Free radical damage in facsimile synovium: correlation with adhesion formation in osteoarthritic TMJs.

摘要: PURPOSE: The purpose of this study was to use the rat air pouch model facsimile synovium evaluate oxidative stress as a primary mechanism in pathogenesis degenerative temporomandibular joint (TMJ) disease. MATERIALS AND METHODS: Forty-nine Sprague-Dawley adult female rats were used generate standard synovium. This accomplished by daily injections (20 cc) subdermally through dorsal skin. Hydrogen peroxide and ferrous iron (components Fenton reaction which free radicals) introduced into pouches 4-, 7-, 14-day groups stress. Control injected with phosphate-buffered solution (PBS), pH 7.4. Either N-acetylcysteine (NAC), powerful radical scavenger, or ibuprofen simultaneously reagents treatment modulate radical-mediated protein damage Animals euthanized at appropriate experimental intervals biopsies obtained from specimens analyze: (1) proteins' amino acid modification (carbonyl group formation), (2) hydrophobicity, (3) detection low molecular weight degradation products, (4) histological gross anatomical observations. RESULTS: Free radicals interacted synovial tissues causing oxidation breakdown proteins. Clinical evidence adhesion formation consistent features found osteoarthritis TMJ developed. subjected experienced statistically significant (p < 0.05) increases carbonyl formation, carbonyls/protein, fragments. These also showed hydrophobicity changes attack. undamaged. NAC decreases total hydrophobicity. Histological observations damaged exhibited known arthoscopic arthrocentesis findings diseased TMJs. CONCLUSIONS: suggests that develops clinical adhesions biochemical signs when prevented well indicative are human Future direction may be taken postulate new analysis techniques modalities for patients