Luzia Hermínia Teixeira Sousa1, Eveline Valeriano Moura1, Ana Larissa Queiroz2, Danielle Val3, Hellíada Chaves4, Mario Lisboa5, Flávia Furlaneto6, Gerly Anne Brito7, Paula Goes8. 1. Post-graduation Program of Health Science, Medical School, Federal University of Ceará - Sobral, Avenida Comandante Maurocelio Rocha Pontes, 100 - Derby, Sobral, CE, 62.042-280, Brazil. 2. School of Dentistry, Federal University of Ceará - Sobral, R. Cel. Estanislau Frota - Centro, Sobral, CE, 62.010-560, Brazil. 3. Post Graduation Program RENORBIO, Federal University of Pernambuco, Av. Professor Morais Rego, 1235 - Cidade Universitária, Recife, PE, 50670-901, Brazil. 4. Post-graduation Program of Health Science, Medical School, Federal University of Ceará - Sobral, Avenida Comandante Maurocelio Rocha Pontes, 100 - Derby, Sobral, CE, 62.042-280, Brazil; School of Dentistry, Federal University of Ceará - Sobral, R. Cel. Estanislau Frota - Centro, Sobral, CE, 62.010-560, Brazil. 5. Post-graduation Program of Morphological Science, Department of Morphology, Medical School, Federal University of Ceará - Fortaleza, Rua Delmiro de Farias, s/n - Rodolfo Teófilo, Fortaleza, CE, 60.430-170, Brazil. 6. Department of Oral & Maxillofacial Surgery and Periodontology, Ribeirão Preto School of Dentistry, University of São Paulo, Av. do Café, s/n - Vila Amelia, Ribeirão Preto, São Paulo, 14050-904, Brazil, Brazil. 7. Post-graduation Program of Morphological Science, Department of Morphology, Medical School, Federal University of Ceará - Fortaleza, Rua Delmiro de Farias, s/n - Rodolfo Teófilo, Fortaleza, CE, 60.430-170, Brazil; Department of Morphology, Medical School, Federal University of Ceará - Fortaleza, Rua Delmiro de Farias, s/n - Rodolfo Teófilo, Fortaleza, CE, CEP 60.430-170, Brazil. 8. Post-graduation Program of Health Science, Medical School, Federal University of Ceará - Sobral, Avenida Comandante Maurocelio Rocha Pontes, 100 - Derby, Sobral, CE, 62.042-280, Brazil; Department of Pathology and Legal Medicine, Medical School, Federal University of Ceará - Fortaleza, Rua Monsenhor Furtado, S/N - Rodolfo Teófilo, Fortaleza, CE, 60.441-750, Brazil. Electronic address: paulagpinheiro@yahoo.com.br.
Abstract
OBJECTIVE: To evaluate the effects of osteoporosis induced by glucocorticoid (GIOP) on bone tissue of rats with experimental periodontitis (EP). DESIGN: 48 male Wistar rats divided into groups: Naïve, EP, GIOP and GIOP+EP. Rats of GIOP and GIOP+EP groups received 7mg/kg of dexamethasone intramuscularly once a week for 5 weeks. Following, EP and GIOP+EP groups were subjected to ligature-induced periodontitis. Naïve group experienced no manipulation. After 11 days, the animals were euthanized and left maxillae collected for macroscopic, radiographic, micro-tomographic and microscopic analysis of alveolar bone loss (ABL). Blood samples were collected for determination of bone-specific alkaline phosphatase (BALP) levels and the right femurs were removed for radiographic and biomechanical analysis. RESULTS: EP caused ABL and reduced BALP levels (p<0,05), but it did not change the architecture or biomechanics of femur, compared to Naïve. GIOP did not cause ABL, but it significantly decreased alveolar bone mineral density (ABMD), bone percentage and trabecular thickness (Tb.Th) and increased alveolar bone porosity (p<0.05) and significantly reduced BALP serum levels, as well as radiographic density and Young's module of femur, compared to Naïve. There was a greater ABL in group GIOP+EP when compared to EP (p<0.05). GIOP+EP caused a greater decrease on ABMD, Tb.Th, bone percentage and increased bone porosity (p<0.05) and also presented a significant reduction in BALP levels (p<0.05), in radiographic density and in Young's module of femur compared to EP (p<0.05). CONCLUSIONS: GIOP can potentiate the destructive effects of EP on alveolar bone and alter the systemic bone loss, by promoting bone resorption and reducing osteoblast activity.
OBJECTIVE: To evaluate the effects of osteoporosis induced by glucocorticoid (GIOP) on bone tissue of rats with experimental periodontitis (EP). DESIGN: 48 male Wistar rats divided into groups: Naïve, EP, GIOP and GIOP+EP. Rats of GIOP and GIOP+EP groups received 7mg/kg of dexamethasone intramuscularly once a week for 5 weeks. Following, EP and GIOP+EP groups were subjected to ligature-induced periodontitis. Naïve group experienced no manipulation. After 11 days, the animals were euthanized and left maxillae collected for macroscopic, radiographic, micro-tomographic and microscopic analysis of alveolar bone loss (ABL). Blood samples were collected for determination of bone-specific alkaline phosphatase (BALP) levels and the right femurs were removed for radiographic and biomechanical analysis. RESULTS: EP caused ABL and reduced BALP levels (p<0,05), but it did not change the architecture or biomechanics of femur, compared to Naïve. GIOP did not cause ABL, but it significantly decreased alveolar bone mineral density (ABMD), bone percentage and trabecular thickness (Tb.Th) and increased alveolar bone porosity (p<0.05) and significantly reduced BALP serum levels, as well as radiographic density and Young's module of femur, compared to Naïve. There was a greater ABL in group GIOP+EP when compared to EP (p<0.05). GIOP+EP caused a greater decrease on ABMD, Tb.Th, bone percentage and increased bone porosity (p<0.05) and also presented a significant reduction in BALP levels (p<0.05), in radiographic density and in Young's module of femur compared to EP (p<0.05). CONCLUSIONS: GIOP can potentiate the destructive effects of EP on alveolar bone and alter the systemic bone loss, by promoting bone resorption and reducing osteoblast activity.
Authors: Paula Goes; Caio Dutra; Lennart Lösser; Lorenz C Hofbauer; Martina Rauner; Sylvia Thiele Journal: Front Immunol Date: 2019-12-10 Impact factor: 7.561