C Robinson, J Kirkham, S J Brookes, W A Bonass and R C Shore
Leeds Dental Institute, Division of Oral Biology, United Kingdom.
The central problems of enamel biochemistry are the mechanisms concerned with initiation and development of the mineral crystals, together with their architectural arrangement within the tissue. These processes are mediated by the extracellular matrix as well as the composition of the mineral itself. Initial mineral deposition occurs at the dentine surface, nucleated either by dentinal components or early enamel matrix, possibly non-amelogenin molecules. The early crystals are small in size and rich in magnesium and carbonate resulting in relatively poor crystallinity. This is in spite of the fact that fluoride is high at this stage. Crystal development includes a reduction in magnesium, carbonate and fluoride as crystals increase in length following the retreating ameloblasts from the dentine. The matrix acquires increasing concentrations of amelogenin and albumin. Prismatic structure begins to develop together with some growth of crystals in width and thickness. Degradation of amelogenin and non-amelogenin molecules generates a series of specific molecular fragments possibly concerned with modulating crystal growth and morphology and the creation of prismatic and interprismatic structures. Towards the end of secretion, matrix, now almost completely degraded, is replaced by fluid followed by massive crystal growth during maturation. Degradation of albumin also occurs at this stage, probably as a result of comprehensive destruction of molecules which might impair crystal growth. Selective acquisition of magnesium and fluoride at this stage may reflect the hydrated state of the tissue as well as cell changes. Fluid is displaced as crystals grow and the enamel acquires concentrations of mineral characteristic of mature tissue.