RESUMO
Vertebroplasty was performed using hydroxyapatite blocks to examine the course of compressive strength and histological features in a dog model. The vertebral fracture model was prepared by punching a hole in the center of the vertebra and at 4 sites around the vertebra (5 holes in total) from the front side of the vertebra using an air drill and hollowing the holes. Measurements were made on healthy vertebrae, vertebrae from the vertebral fracture model, vertebrae removed from animals immediately after vertebroplasty, vertebrae collected 1 and 2 months after vertebroplasty, and vertebrae untreated for 1 month after vertebral fracture. Histological examinations were also performed 1 and 2 weeks and 1 and 2 months after vertebroplasty with hydroxyapatite blocks. The strength of vertebrae in the fracture model immediately after vertebroplasty was significantly higher than that in the untreated fracture, and the strength of vertebrae 1 month after the procedure was equivalent to that of healthy vertebrae. Histologically, new bone formation was found around hydroxyapatite blocks 2 weeks after the procedure, and strong crosslinking between neighboring hydroxyapatite blocks was found after 1 month.These results suggest that hydroxyapatite blocks may be effective as filling material for vertebral fracture from both biomechanical and histological perspectives.
Assuntos
Durapatita/administração & dosagem , Vértebras Lombares/lesões , Vértebras Lombares/fisiopatologia , Fraturas da Coluna Vertebral/fisiopatologia , Fraturas da Coluna Vertebral/terapia , Vertebroplastia/métodos , Animais , Substitutos Ósseos/administração & dosagem , Cães , Elasticidade/efeitos dos fármacos , Vértebras Lombares/efeitos dos fármacos , Estresse Mecânico , Resistência à Tração/efeitos dos fármacosRESUMO
BACKGROUND: Passive smoking has been reported to induce intervertebral disc degeneration in rats, and the objective of the present study was to histologically investigate changes in smoking-induced intervertebral disc degeneration after cessation of smoking. METHODS: Four-week-old rats were subjected to passive smoking for 8 weeks in a smoking box [20 cigarettes a day: one cigarette an hour (inhaled over 3 minutes and followed by ventilation with room air for 5 minutes)] to induce intervertebral disc degeneration. Smoke-free periods of different lengths were then established, and intervertebral discs were histologically analyzed. RESULTS: Immediately after 8 weeks of passive smoking, intervertebral discs exhibited cracks, tears, and misalignment of the annulus fibrosus, and increased fibrous tissue was seen in the nucleus pulposus. In addition, the level of interleukin-1beta in intervertebral discs was higher in the smoking group than in the non-smoking group. After cessation, progression of degeneration ceased, and the matrix of the nucleus pulposus and annulus fibrosus exhibited increased fibrous connective tissue and proteoglycan. However, there were no changes in annulus fibrosus misalignment. Interleukin-1beta levels also remained significantly elevated after 8 weeks of cessation. CONCLUSIONS: While the annulus fibrosus degeneration caused by smoking was partially irreversible after cessation of smoking, the amount of mucin (proteoglycan) in the nucleus pulposus and annulus fibrosus tended to increase after cessation, thus suggesting the possibility that smoking-induced intervertebral disc degeneration can be repaired to some degree by cessation of smoking.