Format

Send to

Choose Destination
Oral Dis. 2019 Nov 6. doi: 10.1111/odi.13227. [Epub ahead of print]

Gingival crevicular fluid levels of SLIT3 are increased in periodontal disease.

Author information

1
Department of Stomatology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
2
Henan Key Laboratory for Pharmacology of Liver Diseases, Institute of Medical and Pharmaceutical Sciences, Zhengzhou University, Zhengzhou, China.

Abstract

This study aims to investigate the levels of SLIT3 in gingival crevicular fluid (GCF) of healthy and periodontal disease subjects, and their correlations to periodontal disease. A total of 45 periodontal patients and 45 periodontally healthy volunteers were enrolled. The clinical parameters, radiographic bone loss and the levels of SLIT3, receptor activator of NF-κB ligand (RANKL) and osteoprotegerin (OPG) in GCF were measured. The prevalences of Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia in subgingival plaque were also analyzed. The expression of SLIT3 and RANKL was detected in the periodontium of experimental periodontitis in rats and lipopolysaccharide (LPS)-induced mouse macrophage. The total amounts and concentrations of SLIT3 and RANKL were significantly higher in periodontitis than those in healthy, while the level of OPG was significantly lower (p < .05). Significant positive correlations were observed between the level of GCF SLIT3 and clinical attachment level and radiographic bone loss (p < .05). There existed a significant positive correlation between SLIT3 and RANKL (p < .05). Increased expression of SLIT3 and RANKL was observed in the periodontium of periodontal rats. SLIT3 expression was induced by LPS stimulation in macrophages. These results suggest that SLIT3 may act as a diagnostic indicator of periodontal disease and should be further investigated.

KEYWORDS:

SLIT3; gingival crevicular fluid; periodontitis

PMID:
31696592
DOI:
10.1111/odi.13227

Supplemental Content

Full text links

Icon for Wiley
Loading ...
Support Center