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The diphosphonates are a group of synthetic compounds which are adsorbed onto hydroxyapatite crystal surfaces and inhibit both the growth and dissolution of these crystals. They also inhibit mineralisation and resorption of bone in vivo. The effects of diphosphonates were tested on the attachment of macrophages to bone and on the dissolution of bone mineral by macrophages. Attachment was unaffected but resorption was inhibited. Diphosphonates were found to be cytotoxic at much lower concentrations when bone mineral was present, and the most likely explanation for the effects of diphosphonate on bone resorption is that the drug is adsorbed onto the mineral surface where it reaches cytotoxic concentrations.

Thin sections of rat incisor enamel were studied with the electron microscope. Fringe patterns having repeat periods in the range 3.1–8.2 A were seen in individual enamel crystals. These images were interpreted as representing the resolution of corresponding planes in the hydroxyapatite crystal lattice. The lattice spacings and interplanar angles were identified by comparing the observations with available data derived from X-ray diffraction analysis.

Bone serves two distinct functions, viz., (1) it aids to protect part of the body, to support it in rest and in locomotion, and (2) it plays the role of a store of inorganic matter helpful in the mineral homeostasis in the blood and in the extracellular fluids. Bone owes most of its functional characteristics to its mineralization, i.e., to the presence within an organic matrix — gel-like polysaccharides which form a continuous phase and embed collagen fibres — of a system of discrete submicroscopic particles built of a complex mineral substance chiefly composed of calcium, phosphate and carbonate. The mineral phase gives a Roentgen-ray diffraction pattern characteristic of a structure called by the minerologists hydroxyapatite crystal lattice.

The control of hydroxyapatite crystal initiation and growth during enamel development is thought to be mediated via the proteins of the extracellular matrix. However, the precise nature of these matrix-mineral interactions remains obscure. The aim of the present study was to use a combination of atomic and chemical force microscopy to characterize developing enamel crystal surfaces and to determine their relationship with endogenous enamel matrix protein (amelogenin). The results show regular and discrete domains of various charges or charge densities on the surfaces of hydroxyapatite crystals derived from the maturation stage of enamel development. Binding of amelogenin to individual crystals at physiological pH was seen to be coincident with positively charged surface domains. These domains may therefore provide an instructional template for matrix-mineral interactions. Alternatively, the alternating array of charge on the crystal surfaces may reflect the original relationship with, and influence of, matrix interaction with the crystal surfaces during crystal growth.

Previous freeze-etching studies of developing enamel [21] revealed collinear arrays of spherical structures (~50 nM dia) of similar width to the crystals of mature tissue. Concomitant with matrix degradation/processing, spherical structures became less distinct until, coincident with massive matrix loss, only crystal outlines were seen. More recently, using Atomic force microscopy technology [22], early crystals exhibited topology reminiscent of these collinear spherical structures. After matrix loss these were replaced by similarly sized bands of positive charge density on the crystal surfaces [28]. The data suggest enamel crystals may form from mineral-matrix spherical subunits. Matrix processing may generate mineral nuclei and lead to their fusion and transformation into long apatite crystals. Support for this view derives from the appearance of short crystal segments in amelogenesis imperfecta (hypoplastic AI) or abnormally large crystals alongside 50 nM diameter spherical mineral subunits (hypomatura...

Hydroxyapatite crystal deposition and stabilization within the collagen matrix of bone and dentin have been linked to the presence of noncollagenous proteins (NCP). Dentinogenesis imperfecta (DI), a genetic disorder of dentin mineralization, is being studied as a model for the analysis of mineralization mechanisms. A comparative study of the NCP in normal human dentin and dentinogenesis imperfecta Type II (hereditary opalescent dentin) dentin has been performed. The proteins of each tissue were extracted and separated using a variety of techniques. The calcium-binding, highly phosphorylated protein phosphophoryn was one of the principal NCP in normal human teeth dentin, whereas there was no evidence for the presence of such a component in the DI teeth. These data imply that dentin phosphophoryn may be related in function to the mineralization process. A similar calcium-binding protein defect should be sought in the various types of osteogenesis imperfecta.

(2005). Growth Of Hydroxyapatite Crystal On The Surface Of Pure Cotton Fabric Previously Modified Using Titanium Isopropoxide. Materials Research Innovations: Vol. 9, No. 3, pp. 66-67.

Hydroxyapatite crystals cause extensive membrane damage in granulocytes and erythrocytes, as is evident from the leakage of cellular constituents of these cells upon exposure to crystals. In granulocytes this membrane damage is linked to phagocytosis. Both granulocyte and erythrocyte lysis depend on electrostatic interactions of crystals with membranes, in which positive charges on the crystals are involved.