Animating Human Muscle Structure

Graphical simulations of human muscle motion and deformation are of great interest to medical education. In this article, the authors present a technique for simulating muscle deformations by combining physically and geometrically based computations to reduce computation cost and produce fast, accurate simulations

Microstructural analysis of skeletal muscle force generation during aging.

Human aging results in a progressive decline in the active force generation capability of skeletal muscle. While many factors related to the changes of morphological and structural properties in muscle fibers and the extracellular matrix (ECM) have been considered as possible reasons for causing age-related force reduction, it is still not fully understood why the decrease in force generation under eccentric contraction (lengthening) is much less than that under concentric contraction (shortening). Biomechanically, it was observed that connective tissues (endomysium) stiffen as ages, and the volume ratio of connective tissues exhibits an age-related increase. However, limited skeletal muscle models take into account the microstructural characteristics as well as the volume fraction of tissue material. This study aims to provide a numerical investigation in which the muscle fibers and the ECM are explicitly represented to allow quantitative assessment of the age-related force reduction mechanism. To this end, a fiber-level honeycomb-like microstructure is constructed and modeled by a pixel-based Reproducing Kernel Particle Method (RKPM), which allows modeling of smooth transition in biomaterial properties across material interfaces. The numerical investigation reveals that the increased stiffness of the passive materials of muscle tissue reduces the force generation capability under concentric contraction while maintains the force generation capability under eccentric contraction. The proposed RKPM microscopic model provides effective means for the cellular-scale numerical investigation of skeletal muscle physiology. NOVELTY STATEMENT: A cellular-scale honeycomb-like microstructural muscle model constructed from a histological cross-sectional image of muscle is employed to study the causal relations between age-associated microstructural changes and age-related force loss using Reproducing Kernel Particle Method (RKPM). The employed RKPM offers an effective means for modeling biological materials based on pixel points in the medical images and allow modeling of smooth transition in the material properties across interfaces. The proposed microstructure-informed muscle model enables quantitative evaluation on how cellular-scale compositions contribute to muscle functionality and explain differences in age-related force changes during concentric, isometric and eccentric contractions

Articular human joint modelling

Copyright @ Cambridge University Press 2009.The work reported in this paper encapsulates the theories and algorithms developed to drive the core analysis modules of the software which has been developed to model a musculoskeletal structure of anatomic joints. Due to local bone surface and contact geometry based joint kinematics, newly developed algorithms make the proposed modeller different from currently available modellers. There are many modellers that are capable of modelling gross human body motion. Nevertheless, none of the available modellers offer complete elements of joint modelling. It appears that joint modelling is an extension of their core analysis capability, which, in every case, appears to be musculoskeletal motion dynamics. It is felt that an analysis framework that is focused on human joints would have significant benefit and potential to be used in many orthopaedic applications. The local mobility of joints has a significant influence in human motion analysis, in understanding of joint loading, tissue behaviour and contact forces. However, in order to develop a bone surface based joint modeller, there are a number of major problems, from tissue idealizations to surface geometry discretization and non-linear motion analysis. This paper presents the following: (a) The physical deformation of biological tissues as linear or non-linear viscoelastic deformation, based on spring-dashpot elements. (b) The linear dynamic multibody modelling, where the linear formulation is established for small motions and is particularly useful for calculating the equilibrium position of the joint. This model can also be used for finding small motion behaviour or loading under static conditions. It also has the potential of quantifying the joint laxity. (c) The non-linear dynamic multibody modelling, where a non-matrix and algorithmic formulation is presented. The approach allows handling complex material and geometrical nonlinearity easily. (d) Shortest path algorithms for calculating soft tissue line of action geometries. The developed algorithms are based on calculating minimum ‘surface mass’ and ‘surface covariance’. An improved version of the ‘surface covariance’ algorithm is described as ‘residual covariance’. The resulting path is used to establish the direction of forces and moments acting on joints. This information is needed for linear or non-linear treatment of the joint motion. (e) The final contribution of the paper is the treatment of the collision. In the virtual world, the difficulty in analysing bodies in motion arises due to body interpenetrations. The collision algorithm proposed in the paper involves finding the shortest projected ray from one body to the other. The projection of the body is determined by the resultant forces acting on it due to soft tissue connections under tension. This enables the calculation of collision condition of non-convex objects accurately. After the initial collision detection, the analysis involves attaching special springs (stiffness only normal to the surfaces) at the ‘potentially colliding points’ and motion of bodies is recalculated. The collision algorithm incorporates the rotation as well as translation. The algorithm continues until the joint equilibrium is achieved. Finally, the results obtained based on the software are compared with experimental results obtained using cadaveric joints

