UMLS:C0031099 - FACTA Search

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

Porphyromonas gingivalis is a suspected pathogen in rapidly progressive periodontitis (RPP). We have determined the anti-P. gingivalis serum immunoglobulin G (IgG) isotype response and avidity and the subclass titer distributions for 30 RPP patients and 30 age-, sex-, and race-matched healthy subjects by using enzyme-linked immunosorbent assay technology. Patients and control subjects were classified as seropositive if their total IgG response to P. gingivalis was twofold or more than the median response in healthy subjects. The predominant antibody responses for both patients and healthy subjects were IgG2 and IgG3, with a subclass order of IgG2 greater than IgG3 greater than IgG1 greater than IgG4. The avidity of the IgG response was highest for the seropositive healthy subjects and was no different between seronegative and seropositive RPP patients. The subclass antibody responses did not depend on gender, and there were no correlations between titer, avidity, or subclass with disease severity in the RPP patients as measured by pocket depth or bone loss on dental X rays. The seronegative RPP patients exhibited antibody responses that were greater than the responses of seronegative healthy subjects for all four subclasses, while the seropositive RPP patients had higher IgG1 and IgG4 levels than seropositive healthy subjects. These findings are consistent with the hypothesis that both carbohydrate and protein antigens are important in the IgG response to P. gingivalis. The relative predominance of IgG2, a subclass which lacks strong complement fixation and opsonic properties, and the low avidity of patient anti-P. gingivalis IgG antibodies suggest that humoral responsiveness to infection with P. gingivalis may be ineffective in clearing this organism.
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PMID:Serum immunoglobulin G antibody to Porphyromonas gingivalis in rapidly progressive periodontitis: titer, avidity, and subclass distribution. 131 74

Serum levels of IgM, IgG and IgG-antibody subclasses directed against cell envelopes, lipopolysaccharides and cytoplasmic fractions from Capnocytophaga sputigena, C. gingivalis and C. ochracea were examined in age-, race- and sex-matched periodontally healthy (n = 25) subjects and subjects with adult periodontitis (n = 25). The envelopes and cytoplasmic fractions were obtained by ballistic disintegration of the cells and ultracentrifugation. Cell envelopes were treated with DNase, RNase and lysozyme. Lipopolysaccharides were obtained by hot phenol-water extraction and treated with DNase and RNase. The relative levels of the antibodies in response to the cell fractions were measured by the streptavidinbiotin micro enzyme-linked immunosorbent assay. Both groups showed IgM and IgG antibodies to each fraction of the three Capnocytophaga species, but the frequency of positive IgG subclass responses varied. The IgG4 responses were lower than the other subclasses. There were no significant differences between the IgM antibody levels of the two groups. However, the adult periodontitis group had significantly lower IgG antibody titres to the cell envelopes and cytoplasmic fractions of C. gingivalis and C. ochracea, and lipopolysaccharide of C. gingivalis. These results were reflected in the depressed levels of IgG1 and/or IgG2 to these cellular fractions from the same bacterial species. The adult periodontitis group also showed a lower level of IgG1 to the cytoplasmic fractions of C. sputigena without any depression in the total IgG antibody level. There were no significant differences between the groups in IgG3 and IgG4 antibody levels to any of the cellular fractions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serum antibody responses in human periodontitis to cellular components of Capnocytophaga. 141 21

Patients with adult periodontitis (AP) exhibit elevated serum antibody levels to Porphyromonas (Bacteroides) gingivalis; however, it is not known whether these antibodies originate from plasma cells in the local disease site or from peripheral lymphoid tissues. We studied the isotype and subclass levels and origin of antibodies to P. gingivalis fimbriae, since elevated serum anti-fimbriae responses were seen when compared with sera of healthy controls. IgG anti-fibriae titres were dominant and the subclass response was IgG3 much greater than IgG1 greater than IgG2 much greater than IgG4; however, some IgA anti-fimbriae antibodies were also seen. The IgA subclass fimbriae-specific response was mainly IgA1; however, significant IgA2 anti-fimbrae antibodies were seen. We also assessed numbers of anti-fimbriae antibody producing cells from peripheral blood mononuclear cells (PMBC) and from either healthy or inflamed gingiva of AP subjects. Gingival mononuclear cells (GMC) of AP patients exhibited high numbers of immunoglobulin-producing (spot-forming) cells (SFC) including fimbriae-specific antibody secreting cells in a pattern of IgG greater than IgA greater than greater than greater than IgM. However, low numbers of SFC were seen in GMC from healthy gingiva; further, no anti-fimbriae SFC responses were noted in healthy GMC. Although no fimbriae-specific immunoglobulin-producing cells were seen in PBMC, low numbers of antigen-specific SFC were found in pokeweed mitogen-triggered PBMC from AP subjects. Treatment of AP patients for plaque and surgical removal of inflamed gingiva resulted in significant reductions in serum anti-fimbriae responses. These studies show that AP patients exhibit brisk serum IgG and IgA subclass anti-fimbriae antibodies, whose origin appear to be the plasma cells present in the localized inflamed tissues.
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PMID:Porphyromonas gingivalis-specific serum IgG and IgA antibodies originate from immunoglobulin-secreting cells in inflamed gingiva. 167 64

