Histopathologic changes in growth-plate cartilage following ischemic necrosis of the capital femoral epiphysis - An experimental investigation in immature pigs
Histopathologic changes in growth-plate cartilage following ischemic necrosis of the capital femoral epiphysis - An experimental investigation in immature pigs
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DOI：
10.2106/00004623-200105000-00007
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发表时间：
2001-05-01
影响因子：
5.3
通讯作者：
Qiu, YS
中科院分区：
文献类型：
--
作者：
Kim, HKW;Su, PH;Qiu, YS
背景：发育中的股骨头骨骺由次级骨化中心组成，周围环绕着骺软骨。在骺软骨和次级骨化中心之间是生长板，其有助于次级骨化中心在发育期间尺寸的周向增加。本研究的主要目的是描述未成熟猪股骨头骨骺缺血性坏死诱导后的早期和修复阶段，次级骨化中心周围生长板中发生的组织病理学变化。在18只小猪中，通过在股骨颈周围放置不可吸收的缝线结扎，诱导股骨头骨骺缺血性坏死，关节囊切开术和圆韧带横断术。诱导缺血后3天至8周处死动物，进行视觉、影像学和组织学评估。结果：诱导缺血性坏死后2 ~ 4周，次级骨化中心周围的生长板坏死。观察到的组织病理学变化包括软骨细胞死亡、坏死生长板软骨基质的番红-O染色丧失、终末肥大软骨细胞无血管浸润以及原发性海绵体数量减少，表明软骨内骨化停止。在修复阶段，在术后4 - 8周，在坏死生长板软骨周围的骺软骨中观察到软骨细胞簇和强烈的番红-O染色。在股骨头的周边区域，围绕次级骨化中心的坏死生长板软骨被来自骨髓腔的纤维血管组织再吸收。到6周时，在周围骺软骨中观察到新的骨化辅助中心和恢复的软骨内骨化。新的骨化中心促成了第二骨化中心的碎片化影像学表现。在大多数动物中，骨骺基本上是正常的，尽管18只小猪中有5只表现出轻度或中度的组织病理学变化。结论：在这个模型中，股骨头骨骺缺血性坏死导致次级骨化中心周围的生长板坏死。小的新的异位骨化中心出现在骨骺软骨，部分解释了破碎的影像学外观的第二个中心的骨化。临床相关性：这个不成熟的猪模型可能有助于系统研究的细胞和结构的事件，缺血性损伤后的资本股骨头骨骺的顺序。更好地理解缺血后的损伤和修复过程，可能会导致新的治疗策略，以刺激梗死的股骨头骨骺的修复，并恢复骨化的二级中心的正常生长。
Background: The developing capital femoral epiphysis consists of a secondary center of ossification surrounded by epiphyseal cartilage. Between the epiphyseal cartilage and the secondary center of ossification is a growth plate, which contributes to the circumferential increase in size of the secondary center of ossification during development. The main objective of this study was to describe the histopathologic changes that occur in the growth plate surrounding the secondary center of ossification during the early and reparative phases following the induction of ischemic necrosis of the capital femoral epiphysis in immature pigs.Methods: Ischemic necrosis of the capital femoral epiphysis was induced in eighteen piglets by placing a nonabsorbable suture ligature around the femoral neck following a capsulotomy and transection of the ligamentum teres. The animals were killed three days to eight weeks following the induction of ischemia,and visual, radiographic, and histologic assessments were performed.Results: Two to four weeks after the induction of ischemic necrosis, the growth plate surrounding the secondary center of ossification became necrotic. The observed histopathologic changes included chondrocyte death, loss of safranin-O staining of the matrix of the necrotic growth-plate cartilage, an absence of vascular invasion of terminal hypertrophic chondrocytes, and a decrease in the amount of primary spongiosa, indicating cessation of endochondral ossification. In the reparative phase, at four to eight weeks postoperatively, chondrocyte clusters and intense safranin-O staining were observed in the epiphyseal cartilage around the necrotic growth-plate cartilage. in the peripheral region of the femoral head, necrotic growth-plate cartilage surrounding the secondary center of ossification was resorbed by a fibrovascular tissue from the marrow space. By six weeks, new accessory centers of ossification with restored endochondral ossification were observed in the peripheral epiphyseal cartilage. New ossification centers contributed to the fragmented radiographic appearance of the secondary center of ossification. The physis appeared essentially normal in most animals, although five of the eighteen piglets showed mild or moderate histopathologic changes.Conclusions: In this model, ischemic necrosis of the capital femoral epiphysis resulted in necrosis of the growth plate surrounding the secondary center of ossification.: Small new ectopic centers of ossification appeared in the epiphyseal cartilage, explaining in part the fragmented radiographic appearance of the secondary center of ossification.Clinical Relevance: This immature swine model may facilitate systematic study of the sequence of cellular and structural events that follow ischemic injury to the capital femoral epiphysis. Better understanding of the injury and repair processes:;that follow ischemia may lead to novel treatment strategies to stimulate the repair of the infarcted capital femoral epiphysis and to restore normal growth of the secondary center of ossification.