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Clinical Progresses in Regenerative Dentistry and Dental Tissue Engineering
Published in Vincenzo Guarino, Marco Antonio Alvarez-Pérez, Current Advances in Oral and Craniofacial Tissue Engineering, 2020
Regenerative dentistry: Making enamel—Cells that specialize in the making of enamel (ameloblasts) are no longer present in teeth with complete crown development. Therefore, an in situ cell-based strategy to regenerate enamel is not feasible. However, researchers’ creativity and ingenuity have recently allowed for the development of synthetic enamel that is fundamentally based on the use of the principles of tissue engineering and nanotechnology. Amelogenin allowed for the synthesis of elongated crystals. The combination of amelogenin and fluoride allowed for the formation of rod-like apatite crystals with dimensions that resemble the ones observed in natural enamel (Trembley A 1744).
Micromorphology, microstructure and micro-Raman spectroscopy of a case of amelogenesis imperfecta
Published in J. Belinha, R.M. Natal Jorge, J.C. Reis Campos, Mário A.P. Vaz, João Manuel, R.S. Tavares, Biodental Engineering V, 2019
Sebastiana Arroyo Bote, Alfonso Villa-Vigil, M.C. Manzanares Céspedes, Esteban Brau-Aguadé
Amelogenesis Imperfecta (AI) is characterized by presenting enamel defects, without defects in others tissues (Witkop, 1988). Hereditary defects in the enamel development or environmental exposure to chemicals and drugs can damage the ameloblasts (Ferreira et al., 2005). AI is characterized by its heterogeneous phenotypical clinical patterns of variable severity, as well as for its complex genetype (Wright, 2006; Gibson, 2008; Wang et al., 2013) and/or environmental aetiology (Hedge, 2012; Malik et al., 2012). Based on its heredity and clinical evidences, four types and numerous subtypes of AI were described in 1988 by Witkop (hypoplastic, hypomaturation, hypocalcified AI and a combination of them), and today this is the most widely used classification in the clinical practice. The development of enamel starts with the secretion of the enamel protein matrix by the ameloblasts, followed by its calcification and maturation (Sapp et al., 2005; Malik et al., 2012). Less than 1% of the mature enamel is constituted by organic components, while the mineral components constitute more than a 95%. The enamel mineral crystals are deposited in compact hexagonal rod-shaped structure, making this tissue the hardest in the human body (Nanci, 2012). Numerous genes have been reported as responsible of the regulation of this complex process (Sapp et al., 2005; Bailleul-Forestier et al., 2008; Lee et al., 2008; Misiadis & Luder, 2011; Luder et al., 2013; Simmer et al., 2013; Wang et al., 2014; Zhang et al., 2015; Prasad et al., 2016). Mutations of AMELX (amelogenin), ENAM (enamelin) (Misiadis & Luder, 2011), COL17A1 (Prasad et al., 2016) and FAM20A (Wang et al., 2014) have been proven as causes of hypoplastic AI, either with smooth or rough enamel; while the AI with hypomature phenotype has been attributed to genetic defects in AMELX, MMP20, KLK4 and WDR72. Hypocalcified AI have been reported to be caused by FAM83H or C4orf26 (Kim et al., 2008; Parry et al., 2012; Luder et al., 2013) in humans. Additionally, some studies indicate that a mutation in one gene could be related to more than one type of AI; thus CNNM4 mutation is related to hypoplastic/hypomineralized types (Lee et al., 2008), DLX3 mutation is related with and hypomature/hypoplastic types (Wang et al., 2014) and C4orf26 hypomineralized-hypoplastic types (Prasad et al., 2016).
