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PubMed2006

The short vitamin D receptor is associated with increased risk for generalized aggressive periodontitis.

BACKGROUND: Generalized aggressive periodontitis (GAP) exhibits severe inflammation and alveolar bone loss. Vitamin D receptor (VDR) regulates both bone metabolism and inflammation-related genes, and its polymorphisms and haplotypes may affect the functional activity of the VDR protein in GAP. OBJECTIVE: We analysed the genetic effect of VDR start codon, intron, and exon polymorphisms, and their haplotypes on the development of GAP. MATERIALS AND METHODS: The VDR start codon 27823C > T (rs2228570, FokI), intron 8 60890G > A (rs154410, BsmI), and exon 9 61968T > C (rs731236, TaqI) polymorphisms were determined by using the polymerase chain reaction-restriction fragment length polymorphism analysis among 93 GAP patients and 143 healthy controls. RESULTS: The VDR start codon 27823*C/*C genotype was associated with an increased risk for GAP [odds ratio (OR) = 1.83, p = 0.028], but the intron 8 60880G > A and exon 9 61968T > C polymorphisms were not associated with GAP. The VDR haplotype homozygote ht1(C-G-T) carrying 27823*C allele was associated with a 1.8-fold increased risk of GAP (OR = 1.84, p = 0.030). CONCLUSION: These results demonstrate that the short VDR (27823*C/*C) protein may influence GAP susceptibility.

Adenine↗
PubMed2005

CD38 expression in neutrophils from patients with localized aggressive periodontitis.

BACKGROUND: Localized aggressive periodontitis (LAgP) is associated with neutrophil dysfunction including decreased chemotaxis and reduced calcium entry. It has been suggested that CD38 is involved in chemotaxis. Little is known, however, about the relationship of CD38 and LAgP patients. In this study, we focused on the level of CD38 expression between LAgP and normal subjects and examined the involvement of CD38 in abnormal neutrophil chemotaxis of LAgP patients. METHODS: Neutrophils from 12 normal subjects and 12 LAgP patients were isolated from peripheral venous blood. Membrane associated proteins were extracted from cells with or without N-formylmethionine leucyl-phenylalanine (fMLP) stimulation. CD38 expression was measured using Western blotting. Band density was measured using an imaging densitometer. RESULTS: There was no statistical difference between normal subjects and LAgP patients in resting CD38 expression (basal level). However, the fMLP-stimulated neutrophils exhibited a significant decrease of CD38 expression in LAgP subjects compared to normal subjects. The decrease of CD38 was positively correlated with the defect in chemotactic migration to fMLP. CONCLUSION: These data suggest that the lower expression of CD38 in neutrophils may be related to altered neutrophil function in LAgP.

ADP-ribosyl Cyclase 1↗
PubMed2006

Subgingival microbiota of periodontally untreated Mexican subjects with generalized aggressive periodontitis.

BACKGROUND AND AIM: Specific microbial profiles that may distinguish between generalized aggressive-periodontitis (GAgP) and generalized chronic-periodontitis (GCP) have, to date, not been described. The purpose of the present study was to describe the subgingival microbial composition of Mexican subjects with GAgP and compare it with that of individuals with GCP and periodontal health (PH). MATERIAL AND METHODS: Seventy-seven subjects with GAgP (n=19), GCP (n=39) and PH (n=19) were selected. Clinical measurements included plaque accumulation, gingival erythema, bleeding on probing, suppuration, pocket depth and attachment level. Up to 28 subgingival plaque samples were obtained from each subject and analysed using the checkerboard DNA-DNA hybridization technique. RESULTS: GAgP and GCP subjects harboured significantly higher levels and/or proportion of Porphyromonas gingivalis, Tannerella forsythia (levels: p<0.001, proportion: p<0.01), Prevotella nigrescens (p<0.05 levels) and "red" complex species (p<0.001 proportion) than PH subjects. All GAgP subjects were carriers of P. gingivalis and P. nigrescens. No significant differences in any of the 40 microbial species tested were detected between GAgP and GCP subjects. CONCLUSIONS: Our results revealed that the microbial differences between GAgP and GCP subjects were only discrete and none of the bacterial species tested seemed to specifically differentiate the subgingival microbial profile of either periodontitis group.

