[The role of IL-1 beta and TNF-alpha in hyper-reactivity of neutrophils in rapidly progressive periodontitis patients].
OBJECTIVE
Neutrophils (PMNs) from rapidly progressive periodontitis (RPP) was found to generate abnormally high levels of oxygen radicals. Elastase activity in gingival crevicular fluid (GCF) from RPP was also found much higher. It suggested that PMNs in some RPP patients are hyper-reactive. The purpose of this study was to investigate the mechanism of PMN hyper-reactivity by surveying the correlation of TNF-alpha level with elastase activity in GCF and by evaluating the association between PMN infiltration and the expression of IL-1 beta and TNF-alpha in gingival tissues from RPP patients.


METHODS
41 GCF samples from 22 RPP patients and 34 GCF samples from 11 healthy controls were collected. The total amount of TNF-alpha in GCF was detected using ELISA. The elastase activity was measured with a low molecular weight substrate (S2484) specific for granulocyte. The correlation of TNF-alpha level with elastase activity in a GCF sample was analyzed with Spearman correlation. 20 gingival specimens were obtained respectively from 10 RPP patients and 5 periodontally healthy controls. The expression of IL-1 beta and TNF-alpha was detected with immunohistochemistry. The distribution of PMN was observed with hematoxylin and eosin staining.


RESULTS
Total amount of TNF-alpha in GCF was positively correlated with elastase activity (r = 0.44, P < 0.05). The IL-1 beta- and TNF-alpha-positive cells in gingiva were superimposed in areas where PMNs infiltration predominant.


CONCLUSIONS
The hyper-reactivity of PMN in RPP patients was related to locally produced IL-1 beta and TNF-alpha.
Liu
R
R
Department of Periodontology, School of Stomatology, Beijing Medical University, Beijing 100081, China.
Cao
C
C
Meng
H
H
D000328:Adult; D005260:Female; D006801:Humans; D007375:Interleukin-1 / Q000502:physiology*; D008297:Male; D009504:Neutrophils / Q000502:physiology*; D010518:Periodontitis / Q000145:classification / Q000378:metabolism / Q000473:pathology*; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology*
D007375:Interleukin-1; D014409:Tumor Necrosis Factor-alpha