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)

There have been two previous cases reported in which children with a possible history of Prepubertal Periodontitis (PP) developed Generalized Juvenile Periodontitis (GJP) in their permanent dentitions at circumpubescent ages. This paper reports a case in which an apparently healthy 13-year-old girl, whose radiographs at 6 1/2 years of age showed horizontal bone loss around the primary molars, developed GJP. Blood tests (CBC, WBC differential, fasting glucose level, serum alkaline phosphatase) and a gingival biopsy were performed to exclude possible systemic diseases that might have been associated with alveolar bone resorption. Neutrophil (PMN) chemotaxis (CX) and adhesion molecule CD11b levels were also examined. The results of these tests were all within the normal range. This case report illustrates that an apparently healthy patient with PP may develop advanced periodontitis at a circumpubescent age.
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PMID:Generalized juvenile periodontitis in a thirteen-year-old child. 193 5

Soluble endothelial leukocyte adhesion molecule-1 (sE-selectin) levels in peripheral blood (PB) and gingival capillary blood (GCB) of both healthy donors (HD) and patients with adult periodontitis (AP) were assayed by ELISA. Binding of sE-selectin to polymorphonuclear neutrophils (PMN) from PB, GCB and crevicular fluid (GF), and expression of L-selectin and sialyl-Lewisx (sLex) on these cells were analyzed by immunofluorescence and flow cytometry. No significantly enhanced serum levels of sE-selectin in patients with AP, compared to HD (28 +/- 5 ng/ml vs 19 +/- 3 ng/ml, respectively), and no differences in the concentration of sE-selectin in GCB (16 +/- 1 ng/ml vs 16 +/- 2 ng/ml, respectively) were observed. On PB-PMN no significant differences in the expression of L-selectin and sLex were found and binding of sE-selectin to PB-PMN was comparable between HD and patients with AP. Binding of sE-selectin to GCB-PMN was significantly higher in patients with AP compared to HD (mean channel fluorescence (MCF) = 88.5 +/- 13.2 vs MCF = 24.2 +/- 5.3, respectively). The expression of sLex on GCB-PMN did not differ significantly between the two groups. A significant decrease in the expression of the adhesion molecule L-selectin on GCB-PMNs compared to PB-PMN was found in patients with AP but not in HD. CF-PMN showed decreased expression of both L-selectin and sLex compared to PMN from PB and GCB, both in HD and patients with AP. Taken together, these data suggest that PMN from patients with AP had reduced selectin-mediated adhesive capabilities to inflamed gingival endothelium.
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PMID:Influence of sE-selectin and L-selectin on the regulation of cell migration during chronic periodontitis. 747 3

The normal inflammatory response to infections requires the peripheral leukocytes to migrate across the blood vessels to the site of infection in response to chemotactic factors released in the site. The importance of cell to cell adhesion between the leukocytes and vascular endothelial cells in the leukocyte migration across the blood vessels was substantiated by the finding of a recently defined heritable disease called leukocyte adhesion deficiency (LAD). LAD is a disorder characterized by recurrent bacterial infections, impaired pus formation and wound healing, persistent periodontitis, and an abnormally high peripheral leukocyte count. The profound pathogenesis of the LAD has been defined as impairments in adhesion-dependent leukocyte functions such as chemotaxis due to a lack of leukocyte cell-surface expression of adhesion molecules of LFA-1, Mac-1 and p150/95, the beta 2-integrin. Very recently, a new disorder having almost the same clinical features and leukocyte dysfunctions as the LAD but normal expression of the beta 2-integrin was identified. The disease lacks cell-surface carbohydrate components, the sialyl Lewis antigens which are the ligands of another kind of adhesion molecule of selectins expressed on the vascular endothelial cells. The presence of these two diseases indicates that the leukocyte locomotion requires cell to cell adhesion through both the beta 2-integrin and selectins.
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PMID:[Adhesion molecules and leukocyte functions]. 754 65

The adhesion molecule, CD11b/CD18, plays a role in host defense against bacterial infections owing to its involvement in cell migration and phagocytosis. We examined the kinetics of CD11b expression on neutrophils isolated from peripheral blood (PB-PMNs) and gingival crevicular fluid (CF-PMNs) in subjects with healthy gingivae and in patients with advanced periodontitis in order to assess if CF-PMNs respond differently in regard to CD11b expression from PB-PMNs isolated from healthy or periodontitis subjects. CF-PMNs or formylmethionylleucylphenylalanine (fMLP)-stimulated PB-PMNs were incubated in buffer with or without divalent cations for 60, 90, or 110 minutes. Plasma membrane (surface) CD11b as measured by flow cytometry was found to be reduced with time when cells (PB-PMNs or CF-PMNs) from either controls or patients were treated with calcium- and magnesium-free buffer. However, when CF-PMNs were treated with buffer containing Ca++/Mg++, surface CD11b expression increased on cells from both controls and patients. The reduction in CD11b expression on PB-PMNs is significantly greater than that measured on CF-PMNs over time. Therefore, CF-PMNs respond differently from PB-PMNs which have been artificially stimulated with fMLP in regard to kinetics of CD11b expression on the plasma membrane.
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PMID:Kinetics of CD11b expression on neutrophils isolated from subjects with healthy gingivae and patients with advanced periodontitis. 847 86