Deficiency in the number and function of phagocytes is associated with gingival inflammation and periodontitis. A hereditary deficiency in membrane glycoproteins involved in granulocyte adherence causes impaired chemotaxis, reduced phagocytosis and periodontal problems. Virus infections of antigen-presenting cells interfere with immune responses and lead to seriously increased susceptibility to infections with bacteria which cause no problems in normal patients. Increased levels of IgG antibodies may limit penetration of antigens in the tissues, but at the cost of local inflammation and tissue injury. Mucosal inflammatory disease with increased local formation of IgG is more frequent in IgA deficient patients. The immunological homeostasis depends on a balance between the respective classes and subclasses of antibodies. Deficiencies in the IgA system may contribute to a disturbed balance of the humoral immune response to critical antigens from oral bacteria. A disproportional increase in IgG1 and IgG3 antibodies may persistently activate complement, stimulate the inflammatory activity and cause tissue injury.
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PMID:Periodontal disease mechanisms in immunocompromised patients. 189 Feb 24

The level of serum IgM, IgG and IgA antibodies including IgG1, IgG2, IgG3, IgG4, IgA1 and IgA2 subclass-specific antibodies to Bacteroides (Porphyromonas) gingivalis fimbriae and to lipopolysaccharide (LPS) were analysed in patients with different forms of periodontal disease (PD) and control subjects by ELISA. Among PD subjects, sera obtained from adult periodontitis (AP), rapidly progressive periodontitis (RPP) and gingivitis contained high titres of fimbriae-specific IgG antibodies (7500-15,000 ELISA units) followed by IgA (90-700 units) and IgM (30-90 units). In contrast, sera from localized juvenile periodontitis (LJP) subjects exhibited much lower titres of fimbriae-specific IgG (89 +/- 11 units), IgA (31 +/- 5 units) and IgM (17 +/- 3 units) antibodies. A similar response pattern was also seen in sera from normal subjects aged 35-41 years who practice normal oral hygiene, while sera of younger adults (aged 18-24) with superior hygiene did not have any antigen-specific antibodies. Analysis of IgG subclass anti-fimbriae responses revealed that the major response was IgG3 followed by IgG1, IgG2 and IgG4 in AP, RPP and gingivitis. Although lower, a similar pattern of IgG subclass titre was seen in LJP and normal subjects aged 35-41 years. When IgA subclass responses were measured in AP and RPP, higher titres of the fimbriae-specific response were noted with IgA1 when compared with IgA2. However, lower but approximately equal levels of fimbriae-specific IgA1 and IgA2 titres were seen in other PD groups. When anti-B. gingivalis LPS-specific responses were measured, the sera of AP patients contained high levels of IgG antibodies (2265 +/- 224 units) followed by IgA (411 +/- 90 units) and IgM (214 +/- 56 units). Further, IgG anti-LPS responses were mainly IgG2 followed by IgG4, IgG3 and IgG1. For IgA subclass responses, higher titres of anti-LPS-specific antibodies were noted in IgA2 subclass over IgA1. These results showed that higher anti-B. gingivalis antibody responses occur in PD when compared with healthy individuals and protein and lipid-carbohydrate antigens of B. gingivalis induce distinct patterns of antigen-specific IgG and IgA subclass responses.
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PMID:Bacteroides gingivalis-specific serum IgG and IgA subclass antibodies in periodontal diseases. 197 4

