The Journal of Bone and Joint Surgery (American). 2009;91:1149-1158.
doi:10.2106/JBJS.H.00654
© 2009 The Journal of Bone and Joint Surgery, Inc.
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Effects of Disruption of Epiphyseal Vasculature on the Proximal Femoral Growth Plate

Harry K.W. Kim, MD, MSc, FRCSC1, Natalie Stephenson, BSc2, Amanda Garces2, James Aya-ay, MS2 and Haikuo Bian, MD2

1 Texas Scottish Rite Hospital for Children, 2222 Welborn Street, Dallas, TX 75219. E-mail address: harry.kim{at}tsrh.org
2 Shriners Hospitals for Children, 12502 Pine Drive, Tampa, FL 33612

Investigation performed at the Shriners Hospitals for Children, Tampa, Florida

Disclosure: In support of their research for or preparation of this work, one or more of the authors received, in any one year, outside funding or grants in excess of $10,000 from Shriners Hospitals for Children. Neither they nor a member of their immediate families received payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity. No commercial entity paid or directed, or agreed to pay or direct, any benefits to any research fund, foundation, division, center, clinical practice, or other charitable or nonprofit organization with which the authors, or a member of their immediate families, are affiliated or associated.

Background: Proximal femoral growth disturbance is a major complication associated with ischemic osteonecrotic conditions, such as Legg-Calvè-Perthes disease. The extent of ischemic damage and the mechanisms by which ischemic injury to the growing femoral head produces growth disturbance of the proximal femoral growth plate remain unclear. The purpose of this study was to investigate the effects of disruption of the epiphyseal vasculature on the morphology and function of the proximal femoral growth plate in a porcine model.

Methods: Ischemic osteonecrosis of the femoral head was surgically induced in sixty-five piglets by placing a ligature tightly around the femoral neck. Radiographic, histological, micro-computed tomographic, cellular viability, hypoxia marker, and cellular proliferation studies were performed.

Results: Disruption of the epiphyseal vasculature did not lead to diffuse growth plate damage in the majority of the ischemic femoral heads. One of the twelve femoral heads analyzed at four weeks and six of the twenty-six femoral heads analyzed at eight weeks had severe disruption of the growth plate that precluded histological assessment of the growth plate zones. In the remaining animals, the proximal part of the femur continued to elongate following induction of ischemia, albeit at a slower rate than on the normal side. Histologically, normal developmental thinning of the growth plate was seen to be absent on the ischemic side. Severe hypoxia and cellular death were limited to the area of the growth plate bordering on the infarcted osseous epiphysis. Normal chondrocytic organization and continued proliferation were observed in the proliferative zone of the growth plate.

Conclusions: In our porcine model, the proximal femoral growth plate was not diffusely damaged following disruption of the epiphyseal vasculature in the majority of the ischemic femoral heads. The majority of the growth plates remained viable and were able to function despite total disruption of the epiphyseal vasculature. These findings suggest that the source of nutrition for the proximal femoral growth plate is not solely the epiphyseal vasculature as has been traditionally believed.

Clinical Relevance: Longitudinal growth, albeit at a slower rate, may be expected from the majority of proximal femoral growth plates even when there is a total infarction of the osseous epiphysis.


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