Influence of Parstatin on Experimental Periodontal Disease and Repair in Rats. Issue 9 (1st September 2014)

• Record Type: Journal Article
• Authors: Spolidorio, Luís Carlos; Ramalho Lucas, Pablo Dallari; Steffens, Joao Paulo; da Silva, Henrique Aparecido Bueno; Tubero Euzebio Alves, Vanessa; Palomari Spolidorio, Denise M.; Holzhausen, Marinella
• Is Part Of: Journal of periodontology. Volume 85:Issue 9(2014)
• Page Start: 1266
• Page End: 1274
• Publication Date: 2014-09-01
• Subjects: Inflammation -- neovascularization -- physiologic -- PAR‐1 receptor (1‐41) -- human -- periodontal diseases -- rats -- wound healing; Periodontics -- Periodicals; 617.632
• DOI: 10.1902/jop.2014.130619
• Languages: English
• ISSNs: 0022-3492

Abstract

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.