Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0031099 (periodontitis)
 12,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was undertaken to determine the effects of guided tissue regeneration (GTR) with and without citric acid conditioning and autologous fibronectin application. The study subjects were four female beagle dogs with spontaneous periodontitis. The dogs were given thorough root debridement and 4 weeks later, mucoperiosteal flaps were raised on both sides of the mandible involving the 2nd, 3rd, and 4th premolar and 1st molar teeth. After debridement, notches were placed on the roots at the level of supporting bone. Citric acid (pH 1) was topically applied for 3 minutes on the exposed root surfaces of one side (experimental). The roots were irrigated with normal saline solution. Both the root surfaces and the inner surface of the flap were then bathed in autologous fibronectin in saline. Following this, Gore-Tex periodontal material was adapted to the roots of each tooth and sutured. The contralateral side, serving as control, was treated by surgery and application of Gore-Tex periodontal material only. All membranes were removed 1 month after surgery, and the dogs sacrificed at 3 months. Both mesio-distal and bucco-lingual microscopic histological sections were evaluated by descriptive histology, and linear measurements and surface area determination of the furcal tissues were made. Periodontal healing following the use of GTR procedure resulted in an increase in connective tissue and alveolar bone regeneration. Adjunctive critic acid plus autologous fibronectin produced slightly better results, but these differences were not statistically significant for this sample.
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PMID:Periodontal healing following guided tissue regeneration with citric acid and fibronectin application. 200 28

Past studies have suggested that gingival crevicular fluid is produced more readily in persons with severe periodontal diseases than in persons with healthy gingivae. In this study, salivary fibronectin was selected as an index of total gingival crevicular fluid flow. Our purpose was to determine whether a relationship could be found between salivary fibronectin level and periodontal disease status. Unstimulated saliva was collected from 20 healthy and 20 periodontally-diseased naval recruits. The periodontally-diseased subjects included 10 with localized juvenile periodontitis and 10 with moderate to severe periodontitis. Mean subject ages and salivary flow rates were similar for the 2 groups. Although 2 of the periodontally-diseased subjects showed unusually high fibronectin levels, the mean level for the remaining 18 subjects did not differ significantly from the mean of the healthy group, and no association of periodontal disease status with salivary fibronectin content was seen. Consequently, it was not evident from salivary fibronectin levels that the content of gingival crevicular fluid in unstimulated whole saliva differed significantly for persons with or without severe periodontal disease, except possibly for extreme cases of disease.
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PMID:Fibronectin levels of unstimulated saliva from naval recruits with and without chronic inflammatory periodontal disease. 266 47

While fibronectin (FN) has previously been demonstrated to be present in gingival crevicular fluid (GCF), its quality and quantity has not been reported. Since this information is relevant for ongoing studies on the use of FN for gingival reattachment, we performed these measurements and compared plasma levels in healthy subjects, patients with gingivitis and periodontitis, and in patients undergoing maintenance therapy. Plasma and GCF samples were obtained from 4 sites in each subject using a Periotron to permit quantification of samples. FN concentrations were determined in a microELISA using hyperimmune anti-FN antibody. Purified FN served as a reference for quantification. The functional activity of each sample was assessed by examining the natural affinity of FN for gelatin. Subjects with gingivitis and those in maintenance had significantly depressed levels of plasma fibronectin. While little fibronectin could be detected in the GCF of healthy sites regardless of patient category, examination of the most diseased sites in each group revealed that the concentration of FN in the GCF was highest in health and reduced when there was gingival inflammation. In no case was GCF FN found to be biologically active.
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PMID:Concentrations of fibronectin in the sera and crevicular fluid in various stages of periodontal disease. 266 48

The aim of the present review was to evaluate the benefit of coating root cementum of periodontitis involved teeth with an specific agent to promote connective tissue attachment. This agent was fibronectin, a glycoprotein which enhanced periodontal cell migration to previously scaled and demineralized root surfaces.
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PMID:[Fibronectin: a review of its properties and applications]. 270 Mar 97

125I-fibronectin was incubated with extracts having presumably a proteolytic activity. Plaque from children without gingivitis, plaque from adults with chronic periodontitis, human gingival fluid and pooled culture media of human gingival explants were studied. Proteolysis was usually faster with plaque from patients with adult periodontitis than with plaque from children without gingivitis and the inhibition tests showed that several enzymes were implicated in the process. For the culture medium of gingival explants, the electrophoretic profile of the digestion products of fibronectin was different and showed a decreased activity. Nevertheless the gingival fluid gave a very similar degradation to bacterial plaque. The sulcular content was able to assume enzymatic activity capable of destroying fibronectin. These sulcular activities could be important for bacterial colonisation of sulcular surfaces and perhaps also for fibronectin destruction of periodontal tissues.
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PMID:Fibronectin-degrading activity in human crevicular fluid, gingival explants culture medium and bacterial plaques. 304 69

