Biokinetic Mechanisms Linked With Musculoskeletal Health Disparities: Stochastic Models Applying Tikhonov’s Theorem to Biomolecule Homeostasis

摘要

Multiscale technology and advanced mathematical models have been developed to control and characterize physicochemical interactions, respectively, enhancing cellular and molecular engineering progress. Ongoing tissue engineering development studies have provided experimental input for biokinetic models examining the influence of static or dynamic mechanical stimuli (Saha, A. K., and Kohles, S. S., 2010, “A Distinct Catabolic to Anabolic Threshold Due to Single-Cell Nanomechanical Stimulation in a Cartilage Biokinetics Model,” J. Nanotechnol. Eng. Med., >1(3) p. 031005; 2010, “Periodic Nanomechanical Stimulation in a Biokinetics Model Identifying Anabolic and Catabolic Pathways Associated With Cartilage Matrix Homeostasis,” J. Nanotechnol. Eng. Med., >1(4), p. 041001). In the current study, molecular regulatory thresholds associated with specific disease disparities are further examined through applications of stochastic mechanical stimuli. The results indicate that chondrocyte bioregulation initiates the catabolic pathway as a secondary response to control anabolic processes. In addition, high magnitude loading produced as a result of stochastic input creates a destabilized balance in homeostasis. This latter modeled result may be reflective of an injurious state or disease progression. These mathematical constructs provide a framework for single-cell mechanotransduction and may characterize transitions between healthy and disease states.