Surface poisoning of synthetic and biological apatites

Bone mineral consists of small crystals of CO3-containing, Ca-deficient, non-stoichiometric hydroxyapatite (HA) with a large and reactive surface of 100–200m2g−1. This paper reviews the action of various chemical moieties that adsorb on the crystal surfaces of synthetic and biological apatites and which poison their formation and growth. Three biologically relevant in vitro test systems are used to study the inhibition of HA formation: (a) solution transformation of amorphous calcium phosphate (ACP) to HA, (b) direct formation of HA from solution, and (c) growth of HA crystals. Naturally occurring condensed phosphates with POP bonds, such as P2O7 and ATP, are effective in delaying or slowing the onset and/or the rate of formation of HA in all test systems at concentrations as low as 10−5 to 10−6M. Because of these properties, condensed phosphates are thought to be involved in regulating biological mineralization. Diphosphonates (originally developed as detergents), with PCPbonds, act in a similar manner to condensed phosphates in inhibiting HA formation. Both molecular species strongly adsorb to forming HA critical nuclei, blocking growth to HA crystals. The stability of PCP bonds in aqueous media makes diphosphonates effective therapeutic agents for some metabolic bone disorders. Aluminum ion is effective in slowing the HA formation rate in systems (a), (b) and (c) by adsorbing on HA surfaces and blocking growth sites. This observation partly explains the impairment of mineralization (osteomalacia) associated with aluminum accumulation in bone seen in some patients on renal hemodialysis.