Sohn, D. H. | Search bioRxiv

bioRxiv2024

Soft Tissue Mechanics in Hip Distraction after Total Knee Arthroplasty: A Finite Element Analysis

INTRODUCTIONImprovement in diagnostic and surgical techniques in hip arthroscopy have led to a surge in hip distraction procedures over the recent years with the predicted annual frequency being four out of every 10,000 orthopedic procedures in 2017. Due to the large traction force required to achieve the appropriate joint spacing intra-operatively, an emergence of traction-related neurological and soft tissue injuries have surfaced. Pre-existing hip joint pathologies and surgical procedures disrupt the biomechanical stability of the joint and significantly increase the risk of iatrogenic damage. Furthermore, patients with total knee arthroplasties are often subject to intra-articular ligament releases, leading to reduced stability; however, it is not well understood how this may impact their outcomes of hip arthroscopic procedures. The current study aims to investigate the biomechanical behavior of various instrumented knee joints subjected to traction forces to aid clinical understanding and advancements of hip arthroscopy techniques. METHODSA validated finite element (FE) model of the pelvis and lower extremity was developed from computed tomography (CT) scans of a healthy 45-year-old female. Three different models were assembled according to different TKA techniques performed: Bi-Cruciate Retaining (BCR) model, Posterior-Cruciate Retaining (PCR) model, and Posterior Stabilized (PS) model. The BCR model is noted by retaining all native ligaments of the knee joint (ACL, PCL, MCL, and LCL), whereas the PCR model was subject to ACL removal and the PS model required ACL and PCL removal (Figure 1). The pelvis was encastered to prevent translation under the traction forces as motion of the patients trunk is restrained, intraoperatively. To simulate the loading condition of hip distraction, an axial force was coupled to the distal fibula and tibia and incrementally increased from 100N to 500N. Joint spacing and ligament strain in the hip and knee joint were analyzed to assess the effects of traction forces. O_FIG O_LINKSMALLFIG WIDTH=174 HEIGHT=200 SRC="FIGDIR/small/580129v2_fig1.gif" ALT="Figure 1"> View larger version (70K): org.highwire.dtl.DTLVardef@1494014org.highwire.dtl.DTLVardef@e0fdeorg.highwire.dtl.DTLVardef@133cb56org.highwire.dtl.DTLVardef@16aaf02_HPS_FORMAT_FIGEXP M_FIG O_FLOATNOFigure 1.C_FLOATNO Meshed parts of the A.) Posterior Cruciate retaining total knee replacement system and the B.) Bi-cruciate retaining total knee replacement system. C_FIG RESULTSThe medial and lateral compartment stiffness of the knee joint was analyzed under hip distraction for the three different TKA scenarios. The BCR model displayed the greatest average knee complex stiffness. Release of the ACL resulted in a larger decrease of stiffness compared to release of the PCL. There was no change in forces required for hip distraction as result of changes in the knee joint stiffness (Figure 3). The PCR and PS models were subject to excess knee joint distraction that exceeded 12 mm and ligament strain greater than 20% before adequate hip joint distraction of 10 mm was achieved. The BCR model remained below 10 mm of knee distraction and 15% ligament strain at 10 mm of hip joint distraction. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=182 SRC="FIGDIR/small/580129v2_fig3.gif" ALT="Figure 3"> View larger version (90K): org.highwire.dtl.DTLVardef@107c292org.highwire.dtl.DTLVardef@77351corg.highwire.dtl.DTLVardef@40011aorg.highwire.dtl.DTLVardef@88e9c_HPS_FORMAT_FIGEXP M_FIG O_FLOATNOFigure 3.C_FLOATNO FE models of instrumented TKA. A) PCR TKA with simulated ACL release. B) PS TKA with simulated ACL and PCL releases. C) BCR TKA with intact ligaments. C_FIG DISCUSSIONOur study reveals patients undergoing hip distraction with a prior TKA may experience increased soft tissue damage or iatrogenic dislocation due to reduced knee joint stability. The PCR and PS models outline a trend suggesting patients who have undergone ligament sacrificing TKAs experience large reductions in knee joint stability, causing strain levels that are indicative of soft tissue injury. The BCR TKA was indicated to be the safest under the distraction conditions as joint spacing and strain levels were largely reduced comparatively; however, when surpassing 10 mm of knee joint distraction at forces greater than 350 N, the strain levels in the ACL suggest minor injury may occur.

bioengineering↗

bioRxiv2018

TGFβ stimulates fibroblast-like synovial cells to produce ED-A fibronectin in osteoarthritis

IntroductionThe pathophysiology of osteoarthritis (OA) involves wear and tear, and a state of low-grade inflammation. Wear and tear leads to tissue degradation and tissue repair responses, including tissue growth factor beta (TGF{beta})-induced myofibroblast production of extracellular matrix (ECM). Fibronectins are an essential part of the ECM, and injection of fibronectin fragments into rabbit joints is a previously established animal model of OA. Alternatively-spliced fibronectin contains the ED-A domain (ED-A FN) and has been shown to activate Toll-like receptor 4. In this study, we tested the hypothesis that FN fragments containing the ED-A domain could be one mechanism transducing mechanical events into inflammatory signals in OA.\n\nMethodsSamples of synovial membrane and cartilage were obtained from patients with knee OA undergoing joint replacement surgery. Immunostaining for ED-A FN and the myofibroblast marker alpha smooth muscle actin (SMA) was performed on synovial membranes and fibroblast-like synovial cells (FLS). FLS were stimulated with TGF{beta}, TNF, lipopolysaccharide, IL-6, OA synovial fluid, or chondrocyte lysate, and analyzed for ED-A FN. Synovial cells isolated by enzymatic digestion and human monocyte-derived macrophages (MDM) were incubated with recombinant ED-A FN, plasmin, cellular FN, or cellular FN digested with plasmin; and culture supernatants were analyzed for MCP-1 and TNF.\n\nResultsWe hypothesized that ED-A FN is produced by OA FLS in response to factors found in the OA synovial joint. Indeed, the production of ED-A FN by OA FLS was increased by TGF{beta}, OA synovial fluid, and lysed chondrocytes in all experiments (n=3). ED-A FN co- localized with the myofibroblast marker SMA in both the OA FLS (n=3) and in the OA synovial membranes (n=8). We further hypothesized that ED-A FN expression is associated with cellular density and expression of inflammatory molecules in OA. ED-A FN staining was associated with both number of lining layer cells (rho=0.85 and p=0.011) and sublining cells (rho=0.88 and p=0.007) in the OA synovium (n=8), and co-localized with both MCP-1 and TNF (n=5). Recombinant ED-A FN increased the production of both MCP-1 and TNF by MDM (n=3) and OA FLS (n=3). Finally, we demonstrated that the FN fragments containing the ED-A domain generated the same production of both MCP-1 and TNF as recombinant ED-A FN.\n\nConclusionThe disease process in OA shares features with the chronic wound healing response including myofibroblast differentiation and production of mediators that promote myofibroblast production of ED-A FN. We show that recombinant and plasmin-derived ED-A fragments stimulate FLS and MDM to produce pro-inflammatory mediators. Our findings support utilizing ED-A FN for drug delivery or therapeutic targeting of the formation of ED- A FN or the enzymatic fragmentation of FN to reduce pro-inflammatory responses in OA.

immunology↗