Silver diamine fluoride: the science behind the action – a narrative review

Abstract

Background

Silver Diamine Fluoride (SDF) is a caries-arresting agent that gained popularity among clinicians and patients due to its effectiveness within hours of application. However, the exact mechanisms underlying its action are not yet fully understood. This narrative review explores the current knowledge of SDF's role in caries management, focusing on its mechanism of action, application methods, and safety.

Methods

A comprehensive search was conducted in PubMed, MEDLINE, ScienceDirect, and Google Scholar. Out of 820 identified studies, 40 were selected based on relevance to SDF’s chemical properties and clinical application, following duplicate removal and screening of abstracts and full texts.

Results

Although the literature provides insight into SDF’s benefits in managing caries, its exact mechanism of action and long-term outcomes remain insufficiently understood. Furthermore, variations in the composition of commercially available SDF products, particularly in silver, fluoride, and pH levels, may significantly affect their clinical performance. This variability raises concerns about consistency in therapeutic outcomes and underscores the need for formulation standardization.

Conclusion

Understanding SDF antimicrobial and remineralization mechanisms is essential for optimizing its clinical use in caries management. While current evidence supports its efficacy, further studies are needed to standardize formulations, refine application protocols, and clarify its long-term therapeutic outcomes.

Supplementary Information

The online version contains supplementary material available at 10.1186/s12903-025-06107-x.

Introduction

Silver diamine fluoride (SDF) has become a standard treatment option for managing and arresting dental caries, particularly in young children and those with special needs [1–6]. There is a substantial rise in global interest in SDF therapy, driven by growing evidence of its clinical effectiveness [7]. Silver and fluoride can effectively arrest the progression of dental caries and prevent the formation of new lesions. One suggested mechanism for SDF is its ability to reduce the colony-forming units (CFUs) of cariogenic bacteria, as demonstrated by in vitro studies showing its potent antibacterial activity and enhanced biofilm characteristics, supporting its role in caries prevention [8, 9]. In addition to its antibacterial effects, SDF also demonstrates anti-Candida activity [10]. Moreover, carious cavities treated with SDF exhibit a significant increase in surface microhardness by increasing the mineral content of hard tooth tissues, enhancing calcium absorption, and reducing dentin demineralization [11–13].

Although repeated administrations of SDF have demonstrated greater efficacy in arresting cavity progression and enhancing fluoride uptake compared with fluoride varnish and gel, some side effects may influence its acceptance [14, 15]. One of the most common is the development of black stains on carious tooth tissue, primarily due to the precipitation of silver phosphate (Ag₃PO₄). Although this staining does not compromise the treatment's effectiveness, it can raise aesthetic concerns, particularly for anterior teeth. Other side effects, such as mild gingival irritation or a transient metallic taste, are generally minor and temporary [16–18].

Healthcare practitioners are increasingly investigating ways to enhance the clinical performance of silver diamine fluoride (SDF) by optimizing its original formulations and application protocols. These modifications aim to improve SDF’s therapeutic outcomes, minimize undesirable side effects such as tooth staining, and expand its applicability across different patient populations [19–24]. Despite these advancements, significant gaps remain in our understanding of how such modifications impact SDF's long-term efficacy, safety, and biological behavior. This highlights the need for continued research to evaluate these effects and the establishment of standardized clinical guidelines.

This narrative review aims to provide a comprehensive overview of silver diamine fluoride (SDF) and its role in caries management. Its objectives are to present current information from the literature by examining SDF's chemical composition and available formulations, explaining its antimicrobial and remineralization mechanisms, and describing its clinical safety and application methods.

Methods

As a narrative review, this study does not follow a systematic methodology, which may introduce selection bias and is inherently limited by the availability and quality of published studies. A comprehensive search was conducted on electronic databases in May 2024, including PubMed, MEDLINE, ScienceDirect, and Google Scholar. The search was performed to include only English-language studies for this review. To identify relevant published articles, the following keywords were used: (SDF) OR (silver diamine fluoride) OR (SMART technique) AND (dental treatment) OR (tooth structure) OR (oral Antimicrobial) OR (Composition) OR (Prevention) OR (Arrest).

