Dynamic Failure Properties of the Porcine Medial Collateral Ligament-Bone Complex for Predicting Injury in Automotive Collisions

The goal of this study was to model the dynamic failure properties of ligaments and their attachment sites to facilitate the development of more realistic dynamic finite element models of the human lower extremities for use in automotive collision simulations. Porcine medial collateral ligaments were chosen as a test model due to their similarities in size and geometry with human ligaments. Each porcine medial collateral ligament-bone complex (n = 12) was held in a custom test fixture placed in a drop tower to apply an axial impulsive impact load, applying strain rates ranging from 0.005 s-1 to 145 s-1. The data from the impact tests were analyzed using nonlinear regression to construct model equations for predicting the failure load of ligament-bone complexes subjected to specific strain rates as calculated from finite element knee, thigh, and hip impact simulations. The majority of the ligaments tested failed by tibial avulsion (75%) while the remaining ligaments failed via mid-substance tearing. The failure load ranged from 384 N to 1184 N and was found to increase with the applied strain rate and the product of ligament length and cross-sectional area. The findings of this study indicate the force required to rupture the porcine MCL increases with the applied bone-to-bone strain rate in the range expected from high speed frontal automotive collisions

PTA and stenting in supra-aortic arch arteries

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Viscoelastic models for ligaments and tendons

Ligaments and tendons serve a variety of important functions in the human body. Many experimental studies have focused on understanding their mechanical behavior, mathematical modeling has also contributed important information. This paper presents a brief review of viscoelastic models that have been proposed to describe the nonlinear and time-dependent behavior of ligaments and tendons. Specific attention is devoted to quasi-linear viscoelasticity (QLV) and to our most recent approach, the single integral finite strain model (SBFS) which incorporates constitutive modeling of microstructural change. An example is given in which the SIFS model is used to describe the viscoelastic behavior of a human patellar tendon

Role of biomechanics in the understanding of normal, injured, and healing ligaments and tendons

Ligaments and tendons are soft connective tissues which serve essential roles for biomechanical function of the musculoskeletal system by stabilizing and guiding the motion of diarthrodial joints. Nevertheless, these tissues are frequently injured due to repetition and overuse as well as quick cutting motions that involve acceleration and deceleration. These injuries often upset this balance between mobility and stability of the joint which causes damage to other soft tissues manifested as pain and other morbidity, such as osteoarthritis

Biomechanics and anterior cruciate ligament reconstruction

For years, bioengineers and orthopaedic surgeons have applied the principles of mechanics to gain valuable information about the complex function of the anterior cruciate ligament (ACL). The results of these investigations have provided scientific data for surgeons to improve methods of ACL reconstruction and postoperative rehabilitation. This review paper will present specific examples of how the field of biomechanics has impacted the evolution of ACL research. The anatomy and biomechanics of the ACL as well as the discovery of new tools in ACL-related biomechanical study are first introduced. Some important factors affecting the surgical outcome of ACL reconstruction, including graft selection, tunnel placement, initial graft tension, graft fixation, graft tunnel motion and healing, are then discussed. The scientific basis for the new surgical procedure, i.e., anatomic double bundle ACL reconstruction, designed to regain rotatory stability of the knee, is presented. To conclude, the future role of biomechanics in gaining valuable in-vivo data that can further advance the understanding of the ACL and ACL graft function in order to improve the patient outcome following ACL reconstruction is suggested

