fibrin and Periodontitis

The hemostatic and inflammatory systems work hand in hand to maintain homeostasis at mucosal barrier sites. Among the factors of the hemostatic system, fibrin is well recognized for its role in mucosal homeostasis, wound healing, and inflammation. Here, we present a basic overview of the fibrinolytic system, discuss fibrin as an innate immune regulator, and provide recent work uncovering the role of fibrin-neutrophil activation as a regulator of mucosal/periodontal homeostasis. We reason that the role of fibrin in periodontitis becomes most evident in individuals with the Mendelian genetic defect, congenital plasminogen (PLG) deficiency, who are predisposed to severe periodontitis in childhood due to a defect in fibrinolysis. Consistent with plasminogen deficiency being a risk factor for periodontitis, recent genomics studies uncover genetic polymorphisms in

Topics: Fibrin; Fibrinolysin; Fibrinolysis; Hemostatics; Humans; Periodontitis; Plasminogen

Topics: Alveolar Bone Loss; Amino Acid Sequence; Bacteroides; Blood Coagulation Factors; Fibrin; Fibrinogen; Gingival Hemorrhage; Gingivitis; Humans; Molecular Sequence Data; Osteoblasts; Periodontal Diseases; Periodontitis; Thrombin; Tissue Plasminogen Activator

Scanning electron microscopy (SEM) was used to evaluate root surface characteristics of human teeth affected with periodontitis following periodontal instrumentation and topical application of tetracycline HCl (TTC-HCl; pH 1.6; 4 min). Specimens were randomly assigned to periodontal instrumentation alone (control 1); periodontal instrumentation plus TTC-HCl (test 1); periodontal instrumentation plus trypsin solution after extraction (control 2); and periodontal instrumentation plus TTC-HCl plus trypsin solution after extraction (test 2). Tetracycline solution was applied with a cotton pellet. Twenty-two single root periodontitis affected human teeth scheduled for extraction were selected. Mucoperiosteal flaps were raised, root surfaces were mechanically and chemically treated, flaps were repositioned and maintained in place for 20 min. Teeth were extracted, rinsed and placed in cold phosphate buffer solution (PBS) and control 2 and test 2 groups were treated with trypsin solution. Specimens were examined using SEM. Smear layer was successfully removed, exposing dentinal tubules; however, fibrin network formation in situ was not improved by application of TTC-HCl.

Topics: Anti-Bacterial Agents; Blood Coagulation; Fibrin; Humans; Periodontitis; Smear Layer; Tetracycline

Plasminogen serves as the precursor to plasmin, an essential element in the fibrinolytic process, and is synthesized primarily in the liver. Plasminogen activation occurs through the action of plasminogen activator, converting it into plasmin. This conversion greatly enhances the fibrinolytic system within tissues and blood vessels, facilitating the dissolution of fibrin clots. Consequently, congenital deficiency of plasminogen results in impaired fibrin degradation. Patients with plasminogen deficiency typically exhibit fibrin deposits in various mucosal sites throughout the body, including the oral cavity, eyes, vagina, and digestive organs. Behcet's disease is a chronic recurrent systemic inflammatory disease with four main symptoms: aphthous ulcers of the oral mucosa, vulvar ulcers, skin symptoms, and eye symptoms, and has been reported worldwide. This disease is highly prevalent around the Silk Road from the Mediterranean to East Asia. We report a case of periodontitis in a patient with these two rare diseases that worsened quickly, leading to alveolar bone destruction. Genetic testing revealed a novel variant characterized by a stop-gain mutation, which may be a previously unidentified etiologic gene associated with decreased plasminogen activity.. This case report depicts a patient diagnosed with ligneous gingivitis during childhood, originating from plasminogen deficiency and progressing to periodontitis. Genetic testing revealed a suspected association with the PLG c.1468C > T (p.Arg490*) stop-gain mutation. The patient's periodontal condition remained stable with brief intervals of supportive periodontal therapy. However, the emergence of Behçet's disease induced acute systemic inflammation, necessitating hospitalization and treatment with steroids. During hospitalization, the dental approach focused on maintaining oral hygiene and alleviating contact-related pain. The patient's overall health improved with inpatient care and the periodontal tissues deteriorated.. Collaborative efforts between medical and dental professionals are paramount in comprehensively evaluating and treating patients with intricate complications from rare diseases. Furthermore, the PLG c.1468C > T (p.Arg490*) stop-gain mutation could contribute to the association between plasminogen deficiency and related conditions.

