疲勞負載對脊骨整形手術後之脊椎形態學影響

Abstract

目的：本實驗目的是想藉由X光照攝和切片的方式觀察經骨水泥強固之椎骨在循環負載下形態的變化，以了解椎骨再破壞的產生原因與機制。 背景簡介：經皮椎骨整型手術( Vertebroplasty )是一種微創的脊椎手術，主要用於治療因骨質疏鬆症所導致的椎骨骨折，其併發症主要為骨水泥溢流及癒後鄰近椎骨破壞。但近年來發現，治療節椎骨再破壞(refracture)的病例越來越多。因此本研究希望了解椎骨再破壞的產生原因與機制，可作為預防與治療之理論基礎。 材料與方法： 使用4節胸椎為一組運動單元，將軟組織切除並在椎骨中埋下鋼珠及塗上鎢粉共10組(T5~T8,N=3;T9~T12,N=5 ;T8~T11,N=1; T4~T7,N=1 )。實驗首先模擬椎骨破壞，再使用經皮椎骨整型手術對其椎節做補強。骨水泥是以5ml的液體和6.5g的粉末的比例調配，另外在加上1.3g的鋇劑使骨水泥在X光下更清楚。固定注射3.5ml的骨水泥於受傷節椎骨。接著使試樣承受650牛頓、950牛頓和1150牛頓的循環負載，頻率5Hz，時間5小時。並在每一個小時對試樣照攝X光，利用鋼珠在X光下的顯影量測椎骨高度、神經腔寬度和椎間盤高度等參數。最後將破壞較嚴重的椎骨以每片3mm的厚度切片。 結果： 循環負載的力量和時間的增加會造成椎骨高度、神經腔寬度和椎間盤高度減少，並在12個小時的休息後會有回復的現象，尤其是在椎間盤高度和受傷節椎骨的神經腔寬度更為明顯。由X光片觀察得知，神經腔寬度變小主要是因為椎骨後側的變形侵入至神經腔。而經由線性迴歸分析發現，循環負載後神經腔寬度和椎骨後側高度、破壞時神經腔寬度皆呈現線性相關，但和骨質、前緣椎骨回復高度並無線性相關。切片觀察發現，椎骨後側的骨小樑呈現鬆散的現象，是造成後側強度減弱的主要原因。 結論：將骨水泥灌注在椎骨的前端，會使得椎骨後側強度因為沒有骨水泥補強而減弱。椎骨後側強度減弱使其無法承受循環負載導致椎骨後側變形和椎骨後側高度減少。當一個病人發生了椎骨破壞，發現其椎骨的後側有嚴重的變形現象，若只以VP手術做治療，會有較高的機率發生椎骨再破壞的現象。將骨水泥注射至椎骨前緣可能會造成椎骨後側強度相對降低，造成後側椎骨變形。

Objective: To explore the refracture mechanism of vertebroplasty. Summary of Background Data: Vertebroplasty is a minimal invasive surgery for spinal compression fracture. The major complications of vertebroplasty are cement leakage and adjacent vertebral failure. In recent year, the incidence of augmented vertebral refracture increases. The mechanism of refracture is, however, not clear. Materials and Methods: Ten fresh 4-level thoracic motion segments (T5~T8,N=3;T9~T12,N=5 ;T8~T11,N=1; T4~T7,N=1) from 6 human spines were used. A series of steel balls (D=1.4 mm) were glued to the canal for determining the canal width in the midsagittal plane. Four steel balls separately embedded into the anterior vertebra for measuring the height of anterior vertebra. Both ends of the specimen were mounted, leaving the center 2 vertebrae free. The lower level of free vertebra was artificially injured and than cement augmented. The injection volume of cement was 3.5 ml and the powder to monomer ratio of the cement was 1.3. All specimens were applied with 650 N, 950 N and 1150 N (mean) compressive fatigue loading. The loading frequency was 5 Hz and the loading period was 5 hours in each loading magnitude. The lateral radiographs were taken in each hour. In the end of the experiment, the failure specimens were cut along the sagittal plane. Results: The vertebral height, spinal canal width and disc height decreased following fatigue loading, and can be partially recovered during 12 hr rest. The vertebral posterior cortex extrusion causes loss of the spinal canal width. The spinal canal width after injury and posterior vertebral height were positively related to the spinal canal width after fatigue, but the bone mineral density and the anterior vertebral height restoration were not correlated to the spinal canal. The dissected specimens showed that the weak posterior bony structure was extruded into spinal canal due to the fatigue loading. Conclusion: The fracture of pre-existed vertebral posterior cortex increases the risk of subsequent fracture post vertebroplasty. The refracture mechanism cannot be correlated with the BMD and the anterior vertebral height restoration in this study.