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Aggressive Periodontitis (aggressive + periodontitis)
Kinds of Aggressive Periodontitis Terms modified by Aggressive Periodontitis Selected AbstractsComments on: M. Zigmond et al. (2006) The Outcome of a Preventive Dental Care Programme on the Prevalence of Localized Aggressive Periodontitis in Down's Syndrome (DS) Individuals (Journal of Intellectual Disability Research, 50(7), pp.JOURNAL OF INTELLECTUAL DISABILITY RESEARCH, Issue 1 2008[source] Aggressive periodontitis is likely influenced by a few small effect genesJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 6 2009Flavia M. De Carvalho Abstract Aim: To evaluate the inheritance mode of aggressive periodontitis in a collection of families with a similar geographic origin. Materials and Methods: Segregation analysis was performed in pedigree data from 74 families by the use of the SEGREG program of SAGE v.5.4.2. Homogeneous no transmission, homogeneous Mendelian transmission, homogeneous general transmission, semi-general transmission and heterogeneous general transmission models were tested assuming the prevalence of aggressive periodontitis as 1% and no deviations from Hardy,Weinberg equilibrium. The parameters of the model were estimated by the method of maximum likelihood, which provides the overall ln (likelihood), -2ln and the AIC (Akaike's score) for each model. The likelihood ratio test (LRT) was used to compare each model against a fully general model (p>0.05). Results: The most parsimonious mode of inheritance was the semi-general transmission model that allows the heterozygote transmission probability to vary. Conclusion: This result provides strong support for the hypothesis that genetic factors play a role in aggressive periodontitis and that a few loci, each with relatively small effects, contribute to aggressive periodontitis, with or without interaction with environmental factors. [source] Gene expression signatures in chronic and aggressive periodontitis: a pilot studyEUROPEAN JOURNAL OF ORAL SCIENCES, Issue 3 2004Panos N. Papapanou This pilot study examined gene expression signatures in pathological gingival tissues of subjects with chronic or aggressive periodontitis, and explored whether new subclasses of periodontitis can be identified based on gene expression profiles. A total of 14 patients, seven with chronic and seven with aggressive periodontitis, were examined with respect to clinical periodontal status, composition of subgingival bacterial plaque assessed by checkerboard hybridizations, and levels of serum IgG antibodies to periodontal bacteria assayed by checkerboard immunoblotting. In addition, at least two pathological pockets/patient were biopsied, processed for RNA extraction, amplification and labeling, and used to study gene expression using Affymetrix U-133 A arrays. Based on a total of 35 microarrays, no significantly different gene expression profiles appeared to emerge between chronic and aggressive periodontitis. However, a de novo grouping of the 14 subjects into two fairly robust clusters was possible based on similarities in gene expression. These two groups had similar clinical periodontal status and subgingival bacterial profiles, but differed significantly with respect to serum IgG levels against the important periodontal pathogens Porphyromonas gingivalis, Tannerella forsythensis and Campylobacter rectus. These early data point to the usefulness of gene expression profiling techniques in the identification of subclasses of periodontitis with common pathobiology. [source] Aggressive periodontitis is likely influenced by a few small effect genesJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 6 2009Flavia M. De Carvalho Abstract Aim: To evaluate the inheritance mode of aggressive periodontitis in a collection of families with a similar geographic origin. Materials and Methods: Segregation analysis was performed in pedigree data from 74 families by the use of the SEGREG program of SAGE v.5.4.2. Homogeneous no transmission, homogeneous Mendelian transmission, homogeneous general transmission, semi-general transmission and heterogeneous general transmission models were tested assuming the prevalence of aggressive periodontitis as 1% and no deviations from Hardy,Weinberg equilibrium. The parameters of the model were estimated by the method of maximum likelihood, which provides the overall ln (likelihood), -2ln and the AIC (Akaike's score) for each model. The likelihood ratio test (LRT) was used to compare each model against a fully general model (p>0.05). Results: The most parsimonious mode of inheritance was the semi-general transmission model that allows the heterozygote transmission probability to vary. Conclusion: This result provides strong support for the hypothesis that genetic factors play a role in aggressive periodontitis and that a few loci, each with relatively small effects, contribute to aggressive periodontitis, with or without interaction with environmental factors. [source] TLR4 and IL-18 gene variants in aggressive periodontitisJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 12 2008Barbara Noack Abstract Aim: We aimed to assess the association of different genotypes with increased aggressive periodontitis susceptibility by studying functional relevant variants in the pathogen-recognition receptor Toll-like receptor 4 (TLR4) and variants in the promoter region of the pro-inflammatory cytokine interleukin-18 (IL-18). Material and Methods: One hundred and eleven patients with aggressive periodontitis and 80 periodontally healthy controls were genotyped for four functional variants in the TLR4 gene (c.896A>G and c.1196C>T) and in the IL-18 promoter (c.,368G>C and c.,838C>A). The genotype and allele frequencies, as well as the frequency of combined genotypes were compared between study groups. Results: There were no statistical differences in genotype and allele frequencies within the four variants between the groups. All study subjects were further classified into carriers and non-carriers of at least one variant of both genes. The logistic regression analysis adjusted for gender and smoking showed no association between carrier status of at least one variant of both genes and periodontal status (OR=1.41, 95% CI: 0.43,4.70). Conclusions: Our results reject the hypothesis that functionally relevant IL-18 and TLR4 gene mutations have a major effect on aggressive periodontitis susceptibility alone or in combination. [source] Association between interleukin-6 promoter haplotypes and aggressive periodontitisJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 3 2008Luigi Nibali Abstract Background: Interleukin-6 (IL-6) polymorphisms have been shown to affect IL-6 promoter activity. This study investigated the possible role of IL-6 genetic polymorphisms and haplotypes in the predisposition to aggressive periodontitis (AgP). Material and Methods: A case,control association study on 224 AgP patients and 231 healthy controls was performed in order to detect differences in genotype distributions of five single nucleotide polymorphisms (SNPs) located in the promoter region of the IL-6 gene. Results: The IL-6 ,1363 polymorphism was associated with a diagnosis of AgP in subjects of all ethnicities (p=0.006, adjusted