Actinomyces↗
PubMed2002

Three case reports of aggressive periodontitis associated with Porphyromonas gingivalis in younger patients.

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.

Adolescent↗
PubMed2003

Neutrophil-mediated tissue injury in periodontal disease pathogenesis: findings from localized aggressive periodontitis.

Neutrophils play a major role in the host response against invading periodontopathogenic microorganisms. Localized aggressive periodontitis (LAgP) is associated with various functional abnormalities of neutrophils. Based on the recent findings, LAgP neutrophils are not "hypofunctional" or "deficient." They are "hyperfunctional," and their amplified activity is responsible for the tissue destruction in periodontal disease. Several signal transduction abnormalities are associated with elevated neutrophil function in LAgP. There is a strong correlation between defective chemotaxis and decreased intracellular Ca2+ levels; total calcium-dependent protein Kinase C (PKC) activity of neutrophils is significantly lower than healthy subjects; and there is a marked increase in diacylglycerol (DAG) accompanied by a pronounced decrease in DAG kinase activity. In a separate set of experiments on the involvement of the inducible cyclooxygenase isoform (COX-2) and the role of novel lipid mediators in the pathogenesis of periodontal disease, crevicular fluid samples from LAgP patients were found to contain prostaglandin E2 (PGE2) and 5-LO-derived products, leukotriene B4 (LTB4), and the biosynthesis interaction product, lipoxin LXA4. Neutrophils from peripheral blood of LAgP patients, but not from healthy volunteers, also generated LXA4, suggesting that this immunomodulatory molecule may have a role in periodontal disease. Lipoxin generation and its relationship to PGE2 and LTB4 can be visualized as an important marker for the pathogenesis of periodontal disease. Thus, major advances in our understanding of the role of the neutrophil in host defense against periodontal organisms have been made through studies of LAgP. LAgP is used as an example of a severe periodontal disease that is related to abnormal neutrophil function. In this model, it appears that a hyperresponsiveness of the neutrophil, due to cell priming/predisposition, results in enhanced tissue damage.

Adjuvants, Immunologic↗
PubMed2002

Salivary IgA subclasses and bacteria-reactive IgA in patients with aggressive periodontitis.

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.

Adult↗
PubMedDate not supplied

The use of systemic antibiotics in the treatment of aggressive periodontal disease.

General dentists frequently encounter patients with aggressive periodontal disease and should be able to diagnose and manage this disease properly. Periodontal care in the absence of a comprehensive treatment plan and proper therapy can result in the rapid progression of the disease and, ultimately, tooth loss. It is important for the general dentist to diagnose, inform, and treat the periodontal patient accurately, using referral and nonsurgical, surgical, and antimicrobial/antibiotic therapy. This article provides a brief history of the classification of aggressive periodontal disease, describes the microorganisms associated with aggressive periodontal disease, discusses the selection and use of systemic antibiotics in therapy, and lists the various antibiotic regimens for treating aggressive periodontal disease.

Administration, Oral↗
PubMed2003

Prevalence of periodontopathic bacteria in aggressive periodontitis patients in a Japanese population.

