fibrin and Dental-Plaque

Epidemiological, biological and clinical links between periodontal and cardiovascular diseases are now well established. Several human studies have detected bacterial DNA corresponding to periodontal pathogens in cardiovascular samples. Intraplaque hemorrhage has been associated with a higher risk of atherosclerotic plaque rupture, potentially mediated by neutrophil activation. In this study, we hypothesized that plaque composition may be related to periodontal pathogens.. Carotid culprit plaque samples were collected from 157 patients. Macroscopic characterization was performed at the time of collection: presence of blood, lipid core, calcification and fibrosis. Markers of neutrophil activation released by carotid samples were quantified (myeloperoxidase or MPO, cell-free DNA and DNA-MPO complexes). PCR analysis using specific primers for Porphyromonas gingivalis, Aggregatibacter actinomycetemcommitans, Treponema denticola, Prevotella intermedia and Tannerella forsythia was used to detect DNA from periodontal pathogens in carotid tissues. In addition, bacterial lipopolysaccharide (LPS) and Immunoglobulins G against T. forsythia were quantified in atherosclerotic carotid conditioned medium.. Intraplaque hemorrhage was present in 73/157 carotid samples and was associated with neutrophil activation, reflected by the release of MPO, cell-free DNA and MPO-DNA complexes. LPS levels were also linked to intraplaque hemorrhage but not with the neutrophil activation markers. Seventy-three percent of the carotid samples were positive for periodontal bacterial DNA. Furthermore, hemoglobin levels were associated with the detection of T. forsythia and neutrophil activation/inflammation markers.. This study suggests a potential role of periodontal microorganisms, especially T. forsythia, in neutrophil activation within hemorrhagic atherosclerotic carotid plaques.

Topics: Aged; Aged, 80 and over; Antibodies, Bacterial; Bacteroidaceae; Carotid Artery Diseases; Carotid Artery Thrombosis; Dental Plaque; DNA, Bacterial; Endarterectomy, Carotid; Extracellular Traps; Female; Fibrin; Hemorrhage; Humans; Lipids; Male; Middle Aged; Neutrophil Infiltration; Neutrophils; NF-kappa B; Periodontitis; Peroxidase; Plaque, Atherosclerotic; Respiratory Burst

Platelet-rich plasma (PRP) has been promoted as a surgical adjunct to enhance hard and soft tissue wound healing. Although anecdotally reported to be of value, the results of controlled studies examining the added effects of PRP on surgical procedures have been mixed. The purpose of this study was to test the effect of PRP on flap strength at various post-surgical time points in a minipig animal model.. Twelve Yucatan minipigs provided four sites per animal. PRP was prepared from each animal at the time of surgery. Following reflection of a mucoperiosteal flap in each quadrant, subgingival plaque and calculus were removed. Each surgical site was irrigated with sterile saline; prior to suturing, one randomly selected test quadrant in each arch was treated with PRP. Four animals were euthanized at day 14, and two animals were euthanized at 2, 7, 10, and 28 days. The flap strength in each quadrant was tested by attaching to a loop of 3-0 silk suture through the tissue; the force required to separate the flap from the tooth/bone interface was recorded for each site. A separate portion of each flap site was prepared for descriptive histologic examination, including inflammation, hemorrhage, and new bone growth.. Flap strength was significantly less on day 2 compared to later time points, and there were no significant differences between the test and control groups. No histologic differences in healing between test and control sites were seen at any time point.. PRP did not seem to contribute to greater flap strength at any post-surgical time point, nor was it associated with any histologic differences in wound healing in this Yucatan minipig model. The time points chosen for observation post-surgery, as well as the variability in the PRP platelet count, may have contributed to the lack of positive findings in this study.

Topics: Animals; Biomechanical Phenomena; Dental Calculus; Dental Plaque; Disease Models, Animal; Edema; Female; Fibrin; Gingiva; Gingivitis; Necrosis; Osteoblasts; Osteogenesis; Periodontium; Platelet-Rich Plasma; Postoperative Hemorrhage; Random Allocation; Stress, Mechanical; Subgingival Curettage; Surgical Flaps; Suture Techniques; Swine; Swine, Miniature; Tensile Strength; Time Factors; Wound Healing

