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)

During the past few years, a considerable number of studies have examined different aspects of the host response in gingival crevicular fluid (GCF), including the relationship of specific markers to the active phases of periodontal disease. Various indicators of the acute inflammatory response (the lysosomal enzymes beta-glucuronidase and collagenase, the cytoplasmic enzyme aspartate aminotransferase, and the arachidonic acid metabolite PGE2) have been shown to be associated with clinical attachment loss in chronic adult periodontitis in man and experimental periodontitis in animal models. In contrast, the relationship of indicators of the humoral immune response in GCF to active periodontal disease is equivocal. Furthermore, a number of indicators of the cellular immune response have been identified recently in GCF (i.e., Interleukin-1 alpha, IL-1 beta, tumor necrosis factor-alpha), but their relationship to active phases of periodontal disease have not been studied. The polymorphonuclear leukocyte (PMN) is the cellular hallmark of acute inflammation. Evidence from the GCF studies suggests that hyperreactivity of these cells plays a critical role in the active phases of some forms of periodontal disease. Metabolic activation of PMN can be associated with a number of potentially destructive reactions. The major effector mechanism for tissue destruction that can be specifically identified with the PMN is the synergistic effect of the release of PMN proteases and the generation of reactive oxygen metabolites by these cells. Priming of the PMN, where the PMN response is enhanced by agents that do not initiate the response, may be an important mechanism for PMN activation in the crevicular environment; for example, cytokines such as IL-1 beta and TNF-alpha, and lipopolysaccharides released from subgingival Gram-negative bacteria, can serve this function. The hypothesis proposed here argues that in addition to the severe forms of periodontal disease that have been associated with qualitative or quantitative PMN defects, tissue destruction in the periodontum can be observed with hyperreactivity of these cells. These differing conclusions do not create a dilemma, but may represent opposite ends of a balance that is no longer in equilibrium.
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PMID:Host mediators in gingival crevicular fluid: implications for the pathogenesis of periodontal disease. 173 70

Root canal samples, taken from periapical tissue exudates during routine root canal treatment procedures, were processed for identification of tumor necrosis factor using a mouse anti-human monoclonal antibody and enzyme-linked immunosorbent assay. Detectable levels of tumor necrosis factor were identified in periapical tissue exudates in chronic apical periodontitis.
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PMID:Tumor necrosis factor identified in periapical tissue exudates of teeth with apical periodontitis. 189 33

It seems to be generally agreed that periodontal disease is a local manifestation of a systemic immune response. Interleukin-1 (IL-1), which has multiple biologic activities, is detected in the gingival sulcus fluid of periodontitis sites. Recent investigations have revealed that IL-1 and tumor necrosis factor (TNF) are analogous to osteoclast activating factor and promote bone resorption. These findings have suggested the possibility that IL-1 and TNF may play a significant role in the initiation and development of periodontal disease. However, it remains to be determined whether these cytokines influence periodontal tissue breakdown in periodontitis. To elucidate the mechanisms of tissue breakdown in periodontitis, we examined cytokine production by human periodontitis gingival tissue. Twelve periodontitis patients were included in this study. Control subjects with healthy periodontium consisted of nine individuals. Gingival samples were biopsied from inflamed or healthy gingival tissues. Biopsy specimens were dissected into fragments 3 mm in diameter and plated onto 24 well culture plates with RPMI 1640 medium. IL-1 activity was measured by a growth inhibition assay using melanoma cell line A 375. An enzyme-linked immunosorbent assay (ELIZA) was used for measuring levels of human IL-1 alpha, IL-1 beta. TNF alpha activity was measured by a growth inhibition assay using cell line LM2D6. IL-1 activity was detected in significantly (p less than 0.001) higher levels in culture supernatants from gingival tissues in periodontitis (48.0 +/- 23.3 units/ml) than in control tissues (2.3 +/- 0.6 units/ml), however, levels of IL-1 activity were not associated with periodontal pocket depth or extent of alveolar bone resorption in periodontitis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Study of cytokine production in inflamed human gingival tissues in periodontitis. Interleukin-1 (IL-1 alpha, beta) and tumor necrosis factor (TNF alpha)]. 248 32

The effects of gram-negative bacteria clearly associated with juvenile and adult periodontitis on monokine production were assessed using standard in vitro assay techniques. Actinobacillus actinomycetemcomitans and Bacteroides gingivalis were able to activate human peripheral blood monocytes to produce significant amounts of interleukin-1 (IL-1) and tumor necrosis factor (TNF). These monokines are known to induce osteoclastic bone resorption. An oral gram-positive organism, Staphylococcus epidermidis, was able to induce only modest amounts of IL-1 and TNF, slightly above unstimulated monocyte levels.
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PMID:Actinobacillus actinomycetemcomitans and Bacteroides gingivalis activate human peripheral monocytes to produce interleukin-1 and tumor necrosis factor. 326 71

