Objective Hyaline cartilage degenerative pathologies induce morphologic and biomechanical changes resulting in cartilage tissue damage. In pursuit of therapeutic options, electrical and mechanical stimulation have been proposed for improving tissue engineering approaches for cartilage repair. The purpose of this review was to highlight the effect of electrical stimulation and mechanical stimuli in chondrocyte behavior. Design Different information sources and the MEDLINE database were systematically revised to summarize the different contributions for the past 40 years. Results It has been shown that electric stimulation may increase cell proliferation and stimulate the synthesis of molecules associated with the extracellular matrix of the articular cartilage, such as collagen type II, aggrecan and glycosaminoglycans, while mechanical loads trigger anabolic and catabolic responses in chondrocytes. Conclusion The biophysical stimuli can increase cell proliferation and stimulate molecules associated with hyaline cartilage extracellular matrix maintenance.
Cell membrane is a lipid bilayer that allows the flow of ions through their ionic pumping proteins. The ionic flow can be stimulated with external stimuli to activate specific signaling pathways intracellularly. Although studies have applied electric and magnetic stimuli to modify the cell function, the parameters to stimulate the cell membrane are unknown. Accordingly, a computational model to simulate the effect of electric and magnetic fields on the cell membrane was developed. Cells were stimulated with electric fields from 45 × 103 V/m to 12.6 × 105 V/m and magnetic fields of 2 mT, at frequencies of 60 kHz, 10 MHz, and 1 GHz. Results showed that the electric fields applied to the cell membrane tend to increase according to the frequency used, while magnetic fields do not have any effect on it. It was observed that electric fields generate a high voltage concentrator in the cell membrane of ellipsoidal cells when a frequency window from 1 kHz to 1 GHz was applied. These findings demonstrate that depending on the intensity of the field and frequency, it was possible to stimulate different cell membrane zones. This model is a promising tool to establish the adequate parameters to stimulate cells, and accurately predict if the stimulation modifies the cell membrane potential.
Long bone formation starts early during embryonic development through a process known as endochondral ossification. This is a highly regulated mechanism that involves several mechanical and biochemical factors. Because long bone development is an extremely complex process, it is unclear how biochemical regulation is affected when dynamic loads are applied, and also how the combination of mechanical and biochemical factors affect the shape acquired by the bone during early development. In this study, we develop a mechanobiological model combining: (1) a reaction-diffusion system to describe the biochemical process and (2) a poroelastic model to determine the stresses and fluid flow due to loading. We simulate endochondral ossification and the change in long bone shapes during embryonic stages. The mathematical model is based on a multiscale framework, which consisted in computing the evolution of the negative feedback loop between Ihh/PTHrP and the diffusion of VEGF molecule (on the order of days) and dynamic loading (on the order of seconds). We compare our morphological predictions with the femurs of embryonic mice. The results obtained from the model demonstrate that pattern formation of Ihh, PTHrP and VEGF predict the development of the main structures within long bones such as the primary ossification center, the bone collar, the growth fronts and the cartilaginous epiphysis. Additionally, our results suggest high load pressures and frequencies alter biochemical diffusion and cartilage formation. Our model incorporates the biochemical and mechanical stimuli and their interaction that influence endochondral ossification during embryonic growth. The mechanobiochemical framework allows us to probe the effects of molecular events and mechanical loading on development of bone.
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