Introduction: Patellar instability (PI) is closely correlated with bone loss in the developmental femoral trochlea. However, the molecular mechanism of PI-induced bone loss is not precise. Methods: Four-week-old male C57BL/6 mice were randomly divided into two groups. Mice in the experimental group underwent surgery to induce patellar instability. Distal femurs were collected at 2 and 4 weeks after surgery. Micro-computed tomography and histological observations were conducted to investigate the morphology of the femoral trochlea and the change in bone mass. qPCR, western blot, and immunohistochemistry analyses were performed to evaluate the expression of JAK1 and STAT3 in the subchondral bone.Results: Subchondral bone loss in the femoral trochlea was observed beginning two weeks after surgery in the experimental group and deteriorated over time, with higher expression of JAK1, STAT3, and RANKL, and lower expression of OPG, which resulted in morphological changes in the femoral trochlea, such as a flatter trochlear groove and a larger sulcus angle.Conclusion: Patellar instability could induce subchondral bone loss in developmental femoral trochlea and result in trochlear dysplasia finally with the activation of the JAK1/STAT3 signaling pathway. This study gives insights into the mechanism of bone loss in developmental trochlear dysplasia.