Biomedical subjects

B Ehmke

Publications and source records attributed to B Ehmke.

9 recordsLinked to original sources

PubMed2005

Sequence variations in rgpA and rgpB of Porphyromonas gingivalis in periodontitis.

OBJECTIVE: The aim of the present study was to determine sequence variations in the active centre of the Arg-X-specific protease encoding genes rgpA and rgpB of clinical Porphyromonas gingivalis isolates and to analyse their prevalence in periodontitis patients before and 3 months after mechanical periodontal therapy. BACKGROUND: Genetic diversity at nucleotides 281, 283, 286 and 331 has been shown to result in amino acid substitutions in the catalytic domain of RgpA and RgpB that affect the substrate specificity and thus may influence the efficacy of Arg-X-protease specific inhibitors. METHODS: Sequence analysis of rgpA and rgpB genes in clinical P. gingivalis strains isolated from subgingival plaque samples of 82 periodontitis patients before and 3 months after mechanical supra- and subgingival debridement was performed. RESULTS: No specific variation within the rgpA sequence was observed. However, the rgpB sequence in the region of the active centre showed five different rgpB genotypes, which were named NYPN, NSSN, NSSK, NYPK and DYPN according to the derived amino acid substitution. Porphyromonas gingivalis genotype NYPN was detected in 27 patients (32.9%) before and in 8 patients (9.8%) after therapy, NSSN in 26 (31.7%) and 10 (12.2%), NSSK in 22 (26.8%) and 2 (2.4%), NYPK in 5 (6.2%) and 1 (1.2%), and DYPN in 1 patient (1.2%) and 0 patients (0%), respectively. Only one patient (1.2%) harboured two P. gingivalis rgpB genotypes (NSSK/NYPN) before treatment; these were no longer detected after therapy. CONCLUSION: The results indicate that five rgpB genotypes are maintained in natural populations of P. gingivalis. These data may be of importance with regard to the development of specific rgpB inhibitors.

Adhesins, Bacterial↗

PubMed2003

Guided tissue regeneration using a polylactic acid barrier.

OBJECTIVES: The purpose of this study was to determine the relative impact of various predictors responsible for the variability in treatment outcome after guided tissue regeneration (GTR) in intraosseous periodontal defects. PATIENTS AND METHODS: 30 patients with chronic periodontitis and at least one intraosseous periodontal lesion (> or =4 mm) were enrolled. Following full-mouth scaling, GTR using polylactic acid membranes was performed at one site in each patient. Main periodontal pathogens, defect morphology, membrane exposure and smoking habit were assessed as predictor variables. Alveolar bone level change served as the primary outcome variable in a multiple regression analysis. RESULTS: After 12 months, the 29 patients completing the study showed alveolar bone changes ranging from 4 mm bone gain to 1 mm bone loss (mean: 1.6+/-0.4 mm gain). Active smoking (beta-weight:-0.49, P=0.003) and persistence of subgingival infection with P. gingivalis (P.g.) (beta-weight:-0.25, P=0.11) were associated with poor treatment outcome. Deep initial intraosseous defects (beta-weight: 0.32, P=0.045) were associated with favorable treatment outcome, and membrane exposure had no impact on bone gain. CONCLUSION: Active smoking was the strongest predictor variable negatively affecting alveolar bone gain following GTR in the treatment of periodontal defects. It was followed by a positive influence of a deeper intraosseous defect and by a negative effect by persistent subgingival infection of P. gingivalis. The relative impact of these factors may be useful in assessing the prognosis of GTR in intraosseous periodontal defects.

Adolescent↗

PubMed2003

Guided tissue regeneration using a polylactic acid barrier. Part I: Environmental effects on bacterial colonization.

OBJECTIVES: The purpose of this study was to assess the dynamics of bacterial colonization in intra-osseous defects following guided tissue regeneration (GTR) therapy using a resorbable barrier. PATIENTS AND METHODS: In each of 30 patients, one intra-osseous defect was treated with GTR using a polylactic acid membrane (Guidor). Plaque samples were taken from the defect site, other teeth and mucous membranes following initial therapy (baseline), and at 3, 6 and 12 months after periodontal surgery. Additionally, samples were taken from the defect sites at 1, 2 and 4 weeks. Actinobacillus actinomycetemcomitans (A.a.), Porphyromonas gingivalis (P.g.), and Bacteroides forsythus (B.f.) were detected by polymerase chain reaction (PCR). Supportive periodontal therapy was performed at 3-month intervals. RESULTS: In the 29 patients completing the study, the assessed microflora was detected in 3 (A.a.), 13 (P.g.) and 14 (B.f.) defect sites at baseline, in 2 (A.a.), 2 (P.g.) and 2 (B.f.) following surgical debridement, and in 6 (A.a.), 10 (P.g.) and 22 (B.f.) at 12 months. Defect site colonization following GTR therapy was significantly correlated with presurgical colonization at other assessed teeth (A.a. and P.g.: tau = 0.45 and 0.66, respectively; P < 0.001), or on mucous membranes (B.f.: tau = 0.44, P < 0.001). CONCLUSION: The colonization of periodontal pathogens at sites treated by GTR may correlate with the intra-oral presence of these pathogens before surgery. If colonization of GTR sites by periodontal pathogens is to be prevented, intra-oral suppression/eradication of these pathogens may be required before surgery.

