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Depressed osteoblast activity and increased osteocyte necrosis after closed bone fracture and hemorrhagic shock
M W Wichmann1, S P Arnoczky, C M DeMaso
1Department of Surgery, Michigan State University, East Lansing, USA.
Background:
Although bone fracture and hemorrhagic shock are frequent complications in trauma patients, it remains unknown whether hemorrhagic shock after bone fracture produces any deleterious effects on osteoblast function and osteocyte necrosis.
Methods:
Sham-operation, closed bone fracture (right tibia) with and without hemorrhagic shock (mean arterial blood pressure 35 +/- 5 mm Hg for 90 minutes followed by fluid resuscitation) were induced in 18 male C3H/HeN mice (25 g body weight) At 72 hours after the experiment, all animals were killed, whole blood was obtained by cardiac puncture, and plasma assayed for circulating levels of osteocalcin.
Results:
Plasma osteocalcin levels were found to be significantly depressed after closed bone fracture in conjunction with hemorrhagic shock. Closed bone fracture alone increased plasma osteocalcin. Histologic analysis of the fracture sites revealed that hemorrhagic shock after closed bone fracture significantly increased osteocyte necrosis adjacent to the fracture site, when compared to animals with closed bone fracture alone.
Conclusions:
These findings suggest that severe hemorrhage after closed bone fracture depresses osteoblast activity and increases osteocyte necrosis, which should compromise fracture healing under those conditions.