logistic regression). The ,1480 SNP was associated with LAgP in subjects of all ethnicities (p=0.003). The ,1480 and ,6106 polymorphisms were associated with Localized AgP in Caucasians (n=24) (p=0.007 and 0.010, respectively). Haplotypes determined by the ,1363 and ,1480 polymorphisms were also associated with LAgP (p=0.001) in Caucasians. Conclusions: This study supports the hypothesis of a link between IL-6 genetic factors and AgP and highlights the importance of two IL-6 polymorphisms (,1363 and ,1480) in modulating disease phenotype and susceptibility. [source] Incomplete adherence to an adjunctive systemic antibiotic regimen decreases clinical outcomes in generalized aggressive periodontitis patients: a pilot retrospective studyJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 10 2007Adrian Guerrero Abstract Aim: The objective of this study was to explore the effect of incomplete adherence to the prescribed antibiotic regimen, amoxicillin and metronidazole, in the non-surgical treatment of generalized aggressive periodontitis (GAP). Methods: This retrospective study included 18 GAP subjects who received a conventional course of full-mouth non-surgical periodontal treatment using machine-driven and hand instruments and an adjunctive course of systemic antibiotics (500 mg amoxicillin and 500 mg metronidazole three times a day for 7 days). Clinical parameters were collected at baseline and at 2 months post-treatment. Self-reported adherence to the prescribed medication regimen was recorded at 2 months. Results: All clinical parameters, except for the mean clinical attachment level (CAL) in sites with initial probing pocket depth (PPD) 3 mm, improved at 2 months in all subjects. PPD reduction was 3.7 mm [95% confidence interval (CI) 3.2, 4.3 mm] in deep pockets (7 mm) and 2.2 mm (95% CI 1.9, 2.4 mm) in moderate pockets (4,6 mm), while CAL gain was 2.2 mm (95% CI 1.7, 2.6 mm) and 1.2 mm (95% CI 0.8, 1.5 mm), respectively. However, only 11 subjects (61.1%) reported full adherence to the medication. In deep pockets (7 mm), the difference between an adherent and non-adherent/partially adherent subject was 0.9 mm (95% CI 0.1, 1.7 mm, ancova, p=0.027) in PPD reduction and 0.8 mm (95% CI ,0.2, 1.9, p=0.129) in CAL gain at 2 months. In moderate pockets (4,6 mm) this difference was smaller in magnitude: 0.4 mm (95% CI 0.1, 0.9 mm, p=0.036) in PPD reduction and 0.2 mm (95% CI ,0.3, 0.9 mm, p=0.332) in CAL gain. Conclusions: Within the limits of this design, these data suggest that incomplete adherence to a 7-day adjunctive course of systemic metronidazole and amoxicillin is associated with decreased clinical outcomes in subjects with generalized aggressive periodontitis. [source] Single-nucleotide polymorphisms in the IL-4 and IL-13 promoter region in aggressive periodontitisJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 6 2007J. R. Gonzales Abstract Introduction: IL-4 and IL-13 polymorphisms have been shown to influence the susceptibility to systemic diseases. In this study, possible associations between the IL-4 ,590 C,T, IL-4 ,34 C,T, IL-13 ,1112 C,T and IL-13 ,1512 A,C promoter polymorphisms were investigated in subjects with generalized aggressive periodontitis (AgP) compared with healthy individuals. Material and Methods: Fifty-eight patients with diagnosis of generalized AgP and 51 matched healthy controls participated in the study. Blood samples were collected and DNA isolated. Molecular analyses were performed by PCR-RFLP in a blind fashion. Genotype and allele frequencies among study groups were compared using Fisher's exact test (, value: 0.05). Pearson's ,2 test was used for analysis of Hardy,Weinberg equilibrium. Results: The frequency of the IL-4 ,590 T/T and IL-4 ,34 T/T genotypes differed significantly between groups (p=0.05, 0.02, respectively), although the allele frequencies were similar. There was a higher frequency of the IL-4 ,590 T/T and IL-4 ,34 T/T genotypes in patients with AgP compared with controls. The genotype and allele frequencies of the IL-13 polymorphisms did not differ between groups. Conclusions: This study demonstrated an association between the IL-4 ,590 T/T and IL-4 ,34 T/T genotypes and AgP. Further research is necessary to prove if there is an association of these polymorphisms with AgP, and if the polymorphisms have a functional effect. [source] Gingival crevicular fluid levels of RANKL and OPG in periodontal diseases: implications of their relative ratioJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 5 2007Nagihan Bostanci Abstract Aim: Receptor activator of NF-,B ligand (RANKL) and osteoprotegerin (OPG) are a system of molecules that regulate bone resorption. This study aims to compare the levels of RANKL, OPG and their relative ratio in gingival crevicular fluid (GCF) of healthy and periodontal disease subjects. Material and Methods: GCF was obtained from healthy (n=21), gingivitis (n=22), chronic periodontitis (n=28), generalized aggressive periodontitis (n=25) and chronic periodontitis subjects under immunosuppressant therapy (n=11). RANKL and OPG concentrations in GCF were measured by enzyme-linked immunosorbent assays. Results: RANKL levels were low in health and gingivitis groups, but increased in all three forms of periodontitis. OPG levels were higher in health than all three periodontitis, or gingivitis groups. There were no differences in RANKL and OPG levels between chronic and generalized aggressive periodontitis groups, whereas these were lower in the immunosuppressed chronic periodontitis group. The RANKL/OPG ratio was significantly elevated in all three periodontitis forms, compared with health or gingivitis, and positively correlated to probing pocket depth and clinical attachment level. Conclusion: GCF RANKL and OPG levels were oppositely regulated in periodontitis, but not gingivitis, resulting in an enhanced RANKL/OPG ratio. This ratio was similar in all three periodontitis groups and may therefore predict disease occurrence. [source] Gene polymorphisms of tissue plasminogen activator and plasminogen activator inhibitor-1 in Turkish patients with generalized aggressive periodontitisJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 4 2007Gülnur Emingil Abstract Aim: Tissue plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1) have important roles in proteolytic events in periodontitis. The aim of this study was to investigate TPA and PAI-1 gene polymorphisms in relation to susceptibility to generalized aggressive periodontitis (G-AgP). Methods: Genomic DNA was obtained from peripheral blood of 90 G-AgP patients and 154 periodontally healthy subjects. 