Ogden J A, Ganey T, Light T R, Southwick W O
Shriners Hospitals for Crippled Children, Tampa, FL.
Yale J Biol Med. 1993 May-Jun;66(3):219-33.
Skeletal tissues from children sustaining acute skeletal trauma were analyzed with detailed radiologic and histologic techniques to assess the failure patterns of the developing skeleton. In the physis- and epiphysis-specific fracture propagation varied, usually going through the portion of the hypertrophic zone adjacent to the metaphysis. However, the physeal fracture in types 1 and 2 sometimes involved the germinal zone. There may also be microscopic propagation at oblique angles from the primary fracture plane, splitting cell columns apart longitudinally. The cartilage canals supplying the germinal zone appear to be "weak" areas into which the fracture may propagate, especially in infancy. Incomplete type 1 physeal fractures, which cannot be detected by routine radiography, may occur. Types 1, 2, and 4 physeal injuries may be comminuted. In type 3 injuries, discrete segments of physis that include the germinal zone may "adhere" to the metaphysis, separating the cells from their normal vascularity. In types 2 and 3, comminution may occur at the site of fracture redirection from the physis. Direct type 5 crushing of the physeal germinal zone does not occur, even in the presence of significant pressure-related changes within other areas of the epiphysis. Type 7 separation between cartilage and bone at any chondro-osseous epiphyseal interface may occur, but is similarly impossible to diagnose radiographically. In the metaphysis torus, fractures result from plastic deformation of the cortex, coupled with a partial microfracturing that may be difficult to visualize with clinical radiography. Some of the energy absorption may also be transmitted to the physis, causing metaphyseal hemorrhage adjacent to the growth plate and variable microscopic damage within the physis. In the diaphysis, the greenstick fracture is associated with longitudinal tensile failure through the developing osteons of the "intact" cortex. The inability of these failure patterns to "narrow" after the fracture force dissipates is the probable cause of retained bowing (plastic deformation). In both torus and greenstick fractures, the fractured bone ends show micro-splitting through the osteoid seams. In the diaphysis, metaphysis, and epiphyseal ossification center there may be areas of focal hemorrhage and microfracture that correlate with the reported MRI phenomenon of "bone bruising." Again, such injury cannot be diagnosed during routine radiography.
采用详细的放射学和组织学技术，对遭受急性骨骼创伤的儿童骨骼组织进行分析，以评估发育中骨骼的骨折模式。在生长板和骨骺处，骨折的扩展方式各不相同，通常穿过靠近干骺端的肥大带部分。然而，1型和2型生长板骨折有时会累及生发层。骨折也可能从主骨折平面以斜角进行微观扩展，将细胞柱纵向分开。供应生发层的软骨管似乎是骨折可能扩展进入的“薄弱”区域，尤其是在婴儿期。可能会发生常规X线摄影无法检测到的不完全1型生长板骨折。1型、2型和4型生长板损伤可能会粉碎。在3型损伤中，包括生发层的离散生长板节段可能会“附着”于干骺端，使细胞与正常血供分离。在2型和3型损伤中，骨折从生长板转向的部位可能会发生粉碎。即使在骨骺其他区域存在明显的压力相关变化，也不会发生直接的5型生长板生发层挤压伤。在任何软骨-骨骨骺界面都可能发生7型软骨与骨分离，但同样无法通过X线摄影诊断。在干骺端骨皮质增厚处，骨折是由皮质的塑性变形以及部分微骨折导致的，临床X线摄影可能难以显示这些微骨折。部分能量吸收也可能传递至生长板，导致生长板附近的干骺端出血以及生长板内不同程度的微观损伤。在骨干处，青枝骨折与通过“完整”皮质的发育中的骨单位的纵向拉伸破坏有关。骨折力消散后这些骨折模式无法“变窄”，可能是残留弯曲（塑性变形）的原因。在骨皮质增厚处骨折和青枝骨折中，骨折的骨端都显示出穿过类骨质缝的微裂。在骨干、干骺端和骨骺骨化中心可能存在局灶性出血和微骨折区域，这与报道的“骨挫伤”的MRI现象相关。同样，这种损伤在常规X线摄影时无法诊断。
