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Query: UMLS:C0031099 (periodontitis)
 12,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study was designed to enumerate cell populations before, during and after experimentally induced periodontitis in squirrel monkeys. The clinically healthy gingival connective tissue adjacent to the sulcus contained populations of macrophages, plasma cells, lymphoid cells, and granulocytes, indicating that immune responses were probably in operation. Although these cell populations have been associated with tissue destruction, it is possible that they may serve to confine the antigens to the tissue adjacent to the sulcus, and reduce their spread apically. Active periodontitis was associated with the presence of granulocytes and macrophages in the transseptal fiber region. These cells are capable of causing the localized collagen degradation and bone resorption that occur during the destructive phase of the disease. Eight weeks after etiologic agents were removed, the cell populations in the transseptal fiber area returned to a level comparable with those in the pre-experimental, clinically healthy. This indicates that active periodontitis within the transseptal fiber region had ceased and repair had occurred.
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PMID:Cell populations in the transseptal fiber region before, during and after experimental periodontitis in squirrel monkeys. 10 25

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

Connective tissue fibroblasts undergo cytopathic degenerative changes during certain long-term inflammatory diseases such as rheumatoid arthritis and periodontitis. The failure of inflamed tissues to repair properly may result from functional alterations of fibroblasts within the affected tissues. Numerous previous studies indicate that direct cytotoxicity by bacterial or other substances may be responsible for the cellular alterations observed in vivo. We have tested this hypothesis by exposing cultures of human diploid fibroblasts to homogenates of Actinomyces viscosus (a microorganism associated with periodontitis and capable of causing other chronic inflammatory diseases) and analyzing the effects on cell viability, morphology, and function. The cells bind and subsequently engulf relatively large quantities of the bacterial substances. These substances do not appear to be toxic to fibroblasts as determined by 51Cr release and microcytotoxicity assays, although there is a slight but significant decrease in protein synthesis (P less than 0.01) as measured by the incorporation of [14C]proline. However, collagen production was not altered, and the cytopathic alterations observed in diseased tissues in vivo did not occur in the exposed cells. These findings suggest that A. viscosus substances do not directly cause injury to connective tissue fibroblasts in periodontal disease but may, through cell-surface binding, mark these cells for subsequent immune-mediated damage.
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PMID:Morphological features and functional properties of human fibroblasts exposed to Actinomyces viscosus substances. 62 91

Gingivitis and periodontitis account for more than 95% of all inflammatory diseases of the tissues surrounding the teeth, comprising the principal cause of tooth loss in adults. Gingivitis is a relatively innocuous inflammation of the gums, with associated bleeding and exudation. Gingivitis may convert to periodontitis, a destructive aggressive disease with resorption of alveolar bone, destruction of collagen with fibrosis, and formation of deep pockets around the necks of the teeth. Gingivitis and periodontitis are caused by microorganisms populating the gingival sulcus and periodontal pocket. Treatment is directed toward arresting the progress of the disease through debridement and stabilization of the teeth. Toothbrushing and other measures by which the teeth are mechanically cleaned remain the most effective way to control plaque accumulation and periodontal disease.
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PMID:Chronic inflammatory gingival and periodontal disease. 67 30

Collagen synthesis by fibroblasts obtained from healthy and diseased human gingiva was compared. The cells were labeled with radioactive amino acids and the collagenous proteins synthesized were characterized after NaCl fractionation by CM-cellulose chromatography and cyanogen bromide peptide analysis. Fourteen cell lines, six from healthy gingiva, six from gingiva with chronic inflammatory periodontitis, and two from acutely inflamed gingiva were studied. All of the cell lines synthesized predominantly type I collagen. Type III collagen was a minor product of all cell lines except one from diseased tissue. Five of six cell lines from diseased gingiva and two of two from acutely inflamed tissue synthesized a collagen that was soluble in 2.5 M NaCl. The alpha1/alpha2 ratio and cyanogen bromide peptide pattern indicated that this fraction contained a collagen of the type alpha1[I]3. The alpha1[I]3 collagen was not detectable in the fibroblast lines obtained from healthy gingiva. It appears that inflamed human gingivae contain fibroblasts which differ phenotypically from cells from normal tissue in that they are capable of synthesizing alpha1[I]3 collagen.
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PMID:Collagens synthesized in vitro by diploid fibroblasts obtained from chronically inflamed human connective tissue. 68 92

