Assessment of the effects of diabetes on bone repair and of role of different titanium surfaces on the osseointegration of implants in a model of experimentally-induced diabetes in rabbits

• Grant number: 10/16907-7
• Support Opportunities: Regular Research Grants
• Duration: February 01, 2011 - April 30, 2013
• Field of knowledge: Health Sciences - Dentistry
• Principal Investigator: Elcio Marcantonio Junior
• Grantee: Elcio Marcantonio Junior
• Host Institution: Faculdade de Odontologia (FOAr). Universidade Estadual Paulista (UNESP). Campus de Araraquara. Araraquara , SP, Brazil
• Associated researchers: Carlos Rossa Junior ; José Eduardo Cezar Sampaio ; Silvana Regina Perez Orrico

Abstract

Pre-clinical and clinical studies have shown that some systemic conditions, such as Diabetes, may affect bone homeostasis and healing processes, with severe consequences to these individuals. In the mouth, diabetes has been associated with impairment of osseointegration of dental implants which negatively affects the prognosis of the implant treatment. Modifications of the surface of dental implants to enhance bone healing may circumvent the deleterious influences associated with diabetes. The aims of this proposal are to assess and describe mechanisms for: 1) modulation of bone repair of critical wounds by diabetes; 2) the effects of different surface modifications on osseointegration. Experimental diabetes will be induced in rabbits by alloxan injections and after 8 weeks implants will be inserted in the proximal tíbia and critical defects produced on the calvaria. A total of 54 animals will be randomly distributed into 3 experimental groups of 18 animals each: non-diabetic control (Group C), diabetics (Group D) and controlled diabetics (Group DC) which will be treated by administration of insulin. Four implants will be inserted in each animal (2 in the proximal metaphyses of each tíbia): 2 of a conventional, machined surface and 2 of a Fluoride-treated surface. To assess the influence of diabetes on bone healing processes and obtain insight into the associated mechanisms, a critical defect of 15 mm in diameter will be created on the calvaria of each animal. As a future reference of the original boundaries of this defect, 4 mini-implants will be inserted in diametrically opposing positions. The animals will be humanely killed 2, 4 and 8 weeks after insertion of implants and creation of the critical calvarial defects. The influence of diabetes on bone repair in these defects will be characterized by evaluations of cell proliferation and apoptosis, osteoclastogenesis, osteoblast differentiation, production of extracellular matrix and vascularization. For these evaluations, we will use immunohistochemistry, descriptive histology, stereometry, RT-qPCR and ELISA methods. Osseointegration will be assessed by determination of the ex-vivo removal torque and by the extent of bone-implant contact and bone tissue fill of the implant threads in non-decalcified histological sections. (AU)

Scientific publications

(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)

PIMENTEL LOPES DE OLIVEIRA, GUILHERME JOSE; DURIGAN BASSO, TULIO LUIZ; FONTANARI, LUCAS AMARAL; DE SOUZA FALONI, ANA PAULA; MARCANTONIO JUNIOR, ELCIO; PEREZ ORRICO, SILVANA REGINA. Glycemic control protects against trabecular bone microarchitectural damage in a juvenile male rat model of streptozotocin-induced diabetes. ENDOCRINE RESEARCH, v. 42, n. 3, p. 171-179, 2017. (10/16907-7)