4G/5G polymorphism in the promoter region of the PAI-1 gene and Alu-repeat insertion/deletion (I/D) polymorphism in intron 8 of the TPA gene were genotyped by polymerase chain reaction and endonuclease digestion. Results: The genotype distributions of TPA and PAI-1 genes were similar between G-AgP and healthy subjects (p>0.05). The distribution of TPA genotypes in G-AgP patients was 33.4% D/D, 44.4% I/D, and 22.2% I/I and was 26.3% D/D, 40.4% I/D, and 33.3% I/I in healthy subjects. The D allele was 55.6% in G-AgP and 46.6% in healthy subjects. There was a significant difference among study groups in D allele frequencies (p=0.044). The PAI-1 genotype distribution in G-AgP was 29.1% 4G/4G, 43.0% 4G/5G, and 27.9% 5G/5G, while it was 35.7% 4G/4G, 43.8% 4G/5G, and 20.5% 5G/5G in healthy subjects. Conclusion: These data suggest that the D polymorphic allele of TPA gene polymorphism could be associated with susceptibility to G-AgP in Turkish subjects. [source] Gingival crevicular fluid laminin-5 ,2-chain levels in periodontal diseaseJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 7 2006Gülnur Emingil Abstract Aim: Our study aimed to examine the molecular forms and gingival crevicular fluid (GCF) levels of laminin-5 ,2-chain in patients with different periodontal disease, and compare the effects of P.gingivalis trypsin-like proteinase on intact laminin-5 ,2-chain species. Methods: Eighteen patients with generalized aggressive periodontitis (G-AgP), 29 patients with chronic periodontitis (CP), 20 with gingivitis and 20 periodontally healthy subjects were included. Probing depth, clinical attachment loss, presence of bleeding on probing and plaque were recorded. Molecular forms and GCF laminin-5 ,2-chain levels and the effects of P. gingivalis trypsin-like proteinase on intact laminin-5 ,2-chain were analysed by computer-quantitated Western immunoblotting. Results: Laminin-5 ,2-chain 40 and 70 kDa fragments could be detected in all groups, in varying levels. The CP group had elevated GCF laminin-5 ,2-chain fragment levels compared with the gingivitis and healthy groups (p<0.008). The G-AgP group had GCF laminin-5 ,2-chain fragment levels similar to the gingivitis and healthy groups (p>0.008). GCF laminin-5 ,2-chain fragments differed clearly from the multiple lower molecular size fragments of P.gingivalis trypsin-laminin-5 ,2-chain proteinases. Conclusion: Increased GCF laminin-5 ,2-chain fragments in periodontitis sites with deep periodontal pocket suggest that these cleaved 40 and 70 kDa fragments could reflect the extent of the inflammatory reaction in CP. [source] Clinical and microbiological effects of different antimicrobials on generalized aggressive periodontitisJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 4 2006Christiana Xajigeorgiou Abstract Aim: To evaluate and compare the effects of adjunctive metronidazole plus amoxicillin, doxycycline and metronidazole on clinical and microbiological parameters in patients with generalized aggressive periodontitis. Material and Methods: Forty-three patients participated in this randomized clinical trial divided into four groups. Six weeks after scaling and root planning (SRP), groups 1,3 received adjunctive metronidazole, plus amoxicillin, doxycycline and metronidazole respectively, and group 4 acted as controls. Clinical recordings concerning probing depth, probing attachment level and bleeding on probing were performed at baseline, 6 weeks after SRP and 6 months from baseline. Subgingival samples were analysed using the ,checkerboard' DNA,DNA hybridization for Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans, Tannerella forsythia and Treponema denticola. Results: All treatments resulted in improvement of clinical parameters (ANOVA p>0.05). Systemic administration of metronidazole plus amoxicillin or metronidazole resulted in statistically significant greater reduction of the proportion of sites > 6mm than SRP (z -test, p<0.05). These antimicrobials yielded a significant effect on levels of important periodontal pathogens for 6 months. Conclusion: Adjunctive metronidazole plus amoxicillin or metronidazole alone (when A.actinomycetemcomitans is not involved) is effective in deep pockets of aggressive periodontitis patients. [source] Modulation of clinical expression of plaque-induced gingivitis: response in aggressive periodontitis subjectsJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 2 2006Leonardo Trombelli Abstract Aim: The aim of this study was to characterize the gingival inflammatory response to de novo plaque accumulation in subjects treated for aggressive periodontitis (AP). The gingival inflammatory response of the AP subjects was retrospectively compared with that of periodontally healthy individuals (PH) matched for exposure to plaque and of periodontally healthy subjects previously identified as "high responders" (HR) and "low responders" (LR). Materials and Methods: 13 AP subjects and 26 matched PH subjects participated in a 21-day experimental gingivitis trial. Plaque index (PlI), Gingival index (GI), gingival crevicular fluid volume (GCF) and angulated bleeding score (AngBS) were recorded at days 0, 7, 14 and 21. Cumulative plaque exposure (CPE), i.e. PlI over time, was also calculated. Results: GCF was significantly higher in AP compared with PH group at each observation interval (p0.001). In addition, GCF was significantly higher in AP group compared with either LR or HR groups at each observation interval (p<0.001). Conclusions: These results suggest that susceptibility to gingival inflammation in response to de novo plaque accumulation may be related to susceptibility to periodontitis. [source] Adjunctive benefits of systemic amoxicillin and metronidazole in non-surgical treatment of generalized aggressive periodontitis: a randomized placebo-controlled clinical trialJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 10 2005Adrian Guerrero Abstract Background: The objective of this study was to assess the adjunctive clinical effect of the administration of systemic amoxicillin and metronidazole in the non-surgical treatment of generalized aggressive periodontitis (GAP). Methods: Forty-one systemically healthy subjects with GAP were included in this 6-month double-blind, placebo-controlled, randomized clinical trial. Patients received a course of full-mouth non-surgical periodontal treatment delivered over a 24 h period using machine-driven and hand instruments. Test subjects received an adjunctive course of systemic antibiotic consisting of 500 mg amoxicillin and 500 mg metronidazole three times a day for 7 days. Clinical parameters were collected at baseline, and at 2 and 6 months post-treatment. Results: In both the test and the placebo groups, all clinical parameters improved at 2 and 6 months. In deep pockets (7 mm), the test treatment resulted in an additional 1.4 mm (95% confidence interval 0.8, 2.0 mm) in full-mouth probing pocket depth (PPD) reduction and 1 mm (0.7, 1.3 mm) of life cumulative attachment loss (LCAL) gain at 6 months. In moderate pockets (4,6 mm), the adjunctive benefit was smaller in magnitude: PPD reduction was 0.4 mm (0.1, 0.7 mm) and LCAL gain was 0.5 mm (0.2, 0.8 mm). In addition, the 6-month data showed LCAL gains 2 mm at 25% of sites in test patients compared with 16% in placebo (p=0.028). Similarly, PPD reductions of 2 mm or more were observed in 30% of sites in test and 21% of sites in placebo patients. Seventy-four percent of pockets with PPD 5 mm at baseline were 4 mm or shallower at 6 months in the test group. This compared with 54% in the placebo group (p=0.008). Disease progression at 6 months was observed at 1.5% of test and 3.3% of sites in test and placebo, respectively (p=0.072). Conclusions: These data indicate that a 7-day adjunctive course of systemic metronidazole and amoxicillin significantly improved the short-term clinical outcomes of full-mouth non-surgical periodontal debridement