Mechanical instability induces osteoclast differentiation independent of the presence of a fibrous tissue interface and osteocyte apoptosis in a rat model for aseptic loosening.

Background and purpose - Insufficient initial fixation or early micromotion of an implant is associated with a thin layer of fibrous tissue at the peri-implant interface. It is unknown if bone loss is induced by the fibrous tissue interface acting as an active biological membrane, or as a membrane that will produce supraphysiologic fluid flow conditions during gait, which activates the mechanosensitive osteocytes to mediate osteoclast differentiation. We investigated whether mechanically induced osteolysis is dependent on the fibrous tissue interface as a biologically active scaffold, or if it merely acts as a conduit for fluid flow, affecting the mechanosensitive osteocytes in the peri-prosthetic bone.

GSK-3β inhibition suppresses instability-induced osteolysis by a dual action on osteoblast and osteoclast differentiation.

Currently, there are no medications available to treat aseptic loosening of orthopedic implants. Using osteoprotegerin fusion protein (OPG-Fc), we previously blocked instability-induced osteoclast differentiation and peri-prosthetic osteolysis. Wnt/β-catenin signaling, which regulates OPG secretion from osteoblasts, also modulates the bone tissue response to mechanical loading.

Low Risk of Thromboembolic Events After Routine Administration of Tranexamic Acid in Hip and Knee Arthroplasty.

Background: The blood-conserving effect of intravenous (IV) tranexamic acid (TXA) is well-documented for total hip arthroplasty (THA) and total knee arthroplasty (TKA). However, the risk of thromboembolic (TE) events after routine use of TXA is unclear and the safety profile is debated. This retrospective study investigates patient characteristics, occurrences, and predictors of TE events after routine administration of IV TXA in THA and TKA.