Chronic periodontitis, a common disease of microbial origin, is the major cause of tooth loss in adult humans. The disease serves as a convenient experimental model for analysis of many aspects of chronic inflammation. A consideration of currently available data has permitted the formulation of a new concept of the pathogenesis of this disease. The gingival tissues respond within 2 to 4 days to a beginning accumlation of microbial plaque with a classic acute exudative vasculitis which we have termed the initial lesion. This response, which includes loss of perivascular collagen, is comparable to that elicited in most other tissues subjected to acute injury and may be a consequence of the elaboration and release of chemotactic and antigenic substances by microbial plaque. Within 4 to 10 days, the early lesion develops. It is characterized by a dense infiltrate of lymphocytes and other mononuclear cells, pathologic alteration of fibroblasts, and continuing loss of the connective tissue substance. The structural features of the early lesion are consistent with those expected in some form of cellular hypersensitivity, and a mechanism of this kind may be important in the pathogenesis. The early lesion is followed by the established lesion which develops within 2 to 3 weeks and is distinguished by a predominance of plasma cells in the absence of significant bone loss. The established lesion, which is extremely widespread in humans and in animals, may remain stable for years or decades, or it may become converted into a progressive destructive lesion. Factors causing this conversion are not understood. In the advanced lesion, plasma cells continue to predominate although loss of the alveolar bone and periodontal ligament, and disruption of the tissue architecture with fibrosis are also important characteristics. The initial, early, and established lesions are sequential stages in gingivitis and they, rather than the advanced lesion which is manifest clinically as periodontitis, make up the major portion of inflammatory gingival and periodontal disease in humans.
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PMID:Pathogenesis of inflammatory periodontal disease. A summary of current work. 76 22

Chronic periodontitis results in the destruction of the collagen fibre attachment to cementum, apical migration of the epithelial attachment, contamination of the exposed root surface by plaque and loss of alveolar bone. Regeneration can be defined as the restitution of lost tissues to a state which existed before destruction. As such, it is an ultimate and ideal goal and in most circumstances is currently beyond our capabilities. However, research in periodontology over the last 10 years or so has made considerable advances and is perhaps unique in proposing a new and fundamental treatment modality--guided tissue regeneration.
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PMID:Guided tissue regeneration--why, when and how? 128 60

Mammalian interstitial collagenases (E.C.3.4.24.7) are considered as key initiators of collagen degradation in periodontal diseases. However, the cellular sources of collagenases present in gingival crevicular fluid have not been completely clarified. Resident fibroblasts and epithelial cells as well as infiltrating neutrophils and monocyte/macrophages are potential sources of the enzymes. We have recently found significant differences in tetracycline inhibition between human neutrophil and fibroblast interstitial collagenases. To address the cellular source of collagenase present in gingival crevicular fluid in 2 distinct periodontal diseases, we studied the tetracycline inhibition of collagenase in gingival crevicular fluid of patients with localized juvenile periodontitis and adult periodontitis. Gingival crevicular fluid samples were collected from deep (greater than 5 mm) periodontal pockets and assayed for collagenase in the presence of 0-1000 microM doxycycline as well as a chemically modified tetracycline devoid of antimicrobial activity (4-de-dimethylaminotetracycline). The drug concentration required to inhibit 50% of collagenase activity (IC50) in localized juvenile periodontitis gingival crevicular fluid was 280 microM for doxycycline and 470 microM for 4-de-dimethylaminotetracycline. Significantly lower values, 10-20 microM, were obtained for collagenase in gingival crevicular fluid of patients with adult periodontitis. We propose that systemic tetracycline levels are efficient inhibitors of collagenase in gingival crevicular fluid in affected sites of patients with adult periodontitis but not of patients with localized juvenile periodontitis and that the fibroblast type interstitial collagenase is the predominant collagenase type in gingival crevicular fluid in affected sites of patients with localized juvenile periodontitis and the neutrophil collagenase in adult periodontitis gingival crevicular fluid.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tetracycline inhibition identifies the cellular origin of interstitial collagenases in human periodontal diseases in vivo. 132 40

This study was performed to investigate the frequency and distribution of CD5-positive (CD5+) B cells in inflamed gingival tissues using flow cytometric and immunohistochemical analyses. The ability of CD5+ B cells to produce anti-type I collagen antibody was also examined. CD5+ B cells expressed "low" fluorescence intensity in the peripheral blood of both healthy subjects and patients with adult periodontitis. However, in inflamed gingival tissues the intensity of this surface marker was high. The percentage of B cells bearing CD5 surface marker was statistically higher in gingiva than in peripheral blood obtained from both the patients and healthy subjects. These CD5+ B cells were observed in gingival subepithelial connective tissues from the bottom to the middle of the periodontal pocket. This area showed destruction of collagen fibers and dense cell infiltrations. Anti-collagen IgG antibody level in patients' gingival crevicular fluids (GCF) was higher than that in sera from healthy subjects, and slightly higher than in autologous sera. IgM anti-collagen antibody in GCF was lower than in autologous sera and in sera from healthy subjects. EBV-transformed CD5+ B cells produced considerably more IgM and IgG antibody to collagen than CD5- B cells. Therefore CD5+ B cells may contribute to the pathogenesis of inflamed gingival tissues.
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PMID:Detection of, and anti-collagen antibody produced by, CD5-positive B cells in inflamed gingival tissues. 138 87


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