Different Forms Of Periodontitis Research Articles

General immune status and oral microbiology in patients with different forms of periodontitis and healthy control subjects.

ObjectiveImmunological processes in the etiopathogenesis of periodontitis, especially the aggressive form, are not well understood. This study examined clinical as well as systemic immunological and local microbiological features in healthy controls and patients with different forms of periodontitis.Materials and Methods14 healthy subjects, 15 patients diagnosed with aggressive periodontitis, and 11 patients with chronic periodontitis were recruited. Periodontal examination was performed and peripheral blood was collected from each patient. Lymphocyte populations as well as the release of cytokines by T-helper cells were determined by flow cytometry and enzyme linked immunosorbent spot assay. Subgingival plaque samples were taken from each individual and immediately cultivated for microbiological examination.ResultsWhen stimulating peripheral blood mononuclear cells (PBMCs) with lipopolysaccharide, a higher IL-1β release was found in patients with moderate chronic periodontitis compared to the other groups (p<0.01). Numbers of B-cells, naïve and transitional B-cells, memory B-cells, and switched memory B-cells were within the reference range for all groups, but patients with chronic periodontitis showed the highest percentage of memory B-cells without class switch (p = 0.01). The subgingival plaque differed quantitatively as well as qualitatively with a higher number of Gram-negative anaerobic species in periodontitis patients. Prevotella denticola was found more often in patients with aggressive periodontitis (p<0.001) but did not show an association to any of the systemic immunological findings. Porphyromonas gingivalis, which was only found in patients with moderate chronic periodontitis, seems to be associated with an activation of the systemic immune response.ConclusionDifferences between aggressive periodontitis and moderate chronic periodontitis are evident, which raises the question of an inadequate balance between systemic immune response and bacterial infection in aggressive periodontitis.

Microbial signature profiles of periodontally healthy and diseased patients.

To determine microbial profiles that discriminate periodontal health from different forms of periodontal diseases. Subgingival biofilm was obtained from patients with periodontal health (27), gingivitis (11), chronic periodontitis (35) and aggressive periodontitis (24), and analysed for the presence of >250 species/phylotypes using HOMIM. Microbial differences among groups were examined by Mann-Whitney U-test. Regression analyses were performed to determine microbial risk indicators of disease. Putative and potential new periodontal pathogens were more prevalent in subjects with periodontal diseases than periodontal health. Detection of Porphyromonas endodontalis/Porphyromonas spp. (OR 9.5 [1.2-73.1]) and Tannerella forsythia (OR 38.2 [3.2-450.6]), and absence of Neisseria polysaccharea (OR 0.004 [0-0.15]) and Prevotella denticola (OR 0.014 [0-0.49], p < 0.05) were risk indicators of periodontal disease. Presence of Aggregatibacter actinomycetemcomitans (OR 29.4 [3.4-176.5]), Cardiobacterium hominis (OR 14.9 [2.3-98.7]), Peptostreptococcaceae sp. (OR 35.9 [2.7-483.9]), P. alactolyticus (OR 31.3 [2.1-477.2]), and absence of Fretibacterium spp. (OR 0.024 [0.002-0.357]), Fusobacterium naviforme/Fusobacterium nucleatum ss vincentii (OR 0.015 [0.001-0.223]), Granulicatella adiacens/Granulicatella elegans (OR 0.013 [0.001-0.233], p < 0.05) were associated with aggressive periodontitis. There were specific microbial signatures of the subgingival biofilm that were able to distinguish between microbiomes of periodontal health and diseases. Such profiles may be used to establish risk of disease.

The landscape of protein biomarkers proposed for periodontal disease: markers with functional meaning.