in subjects with GAP. [source] Periodontal dressing (Vocopac®) influences outcomes in a two-step treatment procedureJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 4 2005B. W. Sigusch Abstract Objectives: It is not clear if periodontal dressing influences the long-term results in a non-surgical treatment procedure. Material and Methods: The periodontal parameters (pre-baseline) of 36 patients with aggressive periodontitis were obtained before the patients were treated initially (1st step) by a dental hygienist, who completely removed the supra- and subgingival concrements. Baseline parameters were raised 3 weeks after the 1st step, before the 2nd therapy step was conducted. It consisted of a non-surgical procedure, which comprised a closed full-mouth manual root curettage (root planing), immediate systemic application of metronidazole, and the placement of a periodontal dressing (Vocopac®, Voco). The patients were randomized to two test groups having their periodontal packs removed after 3,4 days (group 1, n=12) and 7,8 days (group 2, n=12), respectively and a control group (n=12) without periodontal dressing. Clinical parameters were raised again after 6 and 24 months. Results: Six and 24 months later, changes in probing pocket depth (PPD) and probing attachment level (PAL) were observed in all three groups compared with baseline, but the difference was significant in group 2 only. In addition, group 2 showed a greater reduction in mean PPD and also a significantly greater gain of attachment in comparison with the controls. Conclusion: Wound dressing has a positive effect on clinical long-term results using a two-step non-surgical procedure. Moreover, removing the dressing after 7,8 days leads to clearly better results than removing it earlier. [source] Five-year maintenance follow-up of early-onset periodontitis patientsJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 6 2003Joanna J. Kamma Abstract Objectives: The purpose of this study was to evaluate the clinical and microbiological status of patients with early-onset or aggressive periodontitis (EOP) who had received supportive periodontal care (SPC) every 3,6 months for a period of 5 years, following active periodontal treatment. Material & Methods: The study population consisted of 25 individuals with early-onset periodontitis. Clinical examination and recordings of probing pocket depth (PPD) and clinical attachment level (CAL) were performed at baseline prior to treatment (T0), 3 months following the termination of active periodontal treatment (T1) and annually at the SPC appointments (T2,T3,T4,T5). Microbiological samples were obtained at the 5-year SPC (T5). Subgingival plaque samples for each individual were collected from one deep pocket (>5 mm), based on pretreatment measurements, randomly selected in each quadrant. The levels of Actinobacillus actinomycetemcomitans, Bacteroides forsythus, Porphyromonas gingivalis and Treponema denticola were determined using oligonucleotide probe hybridization. Results: During the 5-year period, the mean of SPC/patient was 12.7 sessions. A significant improvement was observed in PPD, CAL, gingival bleeding index and suppuration following treatment. However, between T1 and T5, 134 sites in 20 patients deteriorated with a CAL loss of,2 mm. Out of these 134 sites showing disease progression, microbial samples were randomly obtained in 13 sites (9.7%) from 8 patients. Among other factors, smoking and stress were found to have significant predictive value on the future attachment loss. P. gingivalis, T. denticola and total bacterial load were statistically significantly higher in patients who experienced disease progression during the 5-year maintenance period. Conclusions: For most EOP patients, regular SPC was effective in maintaining clinical and microbiological improvements attained after active periodontal therapy. However, a small percentage of sites was identified as progressive in 20 patients. Variables found to be related to periodontal progression were the presence of as well as the high bacterial counts of P. gingivalis, T. denticola and total bacterial load, number of acute episodes, number of teeth lost, smoking and stress. Zusammenfassung Erhaltungstherapie über fünf Jahre bei Patienten mit früh einsetzender Parodontitis (EOP) Ziele: Der Zweck dieser Studie war es, 5 Jahre nach aktiver Parodontalbehandlung den klinischen und mikrobiologischen Zustand von Patienten mit früh einsetzender oder aggressiver Parodontitis (EOP), bei welchen alle 3-6 Monate eine parodontale Erhaltungstherapie (SPC) erfolgte, zu evaluieren. Material & Methoden: Die Studienpopulation bestand aus 25 Individuen mit früh einsetzender Parodontitis. Die klinische Untersuchung und Aufzeichnung der Sondierungstiefe (PPD) sowie des klinischen Attachmentniveaus (CAL) erfolgten bei der Eingangsuntersuchung vor der Behandlung (T0), drei Monate nach Beendigung der aktiven Parodontalbehandlung (T1) und jährlich bei den SPC-Terminen (T2,T3,T4,T5). Die mikrobiologischen Proben wurden bei der 5-Jahres-SPC gewonnen (T5). Für jedes Individuum wurden die subgingivalen Plaqueproben in jedem Quadranten aus einer tiefen Tasche (>5mm) entnommen. Dies geschah randomisiert und auf der Grundlage der Messungen vor der Behandlung. Das Niveau von Actinobacillus actinomycetemcomitans, Bacteroides forsythus, Porphyromonas gingivalis und Treponema denticola wurden unter Verwendung der Hybridisierung mit Oligonukleotid-Sonden bestimmt. Ergebnisse: Während der 5-jährigen Periode betrug die mittlere Anzahl der SPC-Sitzungen pro Patient 12,7. Nach der Behandlung wurden bei PPD, CAL, Gingiva-Blutungs-Index und der Pusentleerung signifikante Verbesserungen beobachtet. Jedoch haben sich zwischen T1 und T5 bei 20 Patienten 134 Taschen mit einem CAL-Verlust von=2mm verschlechtert. Bei 8 Patienten wurden aus diesen 134 Taschen, mit Progression der Erkrankung, von 13 Taschen (9,7%) randomisiert mikrobiologische Proben entnommen. Innerhalb anderer Faktoren wurde bei Rauchen und Stress ein signifikanter Vorhersagewert für zukünftigen Attachmentverlust vorgefunden. Bei den Patienten, die in der 5-jährigen Erhaltungsperiode eine Progression der Erkrankung erfuhren lagen P. gingivalis, T. denticola und die bakterielle Gesamtbelastung höher. Schlussfolgerungen: Für die meisten EOP-Patienten die regelmäßig an der parodontalen Erhaltungstherapie teilnahmen war diese hinsichtlich der Aufrechterhaltung der nach der aktiven Parodontaltherapie erzielten klinischen und mikrobiologischen Verbesserungen erfolgreich. Jedoch wurde bei 20 Patienten ein geringer Prozentsatz von Taschen als fortschreitend identifiziert. Die Variablen, von denen gefunden wurde, dass sie eine Beziehung zur Progression haben waren: sowohl Vorhandensein von P. gingivalis, T. denticola als auch hohe Bakterienzahl von P. gingivalis, T. denticola und die bakterielle Gesamtbelastung, Anzahl der akuten Episoden, Anzahl verlorener Zähne, Rauchen und Stress. Résumé Suivi en maintenance sur 5 ans de patients atteints de parodontites d'apparition précoce. Objectifs: Cette étude se propose d'évaluer l'état clinique et microbiologique de patients atteints de parodontites d'apparition précoce ou agressive (EOP) qui furent suivis en maintenance (SPC) tous les 3-6 mois pendant une période