Fig. 9
From: RUNX2 is essential for maintaining synchondrosis chondrocytes and cranial base growth
RUNX2 is a critical regulator of cranial base synchondrosis organization, maintenance, and fusion. a Postnatal Runx2 deletion causes aberrant development of the craniofacial complex, leading to reductions in anteroposterior elongation, cranial base and vault lengths, and skull width. b Runx2 deletion in synchondrosis chondrocytes causes degradation and premature ossification of the postnatal cranial base synchondroses via reduced cell proliferation, increased chondrocyte hypertrophy and death, osteoclastogenesis associated with localized angiogenesis and FGFR3 downstream signaling, leading to aberrant endochondral ossification and gross craniofacial structural deficiencies
