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PubMed1998

[Periodontitis--a ubiquitous illness].

In recent years, periodontitis has been receiving increasing attention, since it not only impairs the general state of health (loss of the teeth), but also appears to have a relationship with cardiovascular and cerebrovascular illnesses (thrombocyte aggregation, insult). Periodontitis is a very frequent, chronic recurrent, unspecific bacterial inflammation of the periodontium that arises in accumulated plaques on the teeth at the gingiva. It leads to an irreversible destruction of soft tissue followed by loss of bony substance. Three types of periodontitis can be distinguished: 1. adult periodontitis (AP), 2. rapidly progressive periodontitis (RPP) and juvenile periodontitis (JP). Periodontitis appears to have a genetic component. Additional risk factors include juvenile diabetes mellitus and smoking. The diagnosis, prevention and treatment are discussed. The basis for prevention and treatment is individual hygiene and professional dental care.

Adolescent↗
PubMed1989

Depressed helper-to-suppressor T-cell ratios in early-onset forms of periodontal disease.

Helper (CD4+)-to-suppressor (CD8+) T-cell ratios were determined by flow cytometry for 12 patients with early-onset forms of periodontal disease and their appropriate controls. When considered as a group, patients with early-onset periodontal disease showed a markedly depressed CD4+/CD8+ ratio relative to controls (means 0.92 and 1.50 respectively). This difference was significant at the 0.0015% level as determined by the Mann-Whitney test. Separate analysis of patients with either the juvenile or rapidly progressive types of early-onset periodontal disease showed both to have reduced CD4+/CD8+ ratios (means 0.91 and 0.92) relative to their controls (means 1.57 and 1.45) which were both statistically significant (p less than 0.05).

Adolescent↗
PubMed2000

Localisation of a gene for prepubertal periodontitis to chromosome 11q14 and identification of a cathepsin C gene mutation.

Prepubertal periodontitis (PPP) is a rare and rapidly progressive disease of young children that results in destruction of the periodontal support of the primary dentition. The condition may occur as part of a recognised syndrome or may occur as an isolated finding. Both autosomal dominant and recessive forms of Mendelian transmission have been reported for PPP. We report a consanguineous Jordanian family with four members affected by PPP in two nuclear sibships. The parents of the affected subjects are first cousins. We have localised a gene of major effect for PPP in this kindred (Zmax=3.55 for D11S901 at theta=0.00) to a 14 cM genetic interval on chromosome 11q14 flanked by D11S916 and D11S1367. This PPP candidate interval overlaps the region of chromosome 11q14 that contains the cathepsin C gene responsible for Papillon-Lefèvre and Haim-Munk syndromes. Sequence analysis of the cathepsin C gene from PPP affected subjects from this Jordanian family indicated that all were homozygous for a missense mutation (1040A-->G) that changes a tyrosine to a cysteine. All four parents were heterozygous carriers of this Tyr347Cys cathepsin C mutation. None of the family members who were heterozygous carriers for this mutation showed any clinical findings of PPP. None of the 50 controls tested were found to have this Tyr347Cys mutation. This is the first reported gene mutation for non-syndromic periodontitis and shows that non-syndromic PPP is an allelic variant of the type IV palmoplantar ectodermal dysplasias.

Aggressive Periodontitis↗
PubMed1985

Serum and gingival fluid antibodies as adjuncts in the diagnosis of Actinobacillus actinomycetemcomitans-associated periodontal disease.

