Altered Cellular Kinetics in the Growth Plate of the Femoral Head of Spontaneously Hypertensive Rats.
10.3349/ymj.2012.53.3.625
- Author:
Hoon PARK
1
;
Sun Young KONG
;
Hyun Woo KIM
Author Information
1. Department of Orthopaedic Surgery, Severance Children's Hospital, Yonsei University College of Medicine, Seoul, Korea. pedhkim@yuhs.ac
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
Spontaneous hypertensive rats;
growth plate;
avascular necrosis;
apoptosis;
vascular endothelial growth factor
- MeSH:
Animals;
Apoptosis;
Femur Head/metabolism/*pathology;
Femur Head Necrosis/metabolism/pathology;
Growth Plate/*cytology/metabolism;
Osteogenesis/physiology;
Rats;
Rats, Inbred SHR;
Rats, Sprague-Dawley;
Vascular Endothelial Growth Factor A/metabolism
- From:Yonsei Medical Journal
2012;53(3):625-633
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: Pathologic changes in the growth plate remain unknown in Legg-Calve-Perthes (LCP) disease. Spontaneously hypertensive rats have proven to be a good model for studying LCP disease. This study investigated the histopathologic changes and the expression of vascular endothelial growth factor in the growth plate of spontaneously hypertensive rats (SHR). MATERIALS AND METHODS: Sixty SHR rats were divided into two groups: those showing osteonecrosis (SHR+n group: 32), and those showing normal ossification (SHR-n group: 28). Thirty Wister Kyoto rats served as a control. For histomorphological measurement, the length of each zone of the growth plate was measured. Cell kinetics was measured by 5-bromo-2'-deoxyuridin (BrdU) immunohistochemistry and transferase-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL) assays. Vascular endothelial growth factor (VEGF) immunohistochemistry was used to identify of expression of VEGF. RESULTS: The lengths of growth plates of the SHR+n group were significantly shorter in the initial growth period than those of the other groups. The lowest proliferative rate and the highest apoptosis rate were observed in the SHR+n group at the initial growth period. The expression of VEGF in the growth plate of the SHR group was lower than the control group, and it was lower in the SHR+n group than in the SHR-n group. CONCLUSION: The growth plate of the SHR+n group was found to be affected by disease process of ischemic necrosis of the femoral head, and this might explain the relative overgrowth of the greater trochanter in the later stages of LCP disease.
