中国临床康复
中國臨床康複
중국림상강복
CHINESE JOURNAL OF CLINICAL REHABILITATION
2004年
18期
3684-3685
,共2页
张军芳%夏永祥%曹峻岭%毕华银
張軍芳%夏永祥%曹峻嶺%畢華銀
장군방%하영상%조준령%필화은
目的:探讨维甲酸致大鼠骨质疏松对下颌骨骨量的影响.方法:20只3月龄SD雌性大鼠,按随机数字表法分为对照组和模型组,每组10只.采用维甲酸灌胃建立大鼠骨质疏松模型以诱发下颌骨骨丢失,通过下颌骨骨密度测量;血中各项生化指标的检测;下颌骨解剖形态观察以及骨组织形态计量法测量等方法,观测维甲酸诱导的模型对下颌骨骨量的影响.结果:灌胃15d后,立体显微镜下可见,模型组大鼠下颌角下缘和下颌孔上缘有骨膜下骨吸收区存在;模型组大鼠下颌骨磨牙段骨密度为(0.281±0.017)g/cm2,比对照组骨密度[(0.324±0.005)g/cm2]明显降低(t=5.944,P<0.05);骨组织形态计量法结果显示,模型组下颌骨骨小梁平均宽度显著低于对照组(t=26.302,P<0.05);模型组下颌骨骨小梁平均间隔宽度显著高于对照组(t=19.963,P<0.05).与对照组相比,血清雌二醇水平显著降低,血清碱性磷酸酶和抗酒石酸酸性磷酸酶活性显著升高.结论:灌服维甲酸后,颌骨出现了疏松化改变,表明该模型用于研究下颌骨骨丢失是可行的.
目的:探討維甲痠緻大鼠骨質疏鬆對下頜骨骨量的影響.方法:20隻3月齡SD雌性大鼠,按隨機數字錶法分為對照組和模型組,每組10隻.採用維甲痠灌胃建立大鼠骨質疏鬆模型以誘髮下頜骨骨丟失,通過下頜骨骨密度測量;血中各項生化指標的檢測;下頜骨解剖形態觀察以及骨組織形態計量法測量等方法,觀測維甲痠誘導的模型對下頜骨骨量的影響.結果:灌胃15d後,立體顯微鏡下可見,模型組大鼠下頜角下緣和下頜孔上緣有骨膜下骨吸收區存在;模型組大鼠下頜骨磨牙段骨密度為(0.281±0.017)g/cm2,比對照組骨密度[(0.324±0.005)g/cm2]明顯降低(t=5.944,P<0.05);骨組織形態計量法結果顯示,模型組下頜骨骨小樑平均寬度顯著低于對照組(t=26.302,P<0.05);模型組下頜骨骨小樑平均間隔寬度顯著高于對照組(t=19.963,P<0.05).與對照組相比,血清雌二醇水平顯著降低,血清堿性燐痠酶和抗酒石痠痠性燐痠酶活性顯著升高.結論:灌服維甲痠後,頜骨齣現瞭疏鬆化改變,錶明該模型用于研究下頜骨骨丟失是可行的.
목적:탐토유갑산치대서골질소송대하합골골량적영향.방법:20지3월령SD자성대서,안수궤수자표법분위대조조화모형조,매조10지.채용유갑산관위건립대서골질소송모형이유발하합골골주실,통과하합골골밀도측량;혈중각항생화지표적검측;하합골해부형태관찰이급골조직형태계량법측량등방법,관측유갑산유도적모형대하합골골량적영향.결과:관위15d후,입체현미경하가견,모형조대서하합각하연화하합공상연유골막하골흡수구존재;모형조대서하합골마아단골밀도위(0.281±0.017)g/cm2,비대조조골밀도[(0.324±0.005)g/cm2]명현강저(t=5.944,P<0.05);골조직형태계량법결과현시,모형조하합골골소량평균관도현저저우대조조(t=26.302,P<0.05);모형조하합골골소량평균간격관도현저고우대조조(t=19.963,P<0.05).여대조조상비,혈청자이순수평현저강저,혈청감성린산매화항주석산산성린산매활성현저승고.결론:관복유갑산후,합골출현료소송화개변,표명해모형용우연구하합골골주실시가행적.
AIM: To explore the impact of osteoporosis induced by retinoic acid on bone mass of mandible in rats.METHODS: Twenty SD female rats aged three months were randomly allocated into notral group( n = 10) and model group( n = 10). Osteoporosis model was established by retinoic acid through stomach-peffusion in rats to induce mandibular bone loss. The impact of model induced by retinoic acid on mandibular bone mass was observed through the detection of bone mineral density and each serous biochemical index and the observation of the anatomic morphology of mandible as well as bone histomorphological metrological measurements, etc.RESULTS: After 15-day of the administration of retinoic acid, bone resorption regions iii subperiosteum were seen in the lower border of mandibular angle and the upper border of mandibular foramen in the rats of model group under anatomic microscope. The bone mineral density of mandibular molar part in the rats of model group was(0. 281 +0. 017) g/cm2, which was significantly lower compared with(0. 324 ±0. 005)g/cm2 of control group( t=5.944, P<0.05).The trabecular width in model group was significantly lower than that of control group (t =26.302, P<0.05 ). The separation of trabecular in model group was significantly higher than that of control group( t = 19. 963, P < 0.05) .Compared with control group, the serous level of estradiol significantly decreased, the activity of serous alkaline phosphatase(ALP) and tartrate-resistant acid phosphatase(TRAP) was markedly increased in model group.CONCLUSION: Bone mass of mandible decreased in rats with osteoporosis induced by retinoic acid through stomach-peffusion, which indicates that this model is available and feasible in the study of mandibular bone loss.