Extending the intermedullary nail will not reduce the potential risk of femoral head varus in PFNA patients biomechanically: a clinical review and corresponding numerical simulation.

Femoral head varus is an important complication in intertrochanteric fracture patients treated with proximal femoral nail anti-rotation (PFNA) fixation. Theoretically, extending the length of the intramedullary nail could optimize fixation stability by lengthening the force arm. However, whether extending the nail length can optimize patient prognosis is unclear. In this study, a review of imaging data from intertrochanteric fracture patients with PFNA fixation was performed, and the length of the intramedullary nail in the femoral trunk and the distance between the lesser trochanter and the distal locking screw were measured. The femoral neck varus status was judged at the 6-month follow-up. The correlation coefficients between nail length and femoral neck varus angle were computed, and linear regression analysis was used to determine whether a change in nail length was an independent risk factor for femoral neck varus. Moreover, the biomechanical effects of different nail lengths on PFNA fixation stability and local stress distribution have also been verified by numerical mechanical simulations. Clinical review revealed that changes in nail length were not significantly correlated with femoral head varus and were also not an independent risk factor for this complication. In addition, only slight biomechanical changes can be observed in the numerical simulation results. Therefore, commonly used intramedullary nails should be able to meet the needs of PFNA-fixed patients, and additional procedures for longer nail insertion may be unnecessary.

Ligustilide inhibits the proliferation of human osteoblastoma MG63 cells through the TLR4-ERK pathway.

OBJECTIVE: To study the proapoptotic effect of ligustilide on osteoblastoma (OS) and the relative related molecular mechanism. METHODS AND MATERIALS: An MTT was used to examine the proliferation of OS cells, and Flow cytometry was used to analyze apoptosis and the cell cycle. Western blotting was used to detect the signaling pathway of apoptosis, and immunohistochemical (IH) staining was used to detect the apoptosis status of OS cells. A TLR4 inhibitor was used to study the effect of ligustilide on OS. RESULTS: Ligustilide inhibited OS cell proliferation but had no inhibitory effect on normal bone marrow cells. Flow cytometry results showed that ligustilide induced apoptosis in OS cells, and the cell cycle was arrested at the M/G2 phase. Western blot results showed that ERK, P53, P21, Caspase 9, Caspase 8 and Caspase 3 were all activated; cytochrome C and Bax increased; and Bcl-2 decreased when OS was treated with ligustilide. When an ERK or Caspase inhibitor was added to the culture medium, the apoptosis of OS cells decreased to some degree. When OS cells were pretreated with CLI-095, which is a TLR4 inhibitor, the percentage of apoptotic cells and cell cycle arrest were both reversed. IH results also showed that ligustilide induced apoptosis in OS cells, and the effect was blocked by the TLR4 inhibitor. CONCLUSION: Ligustilide selectively inhibited the proliferation of OS cells by inducing apoptosis, which possibly included endogenous and exogenous apoptosis through TLR4.