Type I collagen fibrils provide a structural framework for mineral nucleation, growth, and development during calcification of tissues such as bone, dentin and tendon of many vertebrates. Previous work has described a general mechanistic model of normal collagen- mineral interaction in which nucleation events take place on collagen surfaces and in channels or gaps defined by periodic (64-70 nm) collagen hole and overlap regions. These sites are created in early collagen molecular and macromolecular assembly. The model suggests that, once nucleated, the mineral within channel spaces grows into irregularly shaped platelets of small size and these develop into larger platelets whose detectable crystallographic c-axis direction parallels the long axis direction of the collagen fibrils with which they associate. The fate of mineral nucleated on collagen surfaces is unclear, although it is known that the volume of extracellular tissue space between adjacent collagen fibrils, like that within the fibrils, also becomes mineralized.