| Author | dc.contributor.author | Hernández Ríos, Emma | |
| Author | dc.contributor.author | Gamonal Aravena, Jorge Antonio | es_CL |
| Author | dc.contributor.author | Salo, T. | es_CL |
| Author | dc.contributor.author | Tervahartiala, Taina | es_CL |
| Author | dc.contributor.author | Hukkanen, M. | es_CL |
| Author | dc.contributor.author | Tjäderhane, L. | es_CL |
| Author | dc.contributor.author | Sorsa, Timo | es_CL |
| Admission date | dc.date.accessioned | 2011-09-06T18:12:16Z | |
| Available date | dc.date.available | 2011-09-06T18:12:16Z | |
| Publication date | dc.date.issued | 2011-02 | |
| Cita de ítem | dc.identifier.citation | J Periodont Res 2011; 46: 58–66 | es_CL |
| Identifier | dc.identifier.issn | 0022-3484 | |
| Identifier | dc.identifier.other | DOI: 10.1111/j.1600-0765.2010.01310.x | |
| Identifier | dc.identifier.uri | https://repositorio.uchile.cl/handle/2250/123406 | |
| Abstract | dc.description.abstract | Background and Objective: Matrix metalloproteinase-8 (MMP-8) is a central mediator in chronic periodontitis. Recently developed MMP-8-deficient mice show an impaired polymorphonuclear neutrophil response and more severe alveolar bone loss in Porphyromonas gingivalis-induced experimental periodontitis. The main mediators involved in neutrophil and monocyte/macrophage recruitment and in bone loss include lipopolysaccharide-induced CXC chemokine (LIX/CXCL5), stromal-derived factor-1/CXC chemokine ligand 12 (SDF1/CXCL12) and RANKL. Therefore, the aim of this study was to characterize the expression of LIX/CXCL5, SDF1/CXCL12 and RANKL in Porphyromonas gingivalis-induced experimental periodontitis in MMP-8−/− (knockout) and wild-type mice.
Material and methods: MMP-8 null and WT P. gingivalis-infected and uninfected mice were included. Histopathological changes were assessed and LIX/CXCL5, SDF1/CXCL12 and RANKL were immunodetected and quantified.
Results: Typical histopathological features of chronic periodontitis were seen in P. gingivalis-infected groups. LIX/CXCL5 expression was restricted to the gingival papilla in all four groups. Significantly lower expression of LIX/CXCL5 was seen in the knockout group compared with the wild-type infected group (p < 0.05). SDF1/CXCL12 and RANKL expression was mainly localized to the alveolar crest, including inflammatory leukocytes, vascular endothelium, osteoblasts and osteoclasts. Significant increases of SDF1/CXCL12 and RANKL were seen in both knockout and wild-type P. gingivalis-infected groups compared with uninfected groups (p < 0.05).
Conclusion: RANKL and SDF1/CXCL12 are up-regulated in P. gingivalis-induced periodontitis and they appear to be associated with the pathogenesis of the disease. MMP-8 is associated with a reduced expression of LIX/CXCL5 in the P. gingivalis-induced experimental periodontitis model. | es_CL |
| Patrocinador | dc.description.sponsorship | This work was supported by grants
from the Academy of Finland, the
Research Foundation of the Helsinki
University Central Hospital, and the
Scientific and Technologic Investigation
Resource FONDECYT 1090461,
Santiago, Chile. The authors are
thankful to Professor Carlos Lo´ pez-
Otı´n for providing MMP-8 KO mice | es_CL |
| Lenguage | dc.language.iso | en | es_CL |
| Publisher | dc.publisher | John Wiley & Sons A/S | es_CL |
| Keywords | dc.subject | cytokines | es_CL |
| Título | dc.title | Reduced expression of lipopolysaccharide-induced CXC chemokine in Porphyromonas gingivalis-induced experimental periodontitis in matrix metalloproteinase-8 null mice | es_CL |
| Document type | dc.type | Artículo de revista | |