Topics: Behcet Syndrome; Female; Fibrin; Fibrinolysin; Humans; Periodontitis; Plasminogen; Rare Diseases

The aim of this research was to assess the binding of fibrin clot to the teeth affected by periodontal disease following exposure to different root conditioning agents.. A total of 60 human teeth with a solitary root that were subjected to extraction following severe periodontal disease were used as study samples in this research. Two analogous grooves were prepared on the proximal radicular surface of every sample employing a diamond-tapered fissure bur using an aerator handpiece beneath abundant irrigation. Every sample was assigned to one of the following groups: • Group I: Tetracycline hydrochloride solution • Group II: Ethylenediaminetetraacetic acid (EDTA) gel • Group III: Biopure MTAD™ Subsequent to conditioning, the samples were rinsed for 3 minutes with phosphate-buffered saline (PBS) and permitted to air-dry for 20 minutes. A drop of fresh human whole blood procured from a hale and hearty volunteer was coated onto the dentin blocks in all three groups. A scanning electron microscope under 5000× magnification at 15 kV was used to examine the samples. Kruskal-Wallis test and Mann-Whitney U test were performed to procure the inter- and intragroup assessments Results: The greatest fibrin clot union was noted in the EDTA gel group at 2.86 ± 0.14 in pursuit by Biopure MTAD™ group at 2.39 ± 0.08 as well as tetracycline hydrochloride solution group at 1.82 ± 0.10. A statistically significant difference was noted between the investigational groups (. This research arrived at a conclusion that the dentinal surfaces subjected to conditioning with EDTA gel group as well as coated with human whole blood resulted in appreciably superior fibrin clot bonding to dentin vs Biopure MTAD™ as well as the tetracycline hydrochloride solution group.. Connective tissue attachment subsequent to surgical procedures causing the adhesion of a fibrin clot to the radicular surface as a result of initial wound healing processes is directly related to periodontal regeneration. It depends on biocompatibility for the fibrin clot and the periodontal pathosis-affected radicular surface to stick together, which can be procured with the aid of a variety of root conditioning measures in course of periodontal treatment.

Topics: Cell Adhesion; Dentin; Edetic Acid; Fibrin; Humans; Microscopy, Electron, Scanning; Periodontitis; Smear Layer; Tetracycline; Thrombosis; Tooth Root

Tissue-specific cues are critical for homeostasis at mucosal barriers. Here, we report that the clotting factor fibrin is a critical regulator of neutrophil function at the oral mucosal barrier. We demonstrate that commensal microbiota trigger extravascular fibrin deposition in the oral mucosa. Fibrin engages neutrophils through the α

Topics: Alveolar Bone Loss; Animals; Extracellular Traps; Female; Fibrin; Fibrinogen; Fibrinolysin; Fibrinolysis; Gastrointestinal Microbiome; Gingiva; Humans; Immunity, Mucosal; Macrophage-1 Antigen; Male; Mice; Mouth Mucosa; Neutrophil Activation; Neutrophils; Periodontitis; Plasminogen; Polymorphism, Single Nucleotide; Reactive Oxygen Species; RNA-Seq

A 36-year-old male patient diagnosed with severe chronic periodontitis was treated with novel surgery for his maxillary right lateral incisor. Preoperatively, a 3D printer was used, based on CBCT datasets, to produce a photosensitive resin bony anatomy replica. The patient's blood was centrifuged to obtain advanced platelet-rich fibrin (A-PRF) and injected platelet-rich fibrin (I-PRF), then mixed with Bio-Oss and packed onto the 3D replica to form the ideal shape. The replica was positioned at the planned sites without changes. The A-PRF membrane was applied over the replica as well as a Bio-Gide collagen membrane. Fifteen months after the surgery, clinical and radiographic followup revealed greatly reduced pocket depths and significant 3D alveolar bone fill at the treatment site. Based on these short-term results, the initial 3D printing surgical temple assisted guided tissue regeneration method resulted in significant clinical and radiographic improvements; A-PRF/I-PRF should be considered an ideal biomaterial for regenerative periodontal therapy.

