Elucidating the Effect of Carbonate Location, Cationic Substitutions, and Apatite Maturation on the Dissolution and Recrystallization Mechanisms of Apatites

Aging significantly alters the skeleton and the surrounding body fluids. The electrolyte content changes and the pH of body fluids becomes acidic as we age. Mineralized tissues react to such changes by releasing ions, such as bicarbonate or calcium, to maintain homeostasis between bone/teeth and the surrounding fluid. While this occurs in young healthy individuals without harmful effects, the mineralized tissues in older populations are unable to maintain this balance. It remains unclear why this occurs in older biological mineral. Aging increases carbonate content in mineralized tissues and increases bone-resorption, suggesting that these are not responsible for the reduced output in the older population. Additionally, mineral maturation and crystallinity increases with aging, which is contrary to biomimetic mineral with the same carbonate content. This suggests that the mineral’s structure may be the reason for the decreased inability to mediate the pH back to homeostasis. Therefore, this thesis elucidates how age-related changes within the mineral’s composition and structure as well as the changes in body fluid composition will affect the dissolution and recrystallization mechanism of biomimetic carbonated apatites. To do so, carbonate location with increasing carbonate content and apatite maturity were analyzed at different pHs. Additionally, sodium and potassium in the solution were used to determine how solutes may affect the apatite structure and the dissolution/recrystallization process. Using state-of-the-art techniques, we found that the carbonate location affected the dissolution/recrystallization process with B-type CO32- having the highest solubility and A-type CO32- with the least. Labile CO32- was released into the solution with compositional and structural reversions to non-carbonated biomimetic apatites properties. Sodium provided more apatite dissolution while potassium retained more compositional and structural properties after exposure. Additionally, highly matured apatites had minimal changes to the structural properties even after releasing CO32-. We conclude that increased A-type CO32- and apatite maturity may contribute to the inability of older mineral to buffer body fluids, while sodium and B-type CO32- may support the increased solubility seen in older mineral as well. Understanding the interplay between the age-related changes in mineralized tissues and body fluids will help develop preventative and personalized therapeutics for the aging population.