Abstract

Popularly known as “chalky teeth”, molar hypomineralisation (MH) affects over 1-in-5 children worldwide, triggering massive amounts of suffering from toothache and rapid decay. MH stems from childhood illness and so offers a medical-prevention avenue for improving oral and paediatric health. With a cross-sector translational research and education network (The D3 Group; thed3group.org) now highlighting this global health opportunity, aetiological understanding is urgently needed to enable better awareness, management and eventual prevention of MH. Causation and pathogenesis of “chalky enamel spots” (i.e., demarcated opacities, the defining pathology of MH) remain unclear despite 100 years of investigation. However, recent biochemical studies provided a pathomechanistic breakthrough by explaining several hallmarks of chalky opacities for the first time. This article outlines these findings in context of previous understanding and provides a working model for future investigations. The proposed pathomechanism, termed “mineralisation poisoning”, involves localised exposure of immature enamel to serum albumin. Albumin binds to enamel-mineral crystals and blocks their growth, leading to chalky opacities with distinct borders. Being centred on extracellular fluid rather than enamel-forming cells as held by dogma, this localising pathomechanism invokes a new type of connection with childhood illness. These advances open a novel direction for research into pathogenesis and causation of MH, and offer prospects for better clinical management. Future research will require wide-ranging inputs that ideally should be coordinated through a worldwide translational network. We hope this breakthrough will ultimately lead to medical prevention of MH, prompting global health benefits including major reductions in childhood tooth decay.

Highlights

  • Reviewed by: Heleni Vastardis, National and Kapodistrian University of Athens, Greece Michel Goldberg, Institut National de la Santé et de la Recherche Médicale (INSERM), France

  • molar hypomineralisation (MH) stems from childhood illness and so offers a medical-prevention avenue for improving oral and paediatric health

  • Realising something other than amelogenin must be responsible for blocking enamel hardening, attention turned to our proteomic evidence that serum albumin was uniquely prevalent in “intact” chalky opacities

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Summary

A Breakthrough in Understanding the Pathogenesis of Molar Hypomineralisation

Known as “chalky teeth”, molar hypomineralisation (MH) affects the back teeth (2-year molars, 6-year molars, or both) of 1-in-5 children worldwide, triggering massive amounts of suffering from toothache and rapid decay (Hubbard et al, 2017; Hubbard, 2018, 2020a)1,2 This costly condition appears open to medical prevention as, unlike the relatively rare enamel defects termed “amelogenesis imperfecta”, its cause isn’t primarily genetic. MH seemingly stems from illness earlier in childhood when affected teeth were hardening inside the jaw (Gottlieb, 1920; Hurme, 1949; Suckling, 1989) It follows that aetiological understanding of MH holds remarkable promise as a medical-prevention avenue for improving oral and paediatric health (Hubbard et al, 2017). Attractiveness of a biochemical approach was evident from earlier learnings about the inner workings of ameloblasts, as follows

A PROTEOMIC WINDOW TO THE FRAGILITY OF ENAMEL CELLS
A CATEGORICAL ANSWER ABOUT ENAMEL PROTEINS IN CHALKY ENAMEL
A PATHOMECHANISTIC BREAKTHROUGH FOR MOLAR HYPOMINERALISATION
CONCLUSION
DATA AVAILABILITY STATEMENT

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