Results

This review prioritized studies that contribute to understanding SDF's composition, mechanisms of action, antimicrobial properties, and clinical applications, including those focused on its chemical reactions, remineralization effects, and modifications to its original techniques. Using the predefined search strategy, a total of 820 articles were retrieved. Following manual screening and the application of eligibility criteria, 40 full-text articles were selected based on relevance and scientific quality. Duplicate entries, non-English publications, and studies unrelated to SDF's mechanisms were excluded. The process of study selection, including the number of articles identified, screened, and selected at each stage, is illustrated in Fig. 1.

Fig. 1.

A flow diagram of the number of articles identified at each search stage

SDF composition and commercial forms

Silver diamine fluoride (SDF) is a colorless liquid with an alkaline nature (pH = 8–10). The formation of diamine–silver ions is a chemically reversible yet functionally stable process under physiological conditions [25–27] The proportions of silver, fluoride, and ammonia in SDF solutions vary slightly between manufacturers [28–32]. While most commercially available SDF products are formulated at 38%, lower concentrations (e.g., 10%, 12%, and 30%) are also available as shown in Table 1. The 38% SDF solution, illustrated in Fig. 2, consists of 5% fluoride ions and 25% silver ions dissolved in an 8% ammonia solution. These compositional variations could influence the clinical effectiveness, ion bioavailability, and safety margins across different products. However, their potential impacts have not yet been fully evaluated, underscoring the need for further investigation, careful product selection, and formulation standardization.

Table 1.

Commercially available preparations of silver diamine fluoride and their reported properties [28–32]

F Fluoride, Ag Silver, ppm parts per million, NR Not reported

Fig. 2.

SDF Chemical composition and safety. Box A displays SDF bottle composition and its functional component. Box B illustrates SDF penetration into a caries lesion. Box C shows the composition of a single drop. Table D provides a safety example for a 10 kg child. Created in BioRender, link available in supplementary file

Different available 38% SDF products used for dental procedures have been evaluated, and their pH levels and ion concentrations have been assessed. Research indicated that for the examined bottles of identical products, the average pH levels varied by 0.5% around pH = 10.0 and stayed consistent over a period of three months. The levels of silver and fluoride displayed variability, with silver concentrations between 257,000 and 285,000 ppm and fluoride ranging from 49,400 to 53,360 ppm among the different bottles [28]. Additionally, fluoride concentrations varied from 43,233 to 54,400 ppm, while silver concentrations ranged from 258,841 to 336,149 ppm across different products. The ion concentrations measured in these investigations consistently exceeded the anticipated values in all solutions, with a range of 3.2% to 25.9% increase for silver and 3.5% to 21.4% increase for fluoride [29, 30, 32]. However, some SDF products showed greater consistency in terms of silver and fluoride concentrations than others [29].

Interaction and reactions of SDF

Fluoride and silver ions both play vital roles in maintaining the protective balance of the oral environment. Their combined action results in synergistic interactions that enhance several chemical processes, including calcium fluoride (CaF₂) and silver phosphate (Ag₃(PO₄)) formation. These reactions contribute to the synthesis of fluorapatite (Ca₁₀(PO₄)₆F₂), a mineral highly resistant to degradation. Additionally, the antimicrobial properties of both ions have been demonstrated individually and in combination [33–36]. These compounds are believed to assist in preventing dental caries and in restoring the structural integrity of pre-existing lesions, as illustrated by the following simplified chemical reaction [34]:

$${\mathbf{C}\mathbf{a}}_{10}{({\mathbf{P}\mathbf{O}}_4)}_6{(\mathbf{O}\mathbf{H})}_2+\mathbf{A}\mathbf{g}{({\mathbf{N}\mathbf{H}}_3)}_2\mathbf{F}\to \mathbf{C}\mathbf{a}{\mathbf{F}}_2+{\mathbf{A}\mathbf{g}}_3({\mathbf{P}\mathbf{O}}_4)+{\mathbf{N}\mathbf{H}}_4\mathbf{O}\mathbf{H}$$

Further details will be explained regarding the specific effects of fluoride and silver ions individually and their combined impact. These are elaborated in the following sections and illustrated in Figs. 2, 3, 4 and 5. Tables 2 and 3 outlines the sequential steps of the chemical reaction and links them to their respective mechanisms of action.