Periodontal disease (PD) is characterized by a deregulated inflammatory response which fails to resolve, activating bone resorption. The identification of the proteomes associated with PD has fuelled biomarker proposals; nevertheless, many questions remain. Biomarker selection should favour molecules representing an event which occurs throughout the disease progress. The analysis of proteome results and the information available for each protein, including its functional role, was accomplished using the OralOme database. The integrated analysis of this information ascertains if the suggested proteins reflect the cell and/or molecular mechanisms underlying the different forms of periodontal disease. The evaluation of the proteins present/absent or with very different concentrations in the proteome of each disease state was used for the identification of the mechanisms shared by different PD variants or specific to such state. The information presented is relevant for the adequate design of biomarker panels for PD. Furthermore, it will open new perspectives and help envisage future studies targeted to unveil the functional role of specific proteins and help clarify the deregulation process in the PD inflammatory response.

Prevalence and clinical variety of periodontitis in patients attending dental policlinics in Kazan, Russia

Aim. To determine different periodontal diseases prevalence and distribution in patients attending dental policlinics in Kazan, Russia. Methods. Clinical screening, computed statistical analysis were used as a study methods. 517 medical charts of dental patients (form 043/A) were randomly selected. Different forms of periodontitis were classified according to ICD-10. Results. A high prevalence of periodontal diseases reaching 100% was found among the examined patients who had attended dental policlinics in Kazan, Russia. Chronic (34-89%) and acute (11-44%) apical periodontitis were the most prevalent types of periodontitis in all age groups of patients who had attended dental policlinics. In patients aged 18-39 years acute apical periodontitis was the most common type of periodontitis (11-44%). Conclusion. A high prevalence of periodontal diseases in patients who had attended dental policlinics in Kazan, Russia, was found, with a tendency of chronic periodontitis prevalence to grow, reaching highest levels in elderly patients. Thus, measures for periodontitis prevention and early treatment are vital.

Assessment of transforming growth factor beta one (TGF- β1) immunohistochemical (IHC) expression profile in the gingival tissue of patients with different forms of periodontal diseases

This study evaluate the immunohistochemical expression profile of transforming growth factor beta-1 in inflamed gingival tissue of patients with gingivitis and chronic periodontitis compared to healthy subjects and, determine the correlation between this cytokine and the clinical periodontal parameters, intensity of inflammation and chronic periodontitis severity. Materials and methods: Gingival tissue specimens were taken from 23 chronic periodontitis patients, 20 gingivitis patients and 20 periodontally healthy subjects. The periodontal status was evaluated by dichotomous measurements of the clinical periodontal parameters (PLI, GI, BOP, PPD, CAL). The gingival specimens were fixed immediately in 10% formalin and processed routinely into paraffin blocks for further immunohistochemical analysis. Results: A highly significant statistical difference was observed between the study groups regarding the PLI ,GI ,the percentage of bleeding on probing sites and the intensity of inflammation .TGF-β1 expression profile statistical analysis showed a high statistical significant difference among the study groups , A highly significant statistical difference was found between the PPD Scores while a significant statistical difference was revealed among the CAL Scores when the expression profile of TGF- β1 was compared.TGF-β1 was positively correlated with the clinical periodontal parameters (PLI, GI, and BOP) as well as with the intensity of inflammation in the three study groups. In chronic periodontitis group a highly significant positive linear correlation between the PPD and CAL with the TGF-β1 expression profile. Conclusions: TGF-β1 expression profile showed variations as the destructive character of the periodontal disease changed. Therefore, it could be proposed that TGF-β1 might contribute both to inflammatory regulation and

Periodontal diseases in children and adolescents: a clinician's perspective part 1

Contrasting forms of periodontal disease can affect children and adolescents with varying prevalence, severity and extent, leading to a diverse prognosis in these age groups. For an early diagnosis and treatment of periodontal conditions in young patients, it is essential for the dental practitioner to be able to identify and classify the disease correctly at the earliest opportunity, applying basic principles along with understanding of aetiology and risk factors. The first part of this article discusses the classification, plaque-induced and non-plaque-induced gingival diseases, localized and generalized forms of chronic, as well as aggressive, periodontitis. Knowledge of different forms of periodontal diseases affecting children and adolescents may help to distinguish between different forms of diseases and have value in screening and early diagnosis of the disease.

