RESUMO
BACKGROUND: Failure of glenoid labrum and capsular healing after glenohumeral dislocation can lead to persistent shoulder instability. The purpose of this study was to determine the effect of nonsteroidal anti-inflammatory drugs (NSAIDs) on the healing glenoid labrum and capsule after glenohumeral dislocation in a rat model. METHODS: Sixty-six rats had surgically induced anterior-inferior labral tears and anterior glenohumeral dislocation. Postoperatively, the animals were assigned to either normal (n = 32) or ibuprofen drinking water (n = 31). Animals were euthanized at 2 and 4 weeks postoperatively for biomechanical testing and histologic analysis. RESULTS: The maximum load increased from 2 to 4 weeks after injury in the NSAID groups but not in the control groups. At 2 weeks, the maximum load was lower in the NSAID group compared with the control group. In a matched comparison between injured and uninjured limbs, the maximum load was significantly decreased in the injured limb of the 2-week NSAID group. At 4 weeks, the NSAID group had decreased stiffness compared with the 4-week control group. CONCLUSIONS: In a new rat model of glenohumeral instability, the postinjury administration of ibuprofen resulted in decreased capsulolabral healing. A matched pair analysis of injured to uninjured limbs supported the findings of impaired healing in the NSAID-treated animals. These findings demonstrate that the use of NSAIDs after glenohumeral dislocation may impair capsulolabral healing and should be limited or avoided to optimize glenohumeral stability.
Assuntos
Ibuprofeno/efeitos adversos , Instabilidade Articular/cirurgia , Amplitude de Movimento Articular/fisiologia , Luxação do Ombro/cirurgia , Articulação do Ombro/cirurgia , Cicatrização/efeitos dos fármacos , Animais , Anti-Inflamatórios não Esteroides/efeitos adversos , Modelos Animais de Doenças , Instabilidade Articular/etiologia , Instabilidade Articular/fisiopatologia , Masculino , Período Pós-Operatório , Ratos , Ratos Endogâmicos Lew , Luxação do Ombro/complicações , Luxação do Ombro/fisiopatologia , Articulação do Ombro/efeitos dos fármacos , Articulação do Ombro/fisiopatologiaRESUMO
Androgens play a critical role in the progression of castration-resistant prostate cancer through androgen receptor (AR)-regulated signaling pathways. Progress has been made in the development of potent agents designed to suppress androgen function by blocking the AR, inhibiting the synthesis of androgens, or targeting downstream AR signaling pathways. This review summarizes the development of novel therapies based on current insights into AR signaling pathways in castration-resistant prostate cancer.