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PubMed1987

Genetic analysis of juvenile periodontitis in families ascertained through an affected proband.

Data from 28 families ascertained through a proband with juvenile periodontitis were used to test a series of Mendelian models of inheritance that included both autosomal and X-linked transmission. There was strong evidence of familial aggregation of this progressive dental disease, and the best-fitting model was an autosomal recessive model. Because of the rather limited age range for expression of the disease in this situation, simulations were done, in a model-choice analysis using samples of this size, to assess the chance of mistaking an autosomal dominant disease (with masking of the affected phenotype outside a specified age range) for an autosomal recessive disease. While the rate of Type II error was fairly high (40%) when competing models in these simulations were compared, these data suggest that it is reasonable to infer that juvenile periodontitis is an autosomal recessive disorder.

Adolescent↗
PubMed1996

[Comparison of the evaluation of the periodontium status in 12-year- old children in 6-year interval (years of research 1987 and 1993)].

The comparison of the evaluation results of the periodontium status has been made in 12 years old children from Warsaw, Sulejówek and Wiazowna region at 6 years interval. In both studies the same criteria have been applied. A significant improvement in the periodontium status was observed in the second study. The percentage of different periodontal treatment requirements has been reduced from 81% (in the initial study) to 35% the second study.

Aggressive Periodontitis↗
PubMed1986

Analysis of data from clinical studies of localized juvenile periodontitis.

Data from 27 subjects with localized juvenile periodontitis were used to compute estimates of the intraclass correlation coefficient for initial periodontal pocket depth measurements and total subgingival Actinobacillus actinomycetemcomitans counts, and for changes from pre- to post-treatment in periodontal pocket depth, probing attachment level and Actinobacillus actinomycetemcomitans counts. The estimates for the clinical parameters were considerably higher than those found in a similar study of adult periodontitis. On the average, the estimates for the intraclass correlation coefficients for Actinobacillus actinomycetemcomitans counts did not differ markedly from the corresponding estimates for the clinical parameters. Although the results of this study indicate that the major component of variability in parameters commonly used in studies of periodontal disease can be attributed to site-specific factors, sites within subjects cannot be considered statistically independent. For the analysis of data arising from studies of periodontal disease, it is recommended that statistical techniques, like the nested mixed effects analysis of variance model be employed, which account for this dependence. These techniques will allow meaningful biological questions concerning site-specific phenomenon to be answered. However, changes in clinical and microbiological parameters, when therapeutic measures are employed on localized juvenile periodontitis patients, are often dramatic enough to allow informal data presentation.

Actinobacillus↗
PubMed1996

Occurrence of Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis and Prevotella intermedia in juvenile periodontitis.

The occurrence of Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis and Prevotella intermedia in subgingival plaque in 24 juvenile periodontitis patients was determined using DNA probe. 36 samples of subgingival plaque from 36 pockets having > or = 6 mm depth, > or = 3 mm of loss of attachment, and bleeding on probing and/or suppuration were taken from 18 patients with localized juvenile periodontitis (LJP, age range 12-24 years); and 12 samples from 6 patients with generalized juvenile periodontitis (GJP, age range 23-26 years). As control, an equal numbers of samples from healthy sites in the same patients were studied. P. gingivalis was found in 17 of 18 LJP patients, and in 31 of 36 diseased sites in those patients. P. intermedia was found in 15 out of the 18 LJP patients and in 28 of the 36 diseased sites. A. actinomycetemcomitans was present in 7 of the 18 LJP patients, and in 9 of the 36 diseased sites, and was not found in any GJP patients. All GJP patients had P. gingivalis (11 out of 12 diseased sites) and P. intermedia (all of the diseased sites). None of the three bacterial species was detected in healthy sites of GJP patients, and were found in healthy sites in only 2 of 18 LJP patients. The high prevalence and high levels of P. gingivalis and P. intermedia found in the LJP and GJP patients studied, suggest that there are populations affected by juvenile periodontitis in which this type of periodontitis is more associated with these species than with A. actinomycetemcomitans.

Adolescent↗
PubMed1990

A family study of a mother and daughter with increased susceptibility to early-onset periodontitis: microbiological, immunological, host defensive, and genetic analyses.

