Aspirin is a cyclooxygenase inhibitor commonly used in primary prevention of cardiovascular diseases and cancers. Its users are elderly population susceptible to osteoporosis. It also inhibits the synthesis of prostaglandin E<sub>2</sub> essential in bone remodeling. This prompts the question...
Evidence from cellular and animal studies suggests that
aspirin possesses bone protective effects. Aspirin is able to promote the survival of osteoblast precursor stem cells and differentiation of osteoblast. It also inhibits the NF
κB pathway, reduces the expression of RANKL, and increases OPG, thus suppressing the differentiation of osteoclast. Thus, bone health deterioration is prevented in aspirin-treated animal subjected to bone loss. The skeletal effects of aspirin in human are limited and inconclusive.
Aspirin may increase bone mineral density of the users, but this does not translate to fracture prevention. Data from more large-scale prospective epidemiological studies are essential in validating the relationship between the use of aspirin and fracture.