Abstract
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 E2 essential in bone remodeling. This prompts the question whether it can influence bone health among users. This review aimed to summarize the current literature on the use of aspirin on bone health. A literature search on experimental and clinical evidence on the effects of aspirin on bone health was performed using major scientific databases. In vitro studies showed that aspirin could enhance the survival of bone marrow mesenchymal stem cells, the progenitors of osteoblasts, and stimulate the differentiation of preosteoblasts. Aspirin also inhibited the nuclear factor kappa-B (NFκB) pathway and decreased the expression of receptor activator of NFκB ligand, thus suppressing the formation of osteoclast. Aspirin could prevent bone loss in animal models of osteoporosis. Despite a positive effect on bone mineral density, the limited human epidemiological studies revealed that aspirin could not reduce fracture risk. A study even suggested that the use of aspirin increased fracture risk. As a conclusion, aspirin may increase bone mineral density but its effect on fracture prevention is inconclusive. More data are needed to determine the effects of aspirin and bone health in human.
Highlights
Homeostasis of the skeletal tissue is controlled by three types of bone cells from different lineages
Osteoclasts in command of bone resorption are derived from haematopoietic stem cells and they expressed unique markers such as calcitonin receptor (CTR), tartrateresistant acid phosphatase (TRAP), and cathepsin-K (CTSK)
Osteoblasts secrete receptor activator of nuclear factor kappa-B (RANK) ligand (RANKL), which binds with RANK on preosteoclasts and stimulates their differentiation into osteoclasts
Summary
Homeostasis of the skeletal tissue is controlled by three types of bone cells from different lineages. Osteoblasts responsible for bone formation are derived from mesenchymal stem cells expressing transcription factors runt-related factor 2 and osterix. Osteoclasts in command of bone resorption are derived from haematopoietic stem cells and they expressed unique markers such as calcitonin receptor (CTR), tartrateresistant acid phosphatase (TRAP), and cathepsin-K (CTSK). Osteocytes are terminally differentiated osteoblasts sepulchered in the bone matrix and they are capable of both building and digesting the bone and influencing the activities of other bone cells. Osteoblasts secrete receptor activator of nuclear factor kappa-B (RANK) ligand (RANKL), which binds with RANK on preosteoclasts and stimulates their differentiation into osteoclasts. Osteoblasts release osteoprotegerin (OPG) acting as a decoy receptor to bind with RANKL, inhibiting the differentiation of osteoclasts (reviewed in [1, 2])
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