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Dental caries is a multifactorial disease caused by the interaction of dietary sugars, dental biofilm, and the dental tissue of the host. It results from repeated cycles of demineralization and remineralization at the interface of the biofilm and the tooth surface. Demineralization is the process of removing mineral ions from hydroxyapatite crystals in hard tissues, such as enamel, which can lead to dental caries if left unchecked. The remineralization process can reverse the lost mineral ions that occur during demineralization. The degree of demineralization and remineralization depends on several variables, including the amount of available calcium and phosphate and salivary pH levels. Over the past several decades, remineralizing or calcifying fluids with variable calcium, phosphate, and fluoride formulations have been developed. The management of early caries by remineralization has the potential to significantly advance the noninvasive clinical management of the disease. The chapter outlines the mechanisms by which the demineralization-remineralization process occurs and the use of remineralizing agents that reverse demineralization or enhance remineralization.
Saveetha Dental College, Saveetha Institute of Medical and Technical Sciences, India
Wael I. Ibraheem
College of Dentistry, Jazan University, Saudi Arabia
Abdullah A. Meshni
College of Dentistry, Jazan University, Saudi Arabia
Reghunathan Preethanath*
College of Dentistry, Jazan University, Saudi Arabia
Sukumaran Anil
Department of Dentistry, Oral Health Institute, Hamad Medical Corporation, Qatar
College of Dental Medicine, Qatar University, Qatar
*Address all correspondence to: drpreethanath@gmail.com
1. Introduction
Dental caries is one of the most significant public health issues and a highly prevalent disease worldwide. It is an irreversible, chronic, infectious disease that progresses as a dynamic, multifactorial process and affects the mineralized dental structures. Dental caries is a complex disease caused by the demineralization and remineralization of enamel in the presence of fermentable carbohydrates, saliva, and cariogenic oral flora. When exposed to carbohydrates, oral microorganisms can produce organic acids that lower the pH of dental plaque. Caries progresses through demineralization and remineralization phases on the tooth surface before invading deeper layers [1].
Enamel consists of hydroxyapatite, water, protein, and trace elements, such as fluoride. The organic matrix consists of noncollagenous protein, amelogenin, and inorganic components consists of enamel’s biological apatite. Enamel apatite has a hexagonal unit cell composed of prismatic crystals and contains more inorganic material than dentin, bone, and cementum [2]. Twenty percent of a tooth’s matrix consists of organic material, which makes up the majority of the tooth’s dentine. Most of the organic portion of dentine comprises Type I collagen, while the remainder consists of collagen types III and V [3]. The surface layer of enamel is composed of hydroxyapatite (HA) crystals that form the prism of enamel. HA is a crystalline form of calcium (CA++), hydroxyl (OH), and phosphate ions (PO43−) that compose the mineral structure of bones and teeth. The surface layer’s hardness is primarily the result of a high concentration of phosphate ions, fluorine, calcium, and chlorine. Enamel adjacent to dentine is softer due to its high magnesium, sodium, and potassium ion content [1, 4].
Demineralization refers to the process by which organic acids produced by plaque microorganisms destroy the mineral content from the surface of HA crystals. The most stable form of hydroxyapatite exists in an environment with a pH of 7.4. There is a constant chemical equilibrium between the hydroxyapatite in the enamel (Ca10(PO4)6(OH)2) and the dissolved hydroxyapatite in the plaque biofilm. Mineral crystal dissolution takes place when the pH level of the plaque falls below 5.5 [5, 6]. When the minerals are dissolved, the intercrystalline space expands, and the surface of the enamel becomes softer and more porous, leading to the formation of caries [6]. Due to the acid metabolism of cariogenic microorganisms in dental plaque biofilm, enamel demineralization occurs (Figure 1). The greatest degree of demineralization in enamel caries occurs at a subsurface level covered by a surface layer that appears relatively unaffected by the attack. This means that the majority of the mineral loss during the initial stages of demineralization occurs at a distance away from the enamel surface. This subsurface lesion is commonly referred to as “white spot lesions,” which refers to an opaque white area that can be distinguished from healthy enamel. This stage of the carious lesion is visible as a white spot (WS) during a routine dental clinical examination and is known as initial caries, which can turn brown due to the absorption of pigments into enamel pores.
Figure 1.
Diagrammatic representation showing the equilibrium between dynamic demineralization and remineralization at the plaque-enamel interface. Saliva is a source of mineral and fluoride ions that promote remineralization of lesions.
