BIOMINERALIZATIONChanges in the quality of bone with age and disease
Mineralization profiles are a much more sensitive index of tissue aging than chronological age. In normal physiological conditions, there are shifts in mineralization towards lower densities when turnover is high and towards higher densities with aging. We are studying the correlation between these changes and the lowering of bone mechanical properties which results in fractures. In the case of postmenopausal osteoporosis (high turnover), where we have found a shift to lower mineralization. We are investigating the changes in cancellous bone architecture and material properties as the mechanism leading to vertebral fractures. In the case of age-related osteoporosis, we have shown that there is a non linear increase in mineralization with age in humans together with a decrease in macroscopic density and an increase in porosity. It has also been shown that microcracks accumulate with age in cortical bone. We are therefore investigating the hypothesis that increased mineralization leads to accumulation of microcracks leading to fatigue damages and to cortical bone fractures. Both major functions of the skeletal system (ion homeostasis and mechanical support) are dependent on the chemical nature, size, shape and orientation of the mineral component. It is also dependent on the interaction between the mineral and the organic matrix because soluble, mineral bound and collagen bound proteins have different effects on the fabric of bone. Because of the rates at which calcified tissues are turned over, there are populations of mineral particles of different ages and properties in every sample. Therefore, the changes in chemical and structural characteristics of the mineral component and its interaction with the organic matrix during formation, maturation and resorption need to be understood to interpret changes in the quality of the bone fabric at a molecular and tissue level to distinguish between normal and pathological bone loss. |