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PubMed1996

Potential of diagnostic microbiology for treatment and prognosis of dental caries and periodontal diseases.

Most evidence suggests that only a finite number of bacteria are responsible for dental caries and periodontal diseases. This knowledge led to the development of microbial tests which can identify suspected pathogens. Current evaluation of the diagnostic power of microbial tests has shown that they have a low sensitivity and a low prognostic value. Despite these shortcomings, there are valid indications for microbiological-based diagnosis. Salivary microbial tests for the detection of mutans streptococci and lactobacilli may be useful, for example, in young children, oligosialic patients, and orthodontic patients. These tests can be used to monitor the success of chemopreventive measures or compliance with dietary recommendations. Microbial diagnosis, may also be valuable in the treatment of early-onset periodontitis or in subjects who respond poorly to periodontal therapy. The use of microbial tests to monitor the efficacy of chemotherapy or mechanical treatment is of particular interest.

Aggressive Periodontitis↗
PubMed1995

Smoking and its effects on early-onset periodontitis.

The findings of a recent study show that smoking was more prevalent in a group of patients with generalized early-onset periodontitis and adult periodontitis than in patients with localized juvenile periodontitis or healthy periodontium. In patients with generalized early-onset periodontitis, smoking had a significant effect on periodontal attachment loss; these patients had significantly more teeth with affected sites and a greater mean loss of attachment than patients who did not smoke. Thus, the risk of smoking could greatly accelerate tooth loss in this relatively young group of individuals who are already at high risk for progressive periodontal attachment loss.

Adolescent↗
PubMedDate not supplied

Development of a classification system for periodontal diseases and conditions.

Classification systems are necessary in order to provide a framework in which to scientifically study the etiology, pathogenesis, and treatment of diseases in an orderly fashion. In addition, such systems give clinicians a way to organize the health care needs of their patients. The last time scientists and clinicians in the field of periodontology and related areas agreed upon a classification system for periodontal diseases was in 1989 at the World Workshop in Clinical Periodontics. Subsequently, a simpler classification was agreed upon at the 1st European Workshop in Periodontology. These classification systems have been widely used by clinicians and research scientists throughout the world. Unfortunately, the 1989 classification had many shortcomings, including: (1) considerable overlap in disease categories, (2) absence of a gingival disease component, (3) inappropriate emphasis on age of onset of disease and rates of progression, and (4) inadequate or unclear classification criteria. The 1993 European classification lacked the detail necessary for adequate characterization of the broad spectrum of periodontal diseases encountered in clinical practice. The need for a revised classification system for periodontal diseases was emphasized during the 1996 World Workshop in Periodontics. In 1997 the American Academy of Periodontology responded to this need and formed a committee to plan and organize an international workshop to revise the classification system for periodontal diseases. The proceedings in this volume are the result of this reclassification effort. The process involved development by the Organizing Committee of an outline for a new classification and identification of individuals to write state-of-the-science reviews for each of the items on the outline. The reviewers were encouraged to depart from the preliminary outline if there were data to support any modifications. On October 30-November 2, 1999, the International Workshop for a Classification of Periodontal Diseases and Conditions was held and a new classification was agreed upon (Figure 1). This paper summarizes how the new classification for periodontal diseases and conditions presented in this volume differs from the classification system developed at the 1989 World Workshop in Clinical Periodontics. In addition, an analysis of the rationale is provided for each of the modifications and changes.

Adolescent↗
PubMed1988

Association between HLA antigens and periodontal disease.

HLA-A, B and DR antigen frequencies were determined in three groups of periodontally diagnosed subjects: 49 patients with rapidly progressive periodontitis, 40 elderly subjects with minimal disease (considered as a resistant group) and 30 young subjects with minimal disease. The relative risk for HLA-A9 (previously reported to be associated with periodontal disease) was 15.5. HLA-A9 was present in 36.7% of the patients and 2.5% of the resistant group. HLA-A10 showed a significantly increased incidence in the resistant group (30.0%) compared to a non-periodontally diagnosed control population (9.0%), and was absent from the patient group. These findings provide additional evidence for the involvement of HLA-A9 in susceptibility to periodontitis, and suggest that A10 may play a role in resistance to the disease.

Adult↗
PubMed2000

The in vivo expression of the collagenolytic matrix metalloproteinases (MMP-2, -8, -13, and -14) and matrilysin (MMP-7) in adult and localized juvenile periodontitis.

