title: Influence of parstatin on experimental periodontal disease and repair in rats.
abstract: BACKGROUND
  Parstatin is a 41-amino acid peptide, formed by proteolytic cleavage on activation of the protease activated receptor-1, with antiangiogenic properties. The purpose of this study is to evaluate the influence of synthetic parstatin on experimental periodontal disease and repair in rats.
  
  
  METHODS
  Ligature-induced periodontitis was established in rats and the influence of parstatin administration was assessed after 8 and 15 days for periodontal disease and 24 hours and 8 days after repair after ligature removal.
  
  
  RESULTS
  Parstatin administration significantly inhibited gingival myeloperoxidase activity, interleukin (IL)-1β, tumor necrosis factor-α, and IL-6 levels and led to suppression of macrophages and collagen degradation. At periodontal tissues under repair, parstatin increased the gingival levels of endostatin and decreased vascular endothelial growth factor expression and blood vessel number but did not influence histologic healing. In addition, the tomographic linear bone loss was significantly reduced at 15 days of periodontitis when the rats were treated with parstatin compared to their respective phosphate-buffered saline-treated controls.
  
  
  CONCLUSIONS
  Parstatin suppresses the periodontal tissue breakdown followed by experimental periodontitis in rats and did not impair periodontal tissue repair, despite its antiangiogenic effect. Parstatin may represent a novel approach to modulate host response in chronic periodontal disease.
authors.affiliation: Department of Physiology and Pathology, Dental School at Araraquara, State University of São Paulo, Araraquara, São Paulo, Brazil.
authors.forename: Luís Carlos
authors.initials: LC
authors.lastname: Spolidorio
authors.forename: Pablo Dallari Ramalho
authors.initials: PD
authors.lastname: Lucas
authors.forename: Joao Paulo
authors.initials: JP
authors.lastname: Steffens
authors.forename: Henrique Aparecido Bueno
authors.initials: HA
authors.lastname: da Silva
authors.forename: Vanessa Tubero Euzebio
authors.initials: VT
authors.lastname: Alves
authors.forename: Denise M Palomari
authors.initials: DM
authors.lastname: Spolidorio
authors.forename: Marinella
authors.initials: M
authors.lastname: Holzhausen
mesh_terms: D016301:Alveolar Bone Loss / Q000209:etiology / Q000503:physiopathology; D000539:Alveolar Process / Q000187:drug effects; D020533:Angiogenesis Inhibitors / Q000627:therapeutic use*; D000818:Animals; D001808:Blood Vessels / Q000187:drug effects; D003094:Collagen / Q000187:drug effects; D004195:Disease Models, Animal; D043169:Endostatins / Q000187:drug effects; D005881:Gingiva / Q000187:drug effects / Q000201:enzymology; D053583:Interleukin-1beta / Q000187:drug effects; D015850:Interleukin-6 / Q000032:analysis; D008264:Macrophages / Q000187:drug effects; D008297:Male; D010446:Peptide Fragments / Q000627:therapeutic use*; D010518:Periodontitis / Q000209:etiology* / Q000503:physiopathology; D009195:Peroxidase / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D044463:Receptor, PAR-1 / Q000627:therapeutic use*; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000187:drug effects; D042461:Vascular Endothelial Growth Factor A / Q000187:drug effects; D014945:Wound Healing / Q000187:drug effects; D055114:X-Ray Microtomography / Q000379:methods
chemical_list: D020533:Angiogenesis Inhibitors; D043169:Endostatins; D053583:Interleukin-1beta; D015850:Interleukin-6; D010446:Peptide Fragments; D044463:Receptor, PAR-1; D014409:Tumor Necrosis Factor-alpha; D042461:Vascular Endothelial Growth Factor A; C467498:vascular endothelial growth factor A, rat; D003094:Collagen; D009195:Peroxidase
keywords: Inflammation; PAR-1 receptor (1-41); human; neovascularization; periodontal diseases; physiologic; rats; wound healing