Absorbable Implants↗

PubMed2003

Serum antibody reactivity against recombinant PrtC of Porphyromonas gingivalis following periodontal therapy.

OBJECTIVES: In 34 patients with chronic periodontitis, the presence of IgA, IgG, and IgG subclass serum antibodies against recombinant PrtC (rPrtC) of Porphyromonas gingivalis was assessed by immunoblot analysis 24 months after therapy. METHODS: rPrtC was produced from P. gingivalis ATTC 33277 using the plasmid pGEX-2T. In addition, intraoral colonization with P. gingivalis was detected by PCR in subgingival plaque and swab samples from buccal mucosae, tonsils and tongue at baseline, 10 d, and 3, 6, 9, 12, 18, and 24 months. RESULTS: All patients were found to harbor P. gingivalis in the oral cavity at least once during the observation period. The identified antibody responses against the rPrtC of P. gingivalis were IgA (97%, i.e. 33/34 patients) and IgG (100%, i.e. 34/34), with an IgG subclass distribution of IgG2 (65%, i.e. 22/34 patients) > IgG3 (47%, i.e. 16/34) > IgG1 (38%, i.e. 13/34) > IgG4 (29%, i.e. 10/34). Anti-rPrtC IgA and IgG antibody reactivity was found in all but one patients (anti-rPrtC IgA negative), who tested negative for P. gingivalis at all of the assessed intraoral sites for at least 6 months before sera collection. There was no association between IgG subclass reactivity against the rPrtC of P. gingivalis and progression of periodontal attachment loss. CONCLUSION: The results indicated that anti-rPrtC IgA and IgG antibodies may serve as an indicator for past or present intraoral colonization with P. gingivalis.

Adult↗

PubMed2003

Sequence analysis of kgp in Porphyromonas gingivalis isolates from periodontitis patients.

The aim of the present study was to determine sequence variation in the Lys-x-specific protease (Kgp) encoding gene kgp of Porphyromonas gingivalis and to analyze its association with periodontal disease severity. Pooled subgingival plaque samples were obtained from the six most severely affected sites of 102 patients with periodontitis. Sequence analysis of the kgp gene in 23 clinical P. gingivalis isolates resulted in the identification of two distinct kgp types (kgp-I and kgp-II) according to sequence differences in the region encoding the catalytic domain. Restriction analysis revealed that 59 of the 102 patients were colonized by kgp-I and 43 by kgp-II. Patients harboring kgp-I or kgp-II showed no significant difference in the severity of periodontal disease as assessed by pocket probing depth and bleeding on probing following adjustment for smoking habit and age. Moreover, no differences in proteolytic activity of Kgp-I and Kgp-II were detected. The results indicated that two kgp types are maintained in natural populations of P. gingivalis.

Adhesins, Bacterial↗

PubMed1999

Protective effect of serum antibodies against a 110-kilodalton protein of Actinobacillus actinomycetemcomitans following periodontal therapy.

Thirty-four adult patients with untreated periodontitis were randomly assigned to receive full mouth scaling alone or scaling with an adjunctive antimicrobial therapy, both followed by supportive periodontal therapy. At 24 months, specific serum immunoglobulin A (IgA), IgG and IgG subclass antibody reactivities against a 110-kDa protein of Actinobacillus actinomycetemcomitans were assessed by Western blot. In patients harboring A. actinomycetemcomitans intraorally, the IgG4 antibody reactivity against the 110-kDa protein of A. actinomycetemcomitans was associated with significantly increased survival rates of teeth and of sites not exhibiting 2 mm or more of probing attachment loss. The same trend was found for IgG3 and IgG2 antibody reactivities, but it was statistically insignificant. No association with clinical treatment outcome was observed for IgA, IgG and IgG1 antibody reactivities. The results indicated that systemic IgG4 antibody reactivity against the 110-kDa protein of A. actinomycetemcomitans may have a protective effect against periodontal disease progression in patients harboring A. actinomycetemcomitans and receiving periodontal therapy.