It is well established that increased numbers of plasma cells occur in the localized tissues of chronic inflammatory diseases such as adult periodontitis, and enzymatic isolation has shown that most B lineage cells produce IgG-subclass with some IgA-subclass responses. It would be of importance to determine if excess production of cytokines in the localized lesion account for these responses and in the present study we have assessed gingival mononuclear cell (GMC) supernatants for cytokines that activate B cells including IL-6R expression and for levels of IL-6 present. Inasmuch as limited numbers (approximately 1 to 3 x 10(6) cells) of GMC were obtained from surgically removed tissues (approximately 400 mg), we have focused on the analysis of IL-6 production by GMC in this study. Further, initial evidence of additional cytokines that are produced by GMC and induce expression of IL-6R on resting B cells has been obtained. The GMC and PBMC from individual patients were cultured in the presence (or absence) of Con A. Higher levels of IL-6 were produced spontaneously by GMC when compared with Con A-stimulated PBMC. When PBMC cultures were supplemented with GMC supernatants obtained from the same patient, high numbers of spot-forming cells (SFC), mainly of IgG followed by IgA isotype, were seen. The induction of SFC by GMC supernatants was inhibited by incubation with a goat anti-human IL-6 antibody. When the effect of GMC supernatants on subclasses of PBMC SFC was determined, the response was IgG1 greater than IgG2 greater than IgG3 = IgG4 and IgA1 greater than IgA2, a pattern remarkably similar to the distribution of plasma cells in the GMC itself. To assess for cytokines in GMC supernatants that mediated B cell activation, supernatants containing anti-IL-6 were cultured with PBMC or purified B cells for 72 h. This treatment induced small proliferative B cell responses and elevated expression of IL-6R on B cells, but did not induce SFC responses. Further, incubation of B cells with GMC supernatants induced resting B cells (G0/G1) to enter the cell cycle (S and G2/M). Addition of human rIL-6 to these cultures on day 3 restored IgG- and IgA-subclass SFC responses by day 7. Cytokine-induced IL-6R expression also occurred in vivo because freshly isolated GMC expressed high levels of this receptor.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cytokine regulation of localized inflammation. Induction of activated B cells and IL-6-mediated polyclonal IgG and IgA synthesis in inflamed human gingiva. 200 80

This study was designed to (i) delineate the characteristics of serum antibody responses to Actinobacillus actinomycetemcomitans in patients with periodontitis who are infected with A. actinomycetemcomitans; irrespective of disease classification; (ii) assess the relationship of the elevated antibody levels to colonization of the oral cavity by A. actinomycetemcomitans; and (iii) describe the serotype distribution of A. actinomycetemcomitans and antibodies to the microorganism in infected patients with various clinical classifications. To compare the levels of various isotype-specific antibodies to the different antigens, studies were performed that allowed quantitation of each isotype-specific antibody in a human reference standard. By using this reference standard, it was shown that the levels of immunoglobulin G (IgG), IgM, and IgA responses to A. actinomycetemcomitans were similar among the infected patients, irrespective of disease classification. Also, we demonstrated that the serum antibody response to serotype b was quantitatively greater in all isotypes. Our findings indicate that b was the most frequent A. actinomycetemcomitans serotype detected in the patients and appears to be capable of initiating a substantial serum IgG antibody response that may contain cross-reactive antibodies to other serotypes of A. actinomycetemcomitans. Generally, in cases in which the response to a single serotype was elevated, only that type of A. actinomycetemcomitans was detected in the plaque. Individuals exhibiting elevated antibodies to multiple serotypes were most consistently colonized by the serotype b microorganism. This study represents the first report detailing the distribution of IgG subclass antibodies to A. actinomycetemcomitans in periodontal disease. The results demonstrated that the primary responses of patients with periodontitis to A. actinomycetemcomitans were of the IgG1 and IgG3 subclasses, which is consistent with elicited responses to protein antigens. In contrast, the primary subclass response in normal subjects was limited to the IgG2 subclass and may represent broader cross-reactivity to polysaccharide antigens-lipopolysaccharide from the bacteria.
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PMID:Serum antibody in Actinobacillus actinomycetemcomitans-infected patients with periodontal disease. 201 43