Serum antibody titers to Actinobacillus actinomycetemcomitans were measured in 200 subjects by an enzyme-lined immunosorbent assay (ELISA) using whole microorganisms as antigen. Comparisons were made between titers found in periodontally normal subjects and titers in subjects with localized juvenile periodontitis (LJP), postlocalized juvenile periodontitis, generalized juvenile periodontitis or adult periodontitis. It was found that titers to all three serotypes of A. actinomycetemcomitans were elevated in LJP patients' sera, while serum antibody levels in other diseased groups were not significantly elevated to any of the serotypes. Patient sera were also examined for serum antibody to oral Haemophili previously shown to cross-react with A. actinomycetemcomitans. Similar antibody titers were found in both normal subjects and in patients with various forms of periodontal disease to Haemophilus aphrophilus, H. influenzae and H. parainfluenzae. The A. actinomycetemcomitans antibodies which were elevated in LJP patients could not be correlated with antibody titers to cross-reacting Haemophili, suggesting that these antibodies are A. actinomycetemcomitans-specific. Serum antibody responses in six of the LJP patients were assessed to autologous strains of A. actinomycetemcomitans. Each patient was found to be infected with only a single serotype of A. actinomycetemcomitans, and specific antibodies to the infecting serotype were found in the patients' sera. In families, the LJP patients had significantly elevated IgG, IgA and IgM serum antibody titers to A. actinomycetemcomitans, while the IgG and IgA antibody titers in periodontally normal siblings were at levels comparable to those found in normal subjects. However, IgM serum antibodies were elevated in the periodontally normal siblings of LJP patients suggesting that the formation of IgM antibodies to A. actinomycetemcomitans may precede the clinical appearance of localized juvenile periodontitis. Gingival crevicular fluid and serum antibody levels to A. actinomycetemcomitans were compared in LJP patients. Comparable titers of IgG, IgA and IgM antibodies were found in serum and gingival fluid in most subjects; however, gingival fluid samples sometimes showed higher titers than serum, likely resulting from local antibody synthesis. The value of serum antibody determinations to A. actinomycetemcomitans in the diagnosis of Actinobacillus-associated periodontitis was also assessed. The predictive value of a positive test (significantly elevated anti-A. actinomycetemcomitans IgG) was 86%, while the specificity was 89%.(ABSTRACT TRUNCATED AT 400 WORDS)

Actinobacillus↗
PubMed1995

The possible association between localized juvenile periodontitis and supernumerary teeth.

Supernumerary teeth and localized juvenile periodontitis in the same patient is a very unusual finding. Only 5 cases are reported, 2 of which were identical twins. An additional 2 cases are presented in which localized juvenile periodontitis was associated with multiple supernumerary premolars. These cases are strikingly similar to 3 of the previously reported cases, raising the possibility that this combination of disorders may be more than a chance association.

Adolescent↗
PubMed2002

A novel mutation of the cathepsin C gene in Papillon-Lefèvre syndrome.

BACKGROUND: Papillon-Lefèvre syndrome (PLS) is a disorder that involves destruction of the periodontium and abnormal hyperkeratosis of the palms of the hands and soles of the feet. Mutations of the lysosomal protease cathepsin C gene (CTSC) have been associated with PLS. However, genotypic and phenotypic correlation has not been established. In the present study we investigated the CTSC gene in a Brazilian cohort affected by PLS. METHODS: Eight consanguineous members of a kindred with PLS were studied. DNA was extracted and all exons of the gene amplified by the polymerase chain reaction (PCR) using specific primers. Mutations were identified by DNA sequencing of the coding region and introns of the CTSC gene. RESULTS: Sequence analysis of CTSC from subjects affected by PLS identified a novel mutation (587T --> C) in exon 4, predicted to cause a Leu196Pro amino acid substitution. Three of 3 subjects were homozygous for cathepsin C mutations inherited from a common ancestor. One patient was heterozygous and showed plantar hyperkeratosis without periodontal disease. Two other family members were also heterozygous but did not present palmoplantar hyperkeratosis and/or periodontal disease. CONCLUSIONS: This study describes a novel mutation of the cathepsin C gene in a Brazilian kindred with Papillon-Lefèvre syndrome.

Adolescent↗
PubMed2000

Lipoxin A(4) analogues inhibit leukocyte recruitment to Porphyromonas gingivalis: a role for cyclooxygenase-2 and lipoxins in periodontal disease.

The potential involvement of the inducible cyclooxygenase isoform (COX-2) and the role of novel lipid mediators were investigated in the pathogenesis of periodontal disease. Crevicular fluids from localized juvenile periodontitis (LJP) patients contained prostaglandin (PG)E(2) and 5-lipoxygenase-derived products, leukotriene B(4), and the biosynthesis interaction product, lipoxin (LX)A(4). Neutrophils from peripheral blood of LJP patients, but not from asymptomatic donors, also generated LXA(4), suggesting a role for this immunomodulatory molecule in periodontal disease. To characterize host responses of interest to periodontal pathogens, Porphyromonas gingivalis was introduced within murine dorsal air pouches. In the air pouch cavity, P. gingivalis elicited leukocyte infiltration, concomitant with elevated PGE(2) levels in the cellular exudates, and upregulated COX-2 expression in infiltrated leukocytes. In addition, human neutrophils exposed to P. gingivalis also upregulated COX-2 expression. Blood borne P. gingivalis gave significant increases in the murine tissue levels of COX-2 mRNA associated with both heart and lungs, supporting a potential role for this oral pathogen in the evolution of systemic events. The administration of metabolically stable analogues of LX and of aspirin-triggered LX potently blocked neutrophil traffic into the dorsal pouch cavity and lowered PGE(2) levels within exudates. Together, these results identify PMN as an additional and potentially important source of PGE(2) in periodontal tissues. Moreover, they provide evidence for a novel protective role for LX in periodontitis, limiting further PMN recruitment and PMN-mediated tissue injury that can lead to loss of inflammatory barriers that prevent systemic tissue invasion of oral microbial pathogens.