Adult↗

PubMed1999

Interleukin-1 haplotype and periodontal disease progression following therapy.

The purpose of this study was to assess the prognostic value of the IL-1 haplotype on the progression of periodontal disease following therapy. 48 adult patients with untreated periodontitis harboring Actinobacillus actinomycetemcomitans and/or Porphyromonas gingivalis were randomly assigned to receive full-mouth scaling alone (control) or in combination with systemic metronidazole plus amoxicillin and supragingival irrigation with chlorhexidine digluconate (test). All patients received supportive periodontal therapy at 3 to 6 months intervals. In 33 patients, lymphocyte DNA was analyzed for polymorphism in the IL-1A gene at position -889 and IL-1B gene at position +3953. Overall, 16 of 33 patients (7 of 17 test and 9 of 16 control) carried the IL-1 haplotype. 2 years following initial periodontal therapy, no differences in the survival rates of sites or teeth not exhibiting probing attachment loss of 2 mm or more compared to baseline, were found between patients who tested positive (85% sites, 53% teeth) and patients who tested negative (89% sites, 56% teeth) for the IL-1 haplotype. The results indicated that the IL-1 haplotype may be of limited value for the prognosis of periodontal disease progression following non-surgical periodontal therapy.

Adult↗

PubMed1999

Clonal infection with Actinobacillus actinomycetemcomitans following periodontal therapy.

Mechanical debridement results in a shift of the bacterial composition in the periodontal pocket on the species level. It is unknown, however, whether a clonal change within a species could lead to the emergence of strains with different levels of virulence. Therefore, in the present study, the genetic variability of Actinobacillus actinomycetemcomitans was assessed and strains identified which were associated with periodontal disease progression following periodontal therapy, i.e., refractory periodontitis. Twenty adult patients with untreated periodontitis and subgingival colonization of A. actinomycetemcomitans were randomly assigned to receive full-mouth scaling alone or scaling with an adjunctive antimicrobial therapy. Both groups received supportive periodontal therapy at 3, 6, 9, 12, 18, and 24 months. Subgingival plaque samples were taken at every visit; venous blood was obtained at 24 months only. A. actinomycetemcomitans isolates were typed by the RAPD method, and antibody reactivity against outer membrane proteins was assessed by immunoblot analysis. Eleven distinct RAPD patterns were found in 18 patients completing the study. All patients harbored only one A. actinomycetemcomitans genotype, and within each patient this genotype persisted throughout the 24-month observation period. No differences in the expression of antibody reactivity against outer membrane proteins were found between strains isolated at baseline and at 24 months. Three genotypes were associated with reduced survival rates of teeth without probing attachment loss of 2 mm or more. The results indicated that (i) most patients harbored only one A. actinomycetemcomitans genotype; (ii) the genotype persisted following therapy; and (iii) only some genotypes were associated with refractory periodontitis.

Adult↗

PubMed1998

Long-term maintenance of alveolar bone gain after implantation of autolyzed, antigen-extracted, allogenic bone in periodontal intraosseous defects.

This randomized controlled trial assessed the long-term maintenance of alveolar bone gain after implantation of autolyzed, antigen-extracted, allogenic (AAA) bone. AAA bone is a demineralized freeze-dried bone allograft processed after previously described methods. In each of 14 patients, AAA bone was implanted into the intraosseous defect of 1 tooth (test); a second tooth with an intraosseous defect was treated by modified Widman flap surgery alone (control). All patients were offered supportive periodontal therapy at 3- to 6-month intervals following treatment. Clinical measurements were taken prior to surgery, 6 months, and 3 years following surgery. Of the 14 patients enrolled, 11 patients completed the 6-month and 8 patients the 3-year examination. In test teeth, bone gain was significantly greater compared to control teeth at 6 months (2.2+/-0.5 mm and 1.2+/-0.5 mm, respectively) and 3 years (2.3+/-0.7 mm and 1.1+/-0.8 mm, respectively) (P < 0.05). Also, more probing attachment was gained in test compared to control teeth at 3 years (2.0+/-0.7 mm and 0.8+/-0.5 mm, respectively; P < 0.05). At 3 years, Porphyromonas gingivalis was detected in 3 test and 2 control teeth by polymerase chain reaction, whereas no Actinobacillus actinomycetemcomitans was found. Due to the low detection frequency, there was no clear correlation between the maintenance of alveolar bone during supportive periodontal therapy and subgingival infection with P. gingivalis. The data indicated that alveolar bone gain after implantation of AAA bone may be maintained over a minimum of 3 years in patients receiving periodontal supportive therapy.

Adult↗