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)

Human gingival fibroblast cell lines were initiated in flask cultures from four periodontal patients with the diagnoses of periodontitis (two patients), fibromatosis, and Dilantin hyperplasia. The collagenolytic propensity of these fibroblasts cultivated on collagen-coated cover slips and the inhibitory effect of serum were evaluated by direct microscopic observations.
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PMID:Collagenolysis by human gingival fibroblast cell lines. 26 71

Using 16 human gingival fibroblasts cell lines from patients with periodontitis, Dilantin hyperplasia, and nonpathological gingiva, a microscopic assay was developed to quantitate the cells' ability to lyse collagen substrates. The method employs tissue culture chambers with one cover slip partially coated with a thin layer of undenatured fibrillar bovine collagen. The assay measures the relative numbers and sizes of holes in the collagen within defined regions of the cover slips effected by the phagocytotoc and collagenolytic performance (PCP) of the population of fibroblasts growing on the cover slip for 5 days. The effect on the PCP index by serum, heparin, prostaglandins, and endotoxin was evaluated.
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PMID:Microscopic assay for the phagocytotic-collagenolytic performance (PCP index) of human gingival fibroblasts in vitro. 36 54

Immunoglobulin levels in both Dilantin-induced and idiopathic hyperplastic gingiva were determined and compared with the concentrations in normal gingival tissue. A statistically significant increase in IgG was found in Dilantin hyperplastic tissue, but no significant difference could be shown for idiopathic gingival hyperplasia. IgA levels did not differ significantly in the three types of tissue assayed. IgM was detected in 90% of the Dilantin hyperplastic gingival specimens assayed (mean GI = 1.2) and in 75% of the idiopathic hyperplastic tissue (mean GI = 0.7). This incidence of IgM detection was higher than that reported for normal and inflamed gingiva from periodontitis patients. The significance of these findings and possible correlation with the degree of tissue inflammation are discussed.
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PMID:Immunoglobulins in periodontal tissues. III. Concentrations of immunoglobulins in dilantin-induced and idiopathic gingival hyperplastic tissues. 692 67

Effects of chronic administration of xenobiotics pro-oxidants on the state of periodontal tissues, level of free-radical oxidation of lipids, and antioxidant provision were studied. Diphenin and delagil were found to promote biochemical and morphological changes similar to the manifestations observed in periodontitis. A conclusion is made about an important role of nonenzymatic free-radical oxidation of lipids and biopolymers in the pathogenesis of periodontitis. The principal stages of contribution of autooxidation to the parodontogenesis are presented.
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PMID:[Biochemical and ultrastructural changes in the periodontium during the chronic administration of pro-oxidant xenobiotics]. 773 38

Diphenylhydantoin (DPH) is widely used as an anticonvulsant drug. We examined the effects of DPH on osteoclast differentiation and function using in vivo and in vitro assay systems. Transgenic mice overexpressing a soluble form of RANKL (RANKL Tg) exhibited increased osteoclastic bone resorption. Injection of DPH into the subcutaneous tissue overlying calvaria of RANKL Tg mice suppressed the enhanced resorption in the calvaria. In co-cultures of mouse osteoblasts and bone marrow cells, DPH inhibited lipopolysaccharide (LPS)-induced osteoclast formation. DPH affected neither the mRNA expression of RANKL and osteoprotegerin nor the growth of mouse osteoblasts in culture. On the other hand, DPH inhibited the RANKL-induced formation of osteoclasts in cultures of mouse bone marrow-derived macrophages (BMMphis) and of human peripheral blood-derived CD14(+) cells. DPH concealed LPS-induced bone resorption in mouse calvarial organ cultures and inhibited the pit-forming activity of mouse osteoclasts cultured on dentine slices. DPH suppressed the RANKL-induced calcium oscillation and expression of nuclear factor of activated T cells c1 (NFATc1) and c-fos in BMMphis. Moreover, DPH inhibited the RANKL-induced nuclear localization and auto-amplification of NFATc1 in mature osteoclasts. Both BMMphis and osteoclasts expressed mRNA of a T-type calcium channel, Cav3.2, a target of DPH. Blocking the expression of Cav3.2 by short hairpin RNAs significantly suppressed RANKL-induced osteoclast differentiation. These results suggest that DPH inhibits osteoclast differentiation and function through suppression of NFATc1 signaling. The topical application of DPH may be a therapeutic treatment to prevent bone loss induced by local inflammation such as periodontitis.
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PMID:Diphenylhydantoin inhibits osteoclast differentiation and function through suppression of NFATc1 signaling. 1929 14

Phenytoin-induced gingival overgrowth (PIGO) is a common complication of the continuous use of medications. This paper presents a case of PIGO hindering oral function and compromising oral hygiene and aesthetics, which was treated with a combination of nonsurgical and surgical periodontal therapies. A 39-year-old male patient was referred for dental treatment with several complaints, especially upper and lower gingival overgrowth that hindered speech and swallowing. Generalized deep probing pockets and bone loss were detected. Diagnosis of gingival overgrowth associated with phenytoin and chronic periodontitis was established. The treatment plan consisted of conservative therapy with education on oral health, motivation and meticulous oral hygiene instruction in combination with scaling and root planing. During the revaluation period, a marked reduction in the clinical parameters was noted, particularly probing pocket depth reduction. Surgical therapy for removal of gingival overgrowth was also performed to achieve pocket reduction. Supportive periodontal therapy was proposed and the patient is currently under follow-up for 4 years. Management of PIGO may be obtained by the use of periodontal procedures combined with good oral hygiene and periodontal supportive care.
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PMID:Phenytoin-induced gingival overgrowth management with periodontal treatment. 2567 82