Aggressive Periodontitis↗
PubMed1993

Rapid bony healing in localized juvenile periodontitis: a case report.

A 16-yr-old man with localized juvenile periodontitis was treated in one single surgical treatment visit. No adjunctive chemotherapy, implant material, or guided tissue regeneration (GTR) was used. Excellent bone repair was seen after 14 wk at the sites of the vertical periodontal lesions. The rapid healing could have been due to the treatment method, the youth of the patient, or the type and form of the bony defects. Radiographic control seems to be indicated 12-14 wk after surgical treatment.

Adolescent↗
PubMed1992

Neutrophil modulation by Actinobacillus actinomycetemcomitans. I. Chemotaxis, surface receptor expression and F-actin polymerization.

Localized juvenile periodontitis is an early onset periodontitis, usually localized to molars and incisors. Patients usually present with decreased chemotaxis of systemic neutrophils (PMNs) and infection with Actinobacillus actinomycetemcomitans. The pathogenic mechanisms involved have not been clarified. The purpose of this study was to determine if an extract of A. actinomycetemcomitans could induce changes in PMN chemotaxis similar to those reported in LJP patients. It was demonstrated that the bacterial extract was chemotactic for neutrophils. When neutrophils were pre-incubated with the bacterial extract, chemotaxis toward zymosan-activated serum, FMLP and the bacterial extract was inhibited in two different chemotaxis assays (Boyden chamber and under-agarose). Bacterial extract had no effect on random migration in either assay. Pre-incubation with the extract induced increased expression of CD11b/CD18 (Mac-1), Gp110, and FMLP receptors and increased F-actin polymerization following FMLP or PMA stimulation compared to cells not treated with the extract. Treatment of the bacterial extract with proteinase K or phenol extraction reversed the PMN chemotaxis inhibition activity, but increased significantly the random migration of PMNs. Heating the bacterial extract to 56 degrees C had no effect on its activity. The component(s) in the bacterial extract that inhibits chemotaxis is therefore a protein(s), not sensitive to 56 degrees C, and is not endotoxin. This study suggests that A. actinomycetemcomitans may contribute to the pathogenesis of localized juvenile periodontitis by inhibiting chemotaxis. Interference with chemotaxis by A. actinomycetemcomitans, however, occurs through a mechanism other than inhibition of actin assembly, reduction of CD11b/CD18 or Gp110 expression, or blockage/downregulation of FMLP receptors.

Actins↗
PubMed1997

Racial tropism of a highly toxic clone of Actinobacillus actinomycetemcomitans associated with juvenile periodontitis.

Actinobacillus actinomycetemcomitans strains with enhanced levels of production of leukotoxin are characterized by a 530-bp deletion from the promoter region of the leukotoxin gene operon. Previous isolates with this deletion constituted a single clone belonging to serotype b, although they displayed minor differences among each other. We have analyzed the geographic dissemination of this clone by examining 326 A. actinomycetemcomitans isolates from healthy and periodontally diseased individuals as well as from patients with different types of extraoral infections originating from countries worldwide. A total of 38 isolates, all belonging to the same clone, showed the 530-bp deletion. Comparison of a 440-bp sequence from the promoter region of the leukotoxin gene operon from 10 of these strains revealed complete identity, which indicates that the deletion originates from a single mutational event. This particular clone was exclusively associated with localized juvenile periodontitis (LJP). In at least 12 of 28 families from which the clone was isolated, more than one family member had LJP. Notably, all the subjects carrying this clone had a genetic affiliation with the African population. These observations suggest that juvenile periodontitis in some adolescents with an African origin is associated with a disseminating clone of A. actinomycetemcomitans.

Actinobacillus Infections↗
PubMedDate not supplied

Ultrastructural evidence of a Papova-type viral morphogenesis phenomenon in infiltrating cells from juvenile periodontal lesions. A case report.

Electron optic study of inflammation infiltrating cells in juvenile periodontopathic tissue showed the presence of "nuclear-body"-type structures and of nuclear and cytoplasmic virus-like inclusions, which predominated in cells presenting degenerative modifications commonly encountered in malignant cells. Their significance is discussed.

Aggressive Periodontitis↗
PubMed1985

The thermodynamic behaviour of labial gingiva in patients with destructive periodontal disease.