Endothelial cell activation by endotoxin (LPS), tumor necrosis factor (TNF), Interleukin-1-alpha, beta (IL-1-alpha, beta) and phorbolesters (TPA) results in increased monocyte adhesion. Examination of kinetics of monocyte adhesion shows that the onset of adherence enhancement (AE) is similar in all five agents (about 300% AE at 6 h), while its decrease is delayed in LPS/TNF versus IL-1-alpha, beta/TPA-induced activation (LPS versus IL-1-beta:260% versus 60% at 18 h). Monoclonal antibody (4D10), raised against 24 h LPS-stimulated endothelial cells detects an endothelial cell-specific activation antigen at Mr 81,000 that is induced by LPS, TNF, IL-1-alpha, beta and TPA (within 6 h about 100% positive cells). Decrease in antigen-positive cells is delayed in LPS/TNF versus IL-1-alpha, beta/TPA-induced antigen expression (LPS vs. IL-1-beta: 60% vs. 5% at 24 h). In situ the antigen is not expressed in normal and chronic inflammatory tissues. Acute inflammatory tissues, including contact and atopic dermatitis, psoriasis and periodontitis, however, show endothelial cells staining strongly positive. In contact eczemas at different times after elicitation (0, 6, 24, 72, 96 h), expression of the antigen is first seen after 24 h and is still strong at 96 h. These data indicate that LPS/TNF conduct an endothelial cell activation program in vitro, showing the same prolonged kinetics that is found for endothelial cell activation in the acute inflammatory process in vivo.
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PMID:Characterization and expression kinetics of an endothelial cell activation antigen present in vivo only in acute inflammatory tissues. 331 46

Extensive clinical, microbiological, hematological, and immunological studies were performed on a patient with early onset periodontitis (EOP) and two other members of the family. The proband, a 27-year-old female, had early onset periodontitis and a high level of serum rheumatoid factors (RF) with no diagnosable medical disease. Her mother had lost all her teeth at the age of 50 because of advanced periodontitis, while her elder sister was unaffected by periodontitis. Neither the proband's periodontally-affected mother nor her unaffected sister exhibited a detectable level of RF. In this study, we examined: 1) serum immunoglobulin G (IgG) antibody titers against putative periodontal pathogenic bacteria; 2) peripheral neutrophil functions; 3) phenotypic analyses of peripheral lymphocyte subpopulations; and 4) peripheral lymphocyte functions (T cell proliferative activity, ability of cytokine [interleukin (IL)-2, tumor necrosis factor-alpha, interferon-gamma, IL-6 and IL-8] and IgG and IgM productivity). High antibody titers to Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, and Campylobacter rectus were detected in the sera of the proband, as were high serum antibody titers to P. gingivalis in the mother and to C. rectus in the unaffected sister compared to the non-periodontitis affected subjects. The proband also showed enhanced neutrophil chemotaxis; a high percentage of pan-B cells; and high productivity of IL-6, IgG, and IgM compared to individuals who were not periodontally affected. The mother showed slightly low helper/induced T cells (Th/i) suppressor/cytotoxic T cells (Ts/c) ratios due to the elevated count of Ts/c, and high IFN-gamma productivity compared to control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical and laboratory studies on a patient with early onset periodontitis and her family members. A case report. 762 61

Polymorphonuclear leukocytes (neutrophils) in patients with localized juvenile periodontitis with decreased chemotaxis exhibit increased adherence. The molecular basis of increased adherence of neutrophils in localized juvenile periodontitis is not clear. We show that the neutrophils from localized juvenile periodontitis patients with decreased neutrophil chemotaxis and increased adherence exhibit increased expression of the CD11/CD18 family of adherence molecules, Mac-1, leukocyte function-associated antigen (LFA-1) and p150,95, as compared with neutrophils obtained from systemically and periodontally healthy controls. Treatment of neutrophils obtained from healthy subjects with sera from localized juvenile periodontitis patients resulted in an increased expression of Mac-1, leukocyte function-associated antigen and p150,95 molecules. Sera obtained from health subjects, patients with adult periodontitis or localized juvenile periodontitis patients with normal chemotaxis did not increase the expression of CD11/CD18 molecules on the neutrophils obtained from healthy subjects. The ability of localized juvenile periodontitis sera to induce expression of adherence molecules was at least partially inhibited by pretreatment of localized juvenile periodontitis sera with anti-tumor necrosis factor and anti-interleukin-1 antibodies. Furthermore, increasing concentrations of rh-tumor necrosis factor-alpha and interleukin-1 beta also induced increased expression of the Mac-1 molecule on neutrophils from localized juvenile periodontitis patients and healthy subjects. The increased expression of adherence molecules on neutrophils from localized juvenile periodontitis patients was sustained and could not be reversed by treatment of localized juvenile periodontitis neutrophils with sera obtained from healthy subjects. The upregulation of adherence molecules on neutrophils by localized juvenile periodontitis sera in these experiments emphasizes the physiologic importance of quantitatively small but biologically significant levels of cytokines in the modulation of neutrophil functions in localized juvenile periodontitis.
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PMID:Neutrophil function in juvenile periodontitis: induction of adherence. 780 67