Microbiological, immunological, host-defensive, and genetic analyses were performed on a mother and daughter, both of whom had early-onset periodontitis (rapidly progressive periodontitis in the mother; localized juvenile periodontitis in the daughter). Microscopic examination revealed a greatly elevated percentage of rod-form bacteria in both subjects. Fusobacterium sp. and Porphyromonas gingivalis (formerly Bacteroides gingivalis) were the predominant microorganisms cultured. The humoral immune responses to F. nucleatum, P. gingivalis, and Actinobacillus actinomycetemcomitans were much higher in both subjects than those to any other periodontal bacteria examined. Functional and phenotypic analysis of the peripheral lymphocytes showed no significant abnormalities. However, investigation of neutrophil function showed that the mother had depressed neutrophil chemotaxis and superoxide production. The daughter had depression not only of chemotaxis and superoxide production, but also of neutrophil phagocytosis. Serological typing of HLA antigens revealed the same Class II HLA profile in both subjects. It was concluded that both subjects very probably had an identical condition and that these patients provided a unique model for improving our understanding of the host factors involved in periodontal disease.

Adolescent↗
PubMed1996

Gingival state and dental calculus in early-onset periodontitis.

This study was undertaken to 1) compare the prevalence of gingival inflammation and dental calculus in adolescents with early-onset periodontitis and their matched controls and 2) assess and compare the relationship between the presence of dental calculus and the extent of gingival bleeding and attachment loss in these subjects. The study group consisted of 1,285 13 to 20 year-old individuals, 651 males and 634 females, selected from a national survey of the oral health of U.S. adolescents in 1986/1987. It included 709 (55.2%) Blacks, 224 (17.4%) Hispanics, and 352 (27.4%) Whites. Eighty-nine subjects had localized or generalized juvenile periodontitis (JP), 218 had incidental attachment loss (IAL), and 978 were without clinical attachment loss (controls). The controls were matched to cases on gender, race, age, and geographic location. The subjects were examined clinically to assess the percentage of sites with gingival bleeding and supragingival calculus only and subgingival calculus with or without supragingival calculus. The IAL and JP groups had significantly more gingival bleeding and subgingival calculus than the controls. Also, the JP group had significantly higher prevalence of both conditions than the IAL group. The percentage of sites with supragingival calculus was not different between the groups, but varied by ethnicity. Hispanics with JP had the highest percentage of sites with gingival bleeding and subgingival calculus, and the lowest percentage of sites with only supragingival calculus. The results demonstrate that gingival inflammation and subgingival calculus are associated with early periodontal breakdown, and contradict earlier reports of early-onset periodontitis not being associated with these factors.

Adolescent↗
PubMed1999

[The mechanical action of Dirol chewing gum on the periodontal tissues and masticatory muscles].

Regional hemodynamics, bioelectric activity of masticatory muscles, and compactness of mandibular bone were studied by the rheographic method for measuring periodontal bloodflow, by electromyography, and echo-osteometry in 52 volunteers after 4-week regular chewing of Dirol chewing gum. Congestive hyperemia develops in periodontal tissues; functional activity of masticatory muscles and compactness of mandibular bone are normal.

Adult↗
PubMed2001

Biochemical analysis of total collagen content and collagen types I, III, IV, V and VI in gingiva of various periodontitis categories.

Collagen is one of the chief components of the extracellular matrix of gingival connective tissue, where five different types have been identified to date. The molecular mechanism of collagen loss in periodontitis still needs to be explored. In the present study total collagen content was investigated in gingival connective tissue of adult periodontitis (AP) as well as early onset periodontitis patients (EOP) and clinically healthy subjects. Furthermore, collagen type I, III, IV, V andVI content was evaluated in gingival biopsies obtained from periodontitis patients. There was a statistically significant difference between AP (25.1 +/- 8.1 microg/mg) and EOP (15.6 +/- 4.0microg/mg) groups with regard to the total collagen content (P < 0.05). In the clinically healthy control group the total collagen content was 20.7 +/- 4.6microg/mg. Moreover, the distribution of collagen types exhibited variations in pooled homogenates of each periodontitis group. The total collagen loss seemed to be greater in the EOP patients than in the AP patients. When the ratio of fibril forming collagens to nonfibrillar collagens was evaluated, it seems to be decreased in AP patients in comparison to EOP patients. The findings of the present study suggest that different collagen types present in various periodontitis categories may be related with diverse pathogenic mechanisms acting in these diseases.

Adolescent↗
PubMed1990

[Juvenile periodontitis (microbiology--immunology)].

Juvenile periodontitis is a destructive periodontal disease with young healthy individuals at the age 15-18. Main causative factor is the strain Actinobacillus actinomycetemcomitans (Aa) and is characterized by the rapid periodontal destruction of the incisors and 1st molars in the upper and lower jaw. In this paper is presented the current concepts of the microbiology and immunology of tis disease. However the comparison of the microbiological and immunological picture of juvenile periodontitis to those of the different types of the same disease as well as of the corresponding picture of the adult periodontitis seems to be important in order for the dentists to understand and explain those suffering from juvenile periodontitis. Furthermore, it is concluded that the earliest the diagnosis the better the results of the treatment.