The temperature changes of the labial gingiva and mucosa of the maxillary incisor regions were investigated using computer-assisted thermography. 9 patients with destructive periodontal disease (7 female and 2 male, aged between 12 and 33 years, undergoing periodontal treatment for periods varying from 6 months to 12 years) and 10 volunteers with clinically normal periodontia (6 female and 4 male, aged between 19 and 26 years) took part in this study. The gingivae and mucosae were initially cooled using a homogeneous flow of air (15 l/min at 15 degrees C) for 3 min. 20 s after the cooling phase, temperature increases of these soft tissues were sequentially recorded using 48 thermograms per person. This procedure was repeated 4 times for each person examined. The weighted mean of the time constants of the tissue re-warming curves was significantly higher (p less than 0.025) for the periodontitis group (152 +/- 6 s) compared to the clinically healthy group (110 +/- 9 s). The different thermodynamic behaviour between the 2 groups studied indicated differences in the blood-flow and/or its regulation.

Adolescent↗
PubMed1998

Dissolution of type I collagen fibrils by gingival fibroblasts isolated from patients of various periodontitis categories.

The classification of periodontitis in various disease categories, including juvenile periodontitis, rapidly progressive adult periodontitis and slowly progressive adult periodontitis is based mainly on differences in disease progression and age group susceptibility. Because dissolution of collagen fibers is an integral part of periodontal attachment loss, we investigated whether the clinical differences among these periodontitis/control groups are reflected in the collagen-degrading activity of gingival fibroblasts isolated from affected tissues. All fibroblast strains isolated from the 4 groups (n = 48) displayed cell-associated collagenolytic activity when seeded in contact with a reconstituted film of type I collagen fibrils. Cells from the control group (n = 14) dissolved the collagen fibril film twice as fast as those from each of the 3 disease groups (juvenile periodontitis (n = 13), rapidly progressive adult periodontitis (n = 7), and slowly progressive adult periodontitis (n = 14)). Both interleukin-1 beta and phorbolester accelerated the rate of dissolution 2-4-fold, but even after cytokine or phorbolester stimulation control cells were still considerably more effective in dissolving the collagen fibrils than cells from the disease groups. The observation made in this study, that dissolution of collagen fibrils by gingival fibroblasts from periodontally diseased individuals is significantly slower than by cells from healthy control subjects, challenges disease paradigms based on a direct relationship between collagenolytic potential and disease activity.

Adolescent↗
PubMed2000

Periodontal diagnostics.

Periodontitis affects a subset of the population and our current thinking is that progression of periodontal disease may be either continuous or cyclical (burst hypothesis). These features make screening and diagnostic tools desirable in the management of this disease. Although many potential markers exist, several difficulties hamper our ability to declare them diagnostic tests with proven utility. The 'gold standard' for active periodontal disease is not available and inflammation due to gingivally confined lesions (gingivitis) and periodontal inflammation which results in attachment loss is a potential confounder of any test based on assessing the host response elements of the disease. The current absence of proof for the progression of periodontal disease i.e., whether or not the burst hypothesis is correct, is a further problem. Although much is written about the need for markers of current or future disease which will prevent us from overtreating pockets, the time, effort and cost involved in testing these sites has to be balanced against the relative ease and speed of routine therapy such as root planing. In addition, we are still some way from the development and validation of reliable host or microbial testing methods. In terms of screening tests for diseases such as the early-onset forms of periodontitis, the research and development on diagnostic tools involving genetic polymorphisms, specific genes, systemic antibodies or leucocyte cell surface markers of the patients, may become a clinical reality in time. One could envisage chairside tests using blood from thumb pricks being capable of determining a young individual's risk of developing disease at a later age, and thus the need for a timely prevention programme. Before applying any test we should reconsider what treatment planning effects a positive or negative result will have, and any test which does not influence the treatment plan is redundant. Whether periodontal diagnostic tests will be developed which will indicate to the clinician the need for various treatment regimes other than root planing, is still an open question. For example, in the future, a test of specific antibody levels in patients prior to treatment might indicate their likely response to therapy and thus the need for additional therapeutic agents such as antibiotics. Periodontal diagnostic tests are still at an early stage of development and much work remains to be performed to fully validate their utility such that they become an important and cost effective aspect of clinical treatment planning, screening or patient monitoring.

Aggressive Periodontitis↗
PubMed1989

[A case of prepuberty periodontitis--a classification based on laboratory results].