Biomechanically-Regularized Deformable Image Registration for Head and Neck Adaptive Radiation Therapy

Radiation treatment (RT), one of the best treatments available for head and neck (HN) cancer, may fail to accurately target tumors and spare surrounding healthy tissue that change in shape and location during 5-7 weeks of RT. This anatomical change can be monitored by calculating deformation maps from planning computed tomography (CT) image (taken prior to the start of RT) to treatment CT images (taken at every treatment fractions for patient setup) via deformable image registration (DIR). In response to the deformations estimated by DIR, initial radiation treatment plan established on the planning CT can be adjusted to deliver sufficient radiation dose to the tumors while sparing healthy tissue. However, since DIR is formulated as an optimization problem to find a deformation map that simply maximizes a similarity metric between two images, it may result in physically unreasonable deformations, such as bone warping. Moreover, DIR accuracy of HN soft tissue region is limited and parameter-dependent as reported in previous studies. Finally, previous studies have evaluated DIR accuracy with a limited number of landmarks, with which accuracy of volumetric deformation cannot be rigorously evaluated. The objective of this dissertation is 1) to improve registration accuracy of HN CT images by introducing penalty terms (from biomechanical principles) into B-spline DIR, in which deformation is represented using a linear combinations of B-spline functions, and 2) to develop an improved evaluation method for DIR accuracy based on finite element model (FE) model of HN region. First, a penalty for prevent the bone warping was developed to preserve inter-voxel distances within each of rigid regions. Second, a penalty that prevents resultant deformations from violating the static equilibrium equations of linear elastic material was used for the B-spline DIR of muscle in HN region. Third, a FE HN model was developed to generate deformation maps similar to those seen in patients that can be used as ground-truth for the evaluation of registration accuracy. The outcome of the dissertation would support research/development in RT of HN cancer by enabling the accurate estimation of deformations of healthy tissue surrounding tumor and the rigorous assessment of registration accuracy.PhDMechanical EngineeringUniversity of Michigan, Horace H. Rackham School of Graduate Studieshttp://deepblue.lib.umich.edu/bitstream/2027.42/113532/1/jihun_1.pd

Cancellous bone and theropod dinosaur locomotion. Part II—a new approach to inferring posture and locomotor biomechanics in extinct tetrapod vertebrates

This paper is the second of a three-part series that investigates the architecture of cancellous bone in the main hindlimb bones of theropod dinosaurs, and uses cancellous bone architectural patterns to infer locomotor biomechanics in extinct non-avian species. Cancellous bone is widely known to be highly sensitive to its mechanical environment, and therefore has the potential to provide insight into locomotor biomechanics in extinct tetrapod vertebrates such as dinosaurs. Here in Part II, a new biomechanical modelling approach is outlined, one which mechanistically links cancellous bone architectural patterns with three-dimensional musculoskeletal and finite element modelling of the hindlimb. In particular, the architecture of cancellous bone is used to derive a single ‘characteristic posture’ for a given species—one in which bone continuum-level principal stresses best align with cancellous bone fabric—and thereby clarify hindlimb locomotor biomechanics. The quasi-static approach was validated for an extant theropod, the chicken, and is shown to provide a good estimate of limb posture at around mid-stance. It also provides reasonable predictions of bone loading mechanics, especially for the proximal hindlimb, and also provides a broadly accurate assessment of muscle recruitment insofar as limb stabilization is concerned. In addition to being useful for better understanding locomotor biomechanics in extant species, the approach hence provides a new avenue by which to analyse, test and refine palaeobiomechanical hypotheses, not just for extinct theropods, but potentially many other extinct tetrapod groups as well

Biomechanics of foetal movement.

