Patellar instability-induced bone loss in the femoral trochlea is associated with the activation of the JAK1/STAT3 signaling pathway in growing mice

PI-induced subchondral bone loss in the femoral trochlea and resulted in trochlear dysplasia in growing mice. This bone loss is associated with activation of the JAK1/STAT3 signaling pathway, which weakens the function of osteoblasts and stimulates both formation and function of osteoclasts.

Four-week-old male C57BL/6 mice were randomly divided into two groups (n = 50/group). Mice in the experimental group underwent surgery to induce PI. Distal femurs were collected 2 and 4 weeks after surgery (n = 25 knees/each time point, each group). Microcomputed tomography and histological observations were performed to investigate the morphology of the femoral trochlea and changes in bone mass. qPCR, western blot, and immunohistochemistry analyses were performed to evaluate the expression of JAK1, STAT3, RANKL, and OPG in subchondral bone. A t test was performed for the statistical analysis; a P value < 0.05 was considered to be statistically significant.

In the experimental group, subchondral bone loss in the femoral trochlea was observed two and four weeks after PI; morphological changes, such as a flatter trochlear groove and an increased sulcus angle, were observed in the femoral trochlea; qPCR, western blot, and immunohistochemistry analyses showed higher expression of JAK1, STAT3, and RANKL and lower expression of OPG (P < 0.05).