Earlier in vitro experiments using organic acid buffers as demineralizing media explained the presence of the unaltered surface enamel resistant to acid dissolution by adsorption of organic matter onto the enamel crystallites [1, 7, 8]. Later studies recognized the reprecipitation process with respect to saturation of calcium and phosphates occurring at the underlying enamel layer [9, 10, 11]. According to in vivo microscopic studies, a mineral loss is initiated in the interprismatic regions and later proceeds into the enamel prisms [12, 13]. However, under oral conditions enamel demineralization is affected by a number of factors, such as modification in the microbial activity and changes in the physicochemical properties of the enamel mineral content. Studies using a polarizing microscope revealed that the porous subsurface enamel is positively birefringent, whereas the surface zone retains its negative birefringence [14, 15]. This indicates that the subsurface enamel has a demineralized zone with a pore volume greater than 25%, whereas the surface enamel has a pore volume less than 5% [16].
Remineralization occurs as a process of restoring minerals in the form of mineral ions to the hydroxyapatite latticework structure. Remineralization is a natural repair process for non-cavitated lesions that utilizes calcium and phosphate ions to construct a new surface on existing crystal remnants in subsurface lesions that remain after demineralization. These acid-resistant remineralized crystals are considerably less soluble than the original mineral. The major protein in dentine is predominantly type I collagen, which constitutes 90% of the organic matrix. They provide a scaffold for the deposition of minerals in dentine remineralization. Earlier studies were based on ion-mediated crystallization [17, 18] where epitaxial growth occurs over existing apatite crystallites within the demineralized collagen matrix. Although in vitro studies with a solution containing calcium and phosphorus ions induced calcium phosphate crystal deposition on the collagen surface, other studies with a solution containing fluoride and mineral ions showed better dentine remineralization [19, 20, 21].
These variables may be intrinsic or extrinsic. Diet and medication are examples of extrinsic factors, whereas intrinsic factors are the underlying systemic diseases. Physicochemical changes in enamel surface are also affected by behavior (frequency of tooth brushing and consumption of soft drinks) and socioeconomic status. Modifiable behavioral factors include the types of drinks consumed, the method of drinking, and the frequency of drinking [22]. Several medications cause xerostomia by decreasing salivary flow and pH, thereby diminishing the buffering effect against endogenous and exogenous acids [23, 24]. Intrinsic factors, such as gastroesophageal reflux disease and bulimia nervosa, cause demineralization and erosion of tooth enamel. The pH of endogenous acids is below the critical pH for HA dissolution, resulting in demineralized enamel surface areas [25, 26]. These regions may eventually harbor acid-forming bacteria, resulting in caries formation [27, 28].
The earliest visible symptom caused by the demineralization of enamel is the appearance of white spots. Here, the actual demineralization affects the subsurface layer, while the surface of enamel remains smooth. This defect in the enamel is due to modifications of the chemical composition of the substrate. The translucency of enamel depends on the presence of water around prisms. Demineralization causes the widening of interprismatic space, and the water gets replaced by air. The light scattering effect occurs when there is a difference in refractive index between the two phases. The refractive index of healthy enamel is the same as that of hydroxyapatite (1.62) and therefore, there are no interfaces in healthy enamel (Figure 2). In hypomineralized enamel, light passes through mineral and fluid phases with different refractive indices, resulting in a white optical phenomenon seen as a “white spot” on the enamel surface. During the initial phase, the surface of a tooth has to be dried up in order to see a carious lesion. Microscopic studies report that if the white spot appears only after the tooth surface was dried up with air, the lesion is small, whereas if it is visible even without drying, it means the lesion is more advanced [29, 30].
Figure 2.
White spot lesions after orthodontic treatment with fixed appliances.
The first stages of the carious disease are characterized by hypomineralization without cavity formation and are referred to as white spots (WS). During the initial carious formation, alternating phases of demineralization and remineralization cause the dissolution of mineral salts followed by reprecipitation of minerals on the enamel surface. This results in an intact surface layer, under which the body of the carious lesion extends in a half-moon shape or “cone shape” toward the demineralization zone [31]. The surface layer resembling healthy enamel is usually 20–50 μm deep. Hypomineralization of the subsurface causes enlargement of the enamel pores leading to mineral dissolution [32]. The central layer or body of the lesion is the most affected with 5% mineral loss in the peripheral part to 25% in the central part. The lesion becomes clinically visible when the mineral deficit in this layer compared to healthy enamel reaches 10%. The dark zone at the advancing front of the lesion is considered as a breakdown stage successional to the translucent zone and preceding the body of the lesion. In vitro studies [33, 34] reported large pores in the translucent zone, whereas in the dark zones, a micropore system is found in addition to the large pores, which was explained as areas of demineralization. The deeper translucent layer is seen close to healthy enamel and its occurrence is the first symptom of the pathological process [29]. In vitro studies on human enamel revealed the physical and chemical properties of surface enamel [35, 36]. One probability is the reprecipitation of calcium and phosphate ions released by subsurface dissolution or from the saturated solution in plaque biofilm into the surface enamel. The presence of fluoride ions in the surface enamel also helps in maintaining the surface zone from demineralization [33].
