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Antiresorptive Agent Potentially Prevents Re-fracture after Internal Fixation in Long Bone by Promoting New Cortical Shell Formation in Rat Femora

抗骨質吸收劑透過促進大鼠股骨皮質的形成潛在地防止長骨內固定術後的再骨折

摘要


Re-fracture following open reduction and internal fixation (ORIF) with a bone plate is a prevalent complication in the upper extremities. The use of metal plates for internal fixation of long bone fractures in the upper limbs is a standard procedure. Mechanical forces lead to stress shielding beneath the metal plate and screws and accelerate reduction in bone density (osteopenia). This issue is not only frustrating for patients but also imposes a significant burden on society. However, whether an antiresorptive agent targeting Rankl and Sclerostin could halt the stress shielding effect beneath a metal implant is still not understood. In this study, we developed an animal fracture model using the femur of rats receiving an osteotomy at the mid shaft and fixed with a 1mm miniplate. Rats established with fractures were divided into four groups, those administered with Rankl antibody, Sclerostin antibody, combined Rankl and Sclerostin antibody, or volume-matched saline. Surgery was performed by exposing the femoral bone without osteotomy as a sham group. Micro-CT test and histo-morphological examinations were conducted to evaluate fractures and calluses around the screw holes and the bone mass at the periosteum. These findings highlight potential to prevent re-fracture of the antiresorptive agent in an animal fracture model and suggest this may occur via the increase of bone mineral density and new bone formation.

並列摘要


骨板進行開放復位和內固定(ORIF)後的再次骨折是上肢常見的併發症。在上肢長骨骨折治療中使用金屬板進行內固定是一種標準程序。機械力導致金屬板和螺絲下方出現應力屏蔽效應,加速骨密度(骨質疏鬆)的減少。這個問題不僅讓患者感到沮喪,也給社會帶來了重大負擔。然而,針對Rankl和Sclerostin的抗吸收劑是否能阻止金屬植入物下方的應力屏蔽效應尚未被理解。在本研究中,我們建立一個動物骨折模型,在大鼠股骨中段執行截骨術並以1毫米微型板固定。動物模式分為四組,分別給予Rankl抗體、Sclerostin抗體、合併Rankl和Sclerostin抗體,或等體積生理食鹽水。手術透過暴露股骨骨骼(未進行截骨術)作為假手術組進行。透過微型CT測試和組織形態學檢查來評估骨折、螺釘孔周圍的骨痂和骨膜處的骨質量。本研究發現在動物骨折模型中抗骨質吸收劑可能透過增加骨礦物密度和新皮質骨形成來達到防止再次骨折之潛力。

參考文獻


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