The emergence of cells that produce IgG and IgA subclass antibodies to Bacteroides gingivalis (Porphyromonas gingivalis) fimbriae and lipopolysaccharide (LPS) antigens was examined in mononuclear cells isolated from inflamed gingiva of different stages (slight, moderate or advanced) of adult periodontitis (AP). Antigen-specific IgM, IgG (including IgG1, IgG2, IgG3 and IgG4) and IgA (including IgA1 and IgA2) producing cells were enumerated by the ELISPOT assay and were compared with total Ig-producing cells of each isotype or subclass. In advanced AP, the B. gingivalis fimbriae-specific IgG- and IgA-secreting cells represented 5% of total IgG- or IgA-secreting cells, while those from the moderate stage comprised approximately 1% of these two isotypes. Cells producing antibody specific for B. gingivalis LPS were observed at frequencies of 0.1% and 0.4% for IgG and IgA cells, respectively in the advanced stage. When IgG subclasses were analysed in moderate AP, the anti-fimbriae subclass responses were largely IgG1 (60%), followed by IgG2 (20%), IgG3 (10%) and IgG4 (10%). Fimbriae-specific IgG subclass responses were elevated in the advanced stage of AP, and IgG4 (40%) and IgG1 (30%) were dominant, followed by IgG3 (20%) and IgG2 (10%). IgA1 cells predominated in both the moderate and advanced stages, however a relative increase in IgA2 cells occurred in advanced AP. Mononuclear cells isolated from gingiva of AP patients did not contain cells producing antibody to antigens such as Escherichia coli K235 LPS, cholera toxin or the hapten dinitrophenyl coupled to bovine serum albumin. These results show that local IgG and IgA subclass responses occur to a protein antigen of a major periodontal disease (PD)-associated pathogen, B. gingivalis, and the increase in IgG4 and IgA2 responses may be associated with host protection.
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PMID:Bacteroides-specific IgG and IgA subclass antibody-secreting cells isolated from chronically inflamed gingival tissues. 256 45

Serum IgG1, IgG2, IgG3 and IgG4 antibody levels directed against lipopolysaccharide (LPS) from Bacteroides gingivalis were measured in the sera from systemically healthy subjects with and without periodontitis. An enzyme-linked immunosorbent assay was used that included coating of microtiter plates with LPS, and subsequent incubation with patient sera followed by mouse monoclonal subclass-specific antibodies, biotinylated sheep anti-mouse IgG and alkaline phosphatase conjugated to streptavidin. Anti-LPS IgG antibodies were dominated by IgG2, and moderate amounts only of IgG1, IgG3 and IgG4 were found. The periodontitis patients had significantly higher anti-LPS IgG1, IgG2 and IgG3 levels when compared to the subjects with healthy periodontium (p less than 0.05, Mann-Whitney test).
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PMID:IgG subclass distribution of serum antibodies against lipopolysaccharide from Bacteroides gingivalis in periodontal health and disease. 360 86

Porphyromonas gingivalis is an important oral pathogen with a strong association with adult periodontitis. Significant titers of specific IgG antibodies to P. gingivalis can be found in the sera of both gingivitis and periodontitis patients. Since IgG subclasses have different biological characteristics, the present study dealt with the serum IgG subclass response to outer membrane antigens of P. gingivalis. Western blot analysis of P. gingivalis outer membrane was carried out using 20 adult periodontitis and 20 age- and sex-matched gingivitis patients. Antibodies in sera of both adult periodontitis and gingivitis patients recognized 38 antigen bands, ranging in molecular mass from 11.1 to 161 kDa. IgG2 was the predominant antibody subclass response in both patient groups in terms of the numbers of outer membrane antigens recognized, followed by IgG3, IgG1, and IgG4. More antigens in all IgG subclasses except IgG4 were recognized in adult periodontitis cases. Of the 23 antigens identified by IgG2 antibodies, 9 were recognized predominantly in adult periodontitis and 3 in the gingivitis group. In the IgG1 subclass, 4 antigens were recognized predominantly in the adult periodontitis group while only 1 antigen was recognized significantly more in the gingivitis group. The IgG3 response identified 14 antigens ranging in molecular mass from 11.1 to 61.2 kDa in both groups. Ten antigens were recognized significantly by the adult periodontitis group. The lowest response was seen by IgG4 antibodies, with only 3 antigens of molecular mass 61.2, 52.3, and 38.8 kDa recognized, the latter two significantly in the adult periodontitis group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:IgG antibody subclass response to Porphyromonas gingivalis outer membrane antigens in gingivitis and adult periodontitis. 762 55

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