Abstract: Calcification of octacalcium phosphate on differently packaged intraocular implant lens surfaces has been studied in vitro in solutions supersaturated with respect to OCP. The results of this study indicate that hydrophobic cyclic silicones adsorbed on the IOL surfaces interact strongly with hydrophobic hydrocarbon chains of the fatty acids, creating a layer of amphiphiles oriented with functional carboxylate groups exposed to the aqueous solution and serving as active calcification sites. Furthermore, calcification was observed on implanted intraocular lens (IOL) surfaces when viscoelastic substances were applied during surgery. Three different commercial viscoelastic materials (Viscoat@, OcuCoat@, and Amvisc @ Plus) were investigated in vitro with nanomolar sensitivity using a constant composition method and it was found that different types of Viscoelastics display different calcification properties. The mechanism of additive-brushite crystal growth inhibition depends on the interaction and structure of the additive molecule and the geometric fit between it and particular crystal faces. OPN, with numerous carboxylate-rich functional groups, can effectively interact with most brushite faces, retarding the growth rate when present at very low concentrations. Magnesium ions, which influenced the growth habit and kinetics by inhibiting step movement on different steps, and is almost certainly the result of specific interactions. Citric acid, with several low charged functional carboxylate groups, has a significant inhibition effect by altering mineral surface energies, thus changing the critical step length and delaying the formation of active steps for crystal growth. The in vivo formation of calcium oxalate concretions having CaP nidi is simulated in an in vitro dual constant composition (DCC) system. The brushite dissolution provides calcium ions that raise the supersaturation with respect to COM, which is heterogeneously nucleated either on or near the surface of the dissolving calcium phosphate crystals. The COM crystallites may then form aggregates leading to kidney stone formation. In support of the clinical observations, the results of these studies demonstrate the participation of calcium phosphate phases in COM crystallization and will improve our understanding of the physical chemical mechanisms responsible for kidney stone formation.