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)

Skin biopsies from thirteen patients suffering from Ehlers-Danlos syndrome, including 6 of the mitis type, 4 of the benign hypermobile type, one of the X-linked type, one of the ocular type and one of the periodontitis type, were studied by electron microscopy after routine preparation. Collagen fibrils showed a distorted arrangement of bent, curled or twisted fibrils and thread-like material. Similar changes may be seen in the skin of other hereditary disorders of connective tissue. However, abnormal collagen fibrils in normal skin suggests one of eight types of Ehlers-Danlos syndrome. Clinical variants cannot be differentiated on the basis of ultrastructural findings. Elastic fibres were normal without degenerative changes. Perineurium was lacking in dermal nerves of most patients. Fibroblast-like cells showed no cystic cisterna of endoplasmic reticula.
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PMID:Dermal changes in Ehlers-Danlos syndrome. 673 46

Periodontal disease is one of the most prevalent health problems in the world and is the major cause of tooth loss in the adult population. Its two major subdivisions are gingivitis where disease is confined to the gingiva, and periodontitis where disease is present both in the gingiva and the supporting periodontal tissues. During the first stage there is a vasculitis of vessels subjacent to the junctional epithelium which is followed by exudation of fluid from the gingival sulcus and migration of leukocytes. There is variable expression of this stage throughout the mouth with new areas of involvement appearing in place of healed areas. Mast cells which are present in the gingival connective tissues may participate in this inflammatory response by liberating histamine. Ascorbic acid deficiency has been shown to be a conditioning factor in the development of gingivitis. When humans are placed on ascorbic acid deficient diets there is increased edema, redness and swelling of the gingiva. These changes have been attributed to deficient collagen production by gingival blood vessels. However, this may be due to an antihistamine role of ascorbic acid. This vitamin may act to directly detoxify histamine or effect a change in the level of enzymes responsible for histamine metabolism. This could occur through the influence of ascorbic acid in altering cyclic AMP (c-AMP) levels. Such changes in the level of this regulatory molecule could result in increased histamine-N-methyl transferase and other enzymes responsible for the breakdown of histamine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of ascorbic acid deficiency in human gingivitis--a new hypothesis. 674 85

In an attempt to determine the optimal daily ascorbic acid requirement, the effect of different levels of ascorbic acid intake on collagen synthesis was studied in a double-blind experimental design. By use of electron microscopy, interproximal gingival tissue sections in subjects consuming between 20 to 35 mg of ascorbic acid daily were examined before and after the administration of tablets containing 70 mg of ascorbic acid. The results showed that practically all subjects were affected by progressive periodontitis with marked changes in the connective tissue of the gingival lamina propria. After six weeks of supplementation with ascorbic acid, differences in the shape and activity of fibroblasts in the regenerative tissue of lamina propria were observed. This has resulted in the increased number of collagen bundles in fibroblasts' periphery, increased tonofibril content and an enlarged number of desmosomes between adjacent cells. It is concluded that the obtained results, though suggesting that the optimal daily ascorbic acid intake should be set above the presently recommended 30-50 mg, have to be quantified by a more objective analytical method.
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PMID:The effect of ascorbic acid supplementation on periodontal tissue ultrastructure in subjects with progressive periodontitis. 675 68

The isolation and characterization of cyanogen bromide peptides derived from the human gingival collagen of patients with chronic periodontitis revealed the presence of both Type I and Type III collagens in this tissue. The amount of TYPE III collagen, however, was found to be lower than that in normal gingival tissue. In addition, a non-collagenous protein fraction, accounting for approximately 20% of the insoluble matrix, was relatively rich in acidic, hydrophobic, and hydroxy-containing amino acids. Amino acid analysis, likewise, revealed qualitative and quantitative differences between the normal and diseased tissues.
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PMID:Gingival matrix collagen in chronic periodontitis. 692 81

In order to analyze the conditions for rapidly destructive periodontitis and to describe the early histopathological changes and bone degradation, periodontitis lesions were produced in five male Beagle dogs, 8 to 12 months of age. Cotton floss ligatures were placed around the crowns of upper and lower third and fourth premolars for periods of 4, 7, 14, 21 days. The buccal gingival tissues, being slightly inflamed initially, were clinically scored for various symptoms of inflammation. Block biopsies of premorlars and the adjacent buccal periodontal tissues were taken and processed for light and electron microscopy. Depending on the ligature position in relation to the gingival margin (above, at, deep below) at the day of biopsy harvest, three groups of selected biopsies were formed, and randomly selected sections of these were used for various histometric measurements, for stereological estimation of the size and composition of the connective tissue infiltrate and the osteoclast density, and for general histopathological evaluation. The resulting data and observations implied that (1) onset and maintenance of this periodontitis lesion depend on subgingival ulceration, (2) rapid bone desstruction is the result of osteoclast activity stimulated by acute inflammation, and (3) bone degradation occurs independently of the loss of collagen fiber attachment and the apical migration of the junctional epithelium.
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PMID:Conditions and pathological features of rapidly destructive, experimental periodontitis in dogs. 692 71

