"decreasing 5-lipoxygenase (5-LO) activity during fracture healing increases cyclooxygenase-2 (COX-2) expression in the fracture callus, accelerates chondrogenesis and decreases healing time.
Bilateral, unicortical femoral defects were used in rats. The defect sites were filled with a polycaprolactone (PCL) scaffold containing 5-LO inhibitor (A-79175) at three dose levels, scaffold with drug carrier, or scaffold only. Drug release was assessed in vitro. Osteogenesis was assessed by micro-CT and histology at two endpoints of ten and 30 days.
A-79175, a 5-LO inhibitor, increased bone formation in an apparent dose-related manner."
"The principal function of 5-LO is to convert arachidonic acid into leukotriene A4, which is used to synthesise leukotriene B4 (LTB4) and the cysteinyl leukotrienes. LTB4 and the cysteinyl leukotrienes are lipid signalling molecules that affect many physiological processes, including inflammation, which is an early physiological response to fracture. Arachidonic acid is also the substrate for cyclooxygenase-1 and cyclooxygenase-2 (COX-2), which convert arachidonic acid into prostaglandin (PG)-H2. PGH2 is used to synthesise thromboxane A2, PGD2, PGE2, PGF2α, and PGI2."
"reduced 5-LO activity was associated with enhanced fracture healing, including elevated callus chondrogenesis, increased bone formation and elevated COX-2 expression."
The control group actually seems to have more cartilage.
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