Periodontal inflammation is characterized by irreversible degradation of periodontal ligament collagen fibers leading to loss of tooth attachment. Cultured gingival keratinocytes and fibroblasts express, in vitro, various matrix metalloproteinases (MMPs) which can degrade fibrillar collagens. We hypothesized that several MMPs are also synthesized in vivo by sulcular epithelium, and analyzed the collagenolytic MMPs (MMP-2, -8, -13, and -14) and matrilysin (MMP-7) in gingival tissue specimens and gingival crevicular fluid from adult and localized juvenile periodontitis patients by in situ hybridization, immunohistochemistry, and Western immunoblotting. MMP-2, -7, -8, and -13 were expressed in gingival sulcular epithelium. MMP-7 and -13 were also located in fibroblasts and macrophages, and MMP-8 in neutrophils. MMP-8- and -13-positive cells/mm2 were higher in periodontitis gingiva when compared with healthy control tissue (p < 0.01). In periodontal diseases, gingival sulcular epithelium expresses several, rather than a single, collagenolytic MMPs, and this proteolytic cascade is evidently responsible for the tissue destruction characteristic of adult and juvenile periodontitis.

Adolescent↗
PubMed1989

Clinical and laboratory characterization of early onset periodontitis.

Clinical and laboratory data were compared in 72 patients with localized periodontitis (LP) and 103 patients with generalized periodontitis (GP). Significantly more LP than GP cases had decreased neutrophil chemotaxis (CTX), and were seropositive for Actinobacillus actinomycetemcomitans (Aa). Significantly, more GP cases were seropositive for Bacteroides gingivalis (Bg). All clinical indices were similar on affected teeth in LP and GP, but the attachment loss was greater on clinically unaffected teeth in GP when compared with LP. LP cases with CTX defects had a significantly lower mean age, were more often seropositive for Aa antibodies, and were more often female than LP patients with normal CTX. Significantly more GP cases with CTX defects were seropositive for Aa antibody. GP patients with normal CTX had a higher plaque index on both affected and unaffected teeth than did GP patients with a CTX defect. Our data suggest that chemotaxis and/or specific bacteria may be contributory, but not always necessary, factors in these disorders. The overlap in clinical and laboratory profiles of LP and GP continues to cloud the distinction of these early onset forms of periodontitis.

Adolescent↗
PubMed1997

Role of psychiatric disorders in self-inflicted periodontal injury: a case report.

Self-inflicted or factitious injuries (FI) are not uncommon in psychiatric patients. In general, this kind of behavior is linked to secondary gain. However, the role of underlying psychiatric illness should not be overlooked. Usually, the diagnosis of factitious injury can be confirmed by a careful medical-dental history, clinical appearance of the lesion, laboratory investigations, and response to established treatment protocol. A case is presented in which repetitive injurious behavior resulted in rapid periodontal attachment loss. The lesion responded well to conservative periodontal treatment. The role of underlying psychiatric morbidity leading to repetitive self-injurious behavior is discussed.

Adolescent↗
PubMed1999

One stage full- versus partial-mouth disinfection in the treatment of chronic adult or generalized early-onset periodontitis. I. Long-term clinical observations.

BACKGROUND: A standard treatment strategy for periodontal infections often consists of 4 consecutive sessions of scaling and root planing (per quadrant, at 1- to 2-week intervals), without proper disinfection of the remaining intra-oral niches for periodontopathogens. This could theoretically lead to a reinfection of previously disinfected pockets by bacteria from an untreated region/niche. This study aimed to investigate, over an 8-month period, the clinical benefits of a one stage full-mouth disinfection in the control of severe periodontitis. METHODS: Sixteen patients with early-onset periodontitis and 24 patients with severe adult periodontitis were randomly assigned to test and control groups. The control group was scaled and root planed, per quadrant, at 2-week intervals and given standard oral hygiene instructions. A one stage full-mouth disinfection (test group) was sought by scaling and root planing the 4 quadrants within 24 hours in combination with the application of chlorhexidine to all intra-oral niches for periodontopathogens. Besides oral hygiene, the test group also rinsed twice daily with a 0.2% chlorhexidine solution and sprayed the tonsils with a 0.2% chlorhexidine spray, for 2 months. The plaque index, gingival index, probing depth, bleeding on probing, gingival recession, and clinical attachment level were recorded at baseline and at 1, 2, 4, and 8 months afterwards. RESULTS: The one stage full-mouth disinfection resulted, in comparison to the standard therapy, in a significant (P <0.001) additional probing depth reduction and gain in attachment up to 8 months. For initial pockets > or =7 mm, the "additional" probing depth reduction at the 8 month follow-up was 1.2 mm for single-rooted and 0.9 mm for multi-rooted teeth, with corresponding additional gains in attachment of 1.0 mm and 0.8 mm, respectively. The additional improvements were observed for all subgroups (adult periodontitis, generalized early-onset cases, smokers), with the largest differences in the non-smoking adult periodontitis patients. CONCLUSIONS: These findings suggest that a one stage full-mouth disinfection results in an improved clinical outcome for the treatment of chronic adult or early-onset periodontitis as compared to scaling and root planing per quadrant at 2-week intervals.

