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Immunohistochemical localization of Actinobacillus actinomycetemcomitans in sections of gingival tissue in localized juvenile periodontitis.
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Genetic approach to the study of epidemiology and pathogenesis of Actinobacillus actinomycetemcomitans in localized juvenile periodontitis.
Actinobacillus actinomycetemcomitans isolates from periodontal pockets were examined for restriction fragment-length polymorphism using a characterized 4.7-kb DNA probe. A total of 6 patterns of RFLP was found in 133 isolates originating from 12 subjects. No relatedness was found between RFLP types and serotypes. Different periodontal sites within the same subject and different individuals within the same family sometimes showed only one type of A. actinomycetemcomitans RFLP. When members among the same family showed 2 RFLP types, children were always infected with the A. actinomycetemcomitans strains found in at least one of the parents. These findings support the concept of familial spread of A. actinomycetemcomitans. A. actinomycetemcomitans RFLP type B, corresponding to reference strain JP2, seems to be particularly virulent, as indicated from the presence of RFLP type B in 3 subjects who converted from a healthy periodontal state to localized juvenile periodontitis. RFLP type B was not detected in any of the 21 A. actinomycetemcomitans-infected patients with adult periodontitis. The RFLP method seems to be useful in determining the epidemiology and possibly the potential virulence of periodontal strains of A. actinomycetemcomitans.
Some local and systemic immunological features of prepubertal periodontitis.
OBJECTIVES: The aim of the present investigation was to study local (gingival) and systemic host defense characteristics in a sample of children exhibiting local prepubertal periodontitis (LPP). MATERIAL AND METHODS: 2 groups of subjects were included in the present study. One group consisted of 11 children (9.5+/-2.0 years) with signs of periodontal disease (LPP group). A 2nd group comprised 21 adults (48.1+/-5.8 years) with advanced periodontal disease: adult periodontitis (AP) group. Gingival biopsies and a sample of peripheral blood were obtained in each individual of the AP group and in 7 out of the 11 subjects in the LPP group. The biopsies were prepared for morphometrical and immunohistochemical analysis and the blood samples prepared for immunohistochemical analysis. RESULTS: The cellular infiltrates in the biopsies of the LPP group contained a larger proportion of lymphocytes and, in particular B cells, than was the case in the AP group. The TCR Valpha/Vbeta gene expression in the lesions in the AP group was dominated by Vbeta 17 and in the LPP group by Valpha2. The content in peripheral blood of various lymphocyte sub-populations and TCR Valpha/Vbeta gene expression in the 2 groups was almost similar. CONCLUSION: It is suggested that (i) the systemic host response in children with prepubertal periodontitis has many features in common with that seen in adult patients but that (II) local defense mechanisms in the periodontitis lesion of LPP differ from those in adult periodontitis.
In vivo cleavage of immunoglobulin A1 by immunoglobulin A1 proteases from Prevotella and Capnocytophaga species.
Immunoglobulin A1 (IgA1) proteases secreted by oral Prevotella and Capnocytophaga species specifically cleave IgA1 at the same peptide bond in the hinge region, leaving intact monomeric Fab and Fc fragments. Assuming that Prevotella- and Capnocytophaga-induced Fab fragments of IgA1 expose a specific immunogenic neoepitope at the cleavage site, we established an enzyme-linked immunosorbent assay to measure human serum antibodies to this neoepitope as indirect evidence of in vivo activity of Prevotella and Capnocytophaga IgA1 proteases. The assay used a monoclonal antibody with specificity for the neoepitope, and the ability to block binding of the monoclonal antibody to the neoepitope was investigated. Absorption of sera with Prevotella melaninogenica-induced Fab fragments of IgA1 resulted in removal of antibodies blocking binding of the monoclonal antibody, whereas absorption with Fab fragments induced by bacterial IgA1 proteases of other cleavage specificities did not remove blocking antibodies. Consequently, we assume that the antibodies detected had been induced by a neoepitope an the Fab fragment of IgA1 exposed exclusively after cleavage with IgA1 proteases from Prevotella and Capnocytophaga, indicating in vivo activity of these IgA1 proteases. Evidence, though indirect, of in vivo activity of Prevotella and Capnocytophaga IgA1 proteases was present in 42 of 92 sera examined and in a significantly higher proportion of sera from adults with periodontal disease compared with control individuals. No correlation with disease was observed for the juvenile periodontitis groups.
Suppression of the periodontopathic microflora in localized juvenile periodontitis by systemic tetracycline.
