title: Outcome of periapical lesions in a rat model of type 2 diabetes: refractoriness to systemic antioxidant therapy.
abstract: BACKGROUND
  This study evaluated the development of periapical lesions in a rat model of type 2 diabetes and assessed the potential actions of the antioxidant agent tempol in this model.
  
  
  METHODS
  Male Wistar rats were used; they received tap water (N = 5) or a 20% glucose solution (N = 15) during a period of 9 weeks. At the sixth week, periapical lesions were induced on the first mandibular molars, and the animals were subdivided into 4 groups. The subgroup 1 was composed of nondiabetic rats orally receiving saline solution (10 mL/kg). Chronically glucose-fed rats were divided into the following subgroups: (2) saline-treated animals (10 mL/kg by oral route), and animals treated with tempol by gavage at doses of (3) 50 mg/kg or (4) 100 mg/kg. The body weight was monitored thoroughly. After 21 days of apical periodontitis induction, the animals were killed, and the mandibles were collected and submitted to radiographic and histologic analysis. The livers were collected to determine free radicals, and the blood plasma was used to measure insulin levels.
  
  
  RESULTS
  Type 2 diabetic rats displayed a significant decrease of body weight gain and a slight increase of insulin levels, which were allied to reduced levels of the antioxidant components catalase and reduced glutathione; these alterations were reversed by tempol. Concerning the periapical lesions, neither radiographic nor histologic analysis revealed any significant difference between control and type 2 diabetic rats. In diabetic rats, the apical periodontitis was refractory to tempol treatment.
  
  
  CONCLUSIONS
  The extent and cellularity of periapical lesions in glucose-fed type 2 diabetic rats were similar to those seen in control rats. Despite affecting other parameters related to diabetes, tempol failed to improve the outcome of endodontic lesions in type 2 diabetic animals.
authors.affiliation: Postgraduate Program of Dental College, Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS), Partenon, Porto Alegre, Brazil.
authors.forename: Carlos Frederico B
authors.initials: CF
authors.lastname: Wolle
authors.forename: Luciana A
authors.initials: LA
authors.lastname: Zollmann
authors.forename: Patrícia O
authors.initials: PO
authors.lastname: Bairros
authors.forename: Adriana
authors.initials: A
authors.lastname: Etges
authors.forename: Carlos E
authors.initials: CE
authors.lastname: Leite
authors.forename: Fernanda B
authors.initials: FB
authors.lastname: Morrone
authors.forename: Maria M
authors.initials: MM
authors.lastname: Campos
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage / Q000627:therapeutic use*; D001835:Body Weight; D002374:Catalase / Q000032:analysis / Q000187:drug effects; D003497:Cyclic N-Oxides / Q000008:administration & dosage / Q000627:therapeutic use; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy*; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy*; D004195:Disease Models, Animal; D005609:Free Radicals / Q000032:analysis; D005978:Glutathione / Q000032:analysis / Q000187:drug effects; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance / Q000502:physiology; D008099:Liver / Q000378:metabolism; D008297:Male; D008334:Mandible / Q000000981:diagnostic imaging / Q000473:pathology; D008963:Molar / Q000000981:diagnostic imaging / Q000473:pathology; D018384:Oxidative Stress / Q000502:physiology; D010485:Periapical Periodontitis / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology*; D011859:Radiography; D051381:Rats; D017208:Rats, Wistar; D013113:Spin Labels; D016896:Treatment Outcome
chemical_list: D000975:Antioxidants; D003497:Cyclic N-Oxides; D005609:Free Radicals; D007328:Insulin; D013113:Spin Labels; D002374:Catalase; D005978:Glutathione; C001803:tempol