Evaluation of Fluoride Concentration in Commercially Available Bottled Water in Romania--A Potential Risk Factor for Dental Fluorosis  
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1 Department of Paediatric Dentistry, Faculty of Dental Medicine, \"[PERSON]\" University of Medicine and Pharmacy Iasi, 16 Universitati Str., 700115 Iasi, Romania; [EMAIL_ADDRESS] (E.M.); [EMAIL_ADDRESS] (A.S.); [EMAIL_ADDRESS] (V.T. ); [EMAIL_ADDRESS] (C.S.) [PERSON]  
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2 Department of Paediatric Dentistry, Faculty of Dental Medicine, \"[PERSON]\" University of Medicine and Pharmacy Iasi, 16 Universitati Str., 700115 Iasi, Romania  
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gels or varnishes containing high levels of F results in the formation of a temporary layer resembling calcium fluoride on the surface of the enamel [9]. This layer releases F when the pH decreases due to acid production, enabling it to contribute to enamel remineralisation or affect bacterial metabolism [6; 9]. The primary sources of systemic F exposure include the diet (water and food), as well as fluoride-containing oral hygiene or dental products such as toothpaste, mouthwash, dental floss, gels, foams, varnishes, silver diamine fluoride (SDF), slow-release F beads [3; 5; 7; 9; 10; 11]. While Fs have played a crucial role in promoting oral health over the past 60 years and continue to be an important tool in the fight against dental caries in both children and adults, excessive systemic intake of F during critical periods of dental enamel formation (amelogenesis) can result in dental fluorosis (DF) [5; 9; 10]. The optimal dose of F intake is recommended to be 0.05 mg F/kg body weight (bw)/day [6; 12]. Ameloblasts are the cells responsible for the process of amelogenesis. Amelogenesis comprises four main stages: pre-secretory, secretory, transition, and maturation [11]. During the secretory stage, ameloblasts secrete enamel proteins into the enamel matrix [13]. Some studies suggest that chronic exposure to F at this stage can reduce matrix biosynthesis or disturb vesicular transport in secretory ameloblasts, resulting in a slight reduction in enamel thickness [11; 14]. Furthermore, late secretory ameloblasts may detach from the surface and form subameloblastic cysts, leading to the clinical manifestation of shallow occlusal pits, which are often observed in severe forms of DF [11; 14]. In addition, F exposure during this stage has been linked to the development of accentuated perikymata, which is a clinical sign of a mild form of DF [11]. During the transition and maturation stages, the enamel extracellular matrix undergoes enzymatic modification, enabling the continued deposition of minerals required for the development of mature enamel [14]. Chronic F exposure during the maturation stage can lead to the retention of amelogenin proteins, potentially delaying the final mineralisation of the enamel matrix [11; 13]. This delay in mineralisation can contribute to the development of subsurface hypomineralisation, which is one of the characteristic features of DF [11]. As a result, enamel affected by DF exhibits specific characteristics, such as enlarged intercrystalline spaces within the hydroxyapatite structure. These spaces are filled with residual proteins and water [13]. These alterations are specific to hypomineralised enamel and are clinically manifested by increased porosity (subsurface hypomineralisation), reduced translucency, and increased opacity [2]. Additionally, the excess of F adversely affects the bond strength of both conservative [15] and orthodontic materials [16].