Adolescent↗
PubMed2002

Comparison of microbial cultivation and a commercial PCR based method for detection of periodontopathogenic species in subgingival plaque samples.

OBJECTIVES: Microbiological laboratory procedures are involved in diagnosis and therapy control of progressive and refractory forms of periodontitis. In recent years techniques have been developed based on the detection of nucleic acids. The purpose of this study was to validate the commercially available micro-Dent(R) test which employs probes for A. actinomycetemcomitans, P. gingivalis, P. intermedia, B. forsythus and T. denticola. METHODS: 122 plaque samples obtained from periodontal pockets with various depths from 33 early onset periodontitis (EOP) patients and 15 periodontally healthy subjects were analysed by cultivation and the microDent(R) kit. RESULTS: Both cultivation and the nucleic acid based assay showed a positive correlation of pocket depth with the frequency and quantity of periodontopathogenic species. T. denticola was found only in pockets > 4 mm in EOP patients. Comparison of the two methods revealed that the microDent(R) kit identified both P. gingivalis and B. forsythus more often than did the cultivation method. CONCLUSIONS: Nucleic acid techniques should replace cultivation methods as gold standard in microbiological diagnosis of progressive periodontitis. The micro-Dent(R) kit can be recommended for microbiological laboratories analysing subgingival plaque samples.

Adolescent↗
PubMed2000

Herpesvirus in localized juvenile periodontitis.

Herpesvirus genomic sequences can be detected in gingival crevicular fluid of adult periodontitis lesions. Herpesviruses are immunosuppressive and may facilitate establishment of subgingival pathogens. Electron microscopic studies have identified nuclear and cytoplasmic virus-like inclusions in gingival inflammatory cells from localized juvenile periodontitis (LJP). The present study aimed to determine if herpesviruses occur in LJP lesions and if human cytomegalovirus (HCMV) activation is associated with elevated levels of subgingival Actinobacillus actinomycetemcomitans, the putative bacterial pathogen of LJP. Eleven systemically healthy patients exhibiting LJP (10-23 yr) were studied. In each patient, subgingival samples were pooled from 3 periodontitis lesions around first molar and incisor teeth (5-11 mm periodontal pocket depth) and from 3 gingivitis/healthy sites around canines (2-3 mm periodontal pocket depth). Polymerase chain reaction (PCR) was used to detect herpesvirus DNA and HCMV cDNA of major capsid protein transcripts, indicative of viral activation. Selective culture and 16S rRNA PCR were used to identify A. actinomycetemcomitans. Of 11 deep periodontal samples, 8 showed HCMV, 7 showed Epstein-Barr virus type 1 (EBV-1), 1 showed EBV type 2, 6 showed herpes simplex virus (HSV) and 8 showed viral co-infection. Of 11 shallow periodontal samples, 2 showed HCMV, 2 showed EBV-1, 1 showed HSV and 2 showed viral co-infection. The difference in occurrence of HCMV and viral co-infection between deep and shallow periodontal sites was statistically significant (p =0.031). HCMV activation was detected in deep pockets of all 5 virally positive patients with early LJP (aged 10-14 years) but only in 1 of 3 virally positive LJP patients older than 14 years, and not in any shallow pocket tested. HCMV activation appeared related to absence of radiographic crestal alveolar lamina dura, a possible indication of periodontal disease progression. A. actinomycetemcomitans tended to be more prevalent in samples showing active than latent HCMV infection. The present findings are consistent with the notion that periodontal herpesvirus infection and possibly HCMV activation constitute important features of the etiopathogenesis of LJP.

Adolescent↗
PubMed2003

Application of denaturing gradient gel electrophoresis (DGGE) to the analysis of microbial communities of subgingival plaque.

