Altered loading is an important etiological factor for temporomandibular joint (TMJ) disorders. Studies examining altered loading of the TMJ have been done in rats but the response of the TMJ to altered loading in mice is largely unknown. Therefore, due to the potential usefulness of genetically engineered mice, the goal of this study was to develop a mouse TMJ altered functional loading model.
One hundred and thirty four, 21-day-old CD-1 female mice were divided into two groups: (1) normal loading (hard pellet diet) for 2-6 weeks and (2) altered functional loading (incisor trimming every other day and soft dough diet) for 2-6 weeks. The mandibular condylar cartilage was evaluated by histology, the subchondral bone was evaluated by microcomputed tomography (micro-CT) analysis and gene expression was evaluated by real time polymerase chain reaction (PCR) analysis.
Altered functional loading for 2-6 weeks caused significant reduction in the thickness of the condylar cartilage whereas, only at 4 weeks was there a significant decrease in the bone volume fraction and trabecular thickness of the subchondral bone. Gene expression analysis showed that altered functional loading for 4 weeks caused a significant reduction in the expression of SRY-box containing gene 9 (Sox9), Collagen type X (Col X), Indian hedgehog (Ihh), Collagen type II (Col II) and Vascular endothelial growth factor (Vegf) and altered loading for 6 weeks caused a significant decrease in the expression of Sox9, Col II, Vegf and Receptor activator of NF-kappaB ligand (Rankl) compared to the normal loading group.
Altered functional TMJ loading in mice for 2-6 weeks leads to a loss of the condylar cartilage and a transient loss in the density of the mandibular condylar subchondral bone.