RESUMO
Molar incisor hypomineralisation (MIH) is a qualitative type of enamel defect, which occurs due to a failure in the biomineralisation process of the enamel organic matrix during amelogenesis. The tooth enamel affected by MIH shows changes in its chemical, structural, and mechanical properties, leading to different clinical repercussions. The color of MIH opacities varies from opaque white to yellow/brown, and elemental analyses of these lesions show a lower calcium and phosphate content, minerals that are more abundant in sound enamel. Furthermore, the incorporation of other molecules occurs, such as carbonate, a component that provides a greater degree of solubility, thus making hypomineralised enamel more susceptible to posteruptive fractures. At a structural level, the layer of hydroxyapatite crystals appears to be disorganized, with morphological changes, implying a greater degree of porosity in the structure. The increase in porosity of the structure may be associated with dental hypersensitivity, a common clinical repercussion among patients with MIH. Among the mechanical properties, a decrease in hardness and modulus of elasticity occurs, and this also makes the enamel more fragile. Deficiency in biomineralisation can be caused by changes in the function of ameloblasts or by failures at the intercellular junction that result in lower activity of proteases such as MMP-20 and KLK4. The increase in proteins in the organic matrix of enamel impairs the growth and incorporation of minerals into the hydroxyapatite crystals, so that the enamel becomes hypomineralised and has larger organic content, thus having an impact on its properties. These changes present in the enamel with MIH help to explain the clinical repercussions caused by this condition.
Assuntos
Hipoplasia do Esmalte Dentário , Esmalte Dentário , Humanos , Esmalte Dentário/patologia , Esmalte Dentário/ultraestrutura , Hipoplasia do Esmalte Dentário/patologia , Durapatita , Desmineralização do Dente/patologia , DurezaRESUMO
The aim of this study was to explore the effects of nonsteroidal anti-inflammatory drugs on biomineralization of enamel. Sixty C57Bl6 male mice were used, which were assigned into three groups: celecoxib (n = 20) or indomethacin (n = 20) treatment for a period of 28 days or received no medication (control group, n = 20). Visual inspection and microcomputed tomography were used to analyze enamel morphology. Scanning electron microscopy-Energy dispersive X-ray and Knoop microhardness test were used to quantify chemical element content (Ca, P, C, O) and enamel microhardness, respectively. Tissues were collected to investigate the synthesis, activity or nuclear translocation of metalloproteinase-20, transcription factor Runx2, dentin sialoprotein and cyclooxygenase-2 enzyme by means of immunohistochemistry, in situ zymography and indirect immunofluorescence. Treatment with indomethacin and celecoxib reduced the Ca and P content, microhardness and mineral density in enamel. Treatment with nonsteroidal anti-inflammatory drugs caused an accumulation of metalloproteinase-20 and overall increased enzymatic activity in enamel matrix, while the synthesis of the transcription factor Runx2 was inhibited by these drugs. Interestingly, indomethacin inhibited Runx2 translocation to the nucleus whereas celecoxib did not. Those findings show that non-steroidal anti-inflammatory drugs impact the enamel biomineralization and could be involved in the etiology tooth enamel defects if used during the period of tooth formation and mineralization.