Chondrocyte apoptosis enhanced at the growth plate: a physeal response to a diaphyseal fracture.
Post-traumatic overgrowth of growing long bones is a common clinical phenomenon in paediatric traumatology and is the result of an enhanced stimulation of the nearby growth plate after fracture. To date, the exact post-fractural reactions of the growth plate are poorly understood. The aim of this study has been to determine the impact of fracture on the frequency of chondrocyte apoptosis of the growth plate. Rats sustained a mid-diaphyseal closed fracture of the left tibia or were left untreated. All animals were killed 3, 10, 14 or 29 days after trauma. The left and right tibiae were harvested and apoptotic chondrocytes of the proximal tibial growth plate were detected by TUNEL staining. The apoptosis percentage of physeal chondrocytes was statistically compared among fractured bones, intact contra-lateral bones and control bones. The physeal apoptosis rate of the fractured bone was significantly higher than that of the contra-lateral intact bone (valid for all evaluated days) and the control bone (valid from day 10 onwards). Contra-lateral intact tibiae never showed significantly higher apoptosis rates compared with control tibiae. Thus, mid-diaphyseal fracture influences the nearby growth plate by stimulating chondrocyte programmed cell death, which is associated with cartilage resorption and bone replacement. The lack of a significant difference between the intact contra-lateral and the intact control bone suggests that fracture only has a local effect that contributes to the greater apoptosis rate of the adjacent physis.
Gaber
Sonja
S
Medical University of Graz, Clinic of Paediatric Surgery, Auenbruggerplatz 34, 8036 Graz, Austria.
Fischerauer
Eva Elisa
EE
Fröhlich
Eleonore
E
Janezic
Gregor
G
Amerstorfer
Florian
F
Weinberg
Annelie-Martina
AM
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D016022:Case-Control Studies; D019902:Chondrocytes / Q000166:cytology* / Q000473:pathology; D018483:Diaphyses / Q000166:cytology / Q000473:pathology; D004195:Disease Models, Animal; D017102:Fracture Healing / Q000502:physiology; D050723:Fractures, Bone / Q000473:pathology*; D006132:Growth Plate / Q000166:cytology* / Q000254:growth & development / Q000473:pathology; D020287:In Situ Nick-End Labeling; D008297:Male; D010784:Photomicrography; D051381:Rats; D017207:Rats, Sprague-Dawley; D013977:Tibia / Q000166:cytology* / Q000254:growth & development / Q000473:pathology