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)

HLA-A, B and DR antigen frequencies were determined in three groups of periodontally diagnosed subjects: 49 patients with rapidly progressive periodontitis, 40 elderly subjects with minimal disease (considered as a resistant group) and 30 young subjects with minimal disease. The relative risk for HLA-A9 (previously reported to be associated with periodontal disease) was 15.5. HLA-A9 was present in 36.7% of the patients and 2.5% of the resistant group. HLA-A10 showed a significantly increased incidence in the resistant group (30.0%) compared to a non-periodontally diagnosed control population (9.0%), and was absent from the patient group. These findings provide additional evidence for the involvement of HLA-A9 in susceptibility to periodontitis, and suggest that A10 may play a role in resistance to the disease.
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PMID:Association between HLA antigens and periodontal disease. 316 57

The relationship between human leukocyte antigens (HLA) determinants and periodontitis has been examined by several authors without showing any particular pattern. However, no study has investigated the HLA-D determinants, which are generally associated with immune disorders, and rapidly progressive periodontitis (RPP). The HLA profile of 10 RPP patients was compared with that of a healthy control population (n = 120). Although no significant difference was found for HLA-A, HLA-B, and HLA-C, HLA-DR4 of the HLA-D group was found in 80% of patients but only in 38.3% of controls. A high frequency of HLA-DR4 has been reported in rheumatoid arthritis (RA) patients. This finding may be significant in light of previous reports highlighting similarities between RA and periodontal disease.
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PMID:Human leukocyte antigen (HLA) DR4. Positive association with rapidly progressing periodontitis. 349 13

HLA-A, B, C, DR antigen frequencies and Properdin factor B (Bf) allotypes were studied in a group of 44 patients with rapidly progressive periodontitis. HLA-A9 (A24) was the only antigen with a frequency statistically significantly different from the control population. An increased frequency of HLA-A9 was previously reported in periodontal diseases. Our results in a well characterised group of patients adds to the evidence that HLA-A9 plays a role in the susceptibility to severe periodontitis.
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PMID:Association between HLA-A9 and rapidly progressive periodontitis. 364 78

The beta 2-microglobulin (beta 2-m) pattern in gingival biopsy specimen from 24 patients with chronic severe periodontitis (P), from 11 patients with juvenile periodontitis (JP), and from 24 periodontally healthy subjects (CO) was studied with an indirect immunoperoxidase method. No reactivity for beta 2-m was found in 71% of specimens in the P and CO groups, whereas 82% of the JP specimens showed positive beta 2-m staining in the epithelium. The reactivity was detected mostly in the upper layers of the epithelium. In all the three groups the beta 2-m reactivity was less frequent in the subepithelial connective tissue than in the epithelium proper, and it seemed to be confined to the inflammatory cells. In the JP group, prominent reactivity for beta 2-m was also located in intercellular bridges of the squamous cells. The significance of the results is discussed in terms of the cell differentiation in these diseases, including the function of beta 2-m related to the function of the classical HLA antigens (HLA-A, HLA-B, HLA-C).
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PMID:Gingival beta 2-microglobulin in juvenile and chronic periodontitis. 390 9

Certain human lymphocyte antigen (HLA) haplotypes have been correlated with the presence of certain diseases. To date no significant relationship between periodontitis and HLA haplotype has been demonstrated. The purpose of this study was to determine the frequency of HLA-A, HLA-B and HLA-C haplotypes in patients resistant to chronic periodontitis and to determine if there is any association between specific HLA genes and periodontal health. Twenty-five healthy individuals who demonstrated a high resistance to periodontal disease (mean age 49.9 years) were matched to 25 subjects with chronic periodontitis and to a periodontally undiagnosed population of 22,000 individuals. Peripheral blood was taken and HLA specificity was determined by the microlymphocytotoxicity test. The results indicated a statistically significant increase in the occurrence of HLA-B5 (P = 0.0059) and a trend in the occurrence of HLA-A28 (P = 0.0565) in those patients resistant to periodontal disease when compared to the matched controls. When compared to the large random control group, a significant correlation was observed for HLA-A28 (P less than 0.01) in blacks and HLA-B5 (P less than 0.01) in whites. It is possible that the HLA-A28 and the HLA-B5 individual may have the ability to resist the progression of chronic periodontitis.
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PMID:Human lymphocyte antigen haplotype and resistance to periodontitis. 658 91

HLA-A, B, C and DR antigen frequencies were determined in a group of patients with juvenile periodontitis and rapidly progressive periodontitis. In juvenile periodontitis patients, HLA-A24 and DR4 were found at a significantly higher level than in the control group, and in rapidly progressive periodontitis patients, A9 and DR4 were found at a significantly higher level than the control group. The presence of these antigens gives evidence as to the susceptibility of various forms of early onset periodontitis.
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PMID:Association between HLA antigens and early onset periodontitis. 881 76

Cysteine proteinases (gingipains) elaborated from Porphyromonas gingivalis exhibit enzymatic activities against a broad range of host proteins and are considered key virulence factors in the onset and development of adult periodontitis and host defense evasion. In this study, we examined the ability of arginine-specific gingipains (high molecular mass Arg-specific gingipain (HRGP) and Arg-specific gingipain 2) and lysine-specific gingipain (KGP) to cleave monocyte CD14, the main receptor for bacterial cell surface components such as LPS. Binding of anti-CD14 mAb MY4 to human monocytes was almost completely abolished by 0.3 microM HRGP and KGP treatments for 15 min, and 1 microM RGP2 for 30 min. In contrast, the expressions of Toll-like receptor 4, and CD18, CD54, CD59, and HLA-A, -B, -C on monocytes were slightly increased and decreased, respectively, by 0. 3 microM HRGP and KGP. This down-regulation resulted from direct proteolysis, because 1) gingipains eliminated MY4 binding even to fixed monocytes, and 2) CD14 fragments were detected in the extracellular medium by immunoblot analysis. Human rCD14 was degraded by all three gingipains, which confirmed that CD14 was a substrate for gingipains. TNF-alpha production by monocytes after HRGP and KGP treatments was decreased at 1 ng/ml, but not at 20 microg/ml LPS, indicating that gingipains inhibited a CD14-dependent cell activation. These results suggest that gingipains preferentially cleave monocyte CD14, resulting in attenuation of the cellular recognition of bacteria, and as a consequence sustain chronic inflammation.
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PMID:Proteolysis of human monocyte CD14 by cysteine proteinases (gingipains) from Porphyromonas gingivalis leading to lipopolysaccharide hyporesponsiveness. 1086 Oct 79