Topics: Adult; Alveolar Bone Loss; Bone Regeneration; Fibrin; Guided Tissue Regeneration; Guided Tissue Regeneration, Periodontal; Humans; Male; Periodontitis; Platelet-Rich Fibrin; Printing, Three-Dimensional

Topics: Adult; Biopsy; Conjunctivitis; Diagnosis, Differential; Fibrin; Gingival Hemorrhage; Gingival Hyperplasia; Granulomatosis with Polyangiitis; Humans; Hyalin; Male; Periodontitis; Plasminogen; Sarcoidosis; Skin Diseases, Genetic

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

Certain abnormal products of human tissues are resistant to degradation. The fibrillary ultrastructure of some of these are seen integrated with normal tissue components. The accumulations seen in colloid milium, lichen, and macular amyloidosis are of this type. Apoptosis of keratinocytes and filamentous degeneration of some proteins can be important in the pathogenesis. A similar pathogenetic mechanism is possible in ligneous mucosal disease, which is a rare disorder of plasminogen deficiency characterized by amyloid-like amorphous accumulations. Gingival and conjunctival mucosal pseudomembraneous masses are typical and concomitant involvement of other sites are not unusual. The accumulated substance is thought to be an abnormal fibrin degradation product. In this study, we have examined 6 representative samples from 5 gingival and 1 conjunctival lesions displaying characteristic features. Immunohistochemically, fibrinogen was detected as an early change. TUNEL staining revealed numerous apoptotic keratinocytes in this phase as well. These cells also expressed nuclear factor kappa beta. Apoptotic cells showed loss of epithelial cadherin immunostaining. In the later phase, the subepithelial accumulations failed to stain with antifibrinogen, wide spectrum, and high molecular keratins, type 4 collagen and nuclear factor kappa beta. Our findings suggest that the accumulations in ligneous mucosal disorder result from an abnormal healing process and they probably form as a combination of organised fibrinogen, epithelial fragments, and connective tissue matrix.

Topics: Adolescent; Adult; Apoptosis; Biomarkers; Child; Child, Preschool; Conjunctiva; Female; Fibrin; Fibrinolysis; Gingiva; Humans; Keratinocytes; Male; Mouth Mucosa; NF-kappa B; Periodontitis; Young Adult

Periodontitis involves bacterial infection, inflammation of the periodontium, degradation of gum tissue, and alveolar bone resorption, which eventually leads to loss of teeth. To study the role of the broad-spectrum protease plasmin in periodontitis, we examined the oral health of plasminogen (Plg)-deficient mice. In wild-type mice, the periodontium was unaffected at all time points studied; in Plg-deficient mice, periodontitis progressed rapidly, within 20 weeks. Morphological study results of Plg-deficient mice revealed detachment of gingival tissue, resorption of the cementum layer, formation of necrotic tissue, and severe alveolar bone degradation. IHC staining showed massive infiltration of neutrophils in the periodontal tissues. Interestingly, doubly deficient mice, lacking both tissue- and urokinase-type plasminogen activators, developed periodontal disease similar to that in Plg-deficient mice; however, mice lacking only tissue- or urokinase-type plasminogen activator remained healthy. Supplementation by injection of Plg-deficient mice with human plasminogen for 10 days led to necrotic tissue absorption, inflammation subsidence, and full regeneration of gum tissues. Notably, there was also partial regrowth of degraded alveolar bone. Taken together, our results show that plasminogen is essential for the maintenance of a healthy periodontium and plays an important role in combating the spontaneous development of chronic periodontitis. Moreover, reversal to healthy status after supplementation of Plg-deficient mice with plasminogen suggests the possibility of using plasminogen for therapy of periodontal diseases.

