RESUMO
Defects associated with bone mass loss are frequently treated by autogenous bone grafting. However, synthetic biomaterials such as calcium phosphate ceramics can substitute autologous grafts as long as they are biocompatible with bone tissue. In addition, low-level laser therapy (LLLT) is used to enhance bone regeneration by stimulating the local microcirculation and increasing the synthesis of collagen by bone cells. However, bone health is fundamental for osseointegration of the graft and bone repair. In this respect, excessive tobacco consumption can compromise expected outcomes because of its deleterious effects on bone metabolism that predispose to the development of osteoporosis. The objective of this study was to evaluate the regeneration of bone defects implanted with biomaterial and stimulated by LLLT in rats submitted to passive cigarette smoking. Porous hydroxyapatite granules were implanted into critical-size defects induced experimentally in the distal epiphysis of the right femur of 20 female Wistar rats submitted to passive smoking for 8 months in a smoking box. The defect site was irradiated with a gallium-arsenide laser at an intensity of 5.0 J/cm2. The animals were divided into four groups: control (non-smoking) rates submitted (G2) or not (G1) to laser irradiation, and smoking rats submitted (G4) or not (G3) to laser irradiation. The animals were sacrificed 8 weeks after biomaterial implantation. The right femurs were removed for photodocumentation, radiographed, and processed for routine histology. The results showed good radiopacity of the implant site and of the hydroxyapatite granules. Histologically, formation of new trabecular bone was observed adjacent to the hydroxyapatite granules in G1 and G2. In G3 and G4, the granules were surrounded mainly by connective tissue. In conclusion, passive smoking compromised bone neoformation in the defects and the LLLT protocol was not adequate to stimulate local osteogenesis.
Assuntos
Substitutos Ósseos , Durapatita , Osseointegração , Poluição por Fumaça de Tabaco/efeitos adversos , Animais , Modelos Animais de Doenças , Feminino , Inalação , Terapia a Laser , Osteoporose , Ratos , Ratos WistarRESUMO
1. Mice peritoneal mast cells previously treated with alloantibodies directed against private and public major histocompatibility antigens became partially resistant to subsequent passive sensitization with homologous IgG1-rich serum. 2. Sensitization of the mast cells was evaluated in terms of the percentage of cells that degranulated upon challenge with the specific antigen. 3. The phenomenon was immunologically specific and the responsible alloantigens were shown to be coded by the H-2K or H-2D regions.
Assuntos
Antígenos H-2/imunologia , Liberação de Histamina , Isoanticorpos/farmacologia , Mastócitos/imunologia , Anafilaxia/imunologia , Animais , Feminino , Soros Imunes , Imunização Passiva , Imunoglobulina G/imunologia , Capeamento Imunológico , Camundongos , Camundongos Endogâmicos C3H , Camundongos Endogâmicos C57BL , Camundongos Endogâmicos DBA , Receptores ImunológicosRESUMO
Mice peritoneal mast cells previously treated with alloantibodies directed against private and public major histocompatibility antigens became partially resistant to subsequent passive sensitization with homologous IgG1-rich serum. 2. Sensitization of the mast cells was evaluated in terms of the percentage of cells that de granulated upon challenge with the specifc antigen. 3. The phenomenon was immunologically specific and the responsible alloantigens were shown to be coded by the H-2K or H-2D regions