The rare entity of periodontitis in a 4 1/2-year old child and subsequent changes over a 4-year follow-up period will be presented. Various examinations (among other immunological tests, biochemical differentiation of dermal fibroblasts, and ultrastructural skin biopsies) were made to identify whether this was a case of genuine prepuberty periodontitis or of periodontitis secondary to a general disease. On the basis of the results the case was diagnosed as Ehlers-Danlos Disease Type VIII, although at the same time signs of impaired granulocyte function were observed.

Aggressive Periodontitis↗
PubMed1990

The long-term efficacy of systemic doxycycline medication in the treatment of localized juvenile periodontitis.

The presence of Actinobacillus actinomycetemcomitans in the deep periodontal pockets of patients with localized juvenile periodontitis has been causally associated with active periodontal destruction. Thus, eradication of this microorganism has become the goal of treatment. It has been postulated that such eradication cannot be achieved without systemic antimicrobial treatment. The efficacy of a semisynthetic tetracycline (doxycycline) in a double-blind follow-up study of 14 patients with localized juvenile periodontitis was evaluated. For assessment of the periodontal status, probing depth and bleeding after probing at 4 sites of all teeth were recorded. The treatment consisted of instruction in oral hygiene, scaling and root planing, periodontal surgery and systemic medication for 2 weeks with either doxycycline (Doximycin) or placebo. A. actinomycetemcomitans was cultivated from subgingival samples taken from 4 sites. The periodontal condition and the prevalence of A. actinomycetemcomitans were monitored at the baseline and at 2, 8 and 20 months. The periodontal condition improved in both groups; the only significant difference was a greater reduction in the prevalence of A. actinomycetemcomitans 8 months after treatment with doxycycline as compared with the placebo.

Actinobacillus↗
PubMed1985

Effect of periodontal therapy on spontaneous lymphocyte response and neutrophil chemotaxis in localized and generalized juvenile periodontitis patients.

The etiology and pathogenesis of juvenile periodontitis may involve dysfunctions of the host response. In particular, the neutrophil and the lymphocyte have been implicated in the disease. The purpose of the present study was to examine the in vitro spontaneous lymphocyte response and neutrophil chemotaxis in populations of localized juvenile periodontitis (LJP) and generalized juvenile periodontitis (GJP) patients and age- and sex-matched healthy subjects (HS). These laboratory values were also evaluated immediately following and 1 year after periodontal therapy. The results show that spontaneous lymphocyte responses reflecting the autologous mixed lymphocyte reaction (AMLR) are depressed for GJP patients. The decreased AMLR in the GJP group appears to represent an abnormal T-cell function which may reflect activity of the periodontal lesion. LJP patients have an increased AMLR response, although it was not statistically significant. 1 year following active periodontal therapy, spontaneous lymphocyte responsiveness returned to normal in most GJP patients. The increased spontaneous lymphocyte responsiveness of LJP patients was not changed either immediately following active periodontal therapy or 1 year later. LJP and GJP patients exhibited a neutrophil chemotaxis defect when compared to cells from HS. This neutrophil defect was still observed 1 year following active therapy.

Adolescent↗
PubMed1996

Dental caries and tooth loss in adolescents with early-onset periodontitis.

The aim of this study was to assess the caries experience and tooth loss over 6 years in subjects with early-onset periodontitis as compared to their matched controls, and to describe the characteristics of teeth lost during this period. A multi-stage probability sample representing 8th to 12th grade U.S. schoolchildren were screened during the 1986/1987 school year to identify subjects with early-onset periodontitis (cases). The examination included measuring the clinical attachment level, presence of caries and dental restorations, and tooth loss. A random sample of controls without early-onset periodontitis were selected for a follow-up examination and were matched to cases on gender, race, age, and geographic location. A total of 266 subjects, with a mean age of 16 years at baseline, were examined during the 1992/1993 school year and were classified into localized (LJP) and generalized juvenile periodontitis (GJP), incidental attachment loss (IAL), and control groups. Whites had more caries experience than Blacks and Hispanics, but there were no significant differences in tooth loss between the ethnic groups. The LJP and the IAL groups, respectively, had higher and lower overall caries experience than the control group. The LJP group had a significantly higher number of missing teeth at follow-up, and exhibited more extensive tooth mortality during 6 years than the control group. The GJP group also showed more tooth loss than the control group, but the difference was not statistically significant. In the LJP, GJP, IAL, and control groups, respectively, 43%, 32%, 26%, and 18% of the subjects lost teeth over 6 years due to disease. The findings showed differences in caries activity between the early-onset periodontitis groups and a variation by race. The findings suggest that loss of periodontal support was the principal cause for tooth loss in the LJP and GJP groups, and that dental caries was the principal cause for tooth extraction in the IAL and the control groups.

Adolescent↗