Increased chondrocyte apoptosis in growth plates from children with slipped capital femoral epiphysis

Ultrastructural studies of slipped capital femoral epiphysis (SCFE) growth plates have shown diminished cellularity and marked distortion of the architecture in the proliferative and hypertrophic zones. Chondrocyte degeneration and death were noted at all levels of the hypertrophic and proliferative...

Full description

Saved in:
Bibliographic Details
Published inJournal of pediatric orthopaedics Vol. 25; no. 4; p. 440
Main Authors Adamczyk, Mark J, Weiner, Dennis S, Nugent, Ashleigh, McBurney, Denise, Horton, Jr, Walter E
Format Journal Article
LanguageEnglish
Published United States 01.07.2005
Subjects
Adolescent
Apoptosis
Child
Chondrocytes - metabolism
Chondrocytes - ultrastructure
Collagen Type II - immunology
Collagen Type II - metabolism
DNA - analysis
Epiphyses, Slipped - pathology
Female
Femur - ultrastructure
Growth Plate - ultrastructure
Humans
Immunohistochemistry
In Situ Nick-End Labeling
Male
Proteoglycans - immunology
Proteoglycans - metabolism
Online AccessGet more information

Cover

More Information
Summary:Ultrastructural studies of slipped capital femoral epiphysis (SCFE) growth plates have shown diminished cellularity and marked distortion of the architecture in the proliferative and hypertrophic zones. Chondrocyte degeneration and death were noted at all levels of the hypertrophic and proliferative zones, suggesting an accelerated disturbance in the life-to-death cycle of the chondrocytes. The current study examines the mechanism responsible for the diminished cell number and whether increased programmed cell death (apoptosis) or necrosis was operative. Proximal femoral growth plates from patients with SCFE (three patients) were prepared and sectioned for histochemistry, in situ detection of apoptosis, and immunohistochemistry. The results showed that the diminished cell number is due to an abnormal frequency and distribution of chondrocytes undergoing apoptosis. Although it is unclear whether the increased apoptosis is occurring early or late in the disease, it is highly likely that it is directly linked to pathogenesis.
ISSN:0271-6798
DOI:10.1097/01.mph.0000165138.60991.mL