© 2015, AO Research Institute. All rights reserved.Foetal movements commence at seven weeks of gestation, with the foetal movement repertoire including twitches, whole body movements, stretches, isolated limb movements, breathing movements, head and neck movements, jaw movements (including yawning, sucking and swallowing) and hiccups by ten weeks of gestational age. There are two key biomechanical aspects to gross foetal movements; the first being that the foetus moves in a dynamically changing constrained physical environment in which the freedom to move becomes increasingly restricted with increasing foetal size and decreasing amniotic fluid. Therefore, the mechanical environment experienced by the foetus affects its ability to move freely. Secondly, the mechanical forces induced by foetal movements are crucial for normal skeletal development, as evidenced by a number of conditions and syndromes for which reduced or abnormal foetal movements are implicated, such as developmental dysplasia of the hip, arthrogryposis and foetal akinesia deformation sequence. This review examines both the biomechanical effects of the physical environment on foetal movements through discussion of intrauterine factors, such as space, foetal positioning and volume of amniotic fluid, and the biomechanical role of gross foetal movements in human skeletal development through investigation of the effects of abnormal movement on the bones and joints. This review also highlights computational simulations of foetal movements that attempt to determine the mechanical forces acting on the foetus as it moves. Finally, avenues for future research into foetal movement biomechanics are highlighted, which have potential impact for a diverse range of fields including foetal medicine, musculoskeletal disorders and tissue engineering

Simulating Extraocular Muscle Dynamics. A Comparison between Dynamic Implicit and Explicit Finite Element Methods

The finite element method has been widely used to investigate the mechanical behavior of biological tissues. When analyzing these particular materials subjected to dynamic requests, time integration algorithms should be considered to incorporate the inertial effects. These algorithms can be classified as implicit or explicit. Although both algorithms have been used in different scenarios, a comparative study of the outcomes of both methods is important to determine the performance of a model used to simulate the active contraction of the skeletal muscle tissue. In this work, dynamic implicit and dynamic explicit solutions are presented for the movement of the eye ball induced by the extraocular muscles. Aspects such as stability, computational time and the influence of mass-scaling for the explicit formulation were assessed using ABAQUS software. Both strategies produced similar results regarding range of movement of the eye ball, total deformation and kinetic energy. Using the implicit dynamic formulation, an important amount of computational time reduction is achieved. Although mass-scaling can reduce the simulation time, the dynamic contraction of the muscle is drastically altered

Experimental and theoretical analyses of compression induced muscle damage : aetiological factors in pressure ulcers

