title: Cartilage dysfunction in ALS patients as side effect of motion loss: 3D mechano-electrochemical computational model.
abstract: Amyotrophic lateral sclerosis (ALS) is a debilitating motor neuron disease characterized by progressive weakness, muscle atrophy, and fasciculation. This fact results in a continuous degeneration and dysfunction of articular soft tissues. Specifically, cartilage is an avascular and nonneural connective tissue that allows smooth motion in diarthrodial joints. Due to the avascular nature of cartilage tissue, cells nutrition and by-product exchange are intermittently occurring during joint motions. Reduced mobility results in a change of proteoglycan density, osmotic pressure, and permeability of the tissue. This work aims to demonstrate the abnormal cartilage deformation in progressive immobilized articular cartilage for ALS patients. For this aim a novel 3D mechano-electrochemical model based on the triphasic theory for charged hydrated soft tissues is developed. ALS patient parameters such as tissue porosity, osmotic coefficient, and fixed anions were incorporated. Considering different mobility reduction of each phase of the disease, results predicted the degree of tissue degeneration and the reduction of its capacity for deformation. The present model can be a useful tool to predict the evolution of joints in ALS patients and the necessity of including specific cartilage protectors, drugs, or maintenance physical activities as part of the symptomatic treatment in amyotrophic lateral sclerosis.
authors.affiliation: Group of Structural Mechanics and Materials Modelling (GEMM), Aragón Institute of Engineering Research (I3A), University of Zaragoza, 50018 Zaragoza, Spain ; Mechanical Engineering Department, School of Engineering and Architecture (EINA), University of Zaragoza, María de Luna s/n, Betancourt Building, 50018 Zaragoza, Spain ; Biomedical Research Networking Center in Bioengineering, Biomaterials and Nanomedicine (CIBER-BBN), 50018 Zaragoza, Spain.
authors.forename: Sara
authors.identifier: 0000-0002-6305-9283
authors.initials: S
authors.lastname: Manzano
authors.affiliation: Wolfson Centre for Mathematical Biology (WCMB), Mathematical Institute, Oxford University, Oxford OX1 2JD, UK.
authors.forename: Eamonn A
authors.initials: EA
authors.lastname: Gaffney
authors.affiliation: Group of Structural Mechanics and Materials Modelling (GEMM), Aragón Institute of Engineering Research (I3A), University of Zaragoza, 50018 Zaragoza, Spain ; Mechanical Engineering Department, School of Engineering and Architecture (EINA), University of Zaragoza, María de Luna s/n, Betancourt Building, 50018 Zaragoza, Spain ; Biomedical Research Networking Center in Bioengineering, Biomaterials and Nanomedicine (CIBER-BBN), 50018 Zaragoza, Spain.
authors.forename: Manuel
authors.initials: M
authors.lastname: Doblaré
authors.affiliation: Group of Structural Mechanics and Materials Modelling (GEMM), Aragón Institute of Engineering Research (I3A), University of Zaragoza, 50018 Zaragoza, Spain ; Mechanical Engineering Department, School of Engineering and Architecture (EINA), University of Zaragoza, María de Luna s/n, Betancourt Building, 50018 Zaragoza, Spain ; Biomedical Research Networking Center in Bioengineering, Biomaterials and Nanomedicine (CIBER-BBN), 50018 Zaragoza, Spain.
authors.forename: Mohamed
authors.identifier: 0000-0003-0088-7222
authors.initials: M
authors.lastname: Hamdy Doweidar
mesh_terms: D000690:Amyotrophic Lateral Sclerosis / Q000378:metabolism / Q000473:pathology*; D001696:Biomechanical Phenomena; D002358:Cartilage, Articular / Q000378:metabolism / Q000473:pathology / Q000648:ultrastructure*; D019902:Chondrocytes / Q000473:pathology / Q000648:ultrastructure; D003198:Computer Simulation; D006801:Humans; D009046:Motor Neurons / Q000473:pathology / Q000648:ultrastructure*; D009997:Osmotic Pressure; D010539:Permeability; D011509:Proteoglycans
chemical_list: D011509:Proteoglycans