  The mineralized collagen fibril is the main building block of hard tissues
and it directly affects the macroscopic mechanics of biological tissues such as
bone. The mechanical behavior of the fibril itself is determined by its
structure: the content of collagen molecules, minerals, and cross-links, and
the mechanical interactions and properties of these components.
Advanced-Glycation-Endproducts (AGEs) cross-linking between tropocollagen
molecules within the collagen fibril is one important factor that is believed
to have a major influence on the tissue. For instance, it has been shown that
brittleness in bone correlates with increased AGEs densities. However, the
underlying nano-scale mechanisms within the mineralized collagen fibril remain
unknown. Here, we study the effect of mineral and AGEs cross-linking on fibril
deformation and fracture behavior by performing destructive tensile tests using
coarse-grained molecular dynamics simulations. Our results demonstrate that
after exceeding a critical content of mineral, it induces stiffening of the
collagen fibril at high strain levels. We show that mineral morphology and
location affect collagen fibril mechanics: The mineral content at which this
stiffening occurs depends on the mineral's location and morphology. Further,
both, increasing AGEs density and mineral content lead to stiffening and
increased peak stresses. At low mineral contents, the mechanical response of
the fibril is dominated by the AGEs, while at high mineral contents, the
mineral itself determines fibril mechanics.
