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)

Patients with periodontitis juvenilis and patients with periodontitis were tissue typed. In the juvenile group, frequencies of tissue type specificities HLA-A9, HLA-A28, and HLA-BW15 were significantly increased as compared to the findings in the general population. In the periodontitis groups, no significant tissue type deviations were found.
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PMID:Association between HLA-antigens and periodontal disease. 27 92

Juvenile and rapidly progressive periodontitis are grouped under the heading of early-onset periodontitis. In recent years, much attention has been devoted to studying immunologic factors in early-onset periodontitis. This study was designed to investigate peripheral blood lymphocyte subpopulations, natural killer cells and interleukin-2 receptor positive (IL-2R +) cells in patients with juvenile and rapidly progressive periodontitis. 38 patients with juvenile and 30 patients with rapidly progressive periodontitis, plus 30 normal healthy control subjects were included in the study. Peripheral blood T-lymphocytes, helper T-cells, suppressor T-cells, HLA-DR+ cells, and IL-2R + cells were determined using appropriate monoclonal antibodies and the indirect immunofluorescence method. B-lymphocytes were identified using the direct immunofluorescence technique. Both groups of patients had normal number of total CD3+ T-cells, CD4+ helper T-cells, CD8+ suppressor T-cells, HLA-DR+ cells and IL-2R+ cells. Natural killer cells were found to be significantly elevated in both groups. These findings could contribute to the immunopathogenesis of early-onset periodontitis.
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PMID:Juvenile and rapidly progressive periodontitis. Peripheral blood lymphocyte subpopulations. 169 84

Microbiological, immunological, host-defensive, and genetic analyses were performed on a mother and daughter, both of whom had early-onset periodontitis (rapidly progressive periodontitis in the mother; localized juvenile periodontitis in the daughter). Microscopic examination revealed a greatly elevated percentage of rod-form bacteria in both subjects. Fusobacterium sp. and Porphyromonas gingivalis (formerly Bacteroides gingivalis) were the predominant microorganisms cultured. The humoral immune responses to F. nucleatum, P. gingivalis, and Actinobacillus actinomycetemcomitans were much higher in both subjects than those to any other periodontal bacteria examined. Functional and phenotypic analysis of the peripheral lymphocytes showed no significant abnormalities. However, investigation of neutrophil function showed that the mother had depressed neutrophil chemotaxis and superoxide production. The daughter had depression not only of chemotaxis and superoxide production, but also of neutrophil phagocytosis. Serological typing of HLA antigens revealed the same Class II HLA profile in both subjects. It was concluded that both subjects very probably had an identical condition and that these patients provided a unique model for improving our understanding of the host factors involved in periodontal disease.
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PMID:A family study of a mother and daughter with increased susceptibility to early-onset periodontitis: microbiological, immunological, host defensive, and genetic analyses. 212 13

HLA system plays an important role in the regulation of the immune response. Association between HLA genes and disease has been shown for several disorders, in particular auto-immune diseases. HLA system may also be associated with periodontal diseases. It has been suggested that HLA-A2 is related to resistance in juvenile periodontitis and A9 to susceptibility in juvenile periodontitis (JP) and rapidly progressive periodontitis (RPP). DR2, DR4 and DQw1 may also be susceptibility factors in JP and RPP. If implicated in periodontal diseases, HLA system may be associated with low or non-responsiveness to plaque bacterial antigens which could result in disease progression.
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PMID:Association between HLA system and periodontal diseases. 221 37

Generalized pustular psoriasis in siblings, 31-year-old male and 26-year-old female, is presented. In both cases, pustular lesions appeared in childhood and typical eruption of psoriasis vulgaris was not observed during their clinical course. Cholecystitis and chronic tonsillitis of the brother and periodontitis and chronic tonsillitis of the sister were considered to be possible provocative factors. HLA-A24, Bw52-, DR2, as the common HLA haplotype in our cases, was estimated.
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PMID:[Generalized pustular psoriasis in siblings]. 226 97

The Major Histocompatibility Complex is a relatively poorly explored research area among the various immunological aspects of periodontal diseases. After a recall of general concepts, the authors first describe the general HLA-pathology association and then, the reported HLA-periodontal disease associations. HLA theoretical potential interests are multiple. Typing results show, on one hand, no clear correlation with juvenile periodontitis (diminution of A 2, augmentation of A 9, A 28, Bw 15 and Bw 35) but on the other hand, a more constant correlation between HLA A 9 and rapidly progressive periodontitis. Besides, three resistance factors have been reported: A 10, B 5 and A 28.
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PMID:HLA: a review of actual knowledge and perspectives in periodontology. 263 75

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 cellular infiltrate present in human diseased gingiva was analyzed in biopsies from 12 patients with gingivitis or periodontitis. The samples studied had been obtained in the course of surgery at inflammatory sites remaining after institution of periodontal treatment. Histological and immunological techniques were used to identify macrophages, B-cells, plasma-cells, T-cells and T cell subsets, as well as cells expressing class II HLA membrane antigens. T-cells appeared as the predominant population, but plasma-cells were also visualized in nearly all samples. Both OKT4+ and OKT8+ cells were seen in all cases, the latter being more numerous in periodontitis patients. Interdigitating-like cells were observed, positively labelled for class II antigens, as well as macrophages which were more numerous in periodontitis patients. These results suggest the participation of all components of the immune response in gingival disease, in a way resembling chronic recurrent inflammatory diseases.
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PMID:Immunohistological identification of cell subsets in human gingiva after local treatment for gingivitis or periodontitis. 348 94

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


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