## 1 Introduction  
Untreated tooth decay in primary teeth can lead to pain, bacteremia, and high treatment costs. It can also result in disturbances in growth and development, speech and chewing, reduced self-esteem, and damage to permanent teeth [1]. It has been reported that the presence of decay during the primary dentition period may affect the occurrence of decay during the permanent dentition period and could be used as a risk indicator for predicting caries during this stage [2]. Strategies within the minimally invasive dentistry approach, aimed at maintaining the health of permanent teeth throughout life and ensuring that primary teeth remain healthy and functional until their natural exfoliation, include remineralizing demineralized enamel and implementing caries prevention measures [3]. Dental caries, which is defined as a disease that occurs when the balance between the demineralization and remineralization phases that follow each other in the mouth is disturbed in the direction of demineralization, is still the most common childhood disease today, despite advances in preventive and therapeutic practices [4]. Initial caries lesions are white spot lesions without cavitations observed as areas of subsurface demineralization in enamel. They are considered the first stage, in which dental caries become visible [5]. Demineralization is the dissolution of minerals on the tooth surface when the acids released from the metabolism of fermentable carbohydrates taken with nutrition by bacteria come into contact with the tooth [6]. Both in vitro and in vivo studies have reported that initial caries lesions can be treated through remineralization, defined as the re-accumulation of minerals lost by the demineralization of dental tissue on the enamel surface [3; 7]. A successful remineralization process for lesions is achieved by providing and maintaining supersaturation on the tooth surface with neutral pH, calcium, and phosphate ions at the local level, enabling mineral ions to reach the lesion body at the lesion level, and by regulating both dietary and oral hygiene habits at the patient level [8]. Oral hygiene measures aim to mechanically remove bacterial biofilms on the enamel, one of the key components in caries development, by regular and sufficient behaviors and also chemically, by using various compounds and active agents such as fluoride-containing agents [9]. The primary mechanism of fluoride's action is explained by its ability to significantly control the progression of caries and by remineralization through its low and continuous presence in oral fluids, exerting a topical effect. The topical effect mechanism includes inhibiting demineralization, promoting remineralization, and inhibiting bacterial activity in the plaque [10]. Fluoride in plaque fluid through topical sources adsorbs onto demineralized subsurface crystals, forming a fluorapatite-like structure that is less soluble and more resistant to acid attacks than the original tooth mineral. On the other hand, fluoride combines with the hydrogen ions (H+) from acids produced by bacteria's carbohydrate metabolism, forming hydrofluoric acid (HF). This acid passes through bacterial cell walls and inhibits the glycolytic enzyme enolase, thereby obstructing carbohydrate metabolism and acid production and affecting the production of bacterial adhesive polysaccharides [11]. The caries-preventive effects of fluoride-containing products have been demonstrated in numerous reviews. Among all the active ingredients in toothpaste, the greatest number of evidence-based studies have been carried out on fluoride [12; 13]. Reductions in the prevalence of dental caries recorded in many industrialized countries have been attributed to the widespread use of fluoride in various forms, particularly fluoride-containing toothpaste. Using fluoride-containing toothpaste leads to small but sustained increases in fluoride levels in plaque and saliva [14].