Adult↗
PubMed1990

[Juvenile periodontopathies as a manifestation of an ectodermal abnormality].

By means of three cases of progressive infantile periodontal diseases the author points at simultaneous alteration in the keratinization of the skin in the sense of keratosis palmaris et plantaris (Papillon-Lefèvre-Disease). This complex of anomalies is supposed to be a hereditary acro-ectodermal systemic inferiority, primarily consisting in an epithelial disturbance. But it is also necessary to regard the infantile progressive periodontal insufficiency as an obligatory or facultative attendant symptom of general diseases. The therapy is only symptomatic, complete return to health is not realizable.

Aggressive Periodontitis↗
PubMed1989

[Microbiological changes in subgingival flora after treatment with amoxicillin-clavulanic acid].

The association amoxicillin-clavulanic acid can be employed as an alternative to the usual antibiotic therapy of periodontitis. The purpose of this study was to determine subgingival microbial changes in 33 patients with periodontitis after using amoxicillin (500 mgrs.-t.i.d.) and clavulanic acid (125 mgrs.-t.i.d.) for 5 days. It resulted clinically in a decrease of both gingival index and plaque index (not significant) and microbiologically in absence of the main bacterial pathogens found pretreatment, such as Bacteroides melaninogenicus, Bacteroides intermedius, Eikenella corrodens and Actinomyces sp., although it was not able to eliminate Actinobacillus asinomycetemcomitans from a juvenile periodontitis and from a prepuberal periodontitis patient. Atibiotic susceptibility testing showed that all bacteria tested were sensitive to this antibiotic. Although this short term study shows good microbial response of main periodontal pathogens, long term studies are necessary to assess the effect of this antibiotic in periodontitis therapy.

Adolescent↗
PubMed1999

Humoral immune responses in periodontal disease may have mucosal and systemic immune features.

The humoral immune response, especially IgG and IgA, is considered to be protective in the pathogenesis of periodontal disease, but the precise mechanisms are still unknown. Immunoglobulins arriving at the periodontal lesion are from both systemic and local tissue sources. In order to understand better the local immunoglobulin production, we examined biopsy tissue from periodontitis lesions for the expression of IgM, IgG, IgA, IgE and in addition the IgG and IgA subclasses and J-chain by in situ hybridization. Tissues examined were superficial inflamed gingiva and the deeper granulation tissue from periodontal sites. These data confirm that IgM, and IgG and IgA subclass proteins and J-chain can be locally produced in the periodontitis tissues. IgG1 mRNA-expressing cells were predominant in the granulation tissues and in the gingiva, constituting approx. 65% of the total IgG-expressing plasma cells. There was a significantly increased proportion of IgA-expressing plasma cells in the gingiva compared with the granulation tissue (P < 0.01). Most of the IgA-expressing plasma cells were IgA1, but a greater proportion expressed IgA2 mRNA and J-chain mRNA in the gingival tissues (30.5% and 7.5%, respectively) than in the periodontal granulation tissues (19% and 0-4%, respectively). The J-chain or dimeric IgA2-expressing plasma cells were located adjacent to the epithelial cells, suggesting that this tissue demonstrates features consistent with a mucosal immune response. Furthermore, we were able to detect the secretory component in gingival and junctional epithelial cells, demonstrating that the periodontal epithelium shares features with mucosal epithelium. In contrast, deeper tissues had more plasma cells that expressed IgM, and less expressing IgA, a response which appears more akin to the systemic immune response. In conclusion, this study suggests that immune mechanisms involved in the pathogenesis of periodontitis may involve features of both the mucosal and systemic immune systems, dependent on tissue location.

Adult↗
PubMed1997

CD29 expression on CD4+ gingival lymphocytes supports migration of activated memory T lymphocytes to diseased periodontal tissue.

