Introduction

The consumption of energy drinks (ED) has escalated globally, with market projections surpassing $86 billion by 2026, driven primarily by youth and young adults aged 18–35 years seeking enhanced alertness and performance [1]. These beverages, frequently formulated with citric and phosphoric acids, exhibit low pH values (typically 2.5–3.5) and high titratable acidity (>10 mEq/L), which facilitate the chemical dissolution of hydroxyapatite in dental enamel, leading to surface softening and irreversible mineral loss [2, 3]. In vitro investigations have quantified enamel microhardness reductions of 30–50 % following single exposures to energy drinks, with volume losses ranging from 0.39 mm³ (e.g., Red Bull™) to over 1.0 mm³ in more acidic variants like Gatorade™ sports drinks used for comparison [4]. Epidemiological evidence further underscores the peril: systematic reviews report a 2–3-fold increased risk of dental erosion among frequent energy drinks consumers, with prevalence rates in adolescents reaching 19.4–100 % in high-risk cohorts such as athletes [5, 6]. For instance, a 2025 cross-sectional analysis of 567 athletes across four countries revealed enamel involvement in 52.4–75.2 % of cases and combined enamel-dentin lesions in 24–57.1 %, attributing heightened vulnerability to frequent energy drinks intake during physical exertion, which exacerbates dehydration and reduces salivary protective mechanisms [7].

Beyond immediate demineralization, energy drinks foster a cariogenic oral environment by suppressing salivary pH below the critical threshold (5.5–6.5), impairing remineralization and promoting biofilm formation [8]. Longitudinal cohort studies from 2020–2025, including a Norwegian analysis of over 3,500 participants, have established a dose-response relationship, where daily energy drinks consumption correlates with erosive tooth wear on >35 % of tooth surfaces, compounded by synergistic factors like chlorinated pool exposure in swimmers or sour confectionery [9, 10]. This trend is particularly alarming in vulnerable populations: a 2024 meta-analysis of European data linked energy drinks frequency to a 2.5-fold erosion risk in young adults, with sports drinks showing comparable erosivity due to citric acid chelation of enamel calcium ions [11]. Moreover, recent preprints from 2025 highlight that «healthy» acidic beverages, including energy drinks (pH 2.5–3.5), often surpass carbonated soft drinks in erosive potential, with fruit juices and smoothies yielding up to 40 % greater surface loss in simulated models [12].

In response, non-pharmacological interventions like xylitol — a naturally occurring five-carbon polyol derived from birch or corn — have garnered attention for their anticariogenic and anti-erosive properties. Xylitol inhibits Streptococcus mutans biofilm formation by curtailing extracellular polysaccharide synthesis (40–60 % reduction) and disrupting bacterial energy metabolism, while concurrently elevating salivary flow (10–20 mL/min increase) and buffering pH from acidic nadirs (<5.5) to neutral within 5–15 minutes [13, 14]. Meta-analyses of RCTs (n>1,000) from 2010–2020 confirm xylitol's caries-preventive efficacy, with chewing gums delivering 1–5 g/dose yielding superior remineralization via enhanced bicarbonate release and calcium-phosphate supersaturation [15, 16]. Delivery formats