No association between A. actinomycetemcomitans or P. gingivalis and chronic or aggressive periodontitis diagnosis

Objectives Only a few studies have attempted to detect differences in microbiologic profiles of patients with chronic periodontitis (CP) and aggressive periodontitis (AgP). The aim of this analysis was to assess if clinical diagnosis or other subject factors showed association with the presence of Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis in a cohort of periodontitis patients. Method and materials Statistical analysis for association between bacterial detection and clinical diagnosis was performed on a total of 267 consecutive periodontitis cases diagnosed with either CP (n = 183) or AgP (n = 84). All subjects had microbiologic samples collected from the four deepest pockets and analyzed by nested polymerase chain reaction. Results A actinomycetemcomitans was detected in 54% and 48% of CP and AgP subjects, respectively. A slightly higher detection of P gingivalis was found in CP (67% ) compared with AgP (52%) cases. The detection of P gingivalis was associated with older age (P = .002), less disease severity (P = .015), and IL6-1480 genotypes (P = .026), while A actinomycetemcomitans was associated with IL6-1480 genotypes (P = .001). Conclusion Detection of known periodontopathogenic bacteria is not able to discriminate different forms of periodontitis.

The Micronucleus Test to Evaluate Cytogenetic Damage in Patients with Periodontitis

Background and aims. The role of genetic factors and oxidative damage in the etiopathogenesis of periodontal disease is well documented in the literature. The micronucleus test is a sensitive method that indicates DNA damage. The aim of the present study was to investigate the micronuclei frequency in different forms of periodontitis in comparison with healthy controls. Materials and methods. Micronuclei frequency was analyzed in the peripheral lymphocytes of 10 patients with chronic periodontitis (CP), 10 patients with generalized aggressive periodontitis (GAP) and 10 healthy controls. Various clinical parameters like the probing depth, clinical attachment level, and percentages of sites with bleeding and plaque were recorded. After the slides were processed, they were stained with 5% Geimsa solution and 1000 cells per sample were counted for the presence of micronuclei. Results. The mean micronuclei observed in the control group, CP group, and GAP group were 9.8, 10.1 and 9.9, respectively. The differences between the groups were not significant (P=0.978). Conclusion. The results indicated that the cytogenetic damages in the periodontitis groups were not different from those in the control group. The role of cytogenetic damage in peripheral blood cells may have a limited prognostic value in the etiopathogenesis of periodontal tissues and further studies are necessary to assess cytogenetic damage in periodontal tissues to clarify local tissue destruction in periodontal disease.

Periodontitis and Periodontal Drug Delivery Systems: A Review

Periodontitis is a common disease involving supportive structures of the teeth in all groups, ethnicities, races and both genders. Targeting to periodontal pocket has made an important contribution to treat periodontitis, but has yet to fully achieve its potential for better treating the periodontal diseases. This review highlights the stages of diseases, etiology and different forms of periodontal diseases for better understanding. This article then proceeds to cover the periodontal probes, systemic medications and local therapy. Additionally, we focus on the recent advancements of local drug delivery for treating periodontal diseases. Keywords: Periodontitis, teeth, periodontal probes, systemic medication, local therapy, drug delivery, Periodontal disease, gingivitis, Prepubertal Periodontitis, Juvenile Periodontitis

Genetic polymorphism of Fcγ-receptors IIa, IIIa and IIIb in South Indian patients with generalized aggressive periodontitis

