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 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.
Adamczyk
Mark J
MJ
Children's Hospital Medical Center of Akron, Akron, OH 44302, USA.
Weiner
Dennis S
DS
Nugent
Ashleigh
A
McBurney
Denise
D
Horton
Walter E
WE
D000293:Adolescent; D017209:Apoptosis; D002648:Child; D019902:Chondrocytes / Q000378:metabolism / Q000648:ultrastructure*; D024043:Collagen Type II / Q000276:immunology / Q000378:metabolism; D004247:DNA / Q000032:analysis; D004839:Epiphyses, Slipped / Q000473:pathology*; D005260:Female; D005269:Femur / Q000648:ultrastructure*; D006132:Growth Plate / Q000648:ultrastructure*; D006801:Humans; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D008297:Male; D011509:Proteoglycans / Q000276:immunology / Q000378:metabolism
D024043:Collagen Type II; D011509:Proteoglycans; D004247:DNA