In vitroandin vivoeffects of antibiotics on bone cell metabolism and fracture healing

Current research suggests that these negative results could be due to direct effects of antibiotics on mitochondrial physiology within mammalian cells. Treatment doses of antibiotics, especially those released from topical delivery systems such as bone cements, result in antibiotic concentrations thousands of times higher than those required to inhibit bacterial growth. Our findings suggest a need to develop current antibiotic delivery systems to elute sufficient doses to inhibit bacterial growth without negative effects on bone physiology and fracture repair processes.