The cell surface phenotypes of CD+ cells extracted from inflammatory periodontal disease tissues were analyzed using two- and three-color immunofluorescence and flow cytometry. Cells extracted from both adult periodontal and localized juvenile periodontitis lesions showed a depressed CD4/CD8 ratio (1.0 +/- 0.1 adult periodontitis and 1.1 +/- 0.1 localized juvenile periodontitis) compared with cells recovered from normal/marginal gingivitis tissue (1.8 +/- 0.2) or with normal peripheral blood cells (2.1 +/- 0.1) or periodontal disease blood cells (2.1 +/- 0.1 and 1.7 +/- 0.1 for adult periodontitis and juvenile periodontitis, respectively). The monoclonal antibodies anti-2H4 and anti-4B4 were used to identify the CD45RA and CD29 antigens respectively on CD4+ T cells from the periodontal disease lesions. In peripheral blood. CD29+ cells accounted for 66-77% of the CD4+ population, and CD45RA+ cells accounted for 22-27% of the CD4+ subset. No differences in expression were found between peripheral blood lymphocytes from normal subjects and from periodontal disease patients. Two-color analyses of lymphocytes from periodontal diseased tissues showed that 87-89% of the CD4+ population were CD29+ and that 70-79% of the CD4+ cells were CD45RA+. Normal tissues contained significantly fewer CD4+CD29+ cells (56 +/- 4%) and CD4+CD45RA+ cells (40 +/- 4%) on average, and few, if any double-labelled cells could be accounted for. These data implied that a significant percentage of the CD4+ cells from the diseased tissues were both CD29+ and CD45RA+ and that these populations are found in quite different proportions in diseased periodontal tissue than in peripheral blood or nondiseased tissue. In further analyses using three-color cytometry the mean percentage of CD4+ CD29+ CD45RA+ lymphocytes extracted from periodontal disease lesions was 43 +/- 9% of the CD4+ population. These results suggest that CD4+ T lymphocytes in periodontal disease not only demonstrate varying levels of maturity but also that the accumulation of CD4+ T cells within the periodontal tissues may be a result of increased adhesion and transendothelial migration.

Adult↗
PubMed2004

Microbiological profile of early onset/aggressive periodontitis patients.

OBJECTIVES: The objectives of this study were to characterize the bacterial profile and to seek possible bacterial associations in the subgingival microbiota of early onset periodontitis/aggressive periodontitis patients by using two different techniques, culture and immunofluorescence. MATERIAL AND METHODS: The study group consisted of 66 systemically healthy individuals with evidence of early onset periodontitis - 41 females and 25 males aged 23-35 years (mean 31.1 +/- 3.1 years). Bacterial samples were collected from the deepest site in each quadrant, resulting in a total of 264 sites with a mean probing pocket depth of 6.6 +/- 1.5 mm. Samples were cultured anaerobically and in 10% CO(2) using selective and nonselective media, and isolates were characterized to species level. Indirect immunofluorescence using monoclonal antibodies was applied to detect Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythia (Bacteroides forsythus, Tannerella forsythensis), Prevotella intermedia/Prevotella nigrescens, Campylobacter rectus, Peptostreptococcus micros and Actinomyces israelii. RESULTS: 93.6% of sampled sites showed bleeding on probing and 23.5% were positive for suppuration. P. intermedia/P. nigrescens, P. gingivalis, and C. rectus were detected in 77.3-85.9% of samples using culture methods and in 85.6-91.3% using immunofluorescence. P. micros and A. actinomycetemcomitans were found, respectively, in 63.3% and 25.0% of all sites using culturing and in 58.7% and 27.7% sites using immunofluorescence. Significantly strong positive associations were observed between T. forsythia and C. rectus (odds ratio 109.46), and T. forsythia and P. gingivalis (odd ratio 90.26), whereas a negative association was seen between P. intermedia/P. nigrescens and A. actinomycetemcomitans (odds ratio 0.42). Coinfection by P. gingivalis, T. forsythia, P. intermedia/P. nigrescens and C. rectus was observed in 62.1% of the test sites, and in 89.4% of the studied subjects. The sensitivity of immunofluorescence for T. forsythia, C. rectus, P. intermedia/P. nigrescens and P. gingivalis was found to be very high (0.99-0.94) using culture as the reference detection method. The agreement between culture and immunofluorescence in detecting the presence or absence of the investigated species was 85.2-88.1% for P. gingivalis, P. intermedia/P. nigrescens, C. rectus, and T. forsythia, 75.9% for A. actinomycetemcomitans and 70.4% for P. micros. CONCLUSIONS: The microbial profile of the early onset/aggressive periodontitis population was complex. The agreement between the two detection methods was very high.