Topics: Alkaline Phosphatase; Animals; Disease Models, Animal; Fibrin; Fibrinolysin; Immunohistochemistry; Inflammation; Mice; Mice, Inbred C57BL; Mice, Transgenic; Models, Genetic; Neutrophils; Periodontal Diseases; Periodontitis; Time Factors

Neutrophil extracellular traps (NETs) are extracellular web-like structures produced by activated polymorphonuclear neutrophils. NETs kill bacteria extracellularly, but their role in human pathology remains largely unclear. One possible way of studying NETs is through the SEM approach. However, web-like structures observed with SEM in sites of inflammation have been interpreted either as NETs or as fibrin. Thus, the question arises whether a reliable SEM discrimination between NETs and fibrin is at all possible. NET samples were collected as purulent crevicular exudate from periodontal pockets. DNase-digested controls for SEM were employed to demonstrate the DNA backbone and immuno-staining for confocal laser scanning microscopy was used to show the citrullinated histones of NETs. Blood clot samples were treated in the same way as the exudate samples to demonstrate that fibrin and fibrinolysis can mimic NETs and DNA digestion, respectively. No discrimination between fibrin and NETs based on morphological criteria in SEM was possible. Furthermore, only a vague distinction between DNA digestion and fibrinolysis could be made. These findings unambiguously indicate that the discrimination between NETs and fibrin by means of SEM is untrustworthy for samples of inflammatory exudate.

Topics: Adult; Aged; Cytological Techniques; Female; Fibrin; Gingival Crevicular Fluid; Humans; Male; Microscopy, Electron, Scanning; Middle Aged; Neutrophil Activation; Neutrophils; Periodontitis

Destructive membranous periodontal disease is a rare and poorly defined entity that is a part of a systemic disease due to accumulation of fibrin material. The disease is characterized by gingival enlargement and periodontal tissue destruction that leads to rapid bone loss despite treatment efforts. We present a case with ligneous periodontitis and conjunctivitis.

Topics: Adolescent; Alveolar Bone Loss; Conjunctivitis; Female; Fibrin; Gingival Hemorrhage; Gingival Overgrowth; Humans; Oral Ulcer; Periodontitis; Plasminogen

Ligneous periodontitis (LP) is a rare periodontal disease in which plasminogen deficiency and fibrin deposition both play a part, resulting in characteristic gingival enlargement and periodontal breakdown. Recent data suggest that oxidant/antioxidant changes are significant in the pathology of oral diseases. This study examines the gingival histopathology in 2 cases with LP. To examine the antioxidant (AO) status, the activity of the major AOs glutathione (GSH), catalase (CAT), and glutathione S-transferase (GST) and the malondialdehyde (MDA) levels, a product of lipid peroxidation, were measured and compared with healthy control subjects. The histopathologic examination of the gingiva revealed subepithelial fibrin accumulation and irregular extensive downward proliferation of the epithelium. Biochemical analysis showed that the CAT, GST, and MDA levels were higher in LP patients than in the control subjects, and the GSH level was lower. Our preliminary findings show that in LP, the AO capacity of the gingiva changes or decreases and lipid peroxidation increases, which suggests that oxidative stress is involved in the pathology of the periodontal breakdown observed in this disease.

