Abstract
BACKGROUND CONTEXT: The process of osteogenesis after spinal arthrodesis is similar to that which occurs during fracture healing and heterotopic ossification. Previous work with fracture healing models has demonstrated increased healing rates with 5-lipoxygenase inhibition, which increases the cyclooxygenase pathway leading to increased prostaglandin formation. Although arachidonic acid metabolism has been shown to play a central role in fracture healing, little is known about the effects of modulation of the arachidonic acid pathway on spinal fusion healing.
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