| description abstract | This study examines the theoretical foundations for the damage mechanics of biological tissues in relation to viscoelasticity. Its primary goal is to provide a mechanistic understanding of well-known experimental observations in biomechanics, which show that the ultimate tensile strength of viscoelastic biological tissues typically increases with increasing strain rate. The basic premise of this framework is that tissue damage occurs when strong bonds, such as covalent bonds in the solid matrix of a biological tissue, break in response to loading. This type of failure is described as elastic damage, under the idealizing assumption that strong bonds behave elastically. Viscoelasticity arises from three types of dissipative mechanisms: (1) Friction between molecules of the same species, which is represented by the tissue viscosity. (2) Friction between fluid and solid constituents of a porous medium, which is represented by the tissue hydraulic permeability. (3) Dissipative reactions arising from weak bonds breaking in response to loading, and reforming in a stress-free state, such as hydrogen bonds and other weak electrostatic bonds. When a viscoelastic tissue is subjected to loading, some of that load may be temporarily supported by those frictional and weak bond forces, reducing the amount of load supported by elastic strong bonds and thus, the extent of elastic damage sustained by those bonds. This protective effect depends on the characteristic time response of viscoelastic mechanisms in relation to the loading history. This study formalizes these concepts by presenting general equations that can model the damage mechanics of viscoelastic tissues. | |