Topics: Adolescent; Antioxidants; Case-Control Studies; Catalase; Conjunctivitis; Cyclosporine; Dermatologic Agents; Female; Fibrin; Gingiva; Gingival Overgrowth; Glutathione; Glutathione Transferase; Humans; Malondialdehyde; Periodontitis; Plasminogen; Radiography

Generalized membranous gingival enlargement due to an accumulation of fibrin deposits associated with severe alveolar bone loss (ligneous periodontitis) is a rare condition, and plasminogen deficiency seems to play a central role in its pathogenesis. However, this condition has not been described in association with syndromes. This article reports a case of ligneous periodontitis in a boy with the classic type of Ehlers-Danlos syndrome (EDS).. A 12-year-old white male presented with generalized gingival overgrowth and severe alveolar bone loss. A physical examination revealed clinical signs of EDS (velvety skin with mild hyperextensibility, marked hypermobility of the limb joints, atrophic scars on his knees, and easy bruising), which is associated with a positive family history for joint hypermobility. A biopsy of gingival tissues was submitted for routine histology, hematoxylin and eosin (H&E), and direct immunofluorescence (antifibrinogen). An evaluation of plasminogen activity was also performed.. Histopathology revealed chronic periodontitis with fibrinoid material deposition, and direct immunofluorescence proved to be positive for fibrin. Functional plasminogen was reduced. A conclusive diagnosis of ligneous periodontitis due to plasminogen deficiency associated with the classic type of EDS was rendered.. Ehlers-Danlos syndrome can be associated with ligneous periodontitis. In the present case, the histologic examination represented an important tool in the differential diagnosis, because it ruled out EDS type VIII as the associated systemic factor to periodontal breakdown.

Topics: Alveolar Bone Loss; Biopsy; Child; Coloring Agents; Ehlers-Danlos Syndrome; Fibrin; Fluorescent Antibody Technique, Direct; Gingival Overgrowth; Humans; Male; Periodontitis; Plasminogen

During episodes of dental bacteremia, viridans group streptococci encounter platelets. Among these microorganisms, certain Streptococcus sanguis induce human and rabbit platelets to aggregate in vitro. In experimental rabbits, circulating streptococci induced platelets to aggregate, triggering the accumulation of platelets and fibrin into the heart valve vegetations of endocarditis. At necropsy, affected rabbit hearts showed ischemic areas. We therefore hypothesized that circulating S. sanguis might cause coronary thrombosis and signs of myocardial infarction (MI). Signs of MI were monitored in rabbits after infusion with platelet-aggregating doses of 4 to 40 x 10(9) cells of S. sanguis 133-79. Infusion resulted in dose-dependent changes in electrocardiograms, blood pressure, heart rate, and cardiac contractility. These changes were consistent with the occurrence of MI. Platelets isolated from hyperlipidemic rabbits showed an accelerated in vitro aggregation response to strain 133-79. Cultured from immunosuppressed children with septic shock and signs of disseminated intravascular coagulation, more than 60% of isolates of viridans streptococci induced platelet aggregation when tested in vitro. The data are consistent with a thrombogenic role for S. sanguis in human disease, contributing to the development of the vegetative lesion in infective endocarditis and a thrombotic mechanism to explain the additional contributed risk of periodontitis to MI.

Topics: Animals; Bacteremia; Bacterial Physiological Phenomena; Blood Platelets; Blood Pressure; Cells, Cultured; Child; Coronary Thrombosis; Disseminated Intravascular Coagulation; Electrocardiography; Endocarditis, Bacterial; Fibrin; Heart Diseases; Heart Rate; Humans; Hyperlipidemias; Immunocompromised Host; Mouth; Myocardial Contraction; Myocardial Infarction; Myocardial Ischemia; Periodontitis; Platelet Aggregation; Rabbits; Shock, Septic; Streptococcus sanguis; Thrombosis

