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Oral Dis ; 23(8): 1144-1154, 2017 Nov.
Article in English | MEDLINE | ID: mdl-28686335

ABSTRACT

OBJECTIVE: Evidence of increased apoptosis is observed in periodontitis and may be associated with destruction of the periodontal tissue caused by the increased cell death, with the release of danger signals and subsequent stimulation of the proinflammatory processes. However, the exact mechanisms associated with these processes remain unclear. This study aimed to investigate the presence of the periodontal pathogen Treponema denticola, apoptosis, high mobility group box 1 as a damage-associated molecular pattern, and several inflammatory markers in periodontitis and gingivitis subjects. MATERIALS AND METHODS: Soft tissue specimens from gingival tissues of periodontitis and gingivitis patients were used for immunohistochemical and immunofluorescence staining of T. denticola chymotrypsin-like proteinase (CTLP), apoptosis markers, high mobility group box 1, Toll-like receptor 4, inflammatory cell markers, and proinflammatory cytokines. RESULTS: Treponema denticola was detected in all periodontitis-affected tissues. This was associated with a significant increase in the number of apoptotic cells, including macrophages, alterations in the expression of high mobility group box 1 and its receptor, and increased levels of proinflammatory cytokines compared with gingivitis. CONCLUSIONS: In summary, the presence of T. denticola (especially its CTLP), apoptosis, high mobility group box 1, and inflammatory markers suggests their potential involvement in the pathogenesis of periodontitis.


Subject(s)
Gingivitis/metabolism , HMGB1 Protein/metabolism , Periodontitis/metabolism , Treponema denticola/isolation & purification , Adult , Aged , Antigens, CD/metabolism , Antigens, Differentiation, Myelomonocytic/metabolism , Apoptosis , Caspase 3/metabolism , Female , Gingivitis/microbiology , Gingivitis/physiopathology , Humans , Immunohistochemistry , Interleukin-1beta/metabolism , Interleukin-8/metabolism , Male , Middle Aged , Peptide Hydrolases/metabolism , Periodontitis/microbiology , Periodontitis/physiopathology , Toll-Like Receptor 4/metabolism , Treponema denticola/metabolism
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