Recent evidence suggests that polymorphisms in Fcγ receptors are associated with different forms of periodontitis. However, the FcγR genotypes and their allele frequency differ among subjects from different ethnic backgrounds. The aim of the present study was to determine whether specific FcγRIIa, FcγRIIIa, and FcγRIIIb alleles and/or genotypes are associated with susceptibility to generalized aggressive periodontitits (GAgP) in a South Indian population. Buccal scrapings were obtained from 60 subjects with GAgP and 60 periodontally healthy individuals, and DNA was extracted from each of the samples. FcγRIIa and FcγRIIIa genotyping was performed by polymerase chain reaction (PCR) amplification of DNA with allele-specific primers followed by allele-specific restriction digestion of the products, whereas FcγRIIIb genotyping was done by allele-specific PCR. There was no significant difference in the distribution of the FcγRIIa H/R genotype between GAgP patients and healthy subjects, although significant over-representation of the R allele was noted in GAgP patients. With regard to FcγRIIIa F/V genetic polymorphism, the homozygous V/V genotype and V allele were significantly over-represented in the GAgP group, whereas the F/F genotype and F allele were over-represented in the controls. Furthermore, there was significant over-representation of the FcγRIIIb-NA2 allele and NA2/NA2 genotype in GAgP patients, and of the NA1/NA1 genotype and NA1 allele in the controls. These data suggest that the FcγRIIIa V/V genotype and/or V allele, as well as the FcγRIIIb NA2/NA2 and/or NA2 allele, along with the FcγRIIa- R allele, may be risk factors for GAgP in the population of South India.

N-3 Fatty Acid Intake and Periodontal Disease

Gingivitis and periodontitis are inflammatory diseases characterized by bleeding gums, gum recession, formation of deep pockets between the gum and tooth, and loss of the periodontal ligaments and alveolar bone structure that support the teeth in the jaw. The prevalence and severity of the different forms of periodontal disease vary considerably in the US adult population. Gingival bleeding, the mildest and most readily reversible form, is found in 54% of men and 46% of women age 30 years and older ( 1 Albandar J.M. Kingman A. Gingival recession, gingival bleeding, and dental calculus in adults 30 years of age and older in the United States, 1988-1994. J Periodontol. 1999; 70: 30-43 Google Scholar ). More advanced disease affects a smaller proportion of the population. Overall, approximately 10% of adults have moderate or severe periodontitis, with prevalence increasing from 5% in people age 35 to 49 years to 11% in those age 50 to 64 years, and to 20% in the population age 75 years and older ( 2 Dye B.A. Tan S. Smith V. Lewis B.G. Barker L.K. Thornton-Evans G. Eke P.I. Beltrán-Aguilar E.D. Horowitz A.M. Li C.H. Trends in oral health status: United States, 1988-1994 and 1999-2004National Center for Health Statistics. Vital Health Stat 11. 2007; Apr; : 1-92 Google Scholar ). E. K. Kaye is a professor, Boston University Henry M. Goldman School of Dental Medicine, Boston, MA

Low prevalence of subgingival viruses in periodontitis patients

Viruses such as Human Cytomegalovirus (HCMV) and Epstein-Barr virus (EBV) have been proposed to be periodontal pathogens. The aim of this study was to analyse the presence of herpesvirus DNA in subgingival plaque samples of patients with different forms of periodontitis and in healthy periodontia. A total of 140 ethnically mixed (prevalently Caucasian) subjects took part in the study. Sixteen were affected by localized aggressive periodontitis (LAgP), 64 by generalized aggressive periodontitis (GAgP), 20 by chronic periodontitis (CP) and 40 were periodontally healthy. Polymerase chain reaction (PCR) analyses were performed to detect HCMV and EBV. Sera were tested for anti-HCMV and EBV IgG antibodies. PCRs for herpes simplex (HSV) and varicella zoster virus (VZV) were performed in subgingival samples from a subset of 20 AgP subjects. HCMV DNA was not detected in any plaque samples. EBV DNA was detected in four LAgP (25%), two GAgP (3%) subjects and four healthy individuals (10%). HSV DNA and VZV DNA were not detected in the subset of studied individuals. This study challenges the previously reported high prevalence of herpesvirus DNA in subgingival samples from periodontitis patients and so questions whether they act as pathogens in such patients.