A total of 23 periodontitis-affected sites from seven adults was selected for the study. Crevicular fluid (CF) samples were collected with paper strips before treatment (scaling, root planing, and curettage) and 2, 5, 10, 20, and 40 days after treatment. Each sample was eluted into sterile saline and two aliquots were drawn for gel electrophoresis: one for fibronectin and one for fibrin analysis. Peptides were transferred to nitrocellulose membranes, and molecules were detected by specific antibodies. The proportions of different molecular forms of fibronectin and fibrin were analyzed by laser densitometry. Plaque Index, Papilla Bleeding Index, and pocket depth were recorded before and 40 days after treatment. Radiologic bone loss was estimated from orthopantomograms. Two days after treatment, an increase was seen in the proportions of intact fibronectin, fibronectin fragments larger than 70 kDa, and fibrin-positive material with a greater molecular mass than intact fibrin. Between days 5 and 10, the proportions of these large fragments decreased. The highest fibronectin and fibrin concentrations were seen 10 days after treatment. These changes probably reflect degradation of the subgingival fibrin clot formed after treatment, and indicate resolution of the clot during the first 10 days of healing. This agrees well with previous observations of CF plasmin activity and concentration of collagen synthesis markers in CF after periodontal treatment, and with the histologic changes seen during periodontal healing. Results of the present study, together with earlier reported findings of collagen synthesis after periodontal treatment, also support the hypothesis of sequential appearance of fibronectin and collagens during the process of wound healing.

Topics: Adult; Collagen; Dental Plaque Index; Electrophoresis, Polyacrylamide Gel; Extracellular Matrix; Fibrin; Fibrin Fibrinogen Degradation Products; Fibronectins; Gingival Crevicular Fluid; Humans; Molecular Structure; Periodontal Index; Periodontitis; Wound Healing

A total of 49 crevicular fluid (CF) samples were collected with paper strips from 12 healthy adults. Each sample was eluted into sterile saline and two aliquots were drawn for SDS-PAGE, one for fibronectin and one for fibrin analysis. Peptides were transferred to nitrocellulose membranes, and fibronectin and fibrin were detected using specific antibodies. The relative amounts of different molecular forms of fibronectin and fibrin were analyzed using a laser densitometer. After the sample collection, Plaque Index, Papilla Bleeding Index and pocket depth were measured. Bone loss was estimated from the orthopanthomograms. Fibronectin fragments were seen in all CF samples. Intact fibronectin was seen in 21 samples, of which 76% were collected from periodontitis-affected sites. There was a positive correlation between the proportion of intact fibronectin and the clinical parameters. Intact fibrin and fibrin fragments were seen in all samples. Fibrin-positive material with larger molecular weight than intact fibrin was also seen in all samples. A negative correlation was found between the proportion of intact fibrin and the clinical parameters. There was no correlation between total amounts and concentrations of fibronectin and fibrin. Molecular forms of fibronectin and fibrin may affect the pathogenesis and healing of periodontal diseases, since the biologic effects of the fragments of these molecules differ from those of the intact molecules.

Topics: Adult; Blotting, Western; Dental Plaque Index; Electrophoresis, Polyacrylamide Gel; Fibrin; Fibronectins; Gingival Crevicular Fluid; Humans; Periodontal Pocket; Periodontitis

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

A case is reported showing an iatrogenic, chronic abscess of six years' duration associated with a bony defect between the maxillary right central and lateral incisors. The osseous defect was treated by a guided tissue regeneration procedure with the use of a fibrin and fibronectin sealing system. The system was employed to fix the membranes and keep them apart from the root surface, thereby maintaining room for bone regeneration. This operation resulted in a 9-mm clinical attachment gain and in an 11-mm filling of the osseous defect. The second surgical stage after a three-month reentry procedure was strictly for cosmetic improvement by means of a free gingival graft.

Topics: Adolescent; Alveolar Process; Aprotinin; Bone Resorption; Drug Combinations; Factor XIII; Fibrin; Fibrin Tissue Adhesive; Fibrinogen; Humans; Male; Micropore Filters; Periodontal Abscess; Periodontitis; Periodontium; Regeneration; Surgical Flaps; Thrombin; Tissue Adhesives; Tooth Root

Topics: Bacteroides; Fibrin; Fibrinolysis; Gingival Diseases; Humans; Periapical Abscess; Periodontal Abscess; Periodontitis; Prevotella melaninogenica

Topics: Adolescent; Adult; Diabetes Mellitus; Fibrin; Fibrinogen; Fibrinolysis; Gingiva; Humans; Periodontitis