de 5 ans après un traitement parodontal actif. Matériel & Méthodes: La population étudiée consistait en 25 individus atteints de parodontites d'apparition précoce. L'examen clinique et l'enregistrement des profondeurs de poche (PPD) et du niveau d'attache (CAL) furent réalisés avant le traitement (T0), 3 mois après la fin du traitement actif (T1) et chaque année aux rendez vous de maintenance (T2,T3,T4,T5). Des échantillons microbiologiques furent prélevés lors de la maintenance à 5 ans (T5). La plaque sous-gingivale de chaque patient fut prélevée d'une poche profonde (>5mm), sur la base des examens initiaux, choisis au hasard dans chaque quadrant. Les niveaux d' Actinobacillus actinomycetemcomitans, Bacteroides forsythus, Porphyromonas gingivalis et Treponema denticola furent déterminés par hybridation par sonde d'oligonucleotides. Résultats: pendant la période d'examination de 5 ans, la moyenne des SPC par patient fut de 12.7 sessions. Une amélioration significative fut observée pour PPD, CAL, l'indice de saignement gingival et la suppuration suite au traitement. Cependant, entre T1 et T5, 134 sites chez 20 patients connurent une détérioration avec une perte d'attache de 2 mm. De ces 134 sites qui présentaient une progression de la maladie, des échantillons microbiologiques furent obtenus aléatoirement dans 13 sites (9.7%) chez 8 patients. Parmi d'autres facteurs, le tabagisme et le stress furent reconnus comme ayant une significative valeur prédictive pour de futures pertes d'attache. P. gingivalis, T. denticola et la charge bactérienne totale étaient de façon statistiquement significatif plus importants chez les patients chez qui la maladie progressait au cours des 5 ans de maintenance. Conclusions: pour la plupart des patients atteints d' EOP, des soins parodontaux de soutien réguliers sont efficaces pour maintenir les améliorations cliniques et microbiologiques obtenus par le traitement actif. Cependant, un petit pourcentage de sites progressait chez 20 patients. Les variables en ralation avec cette progression étaient la présence et aussi un comptage important de P. gingivalis, T. denticola et la charge bactérienne totale, le nombre d'épisodes aigus le nombre de dents perdues le tabagisme et le stress. [source] Systemic medications: clinical significance in periodonticsJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 2002Sebastian G. Ciancio Abstract Systemic medications are of value as adjuncts to periodontal therapy. These medications can be divided into two major categories: antibiotics and agents for host modulation. Antibiotics have been shown to be valuable adjuncts in specialized types of periodontal disease, such as localized and generalized aggressive periodontitis, and of possible value in severe chronic periodontitis. Antibiotics have been studied individually, in combination and in sequential therapy. Host modulators include Periostat, non-steroidal anti-inflammatory agents, alendronate (Fosamax), hormone replacement therapy and anti-arthritic medications. These agents produce their beneficial effects by a variety of mechanisms of action, including inhibition of matrix metalloproteinases, inhibition of prostaglandin production, stimulation of osteoblasts, inhibition of osteoclasts, and other anti-inflammatory mechanisms of action. [source] The presence of local and circulating autoreactive B cells in patients with advanced periodontitisJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 4 2002Tord Berglundh Abstract Aim: The aim of the present investigation was to study the local (gingival) and systemic occurrence of autoreactive B cells (CD5+CD19 positive) in subjects with a high or low susceptibility to periodontitis. Material and Methods: 2 groups of subjects (Group A and B) susceptible to periodontitis were included. Group A consisted of 22 adult patients (7 females and 15 males, aged 24,66 years) with advanced and generalized chronic periodontitis and group B comprised 7 children (4 girls and 3 boys aged 9,13 years) with localized aggressive periodontitis. 26 periodontally healthy subjects, Group C (aged 23,80 years, mean 49.6±16.3), were also recruited. Assessment of clinical and radiographical characteristics of periodontal disease was performed. Gingival biopsies and peripheral blood samples were obtained and prepared for immunohistochemical analysis. Blood samples only were obtained from the periodontally healthy subjects (group C). Results: The proportion of autoreactive B cells (CD5+CD19 positive) of peripheral blood lymphocytes was about 6 times higher in group A and 4 times higher in group B than in the samples from the control subjects (group C). About 40,50% of the B cells in the peripheral blood of the periodontitis susceptible individuals expressed markers for autoreactive features while less than 15% of the circulating B cells in the subjects of group C exhibited such markers. The periodontitis lesion in the adult periodontitis patients contained a substantial number of B cells out of which about 30% demonstrated autoreactive features. Conclusion: It is suggested that both circulating and local B cells in periodontitis susceptible individuals have a higher propensity to autoreactive properties than B cells of patients with a low susceptibility to periodontitis. Zusammenfassung Zielsetzungen: Untersuchung des lokalen (in der Gingiva) und systemischen Vorkommens autoreaktiver B-Zellen (CD5 und CD19 positiv) bei Individuen mit hoher und niedriger Anfälligkeit für Parodontitis. Material und Methoden: 2 Gruppen von Personen, die anfällig für Parodontitis waren, nahmen an der Studie teil: Gruppe A: 22 erwachsenen Patienten (im Alter von 24,66 Jahren; 7 weiblich) mit fortgeschrittener generalisierter chronischer Parodontitis; Gruppe B: 7 Kinder (9,13 Jahre; 4 Mädchen) mit lokalisierter aggressiver Parodontitis. Zusätzlich wurden 26 parodontal gesunde Personen (23,80 Jahre) untersucht. Klinische und röntgenologische parodontale Parameter wurden erhoben. In den Gruppen A und B, wurden Gingivabiopsien und periphere Blutproben, in Gruppe C nur Blutproben entnommen. Ergebnisse: Der Anteil autoreaktiver B-Zellen an den Lymphozyten im peripheren Blut war etwa 6 mal höher in gruppe A und 4 mal höher in Gruppe B als in Proben der Kontrollgruppe (Gruppe C). Etwa 40,50% der B-Zellen im peripheren Blut der für Parodontitis anfälligen Patienten exprimierten Marker für autoreaktive Eigenschaften während weniger als 15% der zirkulierenden B-Zellen der Individuen aus Gruppe C solche Marker aufwiesen. Die parodontalen Läsionen der erwachsenen Parodontitispatienten enthielten eine hohe Zahl von B-Zellen, von denen etwa 30% autoreaktive Eigenschaften aufwiesen. Schlussfolgerungen: Sowhol lokale als auch zirkulierende B-Zellen von für Parodontitis anfälligen Patienten zeigen mit größerer Häufigkeit autoreaktive Eigenschaften als die B-Zellen von Patienten mit geringer Parodontitisanfälligkeit. Résumé But: Le but de cette recherche était d'étudier la présence locale (gingivale) et systémique de cellules B auto réactives (CD5+CD19 positives) chez des sujets présentant une forte ou une faible susceptibilitéà la parodontite. Matériaux et méthodes: 2 groupes de sujet (A et B) susceptible à la parodontite furent inclus. Le groupe A était constitué de 22 patients adultes (7 femmes et 15 hommes âgés de 24 a 66 ans) présentant une parodontite chronique avancée et généralisée et le groupe B était constitué de 7 enfants (4 filles et 3 garçons ages de 9 à 13 ans) présentant une pardontite agressive localisée. 