Since recent studies have implicated Actinobacillus actinomycetemcomitans in the etiology of localized juvenile periodontitis, this investigation determined the effectiveness of subgingival debridement, topical Betadine Solution, and systemic tetracycline in suppressing subgingival A. actinomycetemcomitans and other microorganisms. A total of 20 deep periodontal pockets and 10 normal periodontal sites of 6 localized juvenile periodontitis patients was included in the study. Each patient was treated in 3 stages over a period of 22 weeks, and the result of treatment was monitored for an additional 38 weeks. The first stage of treatment included plaque control, as well as thorough scaling and root planing, composed of at least 6 h of debridement. No concomitant periodontal surgery was performed. In the second stage, Betadine saturated cotton gauze was inserted into the periodontal pockets for 10 min. Stage 3 involved systemic tetracycline therapy (1 g/day) for 14 days. The subgingival microflora was determined at frequent intervals by selective culturing of A. actinomycetemcomitans and Capnocytophaga and by direct microscopic examination. The clinical effect was assessed by measuring changes in probing periodontal attachment level, probing periodontal pocket depth, radiographic alveolar bone mass, and other relevant clinical parameters. Scaling and root planing reduced the total subgingival bacterial counts and the proportions of certain Gram-negative bacteria, but no periodontal pocket became free of A. actinomycetemcomitans. Betadine application had little or no effect on the subgingival microflora. In contrast, tetracycline administered via the systemic route suppressed A. actinomycetemcomitans, Capnocytophaga, and spirochetes to low or undetectable levels in all test periodontal pockets. A. actinomycetemcomitans reappeared in 9 of the deep periodontal pockets after the administration of tetracycline. Most of these 9 pockets became free of detectable A. actinomycetemcomitans during the second week of tetracycline administration, whereas pockets which yielded no A. actinomycetemcomitans after tetracycline therapy became free of the organisms during the first week of tetracycline treatment. This data suggests that systemic tetracycline therapy of localized juvenile periodontitis should, as a practical rule, be continued for 3 weeks. Periodontal destruction continued in 4 deep pockets which all showed high posttetracycline A. actinomycetemcomitans counts. All 6 pockets which demonstrated a marked gain in periodontal attachment yielded no cultivable A. actinomycetemcomitans. No association was found between periodontal disease status and subgingival Capnocytophaga, spirochetes or motile rods. The present study indicates that A. actinomycetemcomitans is an important etiologic agent in localized juvenile periodontitis.(ABSTRACT TRUNCATED AT 400 WORDS)
Multiple forms of gelatinases/type IV collagenases in saliva and gingival crevicular fluid of periodontitis patients.
The aim of the present study was to characterize the eventual presence and molecular forms of gelatinase/type IV collagenase activities in gingival crevicular fluid (GCF) and saliva in different forms of periodontitis; patients with clinically healthy periodontium served as controls. Enzyme activities were monitored electrophoretically by zymography using gelatin and type IV collagen as substrates and analyzed visually and/or densitometrically. Both saliva and GCF collected from adult periodontitis, localized juvenile periodontitis and type II diabetes mellitus periodontitis patients contained species moving identically with gelatinase isolated from human neutrophils or MMP-9 (mean 98 kD), and species with mobility similar to gelatinase in fibroblast cell culture supernatants or MMP-2 (mean 76 kD). Hitherto, undescribed high molecular weight forms (mean 128 kD), were found, possibly representing polymerized or complexed enzyme active/activated in situ in the gel matrix. Small molecular forms of gelatinases (mean 51 kD and 46 kD), unable to cleave type IV collagen, were also found, most likely representing in vivo proteolytically activated, truncated enzymes. Although multiple forms of gelatinases/type IV collagenases in saliva and GCF may take part in the tissue destruction in periodontitis, their profile judged according to molecular weights does not differentiate between different forms of periodontitis.
Gingival inflammation and subgingival calculus as determinants of disease progression in early-onset periodontitis.
