2010
DOI: 10.1097/prs.0b013e3181cb63a3
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Testing the Critical Size in Calvarial Bone Defects: Revisiting the Concept of a Critical-Size Defect

Abstract: Background-There is a clinical need for bone replacement strategies because of the shortfalls endemic to autologous bone grafting, especially in the pediatric patient population. For the past 25 years, the animal model that has been used to test bone replacement strategies has been the calvarial critical-sized defect (CSD), based on the initial size of the bone defect. This study was undertaken to test the concept of the critical-size in several different models. A review of the theoretical and scientific base… Show more

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Cited by 196 publications
(156 citation statements)
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“…1-A), then transplanted it into a nonhealing, critical-size skeletal defect 40 that was created in the calvarium of syngeneic host mice ( Fig. 1-B).…”
Section: Bone-marrow Grafts Have Osteogenic Potentialmentioning
confidence: 99%
“…1-A), then transplanted it into a nonhealing, critical-size skeletal defect 40 that was created in the calvarium of syngeneic host mice ( Fig. 1-B).…”
Section: Bone-marrow Grafts Have Osteogenic Potentialmentioning
confidence: 99%
“…19) . In the present study, a calvarial defect with 8 mm was created for the animal examination because this bone defect model has been used as a critical size in rat calvarial bone defects 20,21) . Bone formation in the calvarial defect model occurs under unloaded conditions.…”
Section: Histological Evaluationmentioning
confidence: 99%
“…Interestingly, the effects of A2AR activation are more ambiguous; A2AR stimulation promotes osteoblast proliferation but either has no effect on or inhibits osteoblast differentiation (20,21) or promotes differentiation of mesenchymal stem cells to adipocytes (22) but does alter osteoblast function by changing the ratio of RANKL/osteoprotegerin (OPG) expression both in vivo and in vitro (23). Here we determined whether A2AR stimulation or enhancing adenosine concentrations by blockade of purine transport into cells via ent1 with dipyridamole regulates bone formation in a critical size defect in murine calvaria (24).…”
mentioning
confidence: 99%