General introduction
Published in Abdulai Salifu, Fluoride Removal from Groundwater by Adsorption Technology, 2017
Intake of excess fluoride (beyond 1.5 mg/L) for long periods can, however, result in negative human health effects. Fluoride has several mechanism of toxicity (Firempong et al., 2013; Shin, 2016; Whirtford, 1996). When it enters into the human body, mainly through the intake of water and to some extent food and dental products, about 75 — 90% is adsorbed (Harder, 2008; Shomer, 2004; Fawell et al., 2006). Ingested fluoride ions initially acts on the gastrointestinal musoca to form hydrofluoric acid (HF) in the stomach by combining with hydrogen ions under the acidic condition in the stomach. The formation of hydrofluoric acid leads to nausea, diarrhoea, vomiting, gastricintestinal irritation and abnominal pains. About 40% of the ingested fluoride is adsorbed from the stomach as HF. Fluoride not adsorbed in the stomach is adsorbed in the instestine. Once absorbed into the blood stream, fluoride readily distributes throughout the body and tend to accumulate in calcium rich areas such as bone and teeth (dentin and enamel) (Fawell et al., 2006; Firempong et al., 2013; Shin, 2016; Gessner et al., 1994). At moderately high levels (1.5 — 4 mg/L) of ingestion, it leads to dental fluorosis, particularly in children. According to Whirtford (1996), even though the mechanisms underlying the development of dental fluorosis are not well understood, there is evidence that the processes probably involve effects on the ameloblasts, which deposit tooth enamel. Ameloblast are cells present during tooth development (in childhood), and secretes the anamel proteins (i.e enamelin and amelogenin), that mineralizes to form the tooth enamel. These cells are observed to be very sensitive to their environment, and bodily stressors (during childhood) can affect their function hence, cause interruption in enamel production. Presumably exposure of children (between the ages of 2 to 8 years old) who are still undergoing mineralization in the permanent teeth to excess fluoride (1.5 — 4 mg/L), is a type of stressor that disrupts the enamel production and results in the development of dental fluorosis (Firempong et al., 2013; Whirtford, 1996; Fawell et al., 2006). Dental fluorosis, which is characterized by discoloured, blackened, mottled or chalky-white teeth, is by far the most common manifestation of chronic use of high-fluoride water. A person affected by dental fluorosis is an indication of overexposure to fluoride during childhood when the teeth were developing (Fawell et al. 2006). These effects are, however, not apparent if the teeth are already fully grown prior to the fluoride overexposure. Therefore if an adult shows no signs of dental fluorosis, it does not necessarily mean his or her fluoride intake is within safety limits and could be at risk of other fluoride-related health hazards.
Fluoride and human health: Systematic appraisal of sources, exposures, metabolism, and toxicity
Published in Critical Reviews in Environmental Science and Technology, 2020
Humayun Kabir, Ashok Kumar Gupta, Subhasish Tripathy
The effects of F− on teeth are complex and dose-related. As discussed earlier, ingestion of F− at a low level prevents dental caries. However, ingestion of large amounts may cause dental fluorosis (Celeste & Luz, 2016). Dental fluorosis is characterized by yellowish or brownish striations or mottling of the tooth surface or enamel, signs of F− toxicity. As the development of enamel occurs, the mineralization increases within the developing tooth, accompanied by the loss of matrix protein. Intake of excessive F− interferes with amelogenesis and dentinogenesis processes, thus resulting in deformity in the enamel and dentin (Swarup & Dwivedi, 2002). Fluoride decreases free Ca2+ and interferes with enamel mineralization by hampering protease activity and consequently triggering large gaps in enamel structure, and increasing enamel porosity and the retention of matrix proteins (Aoba & Fejerskov, 2002). The mechanism of F− interactions with calcified tissue is depicted in Figure 6. Fluoride has a cytotoxic effect on ameloblasts (dental pulp cells) and odontoblasts. Excessive exposure to F− causes the localized death of ameloblasts, thus resulting in defects in the enamel. The odontoblasts become atrophic, and a brown discoloration emerges on dentin (Chang & Chou, 2001; Krook & Maylin, 1979 as cited in Ranjan & Ranjan, 2015). Dental fluorosis is more likely in individuals exposed to excess F− while teeth are developing (incisors). The level of dental fluorosis largely depends on the degree of F− exposure until the ages of 8–10 years old. Studies conducted in several districts of India have shown that 70% of adolescents consuming drinking water with F− above 1.5 mg L−1 are affected by dental fluorosis (Chaudhry & Gupta, 2017; Reddy et al., 2017). People exposed to high F− after adulthood have lower frequency and severity of dental lesions than those exposed as teenagers. Once developed, dental lesions mostly remain in the same state and do not indicate the status of the F− intake. The severity of dental fluorosis can be classified according to physical observation of the lesions on incisors (Swarup & Dwivedi, 2002). The concentration of F− in drinking water and the prevalence of dental fluorosis have been systematically reviewed and analyzed by McDonagh et al. (2000). The authors analyzed 88 studies from 33 countries by using univariate regression models and concluded that 1 mg L−1 of additional F− in drinking water is associated with a 48% and 15% prevalence of dental fluorosis in fluoridated and non-fluoridated areas, respectively. Depending on the alterations in two severely affected teeth, Dean (1934) developed a fluorosis index that divides dental fluorosis into five categories. Shupe, Olson, and Sharma (1979) have suggested a 0–5 scale to indicate the severity of dental fluorosis. Another grouping system based on expression of dental lesions in fluorotic cattle has been reported (Krook, Maylin, Lillie, & Wallace, 1983).