Dental caries is a cavity that forms on the tooth surface in the form of a small lesion that progresses and results in the loss of tooth structure (Figure 3). Demineralization causes initial changes at the ultrastructural level, which can only be observed with an electron microscope. Clinically, it cannot be detected in its earliest stages, but as the disease progresses, the dentist will notice a decrease in the enamel’s translucency, which can be detected during an intraoral examination of the patient. When bacteria accumulate in dental plaque and ferment dietary carbohydrates for an extended period of time and the locally produced acids cannot be neutralized by the buffering capacity of saliva, demineralization of the teeth occurs, leading to cavities [37]. Although the ability of low pH to demineralize enamel is well-established [38, 39], dental caries is a multifactorial disease caused by microbes and influenced by dietary habits, tooth characteristics, saliva-buffering capacity, and host immune system [40].
Figure 3.
Dental caries leads to the destruction of tooth structures.
The highly organized pellicle-covered dental plaque biofilm on the tooth surface contains live and dead bacterial cells, end products, desquamated epithelial cells, leukocytes, and glycoproteins from saliva. Cariogenic microorganisms metabolize carbohydrates from food to produce organic acid, primarily lactic or acetic acid. Dental caries initiates with surface roughness or subsurface demineralization, later progressing to cavitation. Initial studies indicated the presence of acidogenic streptococci mutans in dental caries [41, 42], and later lactobacilli species were also proposed to produce acid that causes dental caries [43, 44]. In vitro studies on bacterial species in caries lesions using PCR and specific DNA probes [45, 46] indicated that dental cavities are a complex ecosystem containing multiple cariogenic bacterial species, such as Veillonella or Corynebacterium [47].
Saliva mechanically cleanses the tooth surface of bacteria and food particles. Saliva’s composition and secretion also play a significant role in demineralization. Calcium and phosphorus, the inorganic components of saliva, contribute to maintaining the mineral balance between hydroxyapatite of enamel and saliva. If the acid metabolites of microbes are not neutralized by the buffering properties of saliva, the pH of dental plaque decreases, thereby fostering demineralization of enamel. To preserve tooth structure, it is essential to maintain a balance between demineralization and remineralization of enamel [48].
7. Role of saliva in demineralization and remineralization process
A variety of oral and systemic factors can have a positive or negative effect on the constant cycle of demineralization/remineralization processes. Assessing patients’ caries risk and recommending appropriate remineralization therapies for those deemed at high risk is critical for improving their oral health. Saliva is a critical factor in determining caries risk and remineralization. It is a critical biological and protective factor in the process of enamel remineralization [49]. The buffering capacity and secretion flow of saliva are proportional to the rate and extent of demineralization. Saliva can neutralize acids, form a protective membrane on tooth surfaces, and promote remineralization by providing enamel and dentin with calcium, phosphate, and fluoride [50]. The pH level of saliva directly affects remineralization through the amount of calcium and phosphate ions available to the enamel via saliva in times of acidic challenge [51]. Saliva can act as a replenishing agent and inhibit tooth demineralization during periods of low pH, while simultaneously promoting tooth remineralization once the pH returns to a neutral state. Systemic diseases, inherited disorders, a variety of medications, and other medical interventions can all have a detrimental effect on salivary production, buffering capacity, and the amount of calcium and phosphate available for remineralization [52, 53].
