title: Reduced expression of lipopolysaccharide-induced CXC chemokine in Porphyromonas gingivalis-induced experimental periodontitis in matrix metalloproteinase-8 null mice.
abstract: 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.
  
  
  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).
  
  
  CONCLUSIONS
  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.
authors: Laboratory of Periodontal Biology, Faculty of Dentistry, University of Chile, Santiago, Chile. mhernandezrios@gmail.com
authors: M
authors: M
authors: Hernández
authors: J
authors: J
authors: Gamonal
authors: T
authors: T
authors: Salo
authors: T
authors: T
authors: Tervahartiala
authors: M
authors: M
authors: Hukkanen
authors: L
authors: L
authors: Tjäderhane
authors: T
authors: T
authors: Sorsa
mesh_terms: D016301:Alveolar Bone Loss / Q000378:metabolism* / Q000382:microbiology; D000818:Animals; D054377:Chemokine CXCL12 / Q000096:biosynthesis / Q000235:genetics; D054365:Chemokine CXCL5 / Q000096:biosynthesis* / Q000235:genetics; D055113:Chronic Periodontitis / Q000378:metabolism* / Q000382:microbiology; D005786:Gene Expression Regulation; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D020784:Matrix Metalloproteinase 8 / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D016966:Porphyromonas gingivalis; D053245:RANK Ligand / Q000096:biosynthesis / Q000235:genetics
chemical_list: D054377:Chemokine CXCL12; D054365:Chemokine CXCL5; D008070:Lipopolysaccharides; D053245:RANK Ligand; D020784:Matrix Metalloproteinase 8