生长板损伤的磁共振诊断及其进展

生长板是长骨末端的软骨组织,是骨骼生长发育的基础.生长板损伤是儿童青少年较常见的骨科损伤之一,约占其长骨骨折的6%～30%[1],其后期形成的骨桥可导致生长板早闭和肢体短缩或成角畸形[2],影响儿童的生长发育.此外,感染、肿瘤、损伤后缺血坏死等因素也均可造成生长板损伤.

Salter-Harris fractures 骺离骨折

Salter-Harris fractures,.pediatric fractures invo-lving the growth plate (physis) of bones.The majority heal without growth impairment, however some lead to clinically important shortening and angulation.Growth disorders are a result of a destruction of the epiphyseal circulation (inhibits physeal growth) or by formation of a bone bridge across the physis.TypeⅠ:transverse fracture through physis (increased physeal width) (6% ncidence).Healing is rapid,usually within 2～3 weeks, complications are rare.TypeⅡ: Through physis and metaphysic (most common type) (75% incidence).Healing is rapid,and growth is rarely disturbed; an exception to this are fractures of the distal emur and tibia.

Insufficient insulin production or action in diabetic states is associated with growth retardation and impaired bone healing, while the underling mechanisms are unknown. In this study, we sought to define the role of insulin signaling in the growth plate. Insulin treatment of embryonic metatarsal bones from wild-type mice increased chondrocyte proliferation. Mice lacking insulin receptor (IR) selectively in chondrocytes (CartIR2/2) had no discernable differences in total femoral length compared to control littermates. However, CartIR2/2 mice exhibited an increase in chondrocyte numbers in the growth plate than that of the controls. Chondrocytes lacking IR had elevated insulin-like growth factor (IGF)-1R mRNA and protein levels. Subsequently, IGF-1 induced phosphorylation of Akt and ERK was enhanced, while this action was eliminated when the cells were treated with IGF-1R inhibitor Picropodophyllin. Deletion of the IR impaired chondrogenic differentiation, and the effect could not be restored by treatment of insulin, but partially rescued by IGF-1 treatment. Intriguingly, the size of hypertrophic chondrocytes was smaller in CartIR2/2 mice when compared with that of the control littermates, which was associated with upregulation of tuberous sclerosis complex 2 (TSC2). These results suggest that deletion of the IR in chondrocytes sensitizes IGF-1R signaling and action, IR and IGF-1R coordinate to regulate the proliferation, differentiation and hypertrophy of growth plate chondrocytes.

NF-κBp50/p52 double knockout (dKO) and RANK KO mice have no osteoclasts and develop severe osteopetrosis associated with dwarfism. In contrast, Op/Op mice, which form few osteoclasts, and Src KO mice, which have osteoclasts with defective resorptive function, are osteopetrotic, but they are not dwarfed. Here, we compared the morphologic features of long bones from p50/p52 dKO, RANK KO, Op/Op and Src KO mice to attempt to explain the differences in their long bone lengths. We found that growth plates in p50/p52 dKO and RANK KO mice are significantly thicker than those in WT mice due to a 2-3-fold increase in the hypertrophic chondrocyte zone associated with normal a proliferative chondrocyte zone. This growth plate abnormality disappears when animals become older, but their dwarfism persists. Op/Op or Src KO mice have relatively normal growth plate morphology. In-situ hybridization study of long bones from p50/p52 dKO mice showed marked thickening of the growth plate region containing type 10 collagen-expressing chondrocytes. Treatment of micro-mass chondrocyte cultures with RANKL did not affect expression levels of type 2 collagen and Sox9, markers for proliferative chondrocytes, but RANKL reduced the number of type 10 collagen-expressing hypertrophic chondrocytes. Thus, RANK/NF-κB signaling plays a regulatory role in post-natal endochondral ossification that maintains hypertrophic conversion and prevents dwarfism in normal mice.