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Updated: Jan 6, 2026

Less-Invasive Technique for Non-stabilized Mandibular Fracture in Mouse Models
Published on: September 27, 2024
Biomechanically stimulated chondrocytes promote osteoclastic bone resorption in the mandibular condyle
Bin Kuang1, Zhaobin Zeng2, Qing Qin3
1Department of Stomatology, First People's Hospital, Lanzhou, 730050, China.
Objective:
Chondrocyte signaling is important in osteoclastic bone resorption in mice tibiae. The present study aimed to test whether biomechanically stimulated chondrocytes promote osteoclastic bone resorption in the mandibular condyle.
Methods:
Primary chondrocytes isolated from rat condylar cartilage were stimulated by fluid flow shear stress (FSS) for 30, 60, 120 min at intensities of 10, 20, or 30 dynes/cm2. The levels of pro-osteoclastic factors and pro-osteoclastic function of FSS-stimulated chondrocytes were tested. Abnormal molar occlusion was established in rats, and the relationship between cartilage degeneration and osteoclastogenesis in the subchondral bone of the mandibular condyle, and the expression of pro-osteoclastic factors in condylar cartilage, were evaluated.
Results:
The mRNA and protein levels of SDF-1 and TGFβ-1 increased significantly in all FSS-treated groups; the levels of RANKL and RANKL:OPG increased in all intensities and in 60 and 120 min of FSS; and those of Wnt5 A increased in all time-points and in 20 and 30 dynes/cm2 of FSS-treated groups (all compared with their levels the controls; P < 0.05). The percent area of degenerative cartilage changes correlated positively with osteoclast number and osteoclast surface/bone surface in the mandibular condyles of abnormal occlusion rats (P < 0.05). Abnormal occlusion increased the immune-positive area and the mRNA expression levels of Sdf1, Tgfb1, Rankl, Wnt5a and the RANKL:OPG ratio in rat condylar cartilage compared with those in the controls (all P < 0.05).
Conclusion:
Chondrocytes under mechanical stimulation could express higher levels of pro-osteoclastic factors and induced condylar subchondral bone resorption by promoting osteoclastogenesis.
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