[Risk factors for hip osteoarthritis after arthroscopy in patients with femoroacetabular impingement].

OBJECTIVE: To investigate the risk factors of hip osteoarthritis（HOA） after hip arthroscopy in patients with femoro-acetabular impingement（FAI） syndrome, and to reduce and prevent HOA. METHODS: From September 2018 to September 2020, 106 patients with FAI underwent hip arthroscopy, including 40 males and 66 females, aged from 20 to 55 years old with an average age of （33.05±10.19） years old. The mechanism of injury included 51 cases for sports injury, 36 for traffic accidents, and 19 for blunt object injury. The duration of the disease ranged from 5 to 19 days with an average of （12.02±3.69） days. All patients were followed up for 18 months. Patients were divided into HOA group （23 cases） and non-HOA group （83 cases） according to the occurrence of HOA. Multivariate Logistic regression was used to analyze the risk factors of HOA after hip arthroscopy in FAI patients. RESULTS: By univariate analysis, aged from 50 to 70 years old, female, body mass index（BMI）> 30 kg·m-2, physical labor, cam type, postoperative infection, last follow-up hip degree of motion （range of motion, ROM） （flexion, abduction, adduction, internal rotation） and Tönnis grade 1 and above of the HOA group were higher than those of the non-HOA group （P<0.05）, and the relative appendicular skeletal muscle index （RASM） was lower than that of non-HOA group（P<0.05）. By multiple Logistic regression analysis, cam type, BMI>30 kg·m-2, last follow-up hip internal rotation ROM and Tönnis grade 1 were risk factors for HOA after hip arthroscopy in FAI patients （P<0.05）. CONCLUSION: FAI classification, body mass index, hip ROM and Tönnis grade are all related to HOA after hip arthroscopy in FAI patients. Follow-up and intervention should be strengthened in high-risk FAI patients to reduce the occurrence of HOA.

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

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.