Autophagy, as a fundamental mechanism for cellular homeostasis, is generally involved in the occurrence and progression of various diseases. Osteoarthritis (OA) is the most common musculoskeletal disease that often leads to pain, disability and economic loss in patients. Post-traumatic OA (PTOA) is a subtype of OA, accounting for >12% of the overall burden of OA. PTOA is often caused by joint injuries including anterior cruciate ligament rupture, meniscus tear and intra-articular fracture. Although a variety of methods have been developed to treat acute joint injury, the current measures have limited success in effectively reducing the incidence and delaying the progression of PTOA. Therefore, the pathogenesis and intervention strategy of PTOA need further study. In the past decade, the roles and mechanisms of autophagy in PTOA have aroused great interest in the field. It was revealed that autophagy could maintain the homeostasis of chondrocytes, reduce joint inflammatory level, prevent chondrocyte death and matrix degradation, which accordingly improved joint symptoms and delayed the progression of PTOA. Moreover, many strategies that target PTOA have been revealed to promote autophagy. In this review, we summarize the roles and mechanisms of autophagy in PTOA and the current strategies for PTOA treatment that depend on autophagy regulation, which may be beneficial for PTOA patients in the future.

Infrapatellar fat pad (IPFP) inflammation is a common pathological manifestation in knee osteoarthritis (OA). However, the significance of IPFP signal intensity alteration for clinical diagnosis and treatment of knee OA needs further research. We assessed IPFP signal intensity alteration (0–3), IPFP maximum cross-sectional area (CSA) and IPFP depth, meniscus injury, bone marrow edema, and cartilage injury from magnetic-resonance imaging (MRI) in 41 non-KOA patients (K-L grade 0 and grade I) and 68 KOA patients (K-L grade 2,3 and 4). We found that IPFP signaling was altered in all patients with KOA whose alteration was closely related to the K-L grading. We found that the IPFP signal intensity was increased in most OA patients, especially the ones in the late stage. There were significant differences in IPFP maximum CSA and IPFP depth between groups in KOA and non-KOA patients. Moreover, Spearman correlation analysis showed that IPFP signal intensity was moderately positively correlated with age, meniscal injury, cartilage injury, and bone marrow edema, and negatively correlated with height, while not correlated with visual analogue scale (VAS) scoring and body mass index (BMI). In addition, women have higher IPFP inflammation scores on MRI than men. In conclusion, IPFP signal intensity alteration is associated with joint damage in knee OA, which may have clinical significance for diagnosing and treating KOA.