The purpose of the study was to examine the ultrastructure of plaque contaminating polytetrafluoroethylene (PTFE) membranes used for guided periodontal tissue regeneration. 8 patients treated with Gore-Tex membranes received daily antibiotics (650 mg x 2 Femepen) and rinsed with 10 ml 0.2% chlorhexidine during a healing period of 30 days. Following retrieval, the membranes were processed for electron microscopy. External aspects of 12 portions from 4 partially exposed membranes were selected for detailed ultrastructural examination. The plaque-membrane interface was characterized by the presence of fibrin or discontinuous accumulation of intermicrobial matrix. Adjacent plaque-free areas of membrane surface exhibited no detectable electron-dense material. 3 structurally different groups of bacterial aggregations were observed on the strips: (i) dense layers of gram-positive cocci and rods dominated the external aspect of the open microstructure portion; (ii) cocci, rods and filamentous microorganisms embedded in fibrin filled the spaces of the open microstructure; (iii) a loosely arranged mixed microbiota consisting of gram-positive cocci and rods as well as of gram-negative microorganisms and spirochetes were present on the occlusive portion. Areas with morphologically intact bacteria alternated with areas with empty bacterial cell walls. One specimen also displayed degenerated Candida-like blastospores. This study shows that oral micro-organisms may colonize and extensively invade the open microstructure of PTFE material and that adhesion of plaque to the membrane surface is mediated either by fibrin or a discontinuous layer of intermicrobial matrix.

Topics: Adult; Anti-Bacterial Agents; Chlorhexidine; Dental Plaque; Fibrin; Gram-Negative Bacteria; Gram-Positive Cocci; Gram-Positive Rods; Guided Tissue Regeneration, Periodontal; Humans; Membranes, Artificial; Microscopy, Electron; Periodontitis; Polytetrafluoroethylene; Porosity; Spirochaetales; Surface Properties

The purpose of the study was two-fold: to determine the nature of stainable deposits on periodontally diseased root surfaces subsequent to in vivo scaling and root planing procedures, and to quantify the distribution of residual plaque on instrumented root surfaces. Thirty molar and 30 nonmolar teeth which were condemned for periodontal or prosthetic reasons and had proximal probing depths of 4 to 7 mm were treated. Half of these were instrumented with I.U. curettes and the other half with an ultrasonic scaling device. Instrumentation was continued until the root surface felt hard and smooth to an explorer tip. The location of the gingival margin was recorded by notching the treated proximal surface with a No. 1/2 round bur. Twenty control teeth, 10 molar and 10 nonmolar, were extracted without instrumentation. Control and experimental teeth were irrigated with saline and stored in a 2.5% glutaraldehyde fixative solution until the time of assessment. All teeth were stained with a 0.5% solution of toluidine blue, and the amount of residual stained material and calculus was assessed under the stereomicroscope using an eyepiece fitted with a 10 X 10 optical grid. Stained deposits were marked by placing small V-shaped notches in the adjacent root surface as an aid to identification after the specimens were processed for scanning electron microscopic (SEM) examination. The nature of stained deposits on selected teeth was then characterized using the SEM. Treated root surfaces were also surveyed in detail to assess the quantity and extent of residual plaque deposits. The findings showed that although a large percentage of the treated proximal root surface may possess stainable deposits, these surfaces were often unexpectedly free of microbial organisms. In this study, the majority of stained deposits were composed of adherent fibrin and instrumentation debris. When bacterial plaque was present, it was usually found in small "mini-colonies" smaller than 0.5 mm across. Such findings cast doubt on the validity of using histologic and disclosing stains as an indicator for the presence of bacterial plaque immediately after instrumentation. Although only partially effective in removing subgingival calculus, both methods of instrumentation in this study appeared to be remarkably effective in bacterial debridement of subgingival root surfaces.

Topics: Bacteria; Dental Calculus; Dental Plaque; Dental Prophylaxis; Dental Scaling; Fibrin; Humans; Microscopy, Electron, Scanning; Periodontal Diseases; Tooth Root; Ultrasonic Therapy

Samples were taken from blood accumulated in dental alveoli after surgical removal of mandibular third molars, from subgingival plaque of teeth with advanced periodontal destructions, from teeth with infected necrotic pulps, and from subjects suffering from angular cheilitis. Of the microorganisms subcultured from these samples, 116 strains were assayed for enzymes degrading fibrinogen and fibrin. Enzymes degrading fibrinogen were assayed with the thin-layer enzyme assay cultivation technique. This assay involves the cultivation of microorganisms on culture agars applied over fibrinogen-coated polystyrene surfaces. Enzymes degrading fibrin were assayed with both a plate assay and a tube assay, in which fibrin was mixed with a microbial culture medium. Microorganisms degrading fibrinogen or fibrin or both were isolated from all sampling sites. Activity was mainly detected in strains of Actinomyces, Bacteroides, Fusobacterium, Peptococcus, Propionibacterium, and Staphylococcus aureus. Most Fusobacterium strains degraded fibrinogen only. Enzymes degrading fibrinogen as well as enzymes degrading fibrin via activation of plasminogen were revealed in strains of Clostridium, S. aureus, and Streptococcus pyogenes. It was generally found that fibrinogen was degraded by more strains than was fibrin, which indicates that different proteases may be involved.

Topics: Bacteria; Cheilitis; Dental Plaque; Dental Pulp Diseases; Endopeptidases; Fibrin; Fibrinogen; Fibrinolysis; Humans; Mouth Diseases; Periodontal Pocket; Tooth Diseases