title: Influence of short-term diabetes on osteocytic lacunae of alveolar bone. A histomorphometric study.
abstract: The aim of this study was to evaluate, for the first time, the histomorphometry of the cellular and lacunar features of the osteocytes of alveolar bone in acute streptozotocin-induced diabetic insulin-treated or untreated rats. Eighteen male Wistar rats weighing 200 to 260 g were assigned to one of the following groups: I) control group (C), II) diabetic group (DBT), and III) insulin treated diabetic group (DBT+INS). Experimental diabetes was induced by a single intraperitoneal injection of 60 mg/kg of body weight of streptozotocin. Insulin treatment began 24 h after the streptozotocin injection in animals of group DBT+INS in a dose of 4-6 IU of Humulin NPH insulin given as a single daily subcutaneous (s.c.) injection each morning between 07.00 and 10.00 h. The animals were euthanized on the 8th day. The upper maxillae were removed and fixed in buffered formalin, decalcified in EDTA, embedded in paraffin and stained with H-E for histologic and histomorphometric evaluation. Bone activity and lacunar density, osteocyte and empty lacunar densities, lacunar volume and lacunar shape were evaluated. Differences between variables were assessed by one-way ANOVA. Surface bone activity values revealed that bone resorption was significantly greater in the DBT group than in the C group (p < 0.05). Total lacunar density was significantly reduced in the DBT and DBT+INS groups as compared to control (p < 0.05). Concomitantly, a statistically significant reduction in osteocyte density and an increase, albeit not statistically significant, in empty lacunar density was observed in DBT and DBT+INS groups versus control. Lacunar volume did not exhibit statistically significant differences. The osteocyte lacunae in the DBT group lost their rounded shape and acquired intermediate shapes. This study reveals an early response of osteocytes to hyperglycemia, before systemic compensatory mechanisms are turned on. The effects are not always compensated by insulin treatment.
authors.affiliation: Department of Histology and Embryology, School of Dentistry, University of Buenos Aires, Argentina.
authors.forename: Mariano E
authors.initials: ME
authors.lastname: Villarino
authors.forename: Luciana M
authors.initials: LM
authors.lastname: Sánchez
authors.forename: Carola B
authors.initials: CB
authors.lastname: Bozal
authors.forename: Angela M
authors.initials: AM
authors.lastname: Ubios
mesh_terms: D016301:Alveolar Bone Loss / Q000209:etiology* / Q000473:pathology; D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000139:chemically induced / Q000150:complications* / Q000188:drug therapy; D003922:Diabetes Mellitus, Type 1 / Q000139:chemically induced / Q000150:complications* / Q000188:drug therapy; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007328:Insulin / Q000627:therapeutic use; D008297:Male; D010011:Osteocytes / Q000473:pathology*; D016062:Porosity; D051381:Rats; D017208:Rats, Wistar; D013311:Streptozocin
chemical_list: D007004:Hypoglycemic Agents; D007328:Insulin; D013311:Streptozocin