Acute Disease↗
PubMed1986

The nature of the inflammatory infiltrates in childhood gingivitis, juvenile periodontitis and adult periodontitis: immunocytochemical studies using a monoclonal antibody to HLADr.

Routinely fixed and processed gingival biopsies from childhood gingivitis, juvenile periodontitis and chronic adult periodontitis patients have been stained immunocytochemically with a monoclonal anti HLADr antibody to aid in the identification and quantification of cell types in the inflammatory infiltrates. Using immunoperoxidase staining and morphological criteria, 9 cell types were quantified in 30 patients. Lesions in the 3 groups were found to differ widely both in size and composition. In the small childhood gingivitis lesions, most cells were small lymphocytes, over half of which were HLADr positive, whereas in juvenile periodontitis biopsies, well over half the infiltrate was plasma cells. The chronic adult periodontitis samples showed greater variability in composition between these 2 extremes, perhaps reflecting differences in disease activity. These results suggest that, when disease is quiescent, the volume of inflamed gingival connective tissue is small and is dominated by B-small lymphocytes, whilst on activation, the lesion increases in size and much of the B-lymphocyte population is transformed to plasma cells. This view corroborates the results of other workers with regard to juvenile periodontitis, but suggests a different interpretation of the quiescent lesion of childhood gingivitis from that current in the literature.

Adult↗
PubMed1997

Loss of deciduous teeth and germs of permanent incisors in a 4-year-old child. An atypic prepubertal periodontitis? A clinical, microbiological, immunological and ultrastructural study.

A 4-year-old child was referred, in April 1988, to Rennes Dental School (France) for deciduous tooth mobility with premature loss of 4 deciduous teeth and germs of 2 permanent incisors. Microbiological examinations by culture revealed the presence of the periodontal pathogen Actinobacillus actinomycetemcomitans. Immunofluorescence of plaque samples revealed the presence of Porphyromonas gingivalis that had not been isolated by culture. Neutrophil functions were within normal ranges. Transmission electron microscopy of gingiva showed a disorganised epithelium. The connective tissue was infiltrated by inflammatory cells. The basement membranes were normal, but the connective tissue-epithelium interface was mainly composed of short rete pegs. Scanning electron microscopy of extracted deciduous teeth revealed lack of cementum, lacunae in the cementum and lack of fibrillar insertion on the middle part of the root. Skin lesions, mainly situated on face, were observed. Treatment was by extraction of mobile deciduous teeth combined with 3-week courses of metronidazole. Clinical and microbiological follow-up was continued over a 7-year period. No periodontal lesions have been detected since eruption of the permanent teeth. The present subgingival and lingual microflora (December 1995) is composed of bacteria associated with periodontal health. However, the future appearance of a hitherto undetected systemic disease is still possible.

Aggregatibacter actinomycetemcomitans↗
PubMed1987

Tissue localization of Actinobacillus actinomycetemcomitans in human periodontitis. II. Correlation between immunofluorescence and culture techniques.

Recent immunohistological studies have suggested that Actinobacillus actinomycetemcomitans is present in the gingival tissues in juvenile periodontitis lesions. The present study examined tissue bound A. actinomycetemcomitans by bacterial culture and immunohistological demonstration of antigen in tissue. A total of 14 periodontitis lesions were examined. Eleven biopsies were obtained from gingiva adjacent to A. actinomycetemcomitans infected pockets, while the remaining three control biopsies were obtained from gingiva adjacent to pockets where subgingival A. actinomycetemcomitans infection could not be detected. Each biopsy was hemisected, one half was used for immunofluorescence microscopic examination while the other half was processed for culture of A. actinomycetemcomitans. The latter section was surface-disinfected, repeatedly washed and then minced to release bacteria from within the tissues. Aliquots from the serial washings and the minced tissue suspension were cultured on medium selective for A. actinomycetemcomitans. Surface disinfection and serial washings gradually decreased cultivable A. actinomycetemcomitans in the washings aliquots. Following tissue disruption, an increase in colony-forming units of A. actinomycetemcomitans was seen from eight of the 11 test biopsies. This bacterium could not be detected in washings or minced tissue suspensions from the control biopsies obtained from lesions in which subgingival A. actinomycetemcomitans was previously not detected. A positive correlation was seen between the presence of A. actinomycetemcomitans antigens in the gingival biopsies and; (1) A. actinomycetemcomitans colony-forming units released from the minced tissues (r = 0.90, p = 0.000), as well as; (2) the colony-forming units from the periodontal pocket (r = 0.62, P = 0.017).(ABSTRACT TRUNCATED AT 250 WORDS)

Actinobacillus↗