Unbalanced occlusal loading elicited remodeling responses in growing rat temporomandibular joints and Notch1/Hes1...

We aimed to assess the impact of unbalanced occlusal loading on the TMJ and the expression of the Notch1/Hes1 signaling pathway using a unilateral occlusal loss rat model.

We established a unilateral occlusal defect animal model. At three different times, all female Wistar rats were randomized into three groups (4 weeks, 6 weeks, and 10 weeks): (1) unilateral occlusal loss experiment group (extraction of the left mandibular molars and trimming of the left mandibular incisors every other day), (2) restoring incisal occlusion experiment group (extraction of the left mandibular molars and trimming of the left mandibular incisors every other day for 4 weeks, and then the incisor trimming was stopped until 10 weeks), (3) control group (normal loading). Micro-CT, histological staining, immunofluorescence, immunohistochemistry, and real-time quantitative polymerase chain reaction were used to identify changes in condylar cartilage, subchondral bone, and articular discs.

Temporomandibular joint condylar cartilage degradation was induced by unbalanced occlusal loading, especially on the extraction side. The dropped cartilage thickness, Cyclin D1 positive chondrocytes, TB staining and collagen II positive areas, the decreased expression levels of Notch1, Jagged1, and Hes1 in condylar cartilage, the loss of TMJ subchondral bone were all reversed in the restoring incisal occlusion experiment group at 6 weeks. The experiment group exhibited catabolic degradative alterations at the molecular level in TMJ discs, showing a notable decrease in the mRNA expression levels of Col I, Col II, and ALP.

The growing rat TMJ condyle exhibits a significant remodeling capacity in altered occlusal loading, which can be degenerative and recuperative, respectively, in reaction to decreased occlusal loading and restored occlusal loading. Appropriate occlusal loading is essential for transducing the Notch1/Hes1 signaling pathway and normal metabolism of the TMJ disc.