Calcium phosphate apatites offer outstanding biological adaptability that can be attributed to their specific physico-chemical and structural properties. The aim of this review is to summarize and discuss the specific characteristics of calcium phosphate apatite biominerals in vertebrate hard tissues (bone, dentine and enamel). Firstly, the structural, elemental and chemical compositions of apatite biominerals will be summarized, followed by the presentation of the actual conception of the fine structure of synthetic and biological apatites, which is essentially based on the existence of a hydrated layer at the surface of the nanocrystals. The conditions of the formation of these biominerals and the hypothesis of the existence of apatite precursors will be discussed. Then, we will examine the evolution of apatite biominerals, especially during bone and enamel aging and also focus on the adaptability of apatite biominerals to the biological function of their related hard tissues. Finally, the diagenetic evolution of apatite fossils will be analyzed.

Basic calcium phosphate (BCP) crystals, including hydroxyapatite, octacalcium phosphate (OCP) and carbonate-apatite, have been associated with severe osteoarthritis and several degenerative arthropathies. Most studies have considered the chondrocyte to be a bystander in the pathogenesis of calcium crystal deposition disease, assuming that synovial cell cytokines were the only triggers of chondrocyte activation. In the present study we identified direct activation of articular chondrocytes by OCP crystals, which are the BCP crystals with the greatest potential for inducing inflammation. OCP crystals induced nitric oxide (NO) production and inducible nitric oxide synthase (NOS) mRNA expression by isolated articular chondrocytes and cartilage fragments, in a dose-dependent manner and with variations over time. OCP crystals also induced IL-1β mRNA expression. Using pharmacological and cytokine inhibitors, we observed that OCP crystals induced NO production and inducible NOS mRNA activation were regulated at both the transcriptional and the translational levels; were independent from IL-1β gene activation; and involved p38 and c-Jun amino-terminal kinase (JNK) mitogen-activated protein kinase (MAPK) pathways, as further confirmed by OCP crystal-induced p38 and JNK MAPK phosphorylation. Taken together, our data suggest that the transcriptional inducible NOS response to OCP crystals involved both the p38 and the JNK MAPK pathways, probably under the control of activator protein-1. NO, a major mediator of cartilage degradation, can be directly produced by BCP crystals in chondrocytes. Together with synovial activation, this direct mechanism may be important in the pathogenesis of destructive arthropathies triggered by microcrystals.