Guided tissue regeneration using a polylactic acid barrier. Part I: Environmental effects on bacterial colonization
S. G. Rüdiger
Clinic of Conservative Dentistry, University of Tübingen,
Search for more papers by this authorB. Ehmke
Clinic of Periodontology, Münster University Clinic and
Search for more papers by this authorA. Hommens
Clinic of Periodontology, Münster University Clinic and
Search for more papers by this authorH. Karch
Institute of Infection Control, Münster University Clinic, Germany
Search for more papers by this authorT. F. Flemmig
Clinic of Periodontology, Münster University Clinic and
Search for more papers by this authorS. G. Rüdiger
Clinic of Conservative Dentistry, University of Tübingen,
Search for more papers by this authorB. Ehmke
Clinic of Periodontology, Münster University Clinic and
Search for more papers by this authorA. Hommens
Clinic of Periodontology, Münster University Clinic and
Search for more papers by this authorH. Karch
Institute of Infection Control, Münster University Clinic, Germany
Search for more papers by this authorT. F. Flemmig
Clinic of Periodontology, Münster University Clinic and
Search for more papers by this authorAbstract
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.
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