BACKGROUND: Actinobacillus actinomycetemcomitans is considered a major etiologic agent of aggressive periodontitis. Other periodontopathic bacteria such as Porphyromonas gingivalis are also suspected of participating in aggressive periodontitis, although the evidence is controversial. The aim of the present study was to investigate the prevalence of periodontopathic bacteria and to clarify the microbiological features of aggressive periodontitis in Japanese patients. METHODS: Subgingival plaque was collected from 50 aggressive periodontitis (AgP) patients (localized 10, generalized 40). Samples from 35 generalized chronic periodontitis (CP) patients and 18 healthy subjects were examined as controls. Plaque samples were examined using culture and polymerase chain reaction (PCR) method. RESULTS: The prevalence of A. actinomycetemcomitans was relatively low in the localized (20%) and generalized (17.5%) AgP patients, with no significant difference observed in detection frequencies between AgP and the control groups (CP 8.6%, healthy 0%). On the other hand, Tannerella forsythensis (formerly Bacteroides forsythus), Campylobacter rectus, P. gingivalis, and Treponema denticola were frequently detected in localized as well as generalized aggressive periodontitis patients. The prevalence and proportion of P. gingivalis correlated with severity of clinical attachment loss in both localized and generalized aggressive periodontitis. CONCLUSIONS: T. forsythensis, C. rectus, P. gingivalis, and T. denticola were the predominant periodontopathic bacteria of aggressive periodontitis patients in Japan. Although A. actinomycetem- comitans was also detected in AgP patients, the prevalence of this bacterium was much lower than that of P. gingivalis.

Adolescent↗
PubMed2005

Infection patterns in chronic and aggressive periodontitis.

BACKGROUND: We revisited the postulate that localized aggressive periodontitis (LAP) patients have robust serum antibody (ab) responses to periodontal pathogens while patients with generalized aggressive periodontitis (GAP) show weak responses. We also studied ab responses in localized chronic (LCP) and generalized chronic periodontitis (GCP). METHODS: Fifty-seven patients (14-74 years, 25% male, 70% Hispanic, 26% African American) were studied (15 LAP, 19 GAP, 11 LCP, 12 GCP patients). Three plaque samples/subject were analysed with respect to 15 species, and serum immunoglobulin G (IgG) responses to the same bacteria were determined. Ab responses were expressed as log-transformed titres, and "infection ratios", i.e., log-transformed ratios of ab titre over the subject-based mean bacterial load for the homologous species. RESULTS: The results failed to corroborate the postulate that LAG patients have robust responses to infecting agents while GAP subjects exhibit weak responses. This held true for ab to "red complex", "orange complex", and health-associated species, and for both titres and infection ratios. Similarly, no differences were found between ab titres or infection ratios in chronic and aggressive periodontitis, or their extent-based subdivisions. CONCLUSIONS: A distinction between the two principal categories of the current periodontitis classification cannot be established by the study of infection patterns.

Adolescent↗
PubMed2006

Prognostic factors in the treatment of generalized aggressive periodontitis: I. Clinical features and initial outcome.

AIMS: The aims of this study were to investigate prognostic factors for initial response to non-surgical periodontal treatment for generalized aggressive periodontitis. METHODS: Seventy-nine patients with generalized aggressive periodontitis were included in this prospective follow-up intervention study. Patients' clinical and demographic parameters were collected at baseline and 10 weeks following a standard course of treatment (four visits of non-surgical root surface debridement together with OHI as required). The relationship between clinical variables and treatment outcome were analysed at site-specific level by chi(2) analysis and for patient-specific variables by logistic regression. RESULTS: In general, there was a good response to the treatment provided. In deep sites the mean pocket depth reduction was 2.11+/-2.01 mm. Site-specific analysis showed that the presence of plaque had a small but significant predictive effect on outcome (odds ratio 1.4). Sites on teeth with grade II/III mobility showed a significantly reduced response to treatment. Twenty-five patients were classified as "non-responders". Current smoking was strongly associated with non-responding patients (odds ratio 3.8) in a logistic regression model; plaque, baseline bleeding and initial pocket depth were not significantly associated with treatment outcomes. CONCLUSIONS: Overall, the results emphasize the importance of smoking as a negative prognostic factor, and suggest that treatment outcomes may be determined by a wide range of different determinants requiring further study.

