ABSTRACT
Tibial avulsion fractures comprise a subset of anterior cruciate ligament injuries. Primary fixation methods have traditionally used either screw or suture fixation. New anchor and suture technologies have led to the development of tensionable and retensionable techniques. These newer techniques allow for not only anatomic reduction but also further compression after reduction. The purpose of this technical note is to introduce a tensionable and retensionable construct that uses knotless anchor fixation to produce compression after anatomic reduction of a tibial avulsion fracture.
ABSTRACT
Fixation of proximal humerus fractures (PHFs) with intramedullary (IM) nails potentially is a newer, less invasive technique. The purpose of this study was to report on the early adoption results of IM nail use for PHF. Retrospective chart reviews were performed on the first 60 patients treated with IM nails for acute PHFs by two shoulder surgeons. The first 15 patients treated by each surgeon were compared with the subsequent 15 patients. Surgical and fluoroscopic times, fracture type, union, and varus collapse were compared. The average operating time decreased (p = .002). Fluoroscopy time, radiographic alignment, union rate, complications, and reoperations were not influenced. Three- and four-part fractures had a higher complication rate than two-part fractures (53% vs. 20%). When considering implementing use of IM nails for treatment of PHFs, initial cases can have outcomes and complications similar to those performed with greater experience. IM nailing appears a good treatment option for two-part PHFs. (Journal of Surgical Orthopaedic Advances 28(2):121-126, 2019).
Subject(s)
Fracture Fixation, Intramedullary , Shoulder Fractures , Bone Nails , Humans , Humerus , Retrospective Studies , Shoulder Fractures/surgery , Treatment OutcomeABSTRACT
Bone dissemination and bone disease occur in approximately 80% of patients with multiple myeloma (MM) and are a major cause of patient mortality. We previously demonstrated that MM cell-derived heparanase (HPSE) is a major driver of MM dissemination to and progression in new bone sites. However the mechanism(s) by which HPSE promotes MM progression remains unclear. In the present study, we investigated the involvement of mesenchymal features in HPSE-promoted MM progression in bone. Using a combination of molecular, biochemical, cellular, and in vivo approaches, we demonstrated that (1) HPSE enhanced the expression of mesenchymal markers in both MM and vascular endothelial cells; (2) HPSE expression in patient myeloma cells positively correlated with the expression of the mesenchymal markers vimentin and fibronectin. Additional mechanistic studies revealed that the enhanced mesenchymal-like phenotype induced by HPSE in MM cells is due, at least in part, to the stimulation of the ERK signaling pathway. Finally, knockdown of vimentin in HPSE expressing MM cells resulted in significantly attenuated MM cell dissemination and tumor growth in vivo. Collectively, these data demonstrate that the mesenchymal features induced by HPSE in MM cells contribute to enhanced tumor cell motility and bone-dissemination.
Subject(s)
Cell Movement/physiology , Glucuronidase/metabolism , Mesenchymal Stem Cells/enzymology , Mesenchymal Stem Cells/pathology , Multiple Myeloma/enzymology , Multiple Myeloma/pathology , Animals , Bone Neoplasms/metabolism , Bone Neoplasms/secondary , Cell Growth Processes/physiology , Disease Progression , Endothelial Cells/drug effects , Endothelial Cells/enzymology , Endothelial Cells/pathology , Glucuronidase/antagonists & inhibitors , Heparin/analogs & derivatives , Heparin/pharmacology , Heterografts , Humans , MAP Kinase Signaling System , Male , Mesenchymal Stem Cells/drug effects , Mesenchymal Stem Cells/metabolism , Mice , Mice, SCID , Multiple Myeloma/metabolism , Phenotype , Signal Transduction , Tumor Microenvironment , Vimentin/deficiency , Vimentin/genetics , Vimentin/metabolismABSTRACT
The progression of multiple myeloma (MM) is governed by a network of molecular signals, the majority of which remain to be identified. Recent studies suggest that Runt-related transcription factor 2 (Runx2), a well-known bone-specific transcription factor, is also expressed in solid tumors, where expression promotes both bone metastasis and osteolysis. However, the function of Runx2 in MM remains unknown. The current study demonstrated that (1) Runx2 expression in primary human MM cells is significantly greater than in plasma cells from healthy donors and patients with monoclonal gammopathy of undetermined significance; (2) high levels of Runx2 expression in MM cells are associated with a high-risk population of MM patients; and (3) overexpression of Runx2 in MM cells enhanced tumor growth and disease progression in vivo. Additional studies demonstrated that MM cell-derived Runx2 promotes tumor progression through a mechanism involving the upregulation of Akt/ß-catenin/Survivin signaling and enhanced expression of multiple metastatic genes/proteins, as well as the induction of a bone-resident cell-like phenotype in MM cells. Thus, Runx2 expression supports the aggressive phenotype of MM and is correlated with poor prognosis. These data implicate Runx2 expression as a major regulator of MM progression in bone and myeloma bone disease.
