Biomineralization is a dynamic, complex, lifelong process by which living organisms control precipitations of inorganic nanocrystals within organic matrices to form unique hybrid biological tissues, for example, enamel, dentin, cementum, and bone. Understanding the process of mineral deposition is important for the development of treatments for mineralization-related diseases and also for the innovation and development of scaffolds. This review provides a thorough overview of the up-to-date information on the theories describing the possible mechanisms and the factors implicated as agonists and antagonists of mineralization. Then, the role of calcium and phosphate ions in the maintenance of teeth and bone health is described. Throughout the life, teeth and bone are at risk of demineralization, with particular emphasis on teeth, due to their anatomical arrangement and location. Teeth are exposed to food, drink, and the microbiota of the mouth; therefore, they have developed a high resistance to localized demineralization that is unmatched by bone. The mechanisms by which demineralization-remineralization process occurs in both teeth and bone and the new therapies/technologies that reverse demineralization or boost remineralization are also scrupulously discussed. Technologies discussed include composites with nano- and micron-sized inorganic minerals that can mimic mechanical properties of the tooth and bone in addition to promoting more natural repair of surrounding tissues. Turning these new technologies to products and practices would improve health care worldwide.

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Demineralization–remineralization dynamics in teeth and bone

Dental enamel is the hardest and most mineralized tissue in extinct and extant vertebrate species and provides maximum durability that allows teeth to function as weapons and/or tools as well as for food processing. Enamel development and mineralization is an intricate process tightly regulated by cells of the enamel organ called ameloblasts. These heavily polarized cells form a monolayer around the developing enamel tissue and move as a single forming front in specified directions as they lay down a proteinaceous matrix that serves as a template for crystal growth. Ameloblasts maintain intercellular connections creating a semi-permeable barrier that at one end (basal/proximal) receives nutrients and ions from blood vessels, and at the opposite end (secretory/apical/distal) forms extracellular crystals within specified pH conditions. In this unique environment, ameloblasts orchestrate crystal growth via multiple cellular activities including modulating the transport of minerals and ions, pH regulation, proteolysis, and endocytosis. In many vertebrates, the bulk of the enamel tissue volume is first formed and subsequently mineralized by these same cells as they retransform their morphology and function. Cell death by apoptosis and regression are the fates of many ameloblasts following enamel maturation, and what cells remain of the enamel organ are shed during tooth eruption, or are incorporated into the tooth’s epithelial attachment to the oral gingiva. In this review, we examine key aspects of dental enamel formation, from its developmental genesis to the ever-increasing wealth of data on the mechanisms mediating ionic transport, as well as the clinical outcomes resulting from abnormal ameloblast function.

Dental enamel formation and implications for oral health and disease.

Fluorides are present in the environment. Excessive systemic exposure to fluorides can lead to disturbances of bone homeostasis (skeletal fluorosis) and enamel development (dental/enamel fluorosis). The severity of dental fluorosis is also dependent upon fluoride dose and the timing and duration of fluoride exposure. Fluoride's actions on bone cells predominate as anabolic effects both in vitro and in vivo. More recently, fluoride has been shown to induce osteoclastogenesis in mice. Fluorides appear to mediate their actions through the MAPK signaling pathway and can lead to changes in gene expression, cell stress, and cell death. Different strains of inbred mice demonstrate differential physiological responses to ingested fluoride. Genetic studies in mice are capable of identifying and characterizing fluoride-responsive genetic variations. Ultimately, this can lead to the identification of at-risk human populations who are susceptible to the unwanted or potentially adverse effects of fluoride action and to the elucidation of fundamental mechanisms by which fluoride affects biomineralization.

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Fluoride's Effects on the Formation of Teeth and Bones, and the Influence of Genetics

Fluoride (F−) originating from many natural geologic sources and anthropogenic activities has imposed a substantial environmental health risk. More than 200 million people from more than 35 nations...

Fluoride and human health: Systematic appraisal of sources, exposures, metabolism, and toxicity

Silver diamine fluoride (SDF) is found to promote remineralization and harden the carious lesion Hydroxyapatite crystallization is a crucial process in remineralization; however, the role of SDF in crystal formation is unknown We designed an in vitro experiment with calcium phosphate with different SDF concentrations (038, 152, 266, 380 mg/mL) to investigate the effect of this additive on the nucleation and growth of apatite crystals Two control groups were also prepared-calcium phosphate (CaCl2·2H2O + K2HPO4 in buffer solution) and SDF (Ag[NH3]2F in buffer solution) After incubation at 37 oC for 24 h, the shape and organization of the crystals were examined by bright-field transmission electron microscopy and electron diffraction Unit cell parameters of the obtained crystals were determined with powder X-ray diffraction The vibrational and rotational modes of phosphate groups were analyzed with Raman microscopy The transmission electron microscopy and selected-area electron diffraction confirmed that all solids precipitated within the SDF groups were crystalline and that there was a positive correlation between the increased percentage of crystal size and the concentration of SDF The powder X-ray diffraction patterns indicated that fluorohydroxyapatite and silver chloride were formed in all the SDF groups Compared with calcium phosphate control, a contraction of the unit cell in the a-direction but not the c-direction in SDF groups was revealed, which suggested that small localized fluoride anions substituted the hydroxyl anions in hydroxyapatite crystals This was further evidenced by the Raman spectra, which displayed up-field shift of the phosphate band in all the SDF groups and confirmed that the chemical environment of the phosphate functionalities indeed changed The results suggested that SDF reacted with calcium and phosphate ions and produced fluorohydroxyapatite This preferential precipitation of fluorohydroxyapatite with reduced solubility could be one of the main factors for arrest of caries lesions treated with SDF

Formation of Fluorohydroxyapatite with Silver Diamine Fluoride

This review aims to outline the effects of fluoride on the biological processes involved in the formation of tooth tissues, particularly dental enamel. Attention has been focused on mechanisms which, if compromised, could give rise to dental fluorosis. The literature is extensive and often confusing but a much clearer picture is emerging based on recent more detailed knowledge of odontogenesis. Opacity, characteristic of fluorotic enamel, results from incomplete apatite crystal growth. How this occurs is suggested by other changes brought about by fluoride. Matrix proteins, associated with the mineral phase, normally degraded and removed to permit final crystal growth, are to some extent retained in fluorotic tissue. Fluoride and magnesium concentrations increase while carbonate is reduced. Crystal surface morphology at the nano-scale is altered and functional ameloblast morphology at the maturation stage also changes. Fluoride incorporation into enamel apatite produces more stable crystals. Local supersaturation levels with regard to the fluoridated mineral will also be elevated facilitating crystal growth. Such changes in crystal chemistry and morphology, involving stronger ionic and hydrogen bonds, also lead to greater binding of modulating matrix proteins and proteolytic enzymes. This results in reduced degradation and enhanced retention of protein components in mature tissue. This is most likely responsible for porous fluorotic tissue, since matrix protein removal is necessary for unimpaired crystal growth. To resolve the outstanding problems of the role of cell changes and the precise reasons for protein retention more detailed studies will be required of alterations to cell function, effect on specific protein species and the nano-chemistry of the apatite crystal surfaces.

/pdf/the-effect-of-fluoride-on-the-developing-tooth-1x9w1dshnf.pdf

The Effect of Fluoride on the Developing Tooth

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The Effect of Fluoride on the Developing Tooth