Adult↗
PubMed2005

Rehabilitative management offered Nigerian localized and generalized aggressive periodontitis patients.

This paper highlights the typical clinical features of aggressive periodontitis (formerly known as juvenile periodontitis in the South Western region of Nigeria), the attending psychological effect following tooth loss, and the rehabilitative management offered which included periodontal therapy, psychotherapy, and prosthetic replacement of the missing teeth. The psychotherapy is the main distinguishing treatment in this study from previously reported modes of management of this disease entity. Subjects were from a part of the South Western region of Nigeria, and ages ranged from 15 to 22 years. They all presented very late with subsequent gross periodontal breakdown and subsequent psychological depression. The mean values of the probing depth (mm), degree of mobility, and the amount of bone fill (mm) from the periapical radiographs were recorded pre and post-operatively. The missing teeth were replaced with acrylic dentures, and psychotherapy was offered at three levels (individual, group, and conjoint-family psychotherapy). There was significant improvement of these clinical parameters six months after treatment, and the partial denture replacement of the missing teeth improved their appearance as expected but did not totally improve the initial depressive state. The psychotherapy offered gave the patients positive psychological effects that further restored their ability to socialize in their environment, which added to their positive experience of life. In conclusion the typical clinical features of localized aggressive periodontitis (LAP) and generalized aggressive periodontitis (GAP) patients in our environment are late presentation with gross periodontal tissue breakdown. Psychotherapy is an important aspect in the management of this group of patients in conjunction with the periodontal and prosthetic management, which gives total rehabilitation.

Adolescent↗
PubMed2001

Treatment of aggressive periodontitis by osseointegrated dental implants. A case report.

BACKGROUND: Generalized aggressive periodontitis is described as a clinical entity affecting both deciduous and permanent dentition with extensive alveolar bone loss, mobility, and exfoliation of all or many teeth. Controversy exists on dental implant use to restore missing dentition in younger patients. METHODS: This case report presents a patient diagnosed with aggressive periodontitis who has lost all but 4 of her teeth. Her personal and functional desires led us to include implant therapy in her treatment plan. The hematological data are presented with an analysis of the immunological profile. RESULTS: Dental implants were placed, and following 3 months of osseointegration, an implant-supported prosthesis was completed. The patient was followed up for 36 months. CONCLUSIONS: This case report presents an alternative treatment for rehabilitating dentition in a young patient treated for aggressive periodontitis. Similar case studies may help eliminate some of the controversy that exists regarding the use of dental implants in aggressive periodontitis patients.

Adolescent↗
PubMed2003

[Relevance of FcgammaRIIIb genotype, IgG G2m(23) factor to the susceptibility of aggressive periodontitis].

OBJECTIVE: To investigate the polymorphism of FcgammaRIIIb genotype, IgG G2m(23) factor and their associations with the susceptibility to aggressive periodontitis. METHODS: DNA of white blood cells and serum from 21 aggressive periodontitis patients and 26 healthy controls was extracted. Genotype of FcgammaRIIIb and phenotype of G2m(23) factor was determined by allele-specific PCR and dot immunobinding assay respectively. RESULTS: The frequency of FcgammaRIIIb-NA1/NA1 genotype in aggressive periodontitis patients was significantly higher than in healthy controls (P < 0.05). The ratio of subjects with FcgammaRIIIb-NA1/NA1 genotype and positive G2m(23) factor was higher in aggressive periodontitis patients (11/21) than in health controls (5/26) (P < 0.05). However, no statistical difference in distribution of G2m(23) factor alone was observed between patients and controls. CONCLUSIONS: This study indicates that FcgammaRIIIb-NA1/NA1 genotype may be a susceptible genotype to aggressive periodontitis in Chinese population. Subjects with FcgammaRIIIb NA1/NA1 genotype and positive G2m(23) factor may be more susceptible to aggressive periodontitis.