Bacteroides gingivalis-specific serum IgG and IgA subclass antibodies in periodontal diseases

The level of serum IgM, IgG and IgA antibodies including IgG1, IgG2, IgG3, IgG4, IgA1 and IgA2 subclass-specific antibodies to Bacteroides (Porphyromonas) gingivalis fimbriae and to lipopolysaccharide (LPS) were analysed in patients with different forms of periodontal disease (PD) and control subjects by ELISA. Among PD subjects, sera obtained from adult periodontitis (AP), rapidly progressive periodontitis (RPP) and gingivitis contained high titres of fimbriae-specific IgG antibodies (7500-15,000 ELISA units) followed by IgA (90-700 units) and IgM (30-90 units). In contrast, sera from localized juvenile periodontitis (LJP) subjects exhibited much lower titres of fimbriae-specific IgG (89 +/- 11 units), IgA (31 +/- 5 units) and IgM (17 +/- 3 units) antibodies. A similar response pattern was also seen in sera from normal subjects aged 35-41 years who practice normal oral hygiene, while sera of younger adults (aged 18-24) with superior hygiene did not have any antigen-specific antibodies. Analysis of IgG subclass anti-fimbriae responses revealed that the major response was IgG3 followed by IgG1, IgG2 and IgG4 in AP, RPP and gingivitis. Although lower, a similar pattern of IgG subclass titre was seen in LJP and normal subjects aged 35-41 years. When IgA subclass responses were measured in AP and RPP, higher titres of the fimbriae-specific response were noted with IgA1 when compared with IgA2. However, lower but approximately equal levels of fimbriae-specific IgA1 and IgA2 titres were seen in other PD groups. When anti-B. gingivalis LPS-specific responses were measured, the sera of AP patients contained high levels of IgG antibodies (2265 +/- 224 units) followed by IgA (411 +/- 90 units) and IgM (214 +/- 56 units). Further, IgG anti-LPS responses were mainly IgG2 followed by IgG4, IgG3 and IgG1. For IgA subclass responses, higher titres of anti-LPS-specific antibodies were noted in IgA2 subclass over IgA1. These results showed that higher anti-B. gingivalis antibody responses occur in PD when compared with healthy individuals and protein and lipid-carbohydrate antigens of B. gingivalis induce distinct patterns of antigen-specific IgG and IgA subclass responses.

Expression of suppressors of cytokine signaling in diseased periodontal tissues: a stop signal for disease progression?

Inflammatory cytokines are thought to trigger periodontal tissue destruction. In addition to being regulated by anti-inflammatory mediators, their activity is under the control of suppressors of cytokine signaling (SOCS), which down-regulate the signal transduction as part of an inhibitory feedback loop. We therefore investigated the expression of SOCS-1, -2 and -3, and the cytokines tumor necrosis factor-alpha (TNF-alpha) and interleukin-10, in different forms of human periodontal diseases. Quantitative polymerase chain reaction (RealTime-PCR) was performed with mRNA from gingival biopsies of control subjects and from that of patients with chronic gingivitis and chronic periodontitis. Our results show that patients with chronic gingivitis and chronic periodontitis exhibit significantly higher SOCS-1, -2 and -3, TNF-alpha and interleukin-10 mRNA expression when compared with healthy controls. The data also demonstrate that SOCS-1 and -3 mRNA expression was higher in tissue from patients with chronic gingivitis than chronic periodontitis, while the levels of SOCS-2, TNF-alpha and interleukin-10 mRNA were similar in these groups. The increased expression of SOCS-1, -2 and -3 mRNA in diseased periodontal tissues is believed to be involved in the down-regulation of inflammatory cytokine and Toll-like receptor signaling, and therefore in the attenuation of both the inflammatory reaction and disease severity. Furthermore, it is possible that variation in the levels of SOCS mRNA expressed in different forms of periodontal diseases may determine the stable or progressive nature of the lesions.

