Osteoporosis is a major concern worldwide and can be attributed to an imbalance between

osteoblastic bone formation and osteoclastic bone resorption due to the natural aging process.

Heritable factors account for 60–80% of optimal bone mineralization; however, the finer details of

pathogenesis remain to be elucidated. Micro RNA (miRNA) and long-non-coding RNA (lncRNA)

are two targets that have recently come into the spotlight due to their ability to control gene

expression at the post-transcriptional level and provide epigenetic modification. miRNAs are a class

of non-coding RNAs that are approximately 18–25 nucleotides long. It is thought that up to 60% of

human protein-coding genes may be regulated by miRNAs. They have been found to regulate gene

expression that controls osteoblast-dependent bone formation and osteoclast-related bone remodeling.

lncRNAs are highly structured RNA transcripts longer than 200 nucleotides that do not translate

into proteins. They have very complex secondary and tertiary structures and the same degradation

processes as messenger RNAs. The fact that they have a rapid turnover is due to their sponge

function in binding the miRNAs that lead to a degradation of the lncRNA itself. They can act as

signaling, decoy, and framework molecules, or as primers. Current evidence suggests that lncRNAs

can act as chromatin and transcriptional as well as post-transcriptional regulators. With regards to

osteoporosis, lncRNA is thought to be involved in the proliferation, apoptosis, and inflammatory

response of the bone. This review, which is based on a systematic appraisal of the current literature,

provides current molecular and genetic opinions on the roles of miRNAs and lncRNAs in osteoporosis.

Further research into the epigenetic modification and the regulatory roles of these molecules will bring

us closer to potential disease-modifying treatment for osteoporosis.