The periodontal ligament (PDL) is a mechanosensitive noncalcified fibrous tissue connecting the cementum of the tooth and the alveolar bone. Here, we report that scleraxis (Scx) and osterix (Osx) antagonistically regulate tensile force-responsive PDL fibrogenesis and osteogenesis. In the developing PDL, Scx was induced during tooth eruption and co-expressed with Osx. Scx was highly expressed in elongated fibroblastic cells aligned along collagen fibers, whereas Osx was highly expressed in the perialveolar/apical osteogenic cells. In an experimental model of tooth movement, Scx and Osx expression was significantly upregulated in parallel with the activation of bone morphogenetic protein (BMP) signaling on the tension side, in which bone formation compensates for the widened PDL space away from the bone under tensile force by tooth movement.

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Tenascin‐like molecule major (Ten‐m)/odd Oz (Odz), a type II transmembrane molecule, is well known to modulate neural development. We have reported that Ten‐m/Odz3 is expressed in cartilaginous tissues and cells. Actin cytoskeleton and its regulator ras homolog gene family member A (RhoA) are closely associated with chondrogenesis. The present study aimed to evaluate the function and molecular mechanism of Ten‐m/Odz3 during chondrogenesis, focusing on RhoA and the actin cytoskeleton. Ten‐m/Odz3 was expressed in precartilaginous condensing mesenchyme in mouse limb buds. Ten‐m/Odz3 knockdown in ATDC5 induced actin cytoskeleton reorganization and change of cell shape through modulation of RhoA activity and FGF2 expression. Ten‐m/Odz3 knockdown suppressed ATDC5 migration and expression of genes associated with chondrogenesis, such as Sox9 and type II collagen, via RhoA. On the other hand, Ten‐m/Odz3 knockdown inhibited proliferation of ATDC5 in a RhoA‐independent manner. These findings suggest that Ten‐m/Odz3 plays an important role in early chondrogenesis regulating RhoA‐mediated actin reorganization.