Adult↗
PubMed2006

Evaluation of RANK/RANKL/OPG gene polymorphisms in aggressive periodontitis.

BACKGROUND AND OBJECTIVE: Aggressive periodontitis (AgP) is a specific type of periodontal disease that is characterized by rapid attachment loss and bone destruction. While attempting to identify genetic polymorphisms associated with AgP, previous research has focused on candidate genes that may be involved in immune responses to microbial infections. In this study, the focus was on single nucleotide polymorphisms (SNPs) in the key mediators of osteoclast differentiation and activation, which involve receptor activator of nuclear factor-kappaB (RANK), RANK ligand (RANKL) and osteoprotegrin (OPG), in the Japanese population. The aim of this study was to evaluate the association of RANK/RANKL/OPG gene polymorphisms with AgP in the Japanese population. MATERIAL AND METHODS: We examined 99 patients with AgP and 89 controls from the Japanese population to explore the possibility of RANK/RANKL/OPG loci as candidate regions associated with the disease. All exons and relevant exon-intron boundaries of these three candidate genes were amplified by polymerase chain reaction (PCR) using 19 primers, followed by direct sequencing. The polymorphisms were identified by comparing the sequences obtained from 48 subjects. RESULTS: We identified 27 SNPs in RANK, including 10 novel SNPs and seven SNPs each in both RANKL and OPG. A pairwise linkage disequilibrium analysis using the r2 statistic showed that some SNP pairs from the three loci are in tight linkage disequilibrium. CONCLUSION: An association analysis with allelotypes showed that SNPs identified in the RANK/RANKL/OPG genes have no significant association with AgP in the Japanese population.

Acute Disease↗
PubMed2004

[The relationship between a nucleotide substitution of S100A8 gene and aggressive periodontitis].

OBJECTIVES: To screen polymorphisms in the upstream region of S100A8 gene and to detect whether the polymorphisms were associated with aggressive periodontitis. METHODS: Thirty aggressive periodontitis patients and twenty-eight healthy controls were recruited for the study with informed consent. All subjects were of Chinese descent and systemically healthy. The regions about 800 bp upstream from the ATG start codon in exon 2 of the S100A8 gene of 10 patients and 8 controls were amplified by polymerase chain reaction (PCR) and analyzed by direct sequencing. A single nucleotide polymorphism (SNP) at 94 bp upstream from the ATG start codon was selected, and then the shorter regions (about 250 bp upstream from the ATG start codon) of the rest subjects were also amplified by PCR and analyzed by direct sequencing. The frequency of the SNP and the distribution of the genotype were detected and compared between the two groups. RESULTS: A nucleotide substitution (A-->G) at 94 bp upstream from the ATG start codon was demonstrated in Chinese, which was in a cis-acting element, named gamma interferon response element (gamma-IRE) in intron 1 of S100A8 gene. All of the subjects that carried the polymorphism were heterozygous. There was no statistically significant difference in the frequency of allele 2 (corresponding to the nucleotide G) between patients and controls (11.7% vs. 17.9%, chi2 = 0.887, P > 0.05). The prevalence of the heterozygous genotype was 23.2% and 35.7% (chi2 = 1.07, P > 0.05) in patients and controls, respectively. CONCLUSIONS: This is the first report that a nucleotide substitution of S100A8 gene was demonstrated in Chinese. The frequencies of allele 2 and heterozygous genotype were lower in patients, but there is no statistically significant difference between the aggressive periodontitis patients and healthy controls in this preliminary study.

Aggressive Periodontitis↗
PubMed2005

Characterization of Actinobacillus actinomycetemcomitans isolated from young Chinese aggressive periodontitis patients.