Polymorphonuclear neutrophils (PMN) are the most abundant immune cells in inflammatory gingival sites of patients with early onset periodontitis, localized juvenile periodontitis, and rapidly progressive periodontitis (RPP). In the latter, the large number of PMN in connective tissue may explain the marked gingival destruction. Because interleukin-8 (IL-8) is a potent PMN chemoattractant, we evaluated circulating levels and gingival mRNA expression of IL-8. We found high IL-8 plasma levels as well as strong IL-8 mRNA expression in both epithelial and connective gingival cells from patients with RPP. Moreover, the gingival PMN themselves contained IL-8 mRNA, suggesting an autoamplification of PMN recruitment and activation in the gingiva. We also measured the expression of adhesion molecules at the PMN surface as well as the oxidative burst in whole blood from 14 patients with RPP, using flow cytometry to avoid irrelevant stimulations and to analyze single cells. In RPP patients, resting PMN showed reduced L-selectin, Lewis x, and sialyl Lewis x antigen expression as well as increased H2O2 production. These modifications of PMN adhesion molecule expression, together with their increased basal oxidative burst and excessive IL-8 production, may contribute to the noxious inflammatory reaction, which may in turn be autopotentiated by PMN production of IL-8. In addition, PMN showed a lack of increased response (H2O2 production) to formyl peptides after ex vivo priming with IL-8, possibly owing to IL-8 desensitization that may be involved in the increased susceptibility of RPP patients to infection. After appropriate treatment of RPP, the reduction in inflammation was associated with a return to control levels of both plasma IL-8 and PMN functions, suggesting that these features are linked.
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PMID:Interleukin-8 production by polymorphonuclear neutrophils in patients with rapidly progressive periodontitis: an amplifying loop of polymorphonuclear neutrophil activation. 964 66

Numerous studies of polymorphonuclear leucocyte (PMN) function in patients with adult periodontitis, including rapidly progressive periodontitis, have yielded conflicting findings, perhaps because most of the assays were performed on PMNs that had been separated from whole blood by a variety of procedures. To avoid the problems associated with in vitro analysis of isolated cells, PMN function and antigen expression in live whole unmanipulated blood of eight patients with rapidly progressive periodontitis were compared with those of age-, race-, and sex-matched controls. Using multiparameter flow cytometry, a) L-selectin (CD62L) expression, b) cell size, and c) respiratory burst activity were measured in PMNs in whole blood immediately ex vivo and during incubation with Porphyromonas gingivalis and Staphylococcus aureus. By comparison with PMNs from the control group, PMNs from the patient group expressed significantly lower levels of CD62L and had an increased size before stimulation. PMNs from both groups produced respiratory bursts similar to those of the two bacteria, but in both groups the responses to S. aureus were significantly greater than those to P. gingivalis. The significantly reduced expression of the adhesion molecule CD62L on PMNs in the patient group may lead to reduced tethering of neutrophils at sites of inflammation and may partly explain the susceptibility of these individuals to recurrent and severe periodontal infections.
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PMID:Multiparameter flow cytometric analysis of polymorphonuclear leucocytes in whole blood from patients with adult rapidly progressive periodontitis reveals low expression of the adhesion molecule L-selectin (Cd62L). 969 59

Because of their importance in mediating cellular interactions in chronic inflammatory diseases, this study has examined the expression of a number of adhesion molecules in adult (n=11), generalized early onset (n=5) and localized early onset (n=2) forms of periodontitis. In comparison with immunostaining profiles of cryostat sections of healthy gingival tissue (n=7), the beta 1 integrins VLA-1, VLA-2 and VLA-4 were found to be up-regulated in periodontitis, with VLA-6 being markedly elevated. Although only small differences were observed in ICAM-1 and LFA-3 expression in the gingival epithelium, there was particularly notable up-regulation of these adhesion molecules within the inflammatory infiltrates of the diseased tissues. However, there were no statistically significant differences between the serum levels of a soluble form of LFA-3 in periodontitis patients (n=47) compared with healthy control subjects (n=40), although the generalized early onset and adult periodontitis groups exhibited wider ranges of circulating LFA-3. These findings show that there is localized modulation of adhesion molecule expression in the chronic inflammatory periodontal diseases studied, but that the levels of LFA-3 in the circulation nevertheless remain unaffected.
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PMID:Localized adhesion molecule expression and circulating LFA-3 levels in adult and early onset forms of periodontitis. 1059 6

