Issue 4 2007Ana E. Duran-Pinedo Summary Porphyromonas gingivalis is a Gram-negative oral anaerobe associated with chronic adult periodontitis. Its ecological niche is the gingival crevice, where the organism adapts to the challenges of the infectious process such as host defence and bacterial products. Bacterial responses to environmental changes are partly regulated by two-component signal transduction systems. Several intact systems were annotated in the genome of P. gingivalis, as well as an orphan regulator encoding a homologue of RprY, a response regulator from Bacteroides fragilis. With the goal of defining the environmental cues that activate RprY in P. gingivalis, we used several strategies to identify its regulon. Results from gene expression and DNA,protein binding assays identified target genes that were either involved in transport functions or associated with oxidative stress, and indicated that RprY can act as an activator and a repressor. RprY positively activated the primary sodium pump, NADH : ubiquinone oxidoreductase (NQR), and RprY protein also interacted with the promoter regions of nqrA genes from B. fragilis and Vibrio cholerae. Given that gingival bleeding and infiltration of host defence cells are symptoms of periodontal infection, iron products released from blood and reactive oxygen species from polymorphonuclear leucocytes may be potential inducers of the RprY regulon. [source] Characterization of two outer membrane protein antigens of Porphyromonas gingivalis that are protective in a murine lesion modelMOLECULAR ORAL MICROBIOLOGY, Issue 1 2004B. C. Ross Porphyromonas gingivalis is a key periodontal pathogen that has been implicated in the aetiology of chronic adult periodontitis. The aim of this study was to characterize two potential vaccine candidates (PG32 and PG33) identified from a previous genomic sequence analysis. Gene knockout studies suggested that these proteins play an important role in bacterial growth and are transcriptionally linked. Analysis of 14 laboratory and clinical isolates of P. gingivalis found that in all strains, both genes were present with a high level of conservation and that the two proteins were also expressed in vitro. Truncated recombinant PG32 and PG33 proteins were produced in Escherichia coli in an attempt to increase the solubility of the proteins while retaining their native conformation. While most of the truncated proteins remained insoluble, two truncated proteins showed good solubility and high levels of protection in the P. gingivalis murine lesion model and may be considered as potential vaccine candidates for further testing in models of human periodontal disease. [source] Lipid peroxidation caused by oxygen radicals from Fusobacterium -stimulated neutrophils as a possible model for the emergence of periodontitisORAL DISEASES, Issue 1 2001M Sheikhi OBJECTIVE: The possible contribution of bacteria and polymorphonuclear neutrophils (PMN) to the disease process of periodontitis was evaluated. DESIGN: Fusobacterium nucleatum has been associated with chronic adult periodontitis. Intracellular production and extracellular release of reactive oxygen species (ROS) by PMN stimulated by fusobacteria were evaluated. To estimate the potential extracellular damage that might be caused by the ROS, the lipid peroxidation (LPO) of an exogenous phospholipid, Intralipid, was assayed. METHODS: The ROS production of PMN was studied by the nitroblue tetrazolium and chemiluminescence tests. The levels of malonaldehyde (MDA) and 4-hydroxyalkenals were used to indicate LPO. RESULTS: Fusobacterium nucleatum strains stimulated neutrophils to produce a large amount of ROS, independently of plasma complement factors. The two strains tested induced considerable intracellular, but no extracellular chemiluminescence responses during the first hour, indicating that ROS were released into phagosomes. However an incubation period of 4 h, in the presence of the extracellular lipid resulted in a high degree of LPO, presumably caused by ROS release from the Fusobacterium -stimulated PMN. ROS production and lipid peroxidation could be counteracted by vitamin E. CONCLUSION: In periodontitis local bacteria might stimulate PMN to release ROS, which cause inflammation and destruction. [source] |