RESUMO
A survey was undertaken to analyze implants placed in irradiated tissues. It was found that nine centers had placed 118 implants in 24 patients in Japan. Of 118 implants, 39 were in the maxilla, 71 were in the mandible, and 8 were in the orbital region. Seven patients underwent adjunctive hyperbaric oxygen treatment. The treatment decreased implant loss only in the maxilla. (The success rate without hyperbaric oxygen treatment was 62.5%, and that with hyperbaric oxygen treatment was 80.0% for the maxilla.) Implants 7 and 10 mm in length were at a greater risk of being lost than longer implants in the maxilla.
Assuntos
Implantação Dentária Endóssea , Implantes Dentários , Arcada Osseodentária/efeitos da radiação , Procedimentos Cirúrgicos Ortognáticos , Osseointegração , Planejamento de Prótese Dentária , Falha de Restauração Dentária , Desenho de Equipamento , Feminino , Seguimentos , Humanos , Oxigenoterapia Hiperbárica , Japão , Masculino , Mandíbula/efeitos da radiação , Mandíbula/cirurgia , Maxila/efeitos da radiação , Maxila/cirurgia , Pessoa de Meia-Idade , Órbita/diagnóstico por imagem , Órbita/cirurgia , Próteses e Implantes , Radiografia , Radioterapia/efeitos adversos , Resultado do TratamentoRESUMO
Adjuvant and collagen arthritis in the rat are widely accepted T-cell-dependent counterparts of rheumatoid arthritis and were used to examine the antiinflammatory properties of minocycline. Administration of oral minocycline, a semisynthetic tetracycline, significantly decreased (P < 0.01) the incidence of arthritis in both models. In vivo exposure to minocycline also significantly increased the percentage of splenocytes exhibiting a rise in free intracellular calcium concentration ([Ca2+]i) following concanavalin A stimulation (P < 0.05 in adjuvant and P < 0.01 in collagen). This enhancement was mitogen dose-dependent and supported exclusively by extracellular Ca2+. Resting [Ca2+]i levels were unaffected by minocycline and predominantly the CD4+ subset was involved. No changes were observed in weight, IgG antibodies to collagen, synoviocyte release of collagenase and prostaglandin E2, acute inflammation in an air-pouch system, or cell surface expression of activation markers (interleukin-2 and transferrin receptors) by splenocytes or lymph node cells. As a controlled [Ca2+]i rise is a critical event in normal T cell activation, minocycline's antiarthritic profile in vivo may relate to perturbed Ca2+ influx during T cell activation, an alteration that could promote the development of clinical tolerance to otherwise arthritogenic stimuli.