26 sujets sains d'un point de vue parodontal (groupe C, âgés de 23 à 80 ans, age moyen 49.6±16.3) furent également recrutés. L'observation des caractéristiques cliniques et radiographiques de la maladie parodontale fut réalisée. Des biopsies gingivales et des échantillons sanguins furent prélevées et préparées pour des analyses immunohistochemiques. Seuls des prélèvements sanguins furent pris sur le groupe des patients sains. Résultats: La proportion de cellules B auto réactives (CD5+CD19 positives) des lymphocytes du sang périphérique était 6× plus élevée dans le groupe A et 4× plus élevée dans le groupe B que chez les sujets contrôles du groupe C. Environ 40 a 50% des cellules B du sang périphérique des individus susceptibles à la parodontite exprimaient des marqueurs pour des caractéristiques auto réactives alors que moins de 15% des cellules B circulantes des sujets du groupe C présentaient de tels marqueurs. La lésion parodontale de patients atteints de parodontite de l'adulte contenait un nombre substantiel de cellule B parmi lesquels environ 30% présentaient des caractéristiques auto réactives. Conclusions: Cela suggère que les cellules B locales et circulantes des individus susceptibles à la maladie parodontale aient une puls grande propension aux propriétés auto réactives que les cellules B des patients ayant une susceptibilité faible à la parodontite. [source] The outcome of a preventive dental care programme on the prevalence of localized aggressive periodontitis in Down's syndrome individualsJOURNAL OF INTELLECTUAL DISABILITY RESEARCH, Issue 7 2006M. Zigmond Abstract Background Periodontal disease in Down's syndrome (DS) individuals develops earlier and is more rapid and extensive than in age-matched normal individuals. The present study evaluated a group of DS patients, who had been participating in a 10-year preventive dental programme, for the impact of the programme on their periodontal status. Methods Thirty DS patients (mean age 23.3 ± 4 years) were compared with 28 age-matched healthy controls (mean age 22.8 ± 5 years). The hygiene level, gingival condition and periodontal status (periodontal probing depth, clinical attachment level and radiographic alveolar bone loss) were determined. Results In spite of similar oral hygiene and gingival measures, DS patients, as opposed to the control ones, had a severe periodontal disease. The prevalence, extent and severity of periodontitis in the DS group were significantly greater than in the control group. The teeth most commonly and severely affected were the lower central incisors and the upper first molars. DS patients lost significantly more teeth due to periodontitis. Conclusions The clinical and radiographic picture found in the present DS group is characteristic of localized aggressive periodontitis. Within the limitations of this study, it seems that the preventive dental programme had no effect on periodontal destruction progression of localized aggressive periodontitis in DS individuals and that impaired oral hygiene plays a relatively minor role in the pathogenesis of this disease. Future controlled studies are needed to assess the effectiveness of different preventive dental programmes in preventing the progression of periodontitis in DS patients. [source] Neutrophils in chronic and aggressive periodontitis in interaction with Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitansJOURNAL OF PERIODONTAL RESEARCH, Issue 3 2009A. Guentsch Background and Objective:, This study analyzed the interaction of Porphyromonas gingivalis ATCC 33277 and Aggregatibacter actinomycetemcomitans Y4 with peripheral blood polymorphonuclear neutrophils taken from patients with aggressive periodontitis and chronic periodontitis. Material and Methods:, Peripheral blood polymorphonuclear neutrophils obtained from 12 patients with chronic periodontitis, six patients with aggressive periodontitis and 12 healthy controls were exposed to P. gingivalis and A. actinomycetemcomitans following opsonization of the bacteria using the patient's own serum. Serum immunoglobulin G (IgG) levels against both periodontopathogens were measured. Phagocytosis and killing of the bacteria, as well as the extracellular human neutrophil elastase activity, were quantified. The total amount and the extracellular release of reactive oxygen species were measured using luminol-dependent and isoluminol-dependent chemiluminescence. Results:, Polymorphonuclear neutrophils from patients with chronic (62.16 ± 19.39%) and aggressive (43.26 ± 26.63%) periodontitis phagocytosed more P. gingivalis than the healthy controls (24.43 ± 19.87%) at the 30-min time point after exposure to the bacteria (p < 0.05). High serum IgG levels against P. gingivalis and A. actinomycetemcomitans were detected in subjects with periodontitis. Polymorphonuclear neutrophils from subjects with chronic and aggressive periodontitis released significantly more reactive oxygen species and demonstrated greater human neutrophil elastase activity in the absence of any stimulus than polymorphonuclear neutrophils from healthy controls (p < 0.05). Polymorphonuclear neutrophils in chronic periodontitis released significantly more reactive oxygen species when exposed to P. gingivalis and A. actinomycetemcomitans than polymorphonuclear neutrophils in aggressive periodontitis. Conclusion:, High serum IgG levels against P. gingivalis and A. actinomycetemcomitans promote phagocytosis in periodontitis. The extracellular release of reactive oxygen species and neutrophil elastase by polymorphonuclear neutrophils may also contribute to damage of the surrounding periodontal tissues. [source] E-selectin and L-selectin polymorphisms in patients with periodontitisJOURNAL OF PERIODONTAL RESEARCH, Issue 1 2009B. Houshmand Background amd Objective:, Periodontitis is a multifactorial disease in which environmental and genetic determinant factors contribute to individual subject's susceptibility. A DNA polymorphism in the regulating region of adhesion molecule genes is suggested to modulate the molecule's physiological effects. The aim of this study was to investigate the genetic association between the E-selectin Ser128Arg and L-selectin Phe206Leu polymorphisms and periodontitis. Material and Methods:, DNA was isolated from the whole blood of 88 patients with periodontitis and 139 healthy individuals. All samples were genotyped for the E-selectin Ser128Arg and L-selectin Phe206Leu polymorphisms using the polymerase chain reaction with sequence specific primers. Results:, Our findings revealed a significant difference in the Ser128Arg polymorphism of E-selectin, but not in the L-selectin polymorphism, between periodontal patients and controls. The 128Arg allele was present more frequently in patients than in healthy individuals (31.25% vs. 12.2%, p < 0.0001). In addition, there was an association between the presence of the 128Arg allele and periodontitis (odds ratio 2.9; 95% confidence interval: 1.75,4.4, p < 0.0001). No significant association was found between the polymorphisms