Fig. 3.

Silver diamine fluoride (SDF) chemical reaction scheme. Created in BioRender, link available in supplementary file

Fig. 4.

SDF reaction and interaction, Box A shows the antimicrobial action of the silver phosphate interaction. Box B shows Calcium Fluoride interaction and its effect on the tooth remineralization process. (SDF: Ag(NH₃)₂F; hydroxyapatite: Ca₁₀(PO₄)₆(OH)₂; calcium fluoride: CaF₂; silver phosphate: Ag₃PO₄; fluorapatite: Ca₁₀(PO₄)₆F₂.). Created in BioRender, link available in supplementary file

Fig. 5.

SDF application steps and modifications. The original steps are illustrated in the main box (A). The blue box B shows the 1st modification, the 2-step technique (SDF + KI) used to delay & reduce discoloration for future restoration. Green box C displays a 2nd modification using Light cure to reduce working Time by accelerating SDF drying time (20 s.). Purple box D demonstrations of a 3rd modification of SDF reinforced temporary restoration in case of inability of immediate restoration placement. Created in BioRender, link available in supplementary file

Table 2.

Summary of the functional roles of singular ions in SDF

Ion	Process	Condition/Reaction	Effect description	Ref.
Ag+	Reduction to metallic silver	Ag⁺ → Ag⁰	Forms black precipitate; stabilizes lesion site	[35]
	Formation of silver phosphate	Ag⁺ + PO₄3⁻ → Ag₃PO₄	Initial reaction product from hydroxyapatite	[33]
	Conversion to silver chloride	Ag₃PO₄ + 3 Cl⁻ → 3 AgCl↓ + PO₄3⁻	Highly insoluble; enhances long-term antimicrobial effect	[33, 36]
	Membrane disruption	Ag⁺ causes K⁺ leakage, ATP loss	Disrupts bacterial membrane potential	[8, 9, 37]
	Intracellular damage	Ag⁺ binds to thiol groups in DNA, enzymes	Inhibits DNA replication and protein synthesis	[9, 38, 39]
	Oxidative stress	ROS generation	Damages bacterial components	[37]
	Glucosyltransferase inhibition	Inhibits glucan synthesis	Reduces S. mutans adherence and biofilm formation	[39]
	Cell envelope detachment	Ag⁺ detaches cytoplasmic membrane from wall	Seen in both Gram-positive and Gram-negative bacteria	[40, 41]
	"Zombie effect"	Silver-killed cells kill nearby bacteria	Extends antimicrobial effect	[42]
NH₃	Stabilization	[Ag(NH₃)₂⁺] complex Formation	Contributes to high pH (8–10) and Enhances Stability of SDF	[30, 43, 44]
F−	Fluorohydroxyapatite formation	Alkaline pH (pH 8–10)	Stable mineral; enhances remineralization	[45–47]
	Ion substitution	F⁻ replaces OH⁻ in acid	Improves enamel resistance	[46, 48]
	Alternate products	Acidic pH	Forms Ag₃PO₄, CaF₂ (less stable)	[49]
	Crystal growth	↑ SDF concentration	Larger apatite crystals	[35, 50]
	Nucleation	Residual crystals	Support new crystal formation	[46]

Ag⁺ Silver ion, NH₃ Ammonia, F⁻ Fluoride ion

Table 3.

Simplified chemical reactions and action of SDF [34–36]

Ag⁺ Silver iron, F⁻Fluoride ion, NH₄⁺ Ammonium, Ca² Calcium ion, Cl⁻ Chloride ion, PO₄³⁻ Phosphate ion, CaF₂ Calcium Fluoride, AgCl Silver Chloride, Ag₃(PO₄) Silver Phosphate, Ag⁰ Metallic Silver, FAP Fluorapatite, HA Hydroxyapatite

Silver ions (Ag⁺)

When Silver Diamine Fluoride (SDF) is applied to demineralized tooth surfaces, silver ions (Ag⁺) undergo a sequence of chemical and biological interactions that contribute to both antimicrobial action and remineralization. One key reaction involves the reduction of silver ions, forming metallic silver (Ag⁰), which is commonly observed as a black precipitate on the tooth surface [35].