This study evaluated the effects of citric acid demineralization and autologous fibronectin application in association with a modified Widman flap in the treatment of periodontitis. The study population comprised 29 patients under treatment for moderate to advanced periodontitis who reached the one-year posttherapy evaluation. After thorough scaling and root planing, a split mouth design was used in which two quadrants were treated by modified Widman flap alone, and the other two randomly assigned quadrants were treated by modified Widman flap combined with citric acid demineralization and autologous fibronectin application. Fibronectin, which had previously been isolated from the patient's own plasma, was applied with a tuberculin syringe on the citric acid demineralized root surfaces and the inner aspect of the flap. After suturing provided good flap adaptation, additional fibronectin was again applied under the flap and external pressure was applied. Patients were clinically evaluated at baseline and at one year. Statistical evaluation of the data using paired t test and Chi-square analysis indicated that both approaches, modified Widman flap alone or in combination with citric acid and fibronectin, significantly reduced probing pocket depth and increased clinical attachment. However, the changes achieved with citric acid and fibronectin were statistically greater than those obtained with the flap alone. Furthermore, the number of sites gaining 2 mm or more of clinical attachment were significantly increased. The results suggest that the use of citric acid and fibronectin holds promise in promoting reattachment after periodontal therapy.
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PMID:Clinical evaluation of the use of citric acid and autologous fibronectin in periodontal surgery. 305 48

To determine the effect on new connective tissue attachment of citric acid conditioning and fibronectin-laminin application in treating naturally occurring periodontitis, all 4 quadrants in each of 2 Beagle dogs were used. Each quadrant included: P2, P3, P4, and M1 teeth. 2 treatment modalities were employed and comparatively analyzed for differences in histological healing respponses at 120 days after surgery. The treatments were: (1) surgery (mucoperiosteal flaps) plus citric acid; (2) surgery plus citric acid followed by fibronectin-laminin application. After scaling and root planing, coronal and root surface reference notches were placed for histometric measurements. Following each of the randomly assigned treatments, flaps were sutured. After sacrifice, tissue blocks of treated areas were decalcified and serially cut, obtaining bucco-lingual and mesiodistal sections. Using a Filar micrometer, 5 distances were masured on the buccal aspect: (1) from root surface notch to alveolar bone crest; (2) from root surface notch to coronal extent of the cementum; (3) from root surface notch to apical extent of the junctional epithelium; 84) from free gingival margin to apical extent of junctional epithelium; (5) from the coronal notch to the alveolar bone crest. Results showed no differences among the 5 measurements between the 2 treatments tested. On mesio-distal sections, surface area determinations were made in the furcations, evaluating the space occupied by new connective tissue, with or without bone, or by epithelium. For this, images were digitized using a Zeiss IBAS Image analysis system with a 4mB of array processor memory coupled to a Newvicon TV camera and a microcomputer.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of citric acid and fibronectin and laminin application in treating periodontitis. 347 17

The lesion of chronic periodontitis is characterized by the persistence of perivascular collections of degenerate plasma cells. In this study, immunohistochemical demonstration of amyloid P (AP) component was used to define the distribution of this protein in established periodontitis lesions and in biopsies of non-destructive marginal gingivitis. Quantitative assessment of AP indicated significantly higher levels in periodontitis than in gingivitis for all regions of the tissue. This was associated with pathology as determined by the intensity of plasma cell accumulation and the extent of connective tissue matrix degradation. AP was concentrated in the deep connective tissue areas but perivascular accumulation was also noted, as was deposition associated with nerve bundles and, occasionally, in the extracellular matrix of the lining epithelium. These findings have potential significance in relation to the pathology of chronic periodontitis as AP has been shown to interact in a calcium-dependent manner with a number of ligands including fibronectin, elastic fibres, C-4 binding protein and amyloid fibrils.
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PMID:Association of amyloid P protein with pathology in periodontal tissues. 781 74

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.
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PMID:Molecular forms and concentration of fibronectin and fibrin in human gingival crevicular fluid before and after periodontal treatment. 829 Aug 80

Matrix metalloproteinases (MMP) are a family of proteolytic enzymes that mediate the degradation of extracellular matrix macromolecules, including interstitial and basement membrane collagens, fibronectin, laminin, and proteoglycan core protein. The enzymes are secreted or released in latent form and become activated in the pericellular environment by disruption of a Zn(++)-cysteine bond which blocks the reactivity of the active site. The major cell types in inflamed and healthy periodontal tissues (fibroblasts, keratinocytes, endothelial cells, and macrophages) are capable of responding to growth factors and cytokines, as well as to products released from the microbial flora by induction of transcription of 1 or more MMP genes. Cytokines that are likely to regulate expression of MMP genes in periodontal tissues include IL-1, TNF-alpha, and TGF-alpha. In addition, triggered PMN leukocytes which express only 2 MMP (PMN-CL and Mr 92K GL) release these enzymes from specific granule storage sites in response to a number of stimuli. The evidence that MMP are involved in tissue destruction in human periodontal diseases is still indirect and circumstantial. Cells isolated from normal and inflamed gingiva are capable of expressing a wide complement of MMP in culture and several MMP can be detected in cells of human gingiva in vivo. In addition, PMN-CL and Mr 92K GL are readily detected in gingival crevicular fluid from gingivitis and periodontitis patients. Osteoclastic bone resorption does not appear to directly involve MMP, but a body of evidence suggests that bone resorption is initiated by removal of the osteoid layer by osteoblasts by means of a collagenase-dependent process.
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PMID:Role of matrix metalloproteinases in human periodontal diseases. 831 70


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