Enhanced osteonectin expression in the chondroid matrix of the unloaded mandibular condyle.

Osteonectin provided a spatial and temporal marker for proliferating and differentiating chondrocytes, and during the chondroid matrix formation. The goal of this investigation was to examine early cellular and molecular regulation of mandibular growth. Unloading was induced by anterior functional mastication. The proliferative activity measured by tritiated thymidine incorporation increased 8. 3-fold at 24 hours compared with the corresponding control group. Mandibular unloading for 24 hours increased osteonectin mRNA expression 60% in the condyle over the corresponding control group. Microscopic inspection of the condyle demonstrated osteonectin immunostaining of proliferating, early hypertrophic chondrocytes, and the chondroid matrix across the sagittal section in an anterior-posterior direction. An increasing gradient intensity from a medial-superior to posterior direction was produced with treatment in direct contrast to the control group. The posterior chondroid matrix immunostaining increased 11.7-fold (P = 0.038) after 24 hours treatment over a corresponding control group. Unloading of the mouse mandible caused an increased cellular proliferation, a coincident increase of osteonectin mRNA, and a subsequent increased secretion of the osteonectin protein in the chondroid matrix formation.