Distribution of FcγRIIa and FcγRIIIb Genotypes in Patients With Generalized Aggressive Periodontitis.

Polymorphisms in FcγR have been associated with different forms of periodontitis. This study determined the frequency of FcγRIIa and FcγRIIIb alleles/genotypes in patients with generalized aggressive periodontitis (GAgP). Thirty-one GAgP and 49 periodontally healthy Brazilian subjects participated in the study. Full-mouth periodontal examinations were carried out, and mouthwash samples were collected for human DNA isolation. FcγR genotyping was performed by polymerase chain reaction and hybridization with allele-specific oligonucleotide probes. Significant differences between groups were sought by Mann-Whitney, χ2 , and Fisher exact tests and configural frequency analysis. FcγRIIa-H131 (53.8%) and FcγRIIIb-NA1 (75%) were the most prevalent alleles in this sample population. A significant overrepresentation of FcγRIIIb-NA2 was observed in the GAgP group, whereas FcγRIIIb-NA1 was detected more often in healthy individuals (odds ratio, 32.5; 95% confidence interval [CI], 10.6 to 99.8; P <0.001). No significant differences in the distribution of the FcγRIIa genotypes were observed between the groups. The prevalence of FcγRIIIb-NA2/NA2 was higher in GAgP patients, whereas FcγRIIIb-NA1/NA1 was predominant in the healthy group (χ2 = 45.1; P <0.001). The combination of the genotypes FcγRIIIb-NA2/NA2 plus FcγRIIa-H/H131 was observed more frequently in GAgP subjects than expected from marginal frequencies (χ2 = 12.5; P <0.001). The data suggest that the FcγRIIIb-NA2 allele and/or FcγRIIIb-NA2/NA2 genotype and the composite genotype FcγRIIIb-NA2/NA2 plus FcγRIIa-H/H131 may be associated with GAgP, whereas FcγRIIIb-NA1 and/or FcγRIIIb-NA1/NA1 may be related to periodontal health in this sample of the Brazilian population.

Gingival crevicular fluid transforming growth factor-β 1 in several forms of periodontal disease

Transforming growth factor-beta(1) (TGF-beta(1)) has significant effects on periodontal host response regulation. Limited knowledge on the role of TGF-beta(1) in various periodontal disease types and particularly in advanced periodontitis forms warranted the present study. The aim of the present study was to evaluate the gingival crevicular fluid (GCF) TGF-beta(1) levels in patients with different forms of periodontal disease. GCF TGF-beta(1) levels were investigated in 32 chronic periodontitis (CP), 30 generalized aggressive periodontitis (G-AgP), 15 gingivitis patients and 16 periodontally healthy subjects. Periodontal status was evaluated by measuring probing depth, clinical attachment loss, plaque and bleeding on probing. TGF-beta(1) levels were analyzed by enzyme-linked immunosorbent assay. The results were expressed in terms of total amount (pg) and concentration (pg/microl). G-AgP and CP groups had significantly elevated GCF TGF-beta(1) total amount compared to healthy group (p<0.008). Moreover, GCF TGF-beta(1) total amount of G-AgP group was significantly higher than that of gingivitis group (p<0.008). G-AgP and CP groups had similar GCF TGF-beta(1) total amount (p>0.008). Significant correlation was found between GCF TGF-beta(1) total amount and all clinical periodontal parameters (p<0.05). The results of the present study suggest contribution of TGF-beta(1) to the pathogenesis of advanced chronic and aggressive periodontitis. TGF-beta(1) may thus be one of the components modulating exaggerated host response together with other major mediators of inflammation.

