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The clinical management of incisor hypomineralisation (IH) as it pertains to biophysical and aesthetic recovery, especially in the teeth of young individuals, is fraught with complexity. Treatment modalities are wide and varied, and often, if used in the wrong sequence, can lead to a suboptimal aesthetic result. Approaches, such as chemical micro-abrasion, air particle abrasion and tooth whitening have been used in the past, in addition to resin infiltration for the treatment of affected enamel. The penetration depth of hypomineralised lesions by resin infiltrant has been reported to vary and be dependent on the pre-treatment modalities used. The elimination of brown-coloured aspects of the IH lesion via tray-delivered tooth whitening is critical prior to resin infiltration because once the resin has polymerised, it will be more impermeable and thus less likely to be modified by oxidative action. This case report describes an extended resin infiltration period under diminished ambient light prior to polymerisation that was required for aesthetic success.
CPD/Clinical Relevance: Ideal sequencing of treatment prior to resin infiltration is critical for physico-aesthetic success. The length of resin infiltration can be increased if results are not seen by the manufacturer-prescribed application time.
Article
The aesthetic appearance of the upper anterior sextant is a key determinant in the perceived attractiveness of a smile. It is characterised by a balance between both pink (gingival) and white (dental) elements.1 In a proportion of individuals, there is a defect in mineralisation of the organic matrix component during enamel development. Often, post-eruptive surface breakdown can lead to an increased incidence of hypersensitivity and susceptibility to caries formation. Incisor hypomineralisation is characterised clinically as white spot or combination white-brown lesions. These areas often are the source of anxiety during the expression of a smile, and can instigate negative social interactions especially among the younger population, thereby affecting confidence.
Incisor hypomineralisation is commonly classified as part of the molar–incisor hypomineralisation (MIH) spectrum, with the incidence in the northern European population ranging from 3.5% to 25%, with an average of 16%.2 Often, the mixed white and brown lesions are differentially diagnosed as fluorosis or Turner's hypoplasia.3 MIH differs from hypoplasia in that the former features a defect in mineralisation of the organic matrix, whereas the latter exhibits defective secretion of organic matrix during amelogenesis. The realm of hypomineralised lesions comprises both hypomaturation and hypocalcification. Histotypically, hypomaturation is rich in amelogenin, whereas hypocalcification is amelogenin-poor. MIH is categorised as a hypocalcified lesion, which additionally is albumin rich. Albumin is a protein normally excluded from the enamel matrix during formation because it impedes mineralisation; however, it is almost always present in hypomineralisation.4 There are proteins other than albumin that are naturally present during enamel matrix formation that regulate the size, shape and orientation of the crystals.5 In normal enamel development, enzymes work to progressively eliminate this protein content until the content is &1% by weight, and the space is occupied by tightly bound crystals.6 It is an ongoing conundrum as to how the secreted enamel matrix barrier is breached by albumin in MIH.
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