Approximal plaque pH lowering after sugar intake in a periodontally infected dentition.

OBJECTIVES: The aim of this study was to evaluate the effect of periodontal inflammation on the approximal plaque pH after a sucrose rinse. MATERIALS AND METHODS: Thirty-two periodontitis patients (aged 38-72 years; 9M/23F) were included. All patients were in need of periodontal surgery. Two non-adjacent interdental spaces, one healthy (no bleeding on probing [BoP] and probing pocket depth [PPD] < 4 mm) and one periodontally diseased (BoP and PPD ≥5 mm) were selected. Before and after surgery, the approximal plaque pH was measured before and after 2, 5 and 10 min after a 1-min rinse with sucrose solution. RESULTS: In periodontally diseased interdental spaces, a significant pH drop was seen 5 min after rinsing. In healthy spaces and after surgery, a significant pH drop was seen after 2 min. A multilevel regression analysis showed that greater probing pocket depths were significantly associated with pH change measured 5 min after rinsing (p < .05). Further on, the approximal pH drop after a sucrose rinse tended to be delayed in dentitions with ≥10% of PPD ≥5 mm (p = .052). CONCLUSIONS: The results suggest that an ongoing periodontal inflammation could temporarily neutralize acidic metabolic products after a sugar challenge. This may further suggest that plaque pH measured after a sugar rinse might be used to identify an ongoing periodontal disease.

The mechanism of Hsp90-induced oligomerizaton of Tau.

Aggregation of the microtubule-associated protein Tau is a hallmark of Alzheimer's disease with Tau oligomers suspected as the most toxic agent. Tau is a client of the molecular chaperone Hsp90, although it is unclear whether and how the chaperone massages the structure of intrinsically disordered Tau. Using electron paramagnetic resonance, we extract structural information from the very broad conformational ensemble of Tau: Tau in solution is highly dynamic and polymorphic, although "paper clip"-shaped by long-range contacts. Interaction with Hsp90 promotes an open Tau conformation, which we identify as the molecular basis for the formation of small Tau oligomers by exposure of the aggregation-prone repeat domain to other Tau molecules. At the same time, formation of Tau fibrils is inhibited. We therefore provide the nanometer-scale zoom into chaperoning an amyloid client, highlighting formation of oligomers as the consequence of this biologically relevant interaction.

Bacteria-binding plasma proteins in pellicles formed on hydroxyapatite in vitro and on teeth in vivo.

Previous studies on dental pellicle formation and bacterial adherence have focussed on saliva and its components. The tooth surface is, however, also exposed to the plasma-derived crevicular fluid. In the present study, (i). plasma proteins in in vitro and in vivo pellicles were examined using sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE), immunoblotting and image analysis and (ii). the adherence of periodontopathogenic bacteria to experimental plasma and saliva pellicles was examined using radio-labelled bacteria and liquid scintillation counting. The plasma components fibrinogen, fibronectin, albumin and IgG were incorporated from plasma in the experimental pellicle and mediated the adherence of Porphyromonas gingivalis, Fusobacterium nucleatum and Actinomyces naeslundii. These proteins were also readily detected in in vivo pellicles and were found to a higher extent in pellicles formed at the gingival part of the tooth surface than at the incisal part.

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.

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.

Dental biofilms at healthy and inflamed gingival margins.

OBJECTIVES: The increased plaque formation observed in gingival inflammation is not fully understood. Receptor proteins in the dental pellicle might influence bacterial adhesion and subsequent plaque formation. The purpose of the present study was to examine proteins and microorganisms in dental biofilms, at healthy and inflamed gingival margins. MATERIAL AND METHODS: To see whether marginal inflammation affects the composition of the pellicle and the early dental plaque, samples were taken from the gingival and incisal parts of teeth in periodontally healthy subjects, both in gingival health and during experimental gingivitis. Pellicle proteins were analysed using gel-electrophoresis, immunoblotting and image analysis. Bacteria were analysed by culturing and the PCR technique. RESULTS: During gingivitis, the rate of plaque formation increased significantly. The semiquantitative amounts of proteins and the numbers of bacteria varied considerably between individuals and surfaces. The amount of total and individual pellicle proteins and the total numbers of bacteria were, however, increased during gingivitis and the increase in proteins was statistically significant on the incisal parts of tooth surfaces. Compared to a healthy gingiva, reduced numbers for Actinomyces spp. (incisal parts only) and streptococci and increased numbers of periodontopathogens in the 4 h dental biofilms were seen at the inflamed gingiva. CONCLUSION: Increased gingival crevicular fluid flow during gingivitis affects pellicle formation and increased plasma proteins in the pellicle may modify bacterial attachment and early dental plaque composition.

Mandibular and maxillary furcation tunnel preparations--literature review and a case report.

AIM: The objective of this literature review and subsequent case report is to discuss and illustrate the tunnel preparation procedure as a treatment alternative for furcation-involved molars. REVIEW OF THE LITERATURE: Furcation tunnel preparation, i.e., the creation of access for plaque control between periodontally diseased roots, has not been discussed in the literature as comprehensively as root resective therapy, though success rates appear to fall within the same range. A short root trunk and a wide furcation entrance diameter are prerequisites for the indication of the tunnel preparation procedure. Although accessory canals in the furcation area are frequent findings on extracted teeth, endodontic complications have not been reported to be major complications after tunnel preparation. Caries developed at tunneled teeth even under proper maintenance, but did not necessarily lead to the loss of an affected tooth. CASE REPORT: In the case presented to illustrate the indication for the tunnel preparation procedure, periodontal disease was almost entirely restricted to the furcation sites of molar teeth. Affected teeth were either extracted or left intact and subjected to tunneling procedures. Periodontal health could be established and maintained at both single and double tunnels over a period of 2 years of periodontal supportive therapy.