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.

Therapeutic strategies based on utilizing endogenous BMSCs have been developed for the regeneration of bone, cartilage, and ligaments. We previously found that E7 peptide (EPLQLKM) could enhance BMSC homing in bio-scaffolds and, therefore, promote cartilage regeneration. However, the profile and mechanisms of E7 peptide in cartilage regeneration remain elusive. In this study, we examined the effect of E7 peptide on the BMSC phenotype, including adhesion, viability and chondrogenic differentiation, and its underlying mechanism. The konjac glucomannan microsphere (KGM), a carrier material that is free of BMSC adhesion ability, was used as the solid base of E7 peptide to better explore the independent role of E7 peptide in BMSC behavior. The results showed that E7 peptide could support BMSC adhesion and viability in a comparable manner to RGD and promote superior chondrogenic differentiation to RGD. We examined differentially expressed genes of BMSCs induced by E7 compared to RGD. Subsequently, a real-time PCR validated the significantly upregulated expression of lncRNA H19, and the knockdown of lncRNA H19 or miR675, a downstream functional unit of H19, could significantly obscure the chondrogenic differentiation induced by E7. In conclusion, this study confirmed the independent role of E7 in the adhesion and viability of BMSCs and revealed the pro-chondrogenic effect of E7 on BMSCs via the H19/miR675 axis. These results could help establish new therapeutic strategies based on employing endogenous BMSCs for cartilage tissue regeneration.

Prof. Chitranjan S. Ranawat: tips for young physicians