Chemically, Ag⁺ reacts with hydroxyapatite to form metallic silver (Ag⁰) and silver phosphate (Ag₃PO₄). In the presence of chloride ions, silver phosphate further converts into silver chloride (AgCl), which is more stable and precipitates on the tooth surface [33]. These reactions not only reinforce the structural matrix of carious lesions but also establish a slow-release antimicrobial barrier [35, 51].

Biologically, Silver ions (Ag⁺) display potent antibacterial activity through multiple mechanisms that disrupt bacterial cell integrity and interfere with metabolic processes. Primarily, Ag⁺ ions destabilize the bacterial cell envelope, leading to intracellular potassium ions (K⁺) leakage and a subsequent drop in ATP levels, impairing essential cellular functions [8, 9, 37]. Additionally, silver ions target key intracellular components such as proteins and nucleic acids, hindering DNA replication and protein synthesis. A further mechanism involves the generation of reactive oxygen species, which induce oxidative stress and further damage to cellular structures [37].

A deeper insight into the specific interactions of Ag⁺ and bacterial membranes shows that Ag⁺ ions are known to interact directly with the inner membrane (IM) of bacterial cells, a process considered central to silver's cytotoxicity [52]. Ag⁺ accumulation causes cytoplasmic membrane detachment from the cell wall in both Gram-positive and Gram-negative bacteria [40, 41]. Gram-positive strains required 32 times higher Ag⁺ concentrations for bactericidal effects, likely due to differences in cell wall structure [37].

Ag⁺ disrupts bacterial inner membranes, particularly in Staphylococcus aureus, by binding to thiol groups in proteins and nucleic acids, impairing key metabolic functions [9, 53, 54]. It also interferes with respiration, DNA replication, and cell wall synthesis [38, 53] and inhibits glucosyltransferases, reducing Streptococcus mutans biofilm formation in sucrose-rich environments [38]. Additionally, the"zombie effect"where silver-laden dead bacteria continue to exert antimicrobial effects prolongs silver’s action against biofilms [42].

Ammonia (NH₃)

Ammonia is a key component of silver diamine fluoride (SDF). It forms the diamine-silver complex [Ag(NH₃)₂⁺], which stabilizes silver ions in solution. This stabilization increases silver compounds'solubility and contributes to SDF's alkaline pH (typically between 8 and 10) [30, 43, 44].

Fluoride ions (F⁻)

Silver diamine fluoride (Ag(NH₃)₂F) reacts with calcium and phosphate ions in saliva to form fluorohydroxyapatite, a highly stable, acid-resistant mineral that promotes enamel and dentin remineralization [45–47]. This reaction is enhanced under alkaline conditions (pH 8–10), which favor fluorohydroxyapatite over other byproducts like silver phosphate and calcium fluoride that form in acidic environments [48, 49, 55]. SDF also facilitates fluoride incorporation into apatite, enlarging crystal size in a concentration-dependent manner [35, 50].

Mechanism of action

Silver diamine fluoride (SDF) acts through a dual mechanism, antimicrobial action, and remineralization. This synergy enables SDF to arrest caries, prevent new lesions, and exert broad-spectrum antimicrobial and antifungal effects [44]. Although the exact molecular mechanisms remain under investigation, current evidence supports multiple modes of action for SDF. These processes are explained further in the following section, illustrated in Fig. 4 and detailed in Table 4.

Table 4.

Summary of the reported theories of the effects of silver diamine fluoride (SDF) on oral structure

Action	Theory	Ref.
Arresting	Caries arrest due to synergistic effect of silver and fluoride ions	[16, 44, 56–58]
Antibacterial	Inhibits DNA, enzymes, and biofilm formation	[8, 9, 42, 44, 56]
Antifungal	Effective against multiple Candida species, including resistant strains	[10, 59]
Preventive/ Remineralization	Promotes fluorohydroxyapatite formation, inhibits collagenase, and increases acid resistance to prevent new lesions or further tooth structure loss	[2, 35, 43, 44, 60, 61]