In this study, we sought to determine if human polymorphonuclear leukocytes (PMNs) derived from chronically inflamed tissues can produce inflammatory cytokines in vivo. Human gingival crevicular fluid (GCF) with adult periodontitis was collected, and PMNs in GCF were examined after purified by Ficoll-Hypaque gradient method. Cytokines from peripheral blood (PB) cells stimulated with concanavalin A, LPS, or zymosan were also characterized, since GCF contains predominantly PMNs (> 95%) with a small number of lymphocytes or macrophages. Production of interleukin-1 alpha (IL-1 alpha), IL-1 beta, tumor necrosis factor-alpha (TNF alpha), and IL-6 in GCF or culture supernatants of peripheral blood cells was determined by ELISA. Significant levels of IL-1 alpha and IL-1 beta secretion were found in GCF. PB cells in culture showed prominent cytokine production from monocytes/macrophages, followed by lymphocytes. Human peripheral blood PMNs (PB-PMNs) also produced low levels of IL-1 alpha and IL-1 beta, but not TNF alpha and IL-6. These cells were also examined for cytokine mRNA expression using the reverse transcription-polymerase chain reaction analysis. Highly purified PMNs (> 99.5%) from GCF expressed mRNA for IL-1 alpha, IL-1 beta and TNF alpha, but not for IL-6. PB-PMNs in culture also showed mRNA expression for IL-1 alpha, IL-1 beta, and TNF alpha in a time- and dose-dependent manner, especially after stimulation with zymosan. Therefore, we concluded that human PMNs from inflamed tissues can produce IL-1 alpha, IL-1 beta, and TNF alpha in vivo, but not IL-6.
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PMID:Human polymorphonuclear leukocytes derived from chronically inflamed tissue express inflammatory cytokines in vivo. 802 49

Refractory periodontitis manifests as a rapid, unrelenting, progressive loss of attachment despite the type and frequency of therapy. This study examined possible relationships between cytokine levels in gingival crevicular fluid (GCF), occurrence of specific periodontopathic microflora, and disease activity in patients with refractory periodontitis. Refractory periodontitis patients (7 male and 3 female) were selected on the basis of history and longitudinal clinical observations. In each patient, 2 teeth with pocket depths greater than 6 mm were selected and individual acrylic stents were fabricated with reference grooves for each site. The sites were examined at both baseline and 3 months later. The pattern and amount of alveolar bone resorption were assayed by quantitative digital subtraction radiography. Pocket depth and attachment loss were measured with a Florida Probe. The gingival index was measured at 4 sites around each sample tooth. Sites were divided into active sites (> or = 2.1 mm loss of attachment in 3 months) or inactive sites (< or = 2.0 mm loss of attachment in 3 months). The distribution and prevalence of the predominant microflora in active and inactive sites were compared using anaerobic culture and indirect immunofluorescence. Interleukin-1 beta, 2, 4, 6 and tumor necrosis factor-alpha (TNF-alpha) levels in gingival crevicular fluid (GCF) were quantified by ELISA. Prevotella intermedia and Eikenella corrodens significantly decreased in inactive sites but remained the same in active sites after 3 months. The active sites revealed significantly higher GCF levels of IL-2 and IL-6 than inactive sites at both baseline and at 3 months. IL-1 beta was also significantly greater in active sites than in inactive sites at 3 months. Alveolar bone loss in active sites correlated with increased GCF levels of IL-1 beta and IL-2. These results suggest that GCF levels of IL-1 beta, IL-2 and IL-6 and P. intermedia and E. corrodens in subgingival plaque may serve as possible indicators of disease activity in refractory periodontitis.
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PMID:The subgingival microflora and gingival crevicular fluid cytokines in refractory periodontitis. 855 Aug 66

The bone-resorptive cytokines interleukin 1 (IL-1) and tumor necrosis factor (TNF) have been implicated in the pathogenesis of many chronic inflammatory diseases, including pulpitis and apical periodontitis.To further elucidate their role in these disorders, we have identified cells that express IL-1 alpha and TNF alpha in infected pulps and in developing rat periapical lesions after surgical pulp exposure. As detected by immunohistochemistry, IL-1 alpha- and TNF alpha-positive cells were present as early as 2 days after pulp exposure in both the pulp and periapical region. The numbers of cytokine-expressing cells increased up to day 4 in the pulp and up to day 30 in the periapex. In contrast, cells expressing IL-1 beta and TNF beta, the homologous forms of these mediators, were not found in pulp or periapical lesions during this period. Cells expressing IL-1 alpha and TNF alpha were identified primarily as macrophages and fibroblasts, with occasional staining of polymorphonuclear leukocytes. Osteoblasts and osteoclasts were also positive, whereas lymphocytes were negative. In general, cytokine-expressing cells were located proximal to abscesses and the root apex. These findings demonstrate that cells that express bone-resorptive cytokines IL-1 alpha and TNF alpha are present immediately after pulp exposure in this model, which supports the hypothesis that these mediators play a key role in pulpal and periapical pathogenesis, including the concomitant bone destruction. They also indicate that both resident connective tissue cells as well as infiltrating cells express bone-resorptive cytokines in response to infection in these lesions.
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PMID:Immunolocalization of bone-resorptive cytokines in rat pulp and periapical lesions following surgical pulp exposure. 860 33


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