Saliva’s protective properties are volume dependent. These protective properties can be significantly enhanced or diminished based on the rate of secretion in unstimulated and stimulated conditions. Unstimulated, normal salivary secretion is greater than 0.3 ml/minute, ranging between 0.5 and 1.5 L per day, compared to 0.1–0.7 ml/minute in patients with decreased salivary production [50]. Demineralization causes the loss of mineral ions, but it is reversible via remineralization. Both processes occur on the surface of the tooth, but cavitation necessitates a substantial loss of mineral ions from hydroxyapatite. A number of factors, including the availability of calcium and phosphate ions and the pH of the saliva, determine the degree of demineralization and remineralization. Individuals with decreased salivary flow have more acidic saliva and biofilm, which increases the risk of additional demineralization [54]. Reduced salivary flow also creates an oral environment that is unable to neutralize acids effectively, resulting in prolonged increase in intraoral pH [55]. The remineralization process is frequently hampered in patients with decreased salivary production, and the use of fluoride may be limited due to a deficiency of calcium and phosphate ions [56]. Fluoride, calcium, and phosphate are necessary for remineralization following a cariogenic attack. The focus of remineralization is mainly on detecting early caries lesions when the disease is still reversible. This helps in identifying the patients at risk. Saliva, fluoride therapy, and probiotic bacteria are considered as common regimes for tooth remineralization [57, 58].
Several topical remineralizing agents have been used to inhibit and remineralize enamel (Table 1). For decades, fluoride has been the cornerstone of enamel remineralization. It is known to prevent caries by inhibiting demineralization on the surface of the enamel through the formation of fluorapatite. Fluorapatite is less soluble than hydroxyapatite and increases the enamel’s resistance to dissolution during the acid attack. Varnishes, toothpastes, mouth rinses, solutions, gels, and orthodontic adhesives containing a fluoride source have been utilized as methods and formulations for fluoride delivery [59, 60].
The most common remineralizing agent is fluoride. When acid attacks the enamel surface, the pH begins to rise, and the presence of fluoride in the microenvironment stops enamel dissolution. As pH increases, new and larger fluoride crystals containing fluorhydroxyapatite form, reducing enamel demineralization and promoting remineralization [61, 62]. The fluoride acts on the enamel in several ways [61]. In the first mechanism, fluorapatite crystals have greater resistance to acid attack than hydroxyapatite crystals, which inhibits demineralization. Second, the combination of calcium and phosphate ions promotes remineralization by accelerating the formation of new fluorapatite crystals. It inhibits acid-producing carious bacteria by interfering with the synthesis of phosphoenol pyruvate, a crucial intermediate in the glycolytic pathway of bacteria. In addition, fluoride adheres to oral hard tissue, oral mucosa, and dental plaque, thereby preventing demineralization and promoting remineralization. Fluoride concentrations on the surface of teeth can increase resistance to dental caries and erosion. In contrast, numerous laboratory studies have demonstrated that low levels of fluoride, such as those detected after many hours in resting plaque and saliva and resulting from daily use of fluoride dentifrices, have a significant impact on enamel demineralization and remineralization. Fluoride in the mouth affects the natural dissolution and reprecipitation processes that occur at the interface between the tooth and oral fluid. Trace amounts of fluoride accelerate the remineralization of early carious lesions [63, 64]. Stannous fluoride contains both fluoride and stannous ions, which possess antibacterial properties. It is also capable of forming stannous phosphate fluoride precipitates, which halt the progression of caries but discolor the teeth. The most effective technique for remineralization of early caries was twice-daily use of a 0.5% NaF mouth rinse in conjunction with twice-daily use of fluoride toothpaste. These findings suggest that the efficacy of fluoride is determined by the frequency of rinsing and the ability of the fluoride mouth rinse to reach inaccessible areas, such as interproximal spaces [65].
Studies have shown that fluoride released from a glass-ionomer restoration inhibits bacterial acid production by incorporating it into the biofilm of plaque bacteria [66, 67], in the adjacent tooth enamel and saliva of patients. Conventional and resin-modified glass ionomer can be recharged from external sources, such as topical fluoride application. Compared to resin-modified glass ionomers, glass ionomers emit comparatively greater amounts of fluorides. For effective remineralization, the fluoride release must be maintained at approximately 2–3 g/mL per day; this can be accomplished through fluoride recharge. Micro porosities present in conventional and resin-modified glass ionomers may account for the recharging capacity of these materials [67]. Pit-and-fissure sealants commonly used in preventive dentistry consist of either resin- or glass-ionomer-based materials. They prevent bacteria from settling in deep pits and fissures, thereby playing an important role in preventing dental caries. The incorporation of fluorides into sealant fillers promotes remineralization [23].