This study was undertaken to test the hypothesis that gingival inflammation and dental calculus are important determinants of the development and progression of early-onset periodontitis. The study sample included 156 individuals who were 13-20 years old at baseline and who were examined 2x during 6 years to assess the attachment loss, gingival state and the presence of dental calculus. 33 (21%), 62 (40%), and 61 (39%) individuals were classified as having localized, generalized, or incidental EOP, respectively. The results showed an increase in the % of teeth with overt gingivitis and subgingival calculus, and also an increase in the % of teeth showing attachment loss during the 6-year period in all classification groups. Of teeth with 0-2 mm attachment loss at the beginning of the study and which developed > or = 3 mm attachment loss during the following 6 years, there were 2x as many teeth with overt gingival inflammation, and 4x more teeth with subgingival calculus at baseline than teeth without. Gingivitis and subgingival calculus when present at both examinations resulted in a stronger association with the development of new lesions than presence of these variables at baseline. Teeth with gingivitis at baseline had a significantly higher mean attachment loss during 6 years than teeth without gingivitis (p<0.0001), and teeth with subgingival calculus at baseline had a significantly higher mean attachment loss than teeth without subgingival calculus (p<0.0001). The presence of gingivitis and subgingival calculus at baseline and 6 years later was associated with the occurrence of even higher disease progression during this period. The association between gingival inflammation and subgingival calculus and the development and progression of attachment loss during the study period in the generalized and the localized EOP groups was significantly higher than the association in the incidental EOP group. In an appreciable % of the sites in all 3 groups, however, the presence of the 2 factors was not associated with attachment loss during 6 years. The results suggest a significant association between gingival inflammation and subgingival calculus and the development and progression of early-onset periodontitis.
Increased rate of salivary epidermal growth factor secretion in patients with juvenile periodontitis.
We compared salivary epidermal growth factor (EGF) concentrations in patients with juvenile periodontitis (JP) and periodontally healthy controls. In initial screening of 45 JP patients and a group of healthy controls, significantly higher salivary EGF concentrations were measured in the JP patients. Subsequently, 17 JP patients who had high EGF concentrations in some of their salivary samples were chosen, and a group of age- and sex-matched controls was selected. We then examined their EGF concentrations and EGF secretion rates under standardized conditions in stimulated and unstimulated saliva and studied the expression of EGF receptor (EGF-R) in their gingival tissues. The results showed that the mean EGF concentration (pmol/ml) was slightly higher in JP patients than in controls. However, the difference was statistically significant only in stimulated saliva and when calculated per milligram salivary protein. When EGF release was measured as the rate of EGF secretion (pg/min), significantly higher values were observed in JP patients than in controls both in unstimulated and stimulated saliva. Immunofluorescence microscopy (IF) of gingival samples from JP patients and their controls revealed no quantitative or qualitative differences in the expression of EGF-R. Our results demonstrate the complex nature of salivary EGF release. The elevated rate of salivary EGF secretion in JP patients may be associated with the pathogenetic mechanisms of juvenile periodontitis.
Periodontitis.
The purpose of this review was to assess the scientific and clinical bases for the proposed classification of periodontitis. The clinical and histopathological signs and the etiology of periodontitis were described. Cross-sectional studies were analyzed to determine when onset of periodontitis most frequently occurs in adults. In addition, the progression rates of periodontitis have been assessed from longitudinal studies. No clinical, histopathological, or microbiological features could be identified that would characterize different disease entities of chronic periodontitis. The prevalence, extent, and severity of periodontitis were found to increase continually with higher age and there was no age when onset of disease would most likely occur. The rate of periodontitis progression varies largely between patients and there is no natural threshold for distinguishing various rates of disease progression. The incidence of periodontitis unresponsive to treatment depends on pretreatment progression rate, extent and severity of disease, tooth type, smoking, high levels of putative periodontal pathogens, a deficient immune response, and the type of therapy provided. There is no scientific basis for the classification "adult periodontitis" and "refractory adult periodontitis." Extensive clinical examinations are required for the diagnosis of "rapidly progressive adult periodontitis." It appears unrealistic that these examinations can be performed routinely in clinical practice. Therefore, the classification proposed by the Organizing Committee to define adult, rapidly progressive, and refractory periodontitis as specific disease entities was replaced with a simplified classification of periodontitis based on the scientific data available.
Microbiological study of localized juvenile periodontitis in Panama.
The occurrence of subgingival Actinobacillus actinomycetemcomitans and Capnocytophaga in 12 localized juvenile periodontitis and 10 gingivitis patients from Panama was determined using selective culture techniques. A actinomycetemcomitans was present in all localized juvenile periodontitis lesions studied and was, on average, recovered in hundred-fold-higher numbers from localized juvenile periodontitis lesions than from gingivitis lesions. Capnocytophaga was only recovered in approximately threefold-higher numbers from localized juvenile periodontitis than from gingivitis. The study confirms and extends previous data indicating a close relationship between A actinomycetemcomitans and localized juvenile periodontitis. It is proposed that identification of A actinomycetemcomitans may be a valuable adjunct in the diagnosis of localized juvenile periodontitis.
Immunohistological study with peroxidase-antiperoxidase staining in a case of generalized prepubertal periodontitis.
