Fracture healing is a process independent of p53 function.
We studied the role of the tumor suppressor gene p53 in the process of fracture healing using mice with a p53 gene deficiency. Fractures produced in femoral shafts of mice without a functional p53 gene (p53-/-) healed as well as those in wildtype mice (p53 +/+), and no tumor development was observed at the fracture site even after complete bone union. Formation of granulation tissue and cartilage, ossification and remodeling into mature trabecular and cortical bone showed no abnormalities in p53-/- mice. Apoptotic cells were found to be sparse in the ossifying zone of the fracture callus using in situ DNA nick end-labeling in mice of both genotypes, without any significant difference. These results indicate that apoptosis in fracture healing, even if it does play a significant role, occurs through a p53-independent pathway.
Nakayama
T
T
Department of Orthopaedic Surgery, Faculty of Medicine, Kyoto University, Japan.
Toguchida
J
J
Wadayama
B
B
Kanoe
H
H
Aizawa
S
S
Sasaki
M S
MS
Nakamura
T
T
D000818:Animals; D017209:Apoptosis / Q000502:physiology; D001842:Bone and Bones / Q000166:cytology / Q000378:metabolism; D005264:Femoral Fractures / Q000378:metabolism*; D017102:Fracture Healing / Q000502:physiology*; D006651:Histocytochemistry; D017403:In Situ Hybridization; D051379:Mice; D008822:Mice, Transgenic; D011871:Radiology; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000494:pharmacology*
D016159:Tumor Suppressor Protein p53