The microflora of periodontal pockets and some histopathological characteristics of adjacent tissues from individuals with clinical signs of juvenile periodontitis were studied. Adult individuals with ordinary, rapidly advancing periodontitis served as controls. All of the patients had been referred for specialist treatment. Using criteria defined by Baer (19z1), the patients were assigned to one juvenile periodontitis (eight patients), one post-juvenile periodontitis (seven patients) and one adult periodontitis group (seven patients). Only lesions around the first molars and central incisors were studied. Bacterial samples were obtained from each site and were examined by darkfield microscopy and different morphological forms identified. The soft tissue of the diseased sites was excised. The biopsies were placed in a fixative, cut in 1-mm-thick blocks and embedded in Epon. In semithin sections the infiltrated connective tissue (ICT) was identified and the ICT portion further processed for electron microscopy. The numeric and volumetric densities of different cells and structures of the ICT were determined using a morphometric point-counting procedure. The results showed that juvenile periodontitis lesions are associated with a subgingival microflora, the composition of which is different from that of adult periodontitis. Thus, in patients belonging to the adult periodontitis and post-juvenile periodontitis groups, motile microorganisms dominated the subgingival plaque samples, whereas deep pockets in juvenile periodontitis lesions contained a flora dominated by coccoid cells and straight non-motile rods. The most pronounced difference in the composition of ICT between the juvenile on one hand and the post-juvenile and adult periodontitis lesions on the other, was related to the amount of extracellular structures. Thus, in post-juvenile and adult periodontitis lesions, collagen and residual tissue made up around 50% of the infiltrate. In the juvenile periodontitis lesions, however, extracellular structures occupied only around 20% of the volume. In the ICT of the juvenile periodontitis sites, around 70% of the volume was occupied by plasma cells and blast cells. The corresponding figures for the post-juvenile and adult periodontitis sites were 50 and 30%.
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PMID:Juvenile periodontitis. Some microbiological, histopathological and clinical characteristics. 692 56

PREVIOUS INVESTIGATIONS have demonstrated that application of citric acid to a root surface results in exposure of dentin and/or cementum matrix collagen fibrils. Several studies have suggested a rapid and consistent connective tissue reattachment to citric acid treated roots. This study was initiated to determine if such an attachment was obtainable on human periodontally diseased teeth, in vivo, and could be confirmed through observations using the scanning electron and light microscopes. Full thickness flaps were raised on 18 single rooted teeth with moderate to advanced periodontitis. Citric acid (pH = 1.0) was applied to nine teeth with contralateral teeth serving as controls. Six to fifteen weeks later, the teeth with attached periodontal tissue were removed. Sagittal sections were obtained, with one-half of the root being processed for light microscopy and the remaining half studied by scanning electron microscopy. Six of nine citric acid treated roots provided evidence of fibrous attachment. Connective tissue was apposed directly to old or newly formed cementum, but never directly to dentin. Fibrous attachment was usually functionally oriented, i.e., perpendicular to the root surface. No evidence of fibrous attachment was found among the control specimens.
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PMID:Connective tissue attachment to periodontally diseased roots after citric acid demineralization. 695 15

Scanning electron microscopy was used to evaluate surface characteristics of periodontitis-exposed instrumented human cementum and dentin surfaces following topical application of tetracycline HCl (TTC). Specimens were randomly assigned to application of sterile saline for 1 minute (control); TTC (10 mg/ml) for 1 minute and 4 minutes, respectively; and TTC (100 mg/ml) for 1 minute and 4 minutes, respectively. Solutions were applied with a cotton pellet using a burnishing technique. Control specimens exhibited an amorphous irregular surface smear layer. TTC treatment of cementum for 1 minute resulted in a relatively debris-free, nonhomogeneous surface. The 4-minute application resulted in a surface exhibiting a densely fibrillar, mat-like texture. Dentin specimens conditioned for 1 minute showed a smooth surface with many tubule openings partially occluded by debris. The 4-minute treatment exposed a 3-dimensional network of intertubular and peritubular collagen fibrils. No consistent morphologic differences were observed between cementum or dentin specimens treated with TTC at concentrations of 10 and 100 mg/ml, respectively. The results suggest that topical application of TTC produces morphologic alterations of periodontitis-exposed cementum and dentin that appear related to application interval rather than concentration of the drug.
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PMID:Effect of tetracycline HCl on periodontally-affected human root surfaces. 747 11

One-year follow-up of 20 patients with radicular cysts and 16 ones with medium-severity chronic periodontitis demonstrated the efficacy of hydroxylapatite with collagen. Active formation of osseous tissue at the site of cysts, in the periodontal osseous pockets, and at the apexes of interdental septa was observed 6 to 7 months after the treatment.
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PMID:[A clinical x-ray evaluation of the efficacy of hydroxyapatite with collagen in treating periodontitis and radicular cysts]. 748 5

The effects of various prostaglandins (PGs) on the functions of human gingival fibroblasts (Gin-1 cells; ATCC CRL 1292) were examined by phase-contrast microscopy, cell-counting and radioautographic experiments. Tested PGs were PGA1, PGA2, PGB1, PGB2, PGD2, PGE1, PGE2, PGF1 alpha, PGF2 alpha, PGI2, 6-keto-PGF1 alpha, 9 alpha-11 alpha-methanoepoxy-PGF2 alpha, and thromboxane (TX) B2. PGA1 and PGD2 at 30 microM caused morphological deformation of Gin-1 cells. All the PGs tested at 30 microM suppressed the proliferation of Gin-1 cells in the logarithmic growth phase. Furthermore, all the PGs tested at 10 microM suppressed DNA synthesis, collagen synthesis, and noncollagenous protein synthesis in confluent Gin-1 cells, while exerting no effect on GAG synthesis. The concentrations of PGs used are beyond those found in healthy gingiva. However, in periodontitis the local concentrations of some PGs within the gingiva are expected to be extremely elevated beyond the physiological level. These results suggest that PGs may play an important role as a negative regulator in metabolism and some pathologic gingival conditions by suppressing the functions of gingival fibroblasts.
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PMID:Response of human gingival fibroblasts to prostaglandins. 749 71


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