A case of prepubertal periodontitis was observed and examined immunohistologically with peroxidase-antiperoxidase staining. The patient was an 11-year and 7-month-old Japanese girl, well-developed and well-nourished. Her parents were first cousins. Her chief complaint was the loosening and loss of the permanent teeth. There was a similar history of primary dentition. Her remaining permanent teeth were loosened with severe alveolar bone loss, but calculus deposit was minimal. Significantly, there was no palmar-plantar hyperkeratosis. General examination showed normal data except for the increase of the immunoglobulin concentrations. In neutrophil function tests chemotaxis was depressed, although phagocytosis, random migration and superoxide production were within normal limits. Histologically, neutrophils were seen in the gingival tissue and other findings were also similar to those of adult periodontitis. In immunohistological examination, IgG-bearing cells which mostly consisted of plasma cells predominated in the lesion. Considering the past history, the immunodeficiency and the absence of palmar-plantar hyperkeratosis, the case was diagnosed as prepubertal periodontitis.
The effect of a single application of subgingival antimicrobial or mechanical therapy on the clinical parameters of juvenile periodontitis.
Twenty-six (26) patients, 18 female and 7 male, aged 16 to 25 years (mean age 19.03 +/- 2.2 years) previously diagnosed as suffering from localized juvenile periodontitis were randomly assigned to one of the following treatment groups: 9 patients acted as controls; 8 received subgingival chlorexidine gel; and 9 had subgingival tetracycline paste application. All treatment modalities resulted in a pronounced improvement in PI, GI, and GI-S by 12 weeks (P < 0.001). The mean probing depths also decreased, but there were no significant differences found between the three groups. However, when the interproximal sites of the 3 groups were examined separately from the buccal and lingual sites, it was found that there was a significant (P < 0.05) difference between the probing depths, with the control group showing the greatest reduction of 2.58 mm and the chlorhexidine group showing the least reduction of 1.37 mm. It was concluded that a single application of topical subgingival tetracycline did not result in any short-term improvement over that achieved by standard non-surgical therapy in the clinical parameters of these localized juvenile periodontitis patients.
Bacteriophage infection--a possible mechanism for increased virulence of bacteria associated with rapidly destructive periodontitis.
We have recently isolated several groups of bacteriophages infecting Actinobacillus actinomycetemcomitans from periodontal lesions in patients with rapidly destructive periodontitis. Bacteriophage infection of these bacteria in these patients was restricted to periodontal pockets showing radiographic evidence of recent bone loss and suggests an association between phage-infected A. actinomycetemcomitans and active periodontal disease. On the basis of the biological activity of bacteriophages we propose a working hypothesis to explain the mechanism by which a phage may increase bacterial virulence in periodontal disease.
Comprehensive treatment concept in a young adult patient with severe periodontal disease: a case report.
This case report describes the comprehensive treatment of generalized, advanced periodontal disease in a young patient. In view of the necessary reconstruction, the extensive destruction of the periodontal tissues required a systematic approach to determine the possibilities and the expectations of the patient. The subsequent oral rehabilitation was accomplished with fixed prosthodontics. In the mandible, strategically important anchor teeth were replaced with implants, allowing smaller units to be inserted. The long-term treatment result, however, can only be ensured with the full cooperation of the patient and consistent periodontal maintenance care.
Neutrophil dysfunction in prepubertal periodontitis associated with Papillon-Lefèvre syndrome.
Although prepubertal periodontitis (PP) is often associated with the Papillon-Lefèvre (PLS), the etiopathogenetic mechanism in this disease has not been clarified as yet. A three and half year old female with leukocyte chemotaxis deficiency and decrease of T-lymphocytes is presented. The immunohistochemical evaluation of neutrophils showed a reduction of myeloperoxidase content, whereas ultrastructural studies revealed no particular change. The possible role of such a deficiency in the pathogenesis of the periodontal lesion is discussed.
Circulating immune complexes in localised juvenile periodontitis.
This study determined the quantity and type of circulating immune complexes (CIC) in the sera of 15 patients with localised juvenile periodontitis (LJP). There was a significantly higher level IgG and IgM in LJP patients as compared with the controls. The possible role of CIC in the pathogenesis of juvenile periodontitis is discussed.
[Basement membrane in adult and juvenile/post-juvenile/periodontitis: an ultrastructural study].
Soft tissue changes in the pocket wall in the various forms of periodontitis were studied on an ultrastructural level in 20 patients. Considerable differences were noticed according to the degree of inflammation and severity of the periodontitis.