Effect of SDF on oral microorganisms

Streptococcus mutans and cariogenic bacteria

SDF exhibits potent antimicrobial properties, effectively inhibiting the growth of cariogenic bacteria such as Streptococcus mutans and Actinomyces [44]. It disrupts bacterial cell membranes and impairs metabolism by interacting with cell wall components and intracytoplasmic enzymes through silver ions [44, 62–64]. Additionally, SDF suppresses DNA replication by binding silver ions to phosphorus-containing DNA molecules [65]. Studies have shown that SDF reduces the adherence of S. mutans to tooth surfaces and significantly decreases the count of colony-forming units (CFUs) in multi-species biofilms [8, 9, 66, 67]. Compared with silver ammonium nitrate or sodium fluoride, SDF is more effective at inhibiting the growth of cariogenic bacteria [44, 67–69]. However, SDF did not affect the relative abundance of caries-associated bacteria, suggesting that the mechanism by which SDF inhibits caries is broad and not specific to cariogenic bacteria [67, 70].

Periodontal pathogens

SDF has also demonstrated significant antibacterial activity against major periodontal pathogens, including Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis. Its bactericidal efficacy is concentration-dependent, with P. gingivalis remaining viable at lower concentrations of 0.197% and 0.098% [71]. SDF has demonstrated strong antimicrobial effects against pathogens in subgingival biofilms from patients with severe periodontitis. Interestingly, Streptococcus species, such as Streptococcus oralis, were frequently detected in biofilm samples following SDF exposure, suggesting in vitro resistance. This observation may indicate a shift toward health-associated microbial communities, highlighting the potential role of SDF in biofilm modulation [72].

Kern et al. (2023) further underscored the therapeutic potential of SDF by demonstrating that a single application of 38% SDF significantly reduced gingival inflammation in dogs, supporting its role as a non-invasive treatment for periodontal diseases [73]. However, the majority of studies on SDF's impact on periodontal health have been performed in vitro. Further investigation into its potential cytotoxicity and long-term effects is needed to balance SDF’s therapeutic benefits against possible risks, particularly with repeated use for oral health.

Candida and fungal species

SDF exhibits antifungal activity, inhibiting the synthesis of extracellular phospholipases and the transition from yeast to a hyphal form, thus preventing colonization and pathogenicity [67, 74]. The anti-Candida action of SDF was dose-dependent, effectively inhibiting the growth of Candida albicans on dentin from human teeth, preventing germ tube development even at low concentrations, and exerting lethal effects on Candida cell walls at high doses [10, 59, 67]. Additionally, SDF was more effective against certain Candida species, with C. krusei and C. glabrata being more susceptible than C. albicans and C. tropicalis [10].

Effect of SDF on tooth structure

SDF is reported to work via two major pathways to reduce tooth structural damage: first, it forms calcium fluoride (CaF₂), which aids in the formation of fluorapatite (Ca₁₀(PO₄)₆F₂); second, it protects dentin collagen through enhanced remineralization and collagenase activity inhibition [15, 44, 62, 75].

Impacts on inorganic content

After the administration of SDF, a series of chemical reactions occur, as explained in a previous section. Primarily, SDF interacts with hydroxyapatite (Ca₁₀(PO₄)₆(OH)₂), resulting in the formation of insoluble fluorapatite (Ca₁₀(PO₄)₆F₂) [44, 62]. Furthermore, calcium fluoride (CaF₂) formation acts as a slow-release reservoir, helping to regulate the pH during the acidic media challenge, and is believed to contribute to the formation of fluoridated apatite [44, 62, 76, 77]. Additionally, calcium fluoride is thought to adsorb onto the tooth surface rather than being fully integrated, causing an increase in calcium and phosphorus concentrations from the surface to a depth of 300 μm [78]. In demineralization conditions, SDF treatment shows reduced calcium dissolution from enamel, indicating its protective role against mineral loss [44].

Impacts on organic content

Fluoride protects dentin collagen through two primary mechanisms: inhibiting collagenases [44, 62, 79], and stimulating remineralization [35, 44, 62, 76, 79], which helps cover and protect the collagen. In primary teeth, fluoride treatment promoted remineralization, the arrested caries lesions exhibited smoother surfaces with fewer exposed collagen fibers, whereas active dentin lesions displayed porous, rough surfaces with disorganized and sparsely dispersed collagen fibers [80].