Pressure ulcers form a major problem in health care. They often occur when patients are bedridden, wheelchair bound or wearing prostheses. The ulcers can be very painful for the patient and often lead to prolonged hospitalization. In addition, the huge costs involved with treatment and prevention put a heavy burden on heath care budgets. Pressure ulcers occur often: between 14% and 33% of the patients in health care institutions develop an ulcer, ranging from discolouration of the skin to severe wounds involving necrosis of epidermis, extending to underlying bone, tendon and joints. It is clear that pressure ulcers are caused by prolonged mechanical loading, applied at the interface between skin and support surfaces. However, the aetiology of pressure ulcers is poorly understood. This forms an important obstacle in decreasing the unacceptably high prevalence figures. It is anticipated that a better understanding of the mechanobiological pathways leading to cell and tissue damage can lead to a breakthrough in reducing pressure ulcer prevalence. In addition, a solid scientific base may establish tools for objective risk assessment and judgement of preventive measures. The present study focuses on deep ulcers that initiate in skeletal muscle tissue, since deep ulcers are more extensive and often difficult to prevent. To obtain insight into the aetiology of these deep ulcers, it is necessary to understand the transfer from externally applied loads at the skin, to the local conditions that the cells experience within the tissue. In addition, the question which local conditions are harmful to the cell needs to be investigated. By combining knowledge on "what a cell feels" with knowledge on potentially harmful conditions, a better judgement of dangerous situations may be achieved. Although several causes of cell damage may play a role in the initiation of pressure ulcers, the present study focussed on the impact of cell deformations. To investigate the hypothesis that prolonged cell deformations lead to cell damage at clinically relevant strains, an experimental model system was developed. A key requirement of this experimental model is the possibility to study the role of cell deformation on cell damage independently of other possible causes of damage. To achieve this, in-vitro engineered muscle tissue constructs were developed. These constructs were compressed using a newly developed compression device. A custom made incubator system was developed to allow monitoring of the constructs for extended periods of time. In addition, a novel assay was developed to determine the viability of the cells during compression. This assay provides quantitative and spatial information on cell damage throughout a construct in a non-invasive manner, making use of fluorescent dyes which are visualized by confocal microscopy. The compression of the engineered muscle tissue constructs indicated that a significant increase in cell death occurs within 1-2 hours and that higher strain levels led to an earlier increase in damage. In addition, it was demonstrated that cell damage was uniformly distributed across the indented area of the construct, without a gradient in percentage dead cells between the centre and periphery of the constructs. The results strongly suggest that prolonged cell deformation was the predominant cause of cell damage in these experiments. This puts a new light on observations in literature which suggested that ischaemia is not the sole determinant for the onset of pressure ulcers. Nevertheless, more experiments are needed to clarify the role of prolonged cell deformations on cell damage. First, it is recommended that the actual local cell deformations are quantified during compression of the constructs. Furthermore, from the present experiments it could not be excluded that the compression of the constructs decreased the permeability of the construct and hence affected cellular metabolism. In future, measuring diffusion pathways of both small molecules and larger vital molecules, may indicate whether this change in permeability is significant. A numerical model was developed to predict local cell deformations, in response to tissue compression. Since the local cell deformations cannot be a-priori determined on the basis of homogenized tissue deformations, a multilevel finite element approach was adopted. In this approach, cell deformations are predicted from detailed nonlinear finite element analyses of the local microstructures of the tissue, which consist of an arrangement of cells embedded in a matrix material. To avoid unacceptably large computational times, the multilevel model was designed to run on a parallel computer system. Application of the multilevel model showed that the heterogeneity of the microstructure of the tissue has a profound impact on local cell deformations, which highly exceeded macroscopic tissue deformations. Moreover, microstructural heterogeneity led to complex cell shapes and caused non-uniform deformations within the cells. To investigate the evolution of compression induced damage in skeletal muscle tissue, the multilevel model was extended with a damage law, which was derived from the in-vitro experiments. With this model, the compression of muscle tissue against a bony prominence was simulated. The percentage of cell damage in the microstructure of the tissue was computed, which could be extrapolated to the bulk tissue level. In the present form, a schematic geometry was considered that intended to elucidate general patterns of tissue damage evolution. The simulations confirmed that it is not feasible to predict the onset of tissue damage on the basis of externally applied loading conditions at the skin surface alone, since these externally applied loads are not indicative of the local mechanical conditions that the cells experience within the tissue. In addition, the simulations showed that it is necessary to consider the local load history of the cells, and the tolerance of the tissue. These findings may explain why a strikingly large variability in load/time threshold values was found in animal studies, which attempted to relate external mechanical to tissue damage, thereby ignoring the local mechanical conditions within the tissue. At present, it is premature to utilize the models presented in this thesis in clinical practice, since the extrapolation towards human patients requires more research. Clearly, further extensions and validation of the numerical model with experimental animal models will be required. This should finally lead to the application in more realistic cases, involving patient data on geometry and tissue properties. Nevertheless, the present models provided an essential step towards evidence based risk assessment and prevention