A Newly Identified lncRNA Axis Explains Delayed Tooth Eruption in Cleidocranial Dysplasia
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Summary
<img src="https://www.newswise.com/legacy/image.php?image=https://media.newswise.com/pio/articles/857703/6ae4950fbd2e8_1_857703.jpg&width=100&height=150" alt="Newswise image" />Delayed tooth eruption in cleidocranial dysplasia (CCD) has been linked to RUNX2 (Runt-related transcription factor 2) haploinsufficiency; however, the mechanisms by which this transcription factor regulates the bone-resorbing osteoclasts to create a pathway for tooth eruption remain poorly understood. This study shows that RUNX2 directly promotes osteoclast differentiation and alveolar bone resorption by activating a newly identified long noncoding RNA (lncRNA), LncRNA-ROD (Regulator of Osteoclast Differentiation). LncRNA-ROD sequesters Quaking (QKI) to stabilize Csf1r (colony-stimulating factor 1 receptor) mRNA, thereby supporting osteoclastogenesis. These findings link a CCD- associated gene to an RNA-protein regulatory axis that governs alveolar bone remodeling and identify a candidate therapeutic target for eruption disorders and broader bone loss.
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