SDF plays a crucial role in protecting collagen in demineralized dentin, as approximately 90% of the organic component in dentin is type I collagen [81]. It inhibits the breakdown of matrix metalloproteinases (MMPs) [79], and reduces cysteine cathepsin activity, an enzyme involved in collagen degradation [57]. Immunolabeling has shown more intact dentin collagen after SDF treatment [66].

Safety considerations and clinical concerns of Silver Diamine Fluoride (SDF)

While SDF is generally safe and has no significant adverse effects, healthcare providers should exercise caution when using it due to its diverse silver and fluoride content, with some products exhibiting higher concentrations than reported [30–32, 82]. Although the fluoride content of approximately 44,800 parts per million (ppm) may appear high, the actual volume applied is minimal compared to other topical fluorides. For instance, one drop (0.05 mL) of SDF contains around 2.24 mg of fluoride, whereas a typical 5% sodium fluoride varnish unit dose may contain between 5.65 and 11.3 mg of fluoride [83]. An illustration of SDF's composition and safety profile is shown in Fig. 2D. Despite the high concentration, the clinical dosage remains far below toxic thresholds.

Short-term pharmacokinetic studies indicate that fluoride exposure from SDF remains well below the Environmental Protection Agency's (EPA) oral reference dose. Although the silver content per drop (approximately 4.74 mg) exceeds the EPA's recommended lifetime cumulative daily dose, it remains below known toxicity thresholds. A conservative dosing guideline, one drop per 10 kg of body weight, allows safe treatment of up to five or six teeth per session [69].

Clinical trials in both children and adults have reported no serious acute adverse events; the most common effect is the permanent black staining of carious lesions, while mild and transient side effects such as gingival irritation or a metallic taste are infrequently reported [16–18]. Studies indicate that staining is more acceptable on posterior teeth, and despite cosmetic concerns, many caregivers prefer SDF over invasive options such as sedation or general anesthesia [84–88]. Therefore, obtaining informed consent is essential to ensure that parents or guardians fully understand both the benefits and potential drawbacks of SDF treatment [89]. Current evidence on the long-term safety of silver diamine fluoride (SDF) remains limited. Further investigations are crucial to understanding its long-term effects and to balancing the therapeutic benefits of SDF with any potential unforeseen risks, especially when it is used repeatedly for oral health maintenance.

Application techniques and protocol modifications

The original and modified steps of the SDF application are illustrated in Fig. 4. All protocols are performed with proper isolation and stain protection, which involves applying a protective layer (such as petroleum jelly) over the lips and gingiva, followed by partial isolation using a cotton roll. SDF is dispensed from a plastic dappen dish and applied to the carious lesion using a micro-brush. After dip-dabbing the excess, one drop of SDF is painted onto the lesion. To minimize excess SDF, a cotton roll or pellet can be placed on the cavity. The lesion is then dried with a gentle flow of air for 1 to 3 min and left to dry. The recommended frequency for SDF application to reduce caries is once per year or every six months [89, 90]. Since the Food and Drug Administration (FDA) approved SDF in August 2014, several modifications to the original technique have been introduced to enhance its clinical application [19–23, 91–94], as detailed below.

Two-step technique

A modification to reduce staining involves minimizing the precipitation of silver phosphate (Ag₃PO₄), which is the main cause of staining after the SDF treatment [58]. Ngo et al. proposed a solution to SDF staining by coating the first layer of SDF with potassium iodide (KI) [95]. KI reacts with the free silver ions (Ag⁺) in the SDF, inhibiting the production of silver phosphate (Ag₃PO₄) precipitate. Subsequent studies found that adding KI after SDF application prevented tooth discoloration by forming a yellow silver iodide precipitate (AgI) [24, 61, 96]. A dose-dependent reduction in SDF staining was observed immediately after KI treatment; however, this effect was only temporary, with minimal staining detected during a four-week follow-up period in teeth treated with SDF and KI [20, 24, 61]. An excessive amount of KI may reduce the availability of silver ions, diminishing the antibacterial effectiveness of the combination. Moreover, the specific KI-to-SDF ratio used in investigations has not been clearly defined, and current protocols for commercially available SDF + KI lack precise dosage guidelines for KI application following SDF treatment.

