Stepnik Matthew W, Radtke Catherine L, Scollay Mary C, Oshel Philip E, Albrecht Ralph M, Santschi Elizabeth M, Markel Mark D, Muir Peter
Comparative Orthopaedic Research Laboratory, School of Veterinary Medicine, University of Wisconsin-Madison, Madison, WI 53706, USA.
Vet Surg. 2004 Jan-Feb;33(1):2-10. doi: 10.1111/j.1532-950x.2004.04007.x.
To examine the fracture failure surfaces from Thoroughbred horses that had sustained a catastrophic condylar fracture.
Bone specimens from the failure surface were obtained from 12 Thoroughbred racehorses with catastrophic injury and 2 non-racing horses with accidental long bone fracture.
Bone specimens from the failure surface of each fracture were incubated with gold microspheres to label microcracks before examination at x50 to x60,000 using scanning electron microscopy. Microcracking at the failure surface was assessed using a visual analog scale.
Branching arrays or clusters of microcracks were seen over a range of magnifications in adapted subchondral bone in the distal end of the MC3/MT3 bone from racing Thoroughbreds with a catastrophic displaced condylar fracture. In the palmar/plantar region, microcracking was associated with the formation of an array of macroscopic cracks in the condylar groove. A different pattern of microcracking was seen in specimens of bone from distal metaphyseal and diaphyseal MC3/MT3 failure surfaces from Thoroughbred racehorses with catastrophic fracture and non-racing horses with an accidental diaphyseal long bone fracture. Few microcracks were seen and typically did not form branching arrays.
These data suggest that propagation of condylar fracture in Thoroughbred racehorses is initiated by the formation of nanoscale microcracks in adapted subchondral bone that form during exercise-induced bone adaptation.
Accumulation and coalescence of branching microcracks into arrays or clusters appears to eventually lead to the development of macroscopic subchondral cracks in the condylar groove and initiation of a condylar fracture.
检查遭受髁突灾难性骨折的纯种马的骨折断裂面。
从12匹遭受灾难性损伤的纯种赛马和2匹因意外导致长骨骨折的非赛马获取骨折断裂面的骨标本。
将每个骨折断裂面的骨标本与金微球孵育以标记微裂纹,然后使用扫描电子显微镜在50倍至60000倍下进行检查。使用视觉模拟量表评估断裂面的微裂纹情况。
在患有灾难性移位髁突骨折的纯种赛马的MC3/MT3骨远端适应性软骨下骨中,在一系列放大倍数下均可见到微裂纹的分支阵列或簇。在掌侧/跖侧区域,微裂纹与髁突沟中一系列宏观裂纹的形成有关。在患有灾难性骨折的纯种赛马以及因意外骨干长骨骨折的非赛马的MC3/MT3骨干远端和骨干骨折断裂面的骨标本中,观察到不同的微裂纹模式。可见的微裂纹很少,且通常不形成分支阵列。
这些数据表明,纯种赛马髁突骨折的传播是由运动诱导的骨适应性过程中在适应性软骨下骨中形成的纳米级微裂纹引发的。
分支微裂纹聚集并合并成阵列或簇似乎最终导致髁突沟中宏观软骨下裂纹的发展以及髁突骨折的开始。