Background: Increased tibial tuberosity–trochlear groove (TT-TG) distance is an important indicator of medial tibial tubercle transfer in the surgical management of lateral patellar dislocation (LPD). Changes to TT-TG distance are determined by a combination of several anatomical factors. Purpose: To (1) determine the anatomical components related to increased TT-TG distance and (2) quantify the contribution of each to identify the most prominent component. Study Design: Case-control study; Level of evidence, 3. Methods: Included were 80 patients with recurrent LPD and 80 age- and body mass index–matched controls. The 2 groups were compared in TT-TG distance and its related anatomical components: tibial tubercle lateralization (TTL), trochlear groove medialization, femoral anteversion, tibiofemoral rotation (TFR), tibial torsion, and mechanical axis deviation (MAD). The Pearson correlation coefficient ( r) was calculated to evaluate the association between increased TT-TG distance and its anatomical parameters, and factors that met the inclusion criteria of P < .05 and r ≥ 0.30 were analyzed via stepwise multivariable linear regression analysis to predict TT-TG distance. Results: The LPD and control groups differed significantly in TT-TG distance, TTL, TFR, and MAD ( P < .001 for all). Increased TT-TG distance was significantly positively correlated with TTL ( r = 0.376; P < .001), femoral anteversion ( r = 0.166; P = .036), TFR ( r = 0.574; P < .001), and MAD ( r = 0.415; P < .001), and it was signficantly negatively correlated with trochlear groove medialization ( r = −0.178; P = .024). The stepwise multivariable analysis revealed that higher TTL, excessive knee external rotation, and excessive knee valgus were statistically significant predictors of greater TT-TG distance ( P < .001 for all). The standardized estimates that were used for evaluating the predictive values were larger for TFR compared with those for TTL and MAD. Conclusion: TTL, TFR, and MAD were the main independent anatomical components associated with increased TT-TG distance, with the most prominent component being TFR. The association of TT-TG distance to each component analyzed in our study may help guide surgical planning.

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.

Introduction Patellar instability (PI) at an early age is believed closely correlated with bone loss in the development of the femoral trochlea and can cause trochlear dysplasia. However, the molecular mechanism of PI-induced bone loss has not been established. The Janus kinase (JAK)/signal transducers and activators of transcription (STAT) signaling pathway plays an important role in bone development by regulating the expression of osteoprotegerin (OPG) and receptor activator of nuclear factor kappa B ligand (RANKL). The aim of this study was to explore the association of JAK1/STAT3 signaling to PI-induced subchondral bone loss in the femoral trochlea. Methods 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. Results 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). Conclusion 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.