Dentifrices containing fluoride are regarded as the most effective agents for preventing enamel demineralization. Studies have demonstrated the effectiveness of conventional toothpastes containing 1000 ppm fluoride and the evidence suggests that toothpaste containing 5000 ppm fluoride can further reduce demineralization and enhance remineralization [68].
Casein, a milk-derived protein developed by Eric Reynolds, mainly interacts with calcium and phosphate. They are used alone or as CPP-ACP (casein phosphopeptides with amorphous calcium phosphate) or CPP-ACFP (casein phosphopeptides with amorphous calcium fluoride phosphate). CPP-ACP is a two-phase system that precipitates onto the tooth structure and elevates calcium levels in the plaque biofilm and tooth enamel. CPP stabilizes ACP, maintaining a state of supersaturation of calcium and phosphate. As the pH of the material increases, the bound form of amorphous calcium phosphate also increases, thereby facilitating remineralization. The incorporation of casein phosphopeptide–amorphous calcium phosphate (CCP-ACP) into sealants facilitates the release of supersaturated levels of calcium and phosphate ions, which promotes the formation of new hydroxyapatite crystals and the remineralization of enamel subsurface lesions [69]. The advantage of CPPACFP is the availability of calcium, phosphate, and fluoride in one product, which can bind up to 25 calcium ions, 15 phosphate ions, and five fluoride ions, which helps in the remineralization of subsurface lesions in enamel [70, 71, 72]. Studies have shown CPP–ACP incorporated fluoride to a level of 900 ppm in toothpastes, chewing gum, lozenges, and mouth rinses give additive effects in reducing caries [73, 74]. Another in situ study with chewing gum containing CPP-ACP also showed a significant increase in mineral precipitation of initial bovine enamel lesions [75]. A study by Walker et al. [76] reported that the addition of CPP-ACP to milk resulted in enhanced remineralization.
8.3 Bioactive glass
Bioactive glass is a multi-component inorganic compound composed of sodium, calcium, phosphorus, and silica (sodium-calcium phosphosilicate). It helps in the formation of hydroxycarbonateapatite (HCA) crystals when it comes into contact with water, saliva, or other body fluids [72]. It has low cytotoxicity for dental pulp cells and exerts remineralization effects on both enamel and dentin. Additionally, its antimicrobial activity against intraoral bacteria has been established. It demonstrated the ability to neutralize acid and absorb calcium (Ca) ions in physiological conditions via its functional groups. It is a promising remineralization agent due to its biomimetic mineralizing properties. NovaMin®, a product of NovaMin Technology Inc. (NTI) available in the market containing bioactive glass and calcium sodium phosphosilicate has antimicrobial activity toward Streptococcus mutans (S. mutans) and S. sanguis, and also helps in the remineralization of tooth [77].
8.4 Tricalcium phosphate (TCP)
A new remineralizing agent, tricalcium phosphate is incorporated in dentifrices, which release calcium, phosphate, and fluoride when it comes in contact with the enamel surface during tooth brushing [73]. Functionalized TCP is a low-dose calcium phosphate system that is incorporated into a single-phase aqueous or non-aqueous topical fluoride formulation, which facilitates a targeted delivery of TCP when applied to the teeth. Studies have shown that the combination of TCP with fluoride can provide greater enamel remineralization and more acid-resistant mineral than fluoride alone [73].
8.5 Xylitol
The application of xylitol, a sugar alcohol of the pentitol type, on a regular basis has been linked to a marked reduction in caries and tooth remineralization. Xylitol is a nonfermentable sugar alcohol that has been demonstrated to have both noncariogenic and cariostatic properties. Xylitol interferes with the growth and metabolism of S. mutans by inhibiting glycolysis in the mitochondria of these microorganisms. Due to the inability of caries-causing bacteria to ferment xylitol, the acid attack is diminished when xylitol is consumed. As a result, the growth of these bacteria and the concurrent production of acid are inhibited, and the oral pH remains elevated. At high pH, the hydrophilic molecule of xylitol can form complexes with calcium in solution, thereby stabilizing the calcium and phosphates present in saliva. The saturation of calcium ions in saliva stimulates the remineralization of dental tissues through calcium ion deposition [78].
Xylitol increases salivary clearance, buffering capacity, and calcium and phosphate saturation by neutralizing the decreased plaque pH/salivary pH. Increased salivary flow increases acid buffering capacity, and the high mineral content helps in the remineralization of the damaged enamel [78]. There are conflicting reports about the effectiveness of xylitol, especially when taken with fluoride. Fluoride varnish, which contains xylitol-coated calcium and phosphate, released 10 times more fluoride in the first 4 hours than other varnishes like Enamel Pro® (Premier Dental Products, PA, USA) and Duraphat® (Colgate Oral Care, NSW, Australia) [79].