Functional tissue engineering of ligament healing

Ligaments and tendons are dense connective tissues that are important in transmitting forces and facilitate joint articulation in the musculoskeletal system. Their injury frequency is high especially for those that are functional important, like the anterior cruciate ligament (ACL) and medial collateral ligament (MCL) of the knee as well as the glenohumeral ligaments and the rotator cuff tendons of the shoulder. Because the healing responses are different in these ligaments and tendons after injury, the consequences and treatments are tissue- and site-specific. In this review, we will elaborate on the injuries of the knee ligaments as well as using functional tissue engineering (FTE) approaches to improve their healing. Specifically, the ACL of knee has limited capability to heal, and results of non-surgical management of its midsubstance rupture have been poor. Consequently, surgical reconstruction of the ACL is regularly performed to gain knee stability. However, the long-term results are not satisfactory besides the numerous complications accompanied with the surgeries. With the rapid development of FTE, there is a renewed interest in revisiting ACL healing. Approaches such as using growth factors, stem cells and scaffolds have been widely investigated. In this article, the biology of normal and healing ligaments is first reviewed, followed by a discussion on the issues related to the treatment of ACL injuries. Afterwards, current promising FTE methods are presented for the treatment of ligament injuries, including the use of growth factors, gene delivery, and cell therapy with a particular emphasis on the use of ECM bioscaffolds. The challenging areas are listed in the future direction that suggests where collection of energy could be placed in order to restore the injured ligaments and tendons structurally and functionally

Gene expression and matrix turnover in overused and damaged tendons

Chronic, painful conditions affecting tendons, frequently known as tendinopathy, are very common types of sporting injury. The tendon extracellular matrix is substantially altered in tendinopathy, and these changes are thought to precede and underlie the clinical condition. The tendon cell response to repeated minor injuries or “overuse” is thought to be a major factor in the development of tendinopathy. Changes in matrix turnover may also be effected by the cellular response to physical load, altering the balance of matrix turnover and changing the structure and composition of the tendon. Matrix turnover is relatively high in tendons exposed to high mechanical demands, such as the supraspinatus and Achilles, and this is thought to represent either a repair or tissue maintenance function. Metalloproteinases are a large family of enzymes capable of degrading all of the tendon matrix components, and these are thought to play a major role in the degradation of matrix during development, adaptation and repair. It is proposed that some metalloproteinase enzymes are required for the health of the tendon, and others may be damaging, leading to degeneration of the tissue. Further research is required to investigate how these enzyme activities are regulated in tendon and altered in tendinopathy. A profile of all the metalloproteinases expressed and active in healthy and degenerate tendon is required and may lead to the development of new drug therapies for these common and debilitating sports injuries

Factors that influence the intra-articular rupture pattern of the ACL graft following single-bundle reconstruction

The number of revision anterior cruciate ligament (ACL) surgeries performed annually continues to rise. The purpose of this study was to determine the most common rupture pattern in ACL revision cases after previous single-bundle reconstruction. The second aim was to determine the relationship between rupture pattern and patient-specific factors (age, gender, time between the initial ACL reconstruction and re-injury, and etiology/mechanism of failure) and surgical factors (graft type, tunnel angle). This was a cohort study of 60 patients that underwent revision ACL surgery after previous single-bundle ACL reconstruction. Three sports medicine-trained orthopedic surgeons reviewed the arthroscopic videos and determined the rupture pattern of the grafts. The rupture pattern was then correlated to the above-mentioned factors. The inter-observer agreement had a kappa of 0.7. The most common rupture pattern after previous single-bundle ACL reconstruction is elongation of the graft. This is different from the native ACL, which displays more proximal ruptures. With the use of autograft tissue and after a longer period of time, the rupture pattern in revision surgery is more similar to that of the native ACL. The most common rupture pattern after previous single-bundle reconstruction was elongation of the graft. Factors that influenced the rupture pattern were months between ACL reconstruction and re-injury and graft type. Cohort study, Level I

Employment of gene expression profiling to identify transcriptional regulators of hepatic stellate cells

Activated hepatic stellate cells (HSC) play a central role in scar formation that leads to liver fibrosis. The molecular mechanisms underlying this process are not fully understood. Microarray and bioinformatics analyses have proven to be useful in identifying transcription factors that regulate cellular processes such as cell differentiation. Using oligonucleotide microarrays, we performed transcriptional analyses of activated human HSC cultured on Matrigel-coated tissue culture dishes. Examination of microarray data following Matrigel-induced deactivation of HSC revealed a significant down-regulation of myocardin, an important transcriptional regulator in smooth and cardiac muscle development. Thus, gene expression profiling as well as functional assays of activated HSC have provided the first evidence of the involvement of myocardin in HSC activation