tested and the subgroups of periodontal disease (i.e. chronic periodontitis and aggressive periodontitis). Conclusion:, The findings of this study showed that the Ser128Arg polymorphism of E-selectin might contribute to the susceptibility of Iranian individuals to periodontitis. [source] Expression of metalloproteinases and their tissue inhibitors in inflamed gingival biopsiesJOURNAL OF PERIODONTAL RESEARCH, Issue 5 2008L. D. R. Gonçalves Objectives:, Matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs) are known to be involved in the periodontal disease process. Results of in vivo MMPs and TIMPs gene expressions in the gingiva, though, are still controversial. In the present study, we compared the gene expression of MMP-1, -2, -9, -13 and TIMP-1, -2 in healthy and inflamed gingiva. Methods:, 38 gingival samples were collected from gingivitis (n = 10), advanced chronic periodontitis (n = 10), generalized aggressive periodontitis (n = 8) and periodontally healthy individuals (n = 10). Total RNA isolated from those samples was subjected to reverse transcription followed by amplification by polymerase chain reaction (RT-PCR). Products were visualized in agarose gels and quantified by optical densitometry. Samples were also processed for gelatin zymography and Western blotting for MMP-2 and MMP-9 in order to assess for post-transcriptional MMP regulation at the protein level. Results:, The frequencies and levels of transcripts encoding MMPs and TIMPs were found to be not significantly different among groups (p > 0.05, Fisher's Exact and Kruskall-Wallis tests). There is a trend towards higher MMP-2 and -9 gelatinase activities in the inflamed samples, although not statistically significant. In contrast, zymography and Western blotting studies show that MMP-2 is virtually absent in the chronic periodontitis group. Conclusion:, These results could reflect a complex regulation of MMPs and TIMPs' gene expression in the course of gingival inflammation. They also reveal a great biological diversity even among individuals with similar periodontal status. [source] Quantitative analysis of association between herpesviruses and bacterial pathogens in periodontitisJOURNAL OF PERIODONTAL RESEARCH, Issue 3 2008I. Saygun Background and Objective:, The development of human periodontitis may depend upon cooperative interactions among herpesviruses, specific pathogenic bacteria and tissue-destructive inflammatory mediators. This study sought to identify associations among human cytomegalovirus, Epstein,Barr virus and six putative periodontopathic bacteria in periodontitis lesions. Material and Methods:, Fifteen periodontitis patients (nine with aggressive periodontitis and six with chronic periodontitis) and 15 periodontally normal subjects were included in the study. In each study subject, a microbiological sample was collected, using a curette, from the deepest periodontal probing depth of the dentition. A real-time TaqMan® polymerase chain reaction assay was employed to determine the subgingival counts of human cytomegalovirus, Epstein,Barr virus, Porphyromonas gingivalis, Tannerella forsythia, Prevotella intermedia, Aggregatibacter actinomycetemcomitans, Fusobacterium nucleatum and Campylobacter rectus. Statistical analysis was performed using the Student's t -test, the Pearson correlation coefficient test and the single variable logistic regression test for odds ratio-based risk calculation. Results:, Human cytomegalovirus was detected in eight periodontitis lesions and in one normal periodontal site, Epstein,Barr virus was detected in nine periodontitis lesions and in two normal periodontal sites, and the study bacteria were detected in 6,15 periodontitis lesions and in 1,11 normal periodontal sites. Correlations were found between counts of human cytomegalovirus and Epstein,Barr virus, between counts of human cytomegalovirus and P. gingivalis, T. forsythia and C. rectus, and between counts of Epstein,Barr virus and P. gingivalis and T. forsythia. Human cytomegalovirus and Epstein,Barr virus counts were also positively associated with the level of periodontal attachment loss, probing pocket depth and gingival bleeding on probing. Conclusion:, This study confirmed that periodontal human cytomegalovirus and Epstein,Barr virus are associated with major periodontopathic bacteria and with the severity of periodontal disease. The finding of abundant herpesviruses in periodontitis lesions redefines the pathogenic paradigm of the disease. Understanding the interplay between herpesviruses and specific bacterial species in the pathogenesis of periodontitis may form the basis for new approaches to preventing, reducing or delaying tissue breakdown from periodontal infections. [source] Association of vitamin D receptor gene polymorphisms in Chinese patients with generalized aggressive periodontitisJOURNAL OF PERIODONTAL RESEARCH, Issue 3 2008S. Li Background and Objective:, The clinical features suggest that genetic factors may have a strong influence on susceptibility to aggressive periodontitis. The aim of this study was to investigate the association of vitamin D receptor gene polymorphisms with generalized aggressive periodontitis in Chinese patients. Material and Methods:, A restriction fragment length polymorphism (RFLP) for 10,438,141 C to T (rs1544410, BsmI), 10,382,063 A to G (rs731236, TaqI), 10,382,143 C to A (rs7975232, ApaI) and 10,416,201 A to G (rs2228570, FokI) of vitamin D receptor gene was analysed by polymerase chain reaction, followed by digestion with restriction enzymes and gel electrophoresis. The genotypes of 51 generalized aggressive periodontitis patients and 53 periodontally healthy control subjects were analysed. The genotypic and allelic frequencies of each polymorphism site for the patients and control subjects were compared. Results:, The distribution of vitamin D receptor FokI genotypes and alleles between the two groups was significantly different (p = 0.043 and p = 0.012, respectively). The F allele seemed to increase the susceptibility of aggressive periodontitis (odds ratio = 2.02, 95% confidence interval = 1.16,3.50) in Chinese patients. There was no significant difference in the genotype distribution or the allele frequencies of vitamin D receptor BsmI, ApaI and TaqI between two groups. Conclusion:, The study indicates that FokI polymorphism of vitamin D receptor gene might be associated with generalized aggressive periodontitis in Chinese patients. In addition, the carriage of F allele increases the risk of developing generalized aggressive periodontitis. [source] Differential platelet-activating factor synthesis by monocytes and polymorphonuclear leukocytes from subjects with localized aggressive periodontitisJOURNAL OF PERIODONTAL RESEARCH, Issue 3 2007C. R. Shin Background and Objective:, Platelet-activating factor is elevated in localized aggressive periodontitis. We previously demonstrated that the elevated level of platelet-activating factor in localized aggressive periodontitis is at least partially attributable to low levels of platelet-activating factor acetylhydrolase, the enzyme that catabolizes platelet-activating factor. The objective of this study was to determine if platelet-activating factor synthesis was also elevated in localized aggressive