For this reflection blog, I decided to focus on enamel fluorosis. Like I mentioned in my previous post, enamel fluorosis, or mottled teeth, is caused by excessive fluoride intake. In controlled amounts, fluoride can help protect tooth enamel; however, there is a limit where the fluoride concentration can become damaging. The reason I selected this disease out of the three ideas that I mentioned in my last post was because of the environmental factors that are involved. From looking more into the disease, I discovered two important themes being investigated regarding fluorosis: causes for increased susceptibility and effectiveness of current treatment methods.
One reference that I found particularly interesting and useful was “Topics in Dental Biochemistry” by Martin Levine.1 This book contains many chapters on common oral diseases, and I highly recommend it if you have any interest in the subject. I think that this text does a great job of explaining enamel fluorosis, particularly regarding the history, which would make it a great starting point for an investigation into the disease. This text highlights how fluoride in the water supply is a main cause of fluorosis, and describes the path to this discovery. If I were to write a literature report on the topic, I would start with this background and then transition into how enamel fluorosis actually occurs. Conveniently, Levine’s text discusses this.1 The text mentions that fluoride incorporates itself into enamel crystals while also impacting enzymes that are important for enamel formation.1 So, I would use this text to explain exactly how fluoride does this before transitioning into current literature on the disease.
After discussing fluorosis basics, I would transition into other causes of fluorosis. One of the more recent and interesting things I found was the role of polymorphisms in genes important for enamel development. Küchler et al. recently reported that polymorphisms in TIMP1, DLX1, and DLX2 genes all contributed to increased susceptibility to enamel fluorosis.2 TIMP1 stands for tissue inhibitor of metalloproteinases, and is involved in enamel formation and biomineralization regulation.2 DLX1 and DLX2 are distal-less homologs, which also play a role in enamel formation.2 Küchler’s article cites numerous researchers who also found genetic links to susceptibility to enamel fluorosis, so I would dig deeper on this topic to better understand what actually causes increased susceptibility to the disease.2
Next, I would look into some of the possible treatment options. One of the main treatment methods for enamel fluorosis is microabrasion, Microabrasion involves treatment with a hydrochloric acid paste and using an abrasive material to file the affected surface away.3 This method is often followed by application of a composite resin, crown, or veneer to restore the thickness of the enamel and/or improve the appearance. Bassir et al. investigated the impact of fluorosis and microabrasion on the strength of the enamel-composite resin bond.3 The researchers found that fluorosis reduces the bond strength between the resin and enamel after microabrasion as compared to normal teeth.3 Bassir et al. suggested possible techniques for improving the strength, but more research still needs to be done.3 Shafiei et al. investigated different techniques regarding the application of veneers to mottled teeth, specifically focusing on the types of cement/luting agents used.4 While they focused on figuring out which types worked best, I would like to investigate why they worked best, possibly leading to better treatment options.4
If I were to actually carry out this literature review, I would start with the aforementioned texts to work my way from the history of the disease to the causes and eventually the treatment/prevention methods. While I have certainly only scratched the surface of this disease and the relevant literature, I think that this would provide a good starting point for deeper research into the disease. Each of the references listed have cited many other significant papers researching similar topics, which I would look into to better understand where the field is going.
- Levine, M. Topics in dental biochemistry; Oklahoma: Springer Berlin Heidelberg, 2011.
- Küchler, E. C.; Tannure, P. N.; Barroso de Oliveira, D. S.; Charone, S.; Nelson-Fiho, P.; Bezerra da Silva, R. A.; Castro Costa, M.; Antunes, L. S.; Maia, M. D. C.; Antunes, L. A. A. Polymorphisms in genes involved in enamel development are associated with dental fluorosis. Arch. Oral. Biol. 2017, 76, 66-69.
- Bassir, M. M.; Rezvani, M. B.; Ghomsheh, E. T.; Hosseini, Z. M. Effect of different surface treatments on microtensile bond strength of composite resin to normal and fluorotic enamel after microabrasion.
- Shafiei, F.; Memarpour, M.; Jowkar, Z. Marginal sealing of a porcelain laminate veneer luted with three different resin cements on fluorosed teeth. Int. J. Esthet. Dent. 2017, 12, 60-71.
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