8.6 Arginine
Arginine is a semi-essential amino acid found in various proteins and peptides in human saliva. Non-pathogenic bacteria, such as Streptococcus sanguinis, utilize the arginine deiminase system to generate energy, ammonia, and carbon dioxide. The production of ammonia raises the local pH and neutralizes the acidifying effects of sugar metabolism, thereby promoting a more alkaline environment that is unfavorable to cariogenic bacteria and reducing the carcinogenicity of oral biofilms. Research has confirmed that arginine can affect the pH and ecology of oral biofilms. Therefore, it was added to toothpaste (1.5% arginine) containing insoluble calcium and 1450 ppm sodium monofluorophosphate in order to enhance caries lesion prevention via enhanced remineralization [80]. A systematic review concluded that this formulation possesses the potential for a superior anticaries effect [81]. Clinical studies have revealed that the new arginine-containing compound provided significantly greater benefits than conventional fluoride toothpaste alone in halting and reversing caries lesions [82, 83].
8.7 Triclosan
Triclosan is an antibacterial agent that may influence biofilm production, resulting in increased saturation and remineralization. Triclosan binds to bacterial cells and increases the permeability of the cells. High bactericidal concentrations induce membrane lesions that allow cellular content to leak out. There is a linear correlation between acid production inhibition and triclosan adsorption by S. mutans cells. Consequently, the effect of triclosan is not dependent on the concentration of triclosan in solution, but rather on the ratio between the amount of triclosan and the number of cells to be inhibited [84]. Studies conducted have demonstrated that the addition of triclosan to toothpaste formulations can result in modest but statistically significant reductions of coronal and root caries [85]. Silva et al. [86] suggested that it could also have an effect on remineralization.
8.8 Probiotics
WHO defined probiotic bacteria as “live microorganisms which, when administered in adequate amounts, confer a health benefit on the host” [87]. Probiotics is the idea of exploiting “good” bacteria to promote health. The concept is based on the theory of maintaining a healthy flora, which helps in eliminating pathogenic microbiota. Lactobacillus and Bifidobacterium, which are part of normal oral flora, are common examples of probiotics with oral health benefits used in the treatment of dental caries and periodontal disease by reducing the quantity of pathogenic bacteria or inhibiting the virulence genes of S. mutans [88, 89].
8.9 Herbal compounds
Several herbal and other natural compounds have been investigated as potential remineralization agents. Depending on the specific compound, they may influence mineral saturation and precipitation, act as antimicrobials, or stabilize collagen, which may serve as a scaffold for mineral deposition. Proanthocyanidins and calcium phosphate-based compounds may have a synergistic effect when remineralizing in vitro artificial root caries lesions [90]. Ginger rhizome (Zingiber officinale Roscoe, Zingiberaceae) and rosemary (Rosmarinus officinalis L., Lamiaceae) are antimicrobial herbs derived from natural food sources. In addition, they exhibit no toxicity. Several polyphenolic ketones with multiple pharmacological activities are present in the pungent oils of these herbs. Studies documented their antifungal and antimicrobial effects on oral cavity pathogens [91, 92]. Honey is a possible antibacterial agent, and research indicates that manuka honey is probably noncariogenic [93].
An in vitro study revealed that the application of ginger, honey, and rosemary as herbal medicines inhibited demineralization and promoted remineralization of enamel [94].
Several topical remineralizing agents have been used to inhibit and remineralize enamel and white spot lesions specifically. For decades, fluoride has been the cornerstone of enamel remineralization. It is known to prevent caries by inhibiting demineralization on the surface of the enamel through the formation of fluorapatite. Currently, new mineralization agents have been developed to preserve enamel integrity and prevent the formation of carious cavities. Modern dentistry focuses on managing non-cavitated caries lesions noninvasively via remineralization in order to prevent disease progression and improve esthetics, strength, and function. The evidence suggests that initial non-cavitated lesions can be remineralized using appropriate technologies, and even non-fluoride remineralization strategies.
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Written By
Aiswarya Anil, Wael I. Ibraheem, Abdullah A. Meshni, Reghunathan Preethanath and Sukumaran Anil
Submitted: 23 May 2022Reviewed: 14 June 2022Published: 26 September 2022
Open access peer-reviewed chapter