periodontitis. To test this, platelet-activating factor synthesis was quantified in the monocytes and polymorphonuclear neutrophils of periodontally healthy patients and of subjects with localized aggressive periodontitis. Material and Methods:, Cells were labeled with [3H]acetate and treated with vehicle or stimulated with calcium ionophore A23187. Platelet-activating factor was extracted and quantified by scintillation counting. Results:, For both subject groups, resting monocytes and polymorphonuclear neutrophils produced platelet-activating factor, and calcium ionophore A23187 stimulated platelet-activating factor production in both cell types. However, calcium ionophore A23187-activated monocytes from subjects with localized aggressive periodontitis produced less platelet-activating factor than did activated periodontally healthy monocytes (p < 0.0001), suggesting an aberrant calcium ionophore A23187 response in monocytes from subjects with localized aggressive periodontitis. Indeed, when the data were expressed as fold induction of platelet-activating factor synthesis in response to calcium ionophore A23187, monocytes from subjects with localized aggressive periodontitis exhibited only a fourfold increase in platelet-activating factor synthesis, whereas calcium ionophore A23187-stimulated monocytes from periodontally healthy, chronic periodontitis and generalized aggressive periodontitis subjects produced ,,12 times more platelet-activating factor than did resting monocytes. In contrast, both resting and activated localized aggressive periodontitis polymorphonuclear neutrophils synthesized more platelet-activating factor than did periodontally healthy polymorphonuclear neutrophils. Conclusion:, These data suggest that high levels of platelet-activating factor in subjects with localized aggressive periodontitis result from both increased synthesis and reduced catabolism. While localized aggressive periodontitis polymorphonuclear neutrophils contribute to increased platelet-activating factor mass through synthesis, the contribution of monocytes is probably the result of reduced catabolism by platelet-activating factor acetylhydrolase. [source] Real-time polymerase chain reaction quantification of Epstein,Barr virus in chronic periodontitis patientsJOURNAL OF PERIODONTAL RESEARCH, Issue 4 2005Antonis Konstantinidis Background:, Although herpes viruses have been implicated in the pathogenesis of chronic and aggressive periodontitis, few data in the literature refer to quantification of these viruses in periodontal sites, especially in relation to serological findings. Objective:, The aim of the present study was to compare Epstein,Barr virus (EBV) DNA load in subgingival specimens from chronic periodontitis patients and in periodontally healthy subjects, in relation to serologic testing of IgM and IgG antibodies to EBV. Methods:, A total of 22 chronic periodontitis patients and 13 controls participated in the present study. Seventy-nine subgingival specimens (one pooled, one from a deep and one from a shallow site), sampled with paper points, were analysed with real-time polymerase chain reaction for EBV. Subjects were also examined for anti-EBV IgG and IgM levels in serum, using an enzyme-linked immunosorbent assay. Results:, One subject was seronegative for EBV. Three subjects (one patient and two controls) displayed anti-EBV IgM. Their data were excluded from further analysis. All three displayed EBV in their subgingival samples. Nine out of the remaining 20 chronic periodontitis patients and 10 out of 11 controls did not display EBV subgingivally. A statistically significant difference in viral load was observed between pooled and shallow-pocket samples from periodontitis patients but not between samples from deep and shallow pockets (Kruskall,Wallis anova, Dunn's multiple comparisons test). Conclusions:, Data from the present study do not strongly support the pathogenetic significance of EBV in chronic periodontitis lesions. The data do, however, suggest that parallel serological assessments provide a useful insight into the association of viruses with periodontal disease. [source] Three case reports of aggressive periodontitis associated with Porphyromonas gingivalis in younger patientsJOURNAL OF PERIODONTAL RESEARCH, Issue 5 2002Isao Ishikawa The terms ,early onset periodontitis' (EOP) and ,juvenile periodontitis' (JP) were replaced by that of ,aggressive periodontitis' in a recent international workshop for the classification of periodontal diseases and conditions. The chief etiologic agent for aggressive periodontitis is considered to be Actinobacillus actinomycetemcomitans in localized juvenile periodontitis. Porphyromonas gingivalis is also mentioned as the etiologic agent of the aggressive periodontitis, although to date its role remains questionable. This communication describes three cases of aggressive periodontitis found to be associated with P. gingivalis but not A. actinomycetemcomitans by polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA). Our findings clarify the role of P. gingivalis as an etiologic agent in this type of periodontitis and confirm its inclusion in the current definition of aggressive periodontitis. [source] Salivary IgA subclasses and bacteria-reactive IgA in patients with aggressive periodontitisJOURNAL OF PERIODONTAL RESEARCH, Issue 5 2002S. Hägewald The local salivary immunoglobulin A (IgA) response in patients with aggressive periodontitis to oral microorganisms and its role for the pathogenesis has not been determined. This study investigated the hypothesis that aggressive periodontitis patients have impaired oral secretory immunity. Our test group was made-up of 19 aggressive periodontitis patients and 19 age- and gender-matched periodontally healthy controls. Total IgA, IgA subclass 1, IgA subclass 2 and IgA reactive to Actinobacillus actinomycetemcomitans Y4, Treponema denticola ATCC 35404 and Candida albicans DSM 3454 were determined by enzyme-linked immunosorbent assay in whole unstimulated and stimulated saliva. A statistically significantly lower concentration and secretion rate of total salivary IgA (P < 0.01) and IgA1 (P < 0.001) was found in the aggressive periodontitis group in resting and stimulated saliva. A decrease of IgA2 (P < 0.05) was seen in resting saliva. Although only minor differences were detected in the concentration and secretion of bacteria-reactive IgA in both groups, the proportion of bacteria-reactive IgA from the total IgA was significantly higher (P < 0.01) in the aggressive periodontitis group in all three microorganisms tested. Our results indicate an inhibition of total secretory IgA. In particular an IgA subclass 1-specific decrease in aggressive periodontitis was noted, while the bacteria-reactive humoral immune system in saliva was activated. The role of the decrease of IgA1 immunoglobulins in aggressive periodontitis with respect to susceptibility for periodontal diseases has to be elucidated. [source] Epidemiologic patterns of chronic and aggressive periodontitisPERIODONTOLOGY 2000, Issue 1 2010Ryan T. Demmer First page of article [source] Histopathological features of chronic and aggressive periodontitisPERIODONTOLOGY 2000, Issue 1 2010Michael Smith First page of article [source] | ||||||||||