title: Clopidogrel enhances periodontal repair in rats through decreased inflammation.
abstract: OBJECTIVE
  We hypothesized that platelet inactivation induced by drugs might interfere with periodontal repair in experimental periodontitis by suppressing the release of biological mediators from platelets at the site of injury.
  
  
  METHODS
  Sixty rats were randomly assigned to six groups (n = 10) and ligatures were placed around lower first molars of three groups. The other three groups were used as negative controls. Ligatures were removed after 10 days of periodontitis induction and all groups were submitted to treatment with aspirin (Asp) (30 mg/kg), clopidogrel (Clop) (75 mg/kg) or NaCl 0.9% intra-gastrically once daily for 3 days. Periodontal tissue was assessed by the measurement of CXCL12, CXCL4, CCL5 and platelet-derived growth factor (PDGF) by enzyme-linked immunosorbent assay; histomorphometrical analysis of polymorphonuclear (PMN) infiltration, attachment loss, bone loss and osteoclast numbers and quantification of blood vessels by imunnohistochemistry.
  
  
  RESULTS
  During periodontal repair and treatment with NaCl 0.9%, CCL5 was decreased and CXCL12 increased when compared with negative control groups. Asp and Clop did not affect CCL5 expression, decreased CXCL12 but only Clop decreased CXCL4 and PDGF content compared with saline-treated animals. Clop increased blood vessel number, reduced PMN count and decreased attachment and bone loss, also decreased osteoclast number in animals submitted or not to periodontal repair.
  
  
  CONCLUSIONS
  Systemic administration of Clop for 3 days improved the repair process associated with experimental periodontal disease, suggesting that it may have therapeutic value under situations where tissues undergo a transition from inflammation to repair.
authors.affiliation: Department of Physiology and Pathology, Faculdade de Odontologia de Araraquara, UNESP-Univ Estadual Paulista, Araraquara, Brazil.
authors.forename: Leila S
authors.initials: LS
authors.lastname: Coimbra
authors.forename: Joao Paulo
authors.initials: JP
authors.lastname: Steffens
authors.forename: Carlos
authors.initials: C
authors.lastname: Rossa
authors.forename: Dana T
authors.initials: DT
authors.lastname: Graves
authors.forename: Luis C
authors.initials: LC
authors.lastname: Spolidorio
mesh_terms: D016301:Alveolar Bone Loss / Q000188:drug therapy; D000818:Animals; D001241:Aspirin / Q000008:administration & dosage / Q000627:therapeutic use; D002452:Cell Count; D018946:Chemokine CCL5 / Q000187:drug effects; D054377:Chemokine CXCL12 / Q000187:drug effects; D000077144:Clopidogrel; D007263:Infusions, Parenteral; D008297:Male; D055806:Microvessels / Q000187:drug effects; D020556:Neutrophil Infiltration / Q000187:drug effects; D009504:Neutrophils / Q000187:drug effects; D010010:Osteoclasts / Q000187:drug effects; D017622:Periodontal Attachment Loss / Q000188:drug therapy; D010518:Periodontitis / Q000188:drug therapy*; D010519:Periodontium / Q000187:drug effects*; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use*; D010978:Platelet Factor 4 / Q000187:drug effects; D010982:Platelet-Derived Growth Factor / Q000187:drug effects; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D012965:Sodium Chloride; D013988:Ticlopidine / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000627:therapeutic use
chemical_list: C575935:CXCL12 protein, rat; D018946:Chemokine CCL5; D054377:Chemokine CXCL12; D010975:Platelet Aggregation Inhibitors; D010982:Platelet-Derived Growth Factor; D010978:Platelet Factor 4; D012965:Sodium Chloride; D000077144:Clopidogrel; D013988:Ticlopidine; D001241:Aspirin
keywords: chemokines; clopidogrel; inflammation; innate immunity; periodontal repair