Levels of tumor necrosis factor-alpha and interleukin-1beta in saliva of metabolic syndrome patients / 中华口腔医学杂志
Chinese Journal of Stomatology
;
(12): 269-273, 2010.
Artigo
em Chinês
| WPRIM
| ID: wpr-245209
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the association between periodontitis and the low-grade inflammation in metabolic syndrome (MS) patients.</p><p><b>METHODS</b>Fifty-seven MS patients, 26 healthy controls were enrolled. Non-stimulated whole saliva was collected. The levels of tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta was analyzed by radioimmunoassay and enzyme-linked immunosorbent assay, respectively. Concentration of cytokines was compared between MS patients and the healthy controls. Correlations between the cytokines and various periodontal indices, and between the cytokines level and different quantity of metabolic syndrome components were also investigated.</p><p><b>RESULTS</b>Levels of TNF-alpha in saliva of MS patients [(69.30+/-21.01) ng/L] were significantly higher than that in the healthy subjects [(57.85+/-15.69) ng/L, P<0.05], and of IL-1beta in MS patients [(616.42+/-360.05) ng/L] higher than that in healthy subjects [(506.06+/-245.76) ng/L], but the difference was not statistically significant. TNF-alpha was positively correlated with bleeding index (BI). In MS patients, TNF-alpha level and IL-1beta level increased with increasing severity of periodontal disease and increasing component numbers of MS.</p><p><b>CONCLUSIONS</b>Periodontal inflammation may be one of the sources of low-grade inflammation in MS patients. Both systemic and periodontal conditions may influence the level of salivary TNF-alpha and IL-1beta.</p>
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Periodontite
/
Saliva
/
Índice Periodontal
/
Fator de Necrose Tumoral alfa
/
Síndrome Metabólica
/
Interleucina-1beta
/
Metabolismo
Limite:
Adulto
/
Idoso
/
Feminino
/
Humanos
/
Masculino
Idioma:
Chinês
Revista:
Chinese Journal of Stomatology
Ano de publicação:
2010
Tipo de documento:
Artigo
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