Primary cilia regulate limb and axial skeletal formation and hedgehog signaling, 
but their roles in temporomandibular joint (TMJ) development are unknown. Thus, 
we created conditional mouse mutants deficient in ciliary transport protein 
Kif3a in cartilage. In post-natal wild-type mice, primary cilia were 
occasionally observed on the superior, inferior, or lateral side of condylar 
cells. Cilia were barely detectable in mutant chondrocytes but were evident in 
surrounding tissues, attesting to the specificity of chondrocyte Kif3a ablation. 
Mutant condyles from 3-month-old mice were narrow and flat along their 
antero-posterior and medio-lateral axes, were often fused with the articular 
disc, and displayed an irregular bony surface. The polymorphic layer in P15 
mutants contained fewer Sox9-expressing chondroprogenitor cells because of 
reduced mitotic activity, and newly differentiated chondrocytes underwent 
precocious hypertrophic enlargement accompanied by early activation of Indian 
hedgehog (Ihh). Interestingly, there was excessive intramembranous ossification 
along the perichondrium, accompanied by local expression of the hedgehog 
receptor Patched-1 and up-regulation of Osterix and Collagen I. In summary, 
Kif3a and primary cilia are required for coordination of chondrocyte maturation, 
intramembranous bone formation, and chondrogenic condylar growth. Defects in 
these processes in Kif3a condylar cartilage are likely to reflect abnormal 
hedgehog signaling topography and dysfunction.