Osteoclasts are large,multinucleated cells that are responsible for the breakdown or resorption
of bone during bone remodelling. Studies have shown that certain fatty acids (FAs) can increase bone
formation, reduce bone loss, and influence total bone mass. Palmitoleic acid (PLA) is a 16-carbon,
monounsaturated FA that has shown anti-inflammatory properties similar to other FAs. The effects
of PLA in bone remain unexplored. Here we investigated the effects of PLA on receptor activator of
nuclear factor kappa B (NF- B) ligand (RANKL)-induced osteoclast formation and bone resorption in
RAW264.7 murine macrophages. PLA decreased the number of large, multinucleated tartrate resistant
acid phosphatase (TRAP) positive osteoclasts and furthermore, suppressed the osteolytic capability
of these osteoclasts. This was accompanied by a decrease in expression of resorption markers (Trap,
matrix metalloproteinase 9 (Mmp9), cathepsin K (Ctsk)). PLA further decreased the expression of genes
involved in the formation and function of osteoclasts. Additionally, PLA inhibited NF- B activity
and the activation of mitogen activated protein kinases (MAPK), c-Jun N-terminal kinase (JNK) and
extracellular signal–regulated kinase (ERK). Moreover, PLA induced apoptosis in mature osteoclasts.
This study reveals that PLA inhibits RANKL-induced osteoclast formation in RAW264.7 murine
macrophages through suppression of NF- B and MAPK signalling pathways. This may indicate that
PLA has potential as a therapeutic for bone diseases characterized by excessive osteoclast formation.