# Altered Mechano-Electrochemical Behavior of Articular Cartilage in Populations with Obesity
## 1 Introduction  
In the last decade, obesity has become one of the most serious socioeconomic concerns in developed countries [1; 2]. This medical problem is produced by a combination of several factors such as excessive food energy intake, lack of physical activity and/or genetic susceptibility [3; 4; 5]. As a result, an increase in the probability of suffering diseases such as osteoarthritis and bone degeneration has been reported [6; 7; 8]. In particular, overload on joints generates imbalance in tissue homeostasis [9; 10]. This is mainly due to the increment of the force applied on articulations. In the case of normal weight, the applied force is three times the body weight. This force can reach six to ten times the body weight when performing activities such as climbing or running [11]. However, the transmitted force to joints in the case of people with obesity is doubled, generating excessive wear and leading to osteoarthritis [12].  
Since articular cartilage is an avascular tissue, the transport of nutrients from synovial fluid to chondrocytes occurs by diffusion and convection when loading or when chemical conditions are changing [13; 14; 15]. In this sense, cartilage counts on biomolecules also called proteoglycans. They are responsible for the turgid nature of the tissue and provide the osmotic properties needed to resistcompressive loads [16; 17]. This occurs mainly as a consequence of the negative charges attached to them, fixed charge density. These negative charges provide a repulsive force that enhances the compressive stiffness of the cartilage [18].  
Compression cycle due to body weight generates incoming and outgoing fluxes that helps in nutrients and wastes products exchange [11]. In the case of people with obesity, significant alterations are produced in water and ion fluxes as well as in tissue deformation. These fluxes are considered as essential biomarkers that indicate the degree of cartilage degeneration [19; 20]. Therefore, the study of ion fluxes and tissue deformation may reveal alterations in the cartilage tissue.  
Despite the great incidence of obesity, there are no exhaustive studies analyzing the correlation between alterations in the biological processes of cartilage and an increase in body weight. Only [PERSON] et al. [11] have addressed this issue. In their recent work, they describe several changes in protein synthesis and the subsequent reduction in extracellular matrix (ECM) production in hip articular cartilage. They studied these phenomena by means of a self-developed 1D model. However, important questions remain. How does obesity affect water and ion fluxes? Are these alterations a catalyst for osteoarthritis? Is the ion concentration in the tissue similar to that observed in people of normal weight? All these questions need to be addressed.  
To analyze and elucidate tissue behavior under these conditions, a previously described 3D computational model of cartilage behavior [19; 20; 21] is here extended and employed to study the effects of overweight on the articular joints (Figure 1). The present model considers the influence of ions on electrochemical events as well as proteoglycan repulsion in a loaded 3D environment. The main goals of this study are: (i) to analyze the role of proteoglycan repulsion in the cartilage loading problem; (ii) to study the effect of metabolic alterations (fluxes of water and ions) due to obesity on the homeostasis of femoral hip cartilage; and (iii) to quantify and compare cation and water flux in cartilage of both healthy people and those suffering from obesity when a maximal load is applied on the joint.