OBJECTIVES: Denaturing gradient gel electrophoresis (DGGE) was applied to the microbiologic examination of subgingival plaque. MATERIALS AND METHODS: The PCR primers were designed from conserved nucleotide sequences on 16S ribosomal RNA gene (16SrDNA) with GC rich clamp at the 5'-end. Polymerase chain reaction (PCR) was performed using the primers and genomic DNAs of typical periodontal bacteria. The generated 16SrDNA fragments were separated by denaturing gel. RESULTS: Although the sizes of the amplified DNA fragments were almost the same among the species, 16SrDNAs of the periodontal bacteria were distinguished according to their specific sequences. The microflora of clinical plaque samples were profiled by the PCR-DGGE method, and the dominant 16SrDNA bands were cloned and sequenced. Simultaneously, Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis and Prevotella intermedia were detected by an ordinary PCR method. In the deep periodontal pockets, the bacterial community structures were complicated and P. gingivalis was the most dominant species, whereas the DGGE profiles were simple and Streptococcus or Neisseria species were dominant in the shallow pockets. The species-specific PCR method revealed the presence of A. actinomycetemcomitans, P. gingivalis and P. intermedia in the clinical samples. However, corresponding bands were not always observed in the DGGE profiles, indicating a lower sensitivity of the DGGE method. CONCLUSION: Although the DGGE method may have a lower sensitivity than the ordinary PCR methods, it could visualize the bacterial qualitative compositions and reveal the major species of the plaque. The DGGE analysis and following sequencing may have the potential to be a promising bacterial examination procedure in periodontal diseases.

5' Flanking Region↗
PubMed1993

Marginal bone loss in the primary dentition of patients with juvenile periodontitis.

118 patients with juvenile periodontitis (JP), diagnosed when the patients were 13-19 years old, were studied retrospectively with respect to radiographic marginal bone loss in the primary dentition, experienced when the patients were 5-12 years old. 168 other 13-19 year old patients without any signs of bone loss in the permanent teeth were used as a reference group. The JP patients were classified into 2 groups according to the number of sites with bone loss in the permanent dentition: JP group I having 1 site with bone loss (n = 45) and JP group II having > or = 2 sites with bone loss (n = 73). It was found that 35 patients (52%) of JP group II displayed 1 or more sites with bone loss in the primary dentition during the age of 5-12 years. The corresponding numbers for JP group I and the reference group were 9 (20%) and 8 (5%) respectively. These findings indicate that juvenile periodontitis, at least in some individuals, may have its onset already in the primary dentition.

Adolescent↗
PubMed1994

Chemoluminescence generation and MTT dye reduction by polymorphonuclear leukocytes from periodontal disease patients.

Alterations of polymorphonuclear leukocytes (PMNs) functions have been reported in patients with severe forms of some periodontal disease. In this study we evaluated the chemoluminescence generation and MTT dye reduction by human PMN in patients with juvenile periodontitis (JP), rapidly progressive periodontitis (RPP) and adult periodontitis (AP) during protein kinase C (PKC) activation or during the phagocytosis of opsonized zymosan. The results demonstrated that only PMNs of JP patients showed a decreased chemoluminescence generation and MTT dye reduction during the phagocytosis of opsonized zymosan (p < 0.05). The time to reach the maximal peak during the PKC activation on the chemoluminescence reaction was evaluated and JP PMNs patients demonstrated a depressed value (7.0 +/- 0.4 min) compared with healthy volunteers (13.8 +/- 0.5 min). The etiology and importance of such cellular alterations in the immunopathogenesis of the periodontal disease are discussed.

Adolescent↗
PubMed1997

Prevalence of Actinobacillus actinomycetemcomitans serotypes in Japanese patients with periodontitis.

Oral Actinobacillus actinomycetemcomitans strains are serologically classified into 5 distinct groups, a to e. We examined the distribution of A. actinomycetemcomitans serotypes in Japanese patients with periodontitis. A total of 157 A. actinomycetemcomitans clinical isolates from diseased sites of 39 patients with periodontitis were serotyped by using serotype-specific rabbit antisera against A. actinomycetemcomitans serotypes a, b, c, d and e strains. In the immunodiffusion assay, autoclaved extracts of 42, 6, 39, 9 and 41 A. actinomycetemcomitans clinical isolates reacted with serotypes a, b, c, d and e antisera, respectively. Although 37 patients were infected with a serotype strain, 2 patients harbored 2 different serotype strains, b/e and b/untypeable. To establish a correlation between serotype and genotype of A. actinomycetemcomitans clinical isolates from 2 patients who had different serotype strains, we used arbitrarily primed polymerase chain reaction (AP-PCR) to fingerprint clinical isolates of different serotypes. The AP-PCR genotypes among 4 clinical isolates (b/e and b/untypeable) were identical to that of A. actinomycetemcomitans Y4 (serotype b), indicating the presence of multiple A. actinomycetemcomitans serotypes which are genetically homogeneous in the periodontally diseased sites of patients with periodontitis.

Actinobacillus Infections↗