Periodontal diseases, such as gingivitis and periodontitis, are caused by a mixed infection by several types of bacteria in the dental plaque, causing a chronic inflammation of the gingival mucosa. Inflammatory processes in conjunction with immune responses to bacterial attacks are generally protective. In profound periodontitis, however, hyperresponsiveness and hypersensitivity of the immune system are counterproductive because of the destruction of the affected periodontal connective tissues. The intercellular adhesion molecule type 1 (ICAM-1) plays a key role in the onset and manifestation of inflammatory responses. Thus, inhibition of ICAM-1 expression could be of therapeutic relevance for the treatment of destructive periodontitis. Here, antisense oligonucleotides (AS-ON) directed against ICAM-1 suppress protein expression and mRNA levels specifically and effectively in primary human endothelial cells of different tissue origin. Moreover, downregulation of ICAM-1 expression is also observed in AS-ON-transfected inflamed gingival mucosal tissue of patients with periodontal diseases. This work strongly suggests exploiting the local topical application of ICAM-1-directed AS-ON as a therapeutic tool against inflammatory processes of the human gingiva.
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PMID:Antisense-mediated inhibition of ICAM-1 expression: a therapeutic strategy against inflammation of human periodontal tissue. 1207 67

Bovine leukocyte adhesion deficiency (BLAD) in Holstein cattle is an autosomal recessive congenital disease characterized by recurrent bacterial infections, delayed wound healing and stunted growth, and is also associated with persistent marked neutrophilia. The molecular basis of BLAD is a single point mutation (adenine to guanine) at position 383 of the CD18 gene, which caused an aspartic acid to glycine substitution at amino acid 128 (D128G) in the adhesion molecule CD18. Neutrophils from BLAD cattle have impaired expression of the beta2 integrin (CD11a,b,c/CD18) of the leukocyte adhesion molecule. Abnormalities in a wide spectrum of adherence dependent functions of leukocytes have been fully characterized. Cattle affected with BLAD have severe ulcers on oral mucous membranes, severe periodontitis, loss of teeth, chronic pneumonia and recurrent or chronic diarrhea. Affected cattle die at an early age due to the infectious complications. Holstein bulls, including carrier sires that had a mutant BLAD gene in heterozygote were controlled from dairy cattle for a decade. The control of BLAD in Holstein cattle by publishing the genotypes and avoiding the mating between BLAD carriers was found to be successful. This paper provides an overview of the genetic disease BLAD with reference to the disease in Holstein cattle.
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PMID:Bovine leukocyte adhesion deficiency (BLAD): a review. 1564 95

Periodontitis is a response of highly vascularized tissues to the adjacent microflora of dental plaque. Progressive disease has been related to consortia of anaerobic bacteria, with the gram-negative organism Porphyromonas gingivalis particularly implicated. The gingipains, comprising a group of cysteine proteinases and associated hemagglutinin domains, are major virulence determinants of this organism. As vascular expression of leukocyte adhesion molecules is a critical determinant of tissue response to microbial challenge, the objective of this study was to determine the capacity of gingipains to modulate the expression and function of these receptors. Given the potential multifunctional role of platelet endothelial cell adhesion molecule 1 (PECAM-1) in the vasculature, the effect of gingipains on PECAM-1 expression by endothelial cells was examined. Activated gingipains preferentially down-regulated PECAM-1 expression on endothelial cells compared with vascular cell adhesion molecule 1 and endothelial-leukocyte adhesion molecule 1, but the reduction in PECAM-1 expression was completely inhibited in the presence of the cysteine proteinase inhibitor TLCK (Nalpha-p-tosyl-l-lysine chloromethyl ketone). Endothelial monolayers treated with activated gingipains demonstrated progressive intercellular gap formation that correlated with reduced intercellular junctional PECAM-1 expression as determined by Western blotting and immunofluorescence microscopy. This was accompanied by enhanced transfer of both albumin and neutrophils across the monolayer. The results suggest that degradation of PECAM-1 by gingipains contributes to increased vascular permeability and neutrophil flux at disease sites.
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PMID:Functional implication of the hydrolysis of platelet endothelial cell adhesion molecule 1 (CD31) by gingipains of Porphyromonas gingivalis for the pathology of periodontal disease. 1573 Oct 36


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