Low prevalence of interleukin L-1A -899 and IL-1B +3954 genetic polymorphism found in a Thai population group

Original Article Anusaksathien O, Sukboon A, Sitthiphong P, Teanpaisan R. Distribution of interleukin-1beta(+3954) and IL-1alpha(-889) genetic variations in a Thai population group. J Periodontol. 2003 Dec;74(12):1796-802. Level of Evidence 4 Purpose To determine the distribution of IL-1A -899 and IL-1B +3954 genotypes in different forms of periodontal disease in a group of Thai subjects Source of Funding Prince of Songkla University Grant Type of Study/Design Case-control study

Microbiological basis for periodontal therapy

The search for the etiologic agents of periodontal diseases started in the Golden Era of medical bacteriology, when the etiologic agents of many bacterial infections were isolated and characterized. After the initial enthusiasm in establishing the infectious nature and the true agents of periodontal diseases, this concept was virtually ignored for the next four decades. Until the early 1970s treatment regimens based on the non-specific plaque hypothesis were directed towards a non-specific reduction in plaque amount. Later, the specific plaque hypothesis established the role of some microorganisms such as A. actinomycetemcomitans, P. gingivalis, T. forsythensis, T. denticola, P. intermedia and F. nucleatum in different forms of periodontal diseases. It was recently suggested that these suspected periodontal pathogens seem to not act alone and interactions between species, especially the balance between pathogenic and beneficial species affect both progression of disease and response of tissues to periodontal therapy. Nowadays it is well established that one of the goals of therapy is to control such periodontal pathogens. Among the most commonly used therapies to treat periodontal infections are scaling and root planing (SRP), supragingival plaque control and periodontal surgeries. Many studies confirmed the reduction of "red complex" species by SRP, and apically repositioned flap can lead to an additional beneficial effect in the subgingival microbiota by decreasing levels of "red" and "orange complexes" species. Furthermore, the level of plaque control maintained by the patients has been considered a crucial step in preventing recurrence of destructive periodontitis.

Immunoglobulin G profiles in different forms of periodontitis.

Races and Gm(23) allotypes can modify the serum levels of IgG subclasses. The average serum levels of IgG subclasses of African-Americans have been reported to be higher than those of Caucasians in both healthy young adults and patients with aggressive periodontitis; Gm(23)-positive subjects generally had higher IgG2 levels than Gm(23)-negative subjects. We examined serum immunoglobulin G (IgG) concentrations in Taiwanese patients with different forms of periodontitis. The serum levels of four IgG subclasses were determined by enzyme-linked immunosorbent assay and Gm(23) allotypes were verified by radial immunodiffusion tests in 50 patients with chronic periodontitis, 30 patients with aggressive periodontitis, and 74 healthy controls. There were no differences in the concentrations of four IgG subclasses in patients with chronic periodontitis compared with age-matched controls. However, in subjects younger than 35 years, levels of IgG2 were significantly elevated in patients with aggressive periodontitis compared with controls. We also found significant differences in IgG2 levels within the control group when stratified by age (< or = 35 years and > 35 years). Gm(23) allotypes were not correlated with the serum levels of IgG2 in either patient group. Microbial challenge might not provoke significant changes in systemic IgG response in patients with chronic periodontitis. However, in patients with aggressive periodontitis, IgG2 levels were increased when compared with age-matched controls. Gm(23) allotypes had no influence on IgG2 levels in well-established generalized chronic periodontitis or aggressive periodontitis.

HHV-6, HHV-7, HHV-8 in gingival biopsies from chronic adult periodontitis patients. A case-control study.

Recent reports have suggested that various herpesviruses may be involved in the occurrence and progression of different forms of periodontal disease. 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. 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) > or =5 mm and presenting with bleeding upon probing (affected site) at the time of biopsy collection, and the other biopsy from a site with PPD< or =3 mm and without bleeding on probing (nonaffected site). After DNA extraction, nested PCR was used in herpesvirus identification. 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. 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.