OBJECTIVE: This study characterized Actinobacillus actinomycetemcomitans isolates from young Chinese aggressive periodontitis patients. METHODS: Subgingival plaque samples (two/subject) were collected from diseased subjects < 25 years old (n = 9, mean age 21.1 +/- 1.6 years) and age-matched periodontitis-free controls (n = 47, mean age 22.0 +/- 1.1 years). Selective and anaerobic culture were used. The serotype, leukotoxin gene (ltx) operon promoter and the cytolethal distending toxin (cdt) genes complex of the A. actinomycetemcomitans isolates were investigated. Effects of the isolates on non-keratinizing periodontal ligament epithelial cells monolayer were studied. RESULTS: Diseased subjects had significantly higher full-mouth bleeding score (p = 0.002) and total viable counts from plaque samples (7.2 x 10(6) vs. 2.1 x 10(5) CFU/paperpoint, p < 0.005). A. actinomycetemcomitans was isolated from 67%/56% or 6%/4% of diseased or controls subject/sites, respectively (p < 0.001). The proportion of A. actinomycetemcomitans isolatable from aggressive periodontitis or periodontitis-free associated subgingival plaque was low (0.7% vs. 0.1%, p < 0.02). The serotype of the isolates was characterized. All isolates possessed 652-like ltx gene promoter and all but one serotype c isolate from a diseased patient had intact cdtABC genes. That particular strain appeared to confer the least cellular damages on periodontal ligament epithelial monolayer compared to others. CONCLUSION: This preliminary study confirmed the notion of increased prevalence and quantity of A. actinomycetemcomitans associated with aggressive periodontitis in young patients. The overall ltx promoter and cdt characteristics of the A. actinomycetemcomitans isolates, however, were similar among the diseased and control groups. A strain lacking the cdtABC gene appeared to be less damaging to a periodontal ligament epithelial cell model. Further studies therefore are warranted to clarify the pathogenic role and potentials of A. actinomycetemcomitans in aggressive periodontitis.

Actinobacillus Infections↗
PubMed2005

[Localized aggressive periodontitis: a possible site-specific rather than tooth-specific disease?].

The diagnosis of localized aggressive periodontitis includes first molar attachment loss as an obligatory criterion. This tooth-specific based diagnosis has never been questioned or tested previously. We present a rare case of aggressive periodontitis that developed during orthodontic treatment, which included extraction of right lower first molar and bodily movement of the second molar to the original first molar site. At the end of the orthodontic therapy, localized periodontal disease was diagnosed at the site of the lower left first molar and the second lower right molar that was now occupying the site of the former first lower molar. The patient's periodontal condition was stabilized, and the bony defects were filled following periodontal treatment. This report shows that bacterial induced aggressive periodontitis developed during orthodontic treatment in a site-specific manner and suggest the hypothesis that localized aggressive periodontitis was targeted to a specific alveolar site rather than a tooth-specific site.

Acute Disease↗
PubMed2006

Aggressive periodontitis among young Israeli army personnel.

BACKGROUND: The aim of this study was to assess the prevalence of aggressive periodontitis among young Israeli army recruits and to evaluate its association with smoking habits and ethnic origin. METHODS: The study population consisted of 642 young army recruits (562 men [87.5%] and 80 women [12.5%]), aged 18 to 30 years (average: 19.6 +/- 1.6 years), who arrived at a military dental clinic for dental examinations between January and December 2004. Subjects filled out a questionnaire regarding their ethnic origin and family periodontal history, followed by radiographs and a clinical periodontal examination of four first molars and eight incisors. RESULTS: Aggressive periodontitis was found in 5.9% of the subjects (4.3% localized and 1.6% generalized). At least one site with a probing depth > or =5 mm was found in 20.1% of the subjects. A radiographic distance between crestal bone height and the cemento-enamel junction >3 mm was found in 43 (6.7%) subjects. Current smokers (39.9%) (P = 0.03) and subjects of North African origin (P <0.0001) correlated with a high prevalence of aggressive periodontitis. CONCLUSION: A relatively high prevalence of aggressive periodontitis was found in young Israeli army recruits, which was particularly associated with smoking and ethnic origin.

Adolescent↗