Light-cure (LC) technique

A modification to reduce application time involves using light curing (LC) immediately after SDF application, a technique that has gained significant attention for its ability to modify SDF penetration depth while shortening the application time [93]. This technique can alter the hardness of both underlying and overlying dentin surfaces affected by caries [91, 97]. The application of LED light for 20 s post-SDF treatment has been shown to enhance silver ion penetration, resulting in greater deposition in infected dentin while limiting penetration into healthy dentin [19]. However, similar silver penetration depth in sound dentine was also reported for both LC and non-LC specimens [22]. Additionally, light curing did not significantly affect the antibacterial properties of SDF in vitro, with no evidence of enhanced efficacy [98]. Clinical trials are needed to determine the effect of LC on silver penetration and its impact on long-term caries prevention.

The Silver-Modified Atraumatic Restorative Treatment (SMART) technique

The Silver-Modified Atraumatic Restorative Treatment (SMART) concept involves combining SDF with a restorative material to address dental caries. Once SDF is applied, it seals the lesion, depriving the decayed dentin of a nutritional source and thereby inhibiting bacterial survival. Applying potassium iodide (KI) to the initial layer of SDF helps reduce staining prior to placing a restorative material such as glass ionomer cement (GIC) in Atraumatic Restorative Treatment (ART), significantly improving acceptance [21, 23]. Establishing a restoration after SDF treatment also helps prevent fracture of the remaining tooth structure, maintain space, facilitate biofilm removal, and reduce the need for advanced behavior management [99].

Although a black and hardened carious lesion indicates that dental caries progression has been arrested [80], untreated decayed cavities in children's teeth still worry parents. ART restorations have been shown to improve parental satisfaction with their child's oral health regardless of prior SDF treatment [99]. The SMART approach is recognized for its simplicity, effectiveness, affordability, compatibility, and reduced chair time. Moreover, the ART-based method underlying SMART enhances children's cooperation by reducing discomfort and tooth sensitivity, making brushing less painful and improving oral hygiene compliance [94]. Consequently, this method provides a straightforward, cost-effective intervention for resource-constrained healthcare systems and community dental services.

Conclusion

Silver diamine fluoride (SDF) is a potent agent that combines antimicrobial activity with remineralization potential, offering a non-invasive and cost-effective strategy for caries management. Its dual action, Silver ion-mediated microbial inhibition and fluoride-induced apatite formation, makes it particularly useful for high-risk, pediatric, and special-care populations.

This narrative review has explored the chemical interactions, biological mechanisms, and clinical implications of SDF use. While its short-term efficacy and safety are well supported, variations in formulation, application technique, and patient response highlight the need for standardized protocols. Challenges such as tooth staining and uncertainties around long-term exposure remain important considerations.

Modifications to the original technique, such as the use of potassium iodide (KI) to reduce staining and the integration of SDF into atraumatic restorative techniques like the SMART approach, offer promising ways to improve both clinical outcomes and patient acceptance. However, these adaptations require further validation through controlled studies.

Future research may benefit from further investigation to better understand SDF’s mechanism of action evaluate the effectiveness of adjunctive methods, and develop consensus-based guidelines for its optimal use. As the evidence base expands, SDF continues establishing its role as a core tool in modern, minimally invasive dentistry.

Authors’ contributions

DJ: Conceptualisation, Project administration, Writing original draft, review and editing. NA: Conceptualisation, Supervision, Writing original draft, review and editing. AA: Conceptualisation, Supervision, review and editing. TA: Supervision, review and editing final draft. SB: Conceptualisation, Supervision, Writing original draft, review and editing. NB: Conceptualisation, Supervision, Writing original draft, review and editing.

Funding

The project was funded by KAU Endowment (WAQF) at King Abdulaziz University, Jeddah, Saudi Arabia.

Data availability

All data generated or analyzed during this study are included in this published article.

Declarations

Ethics approval and consent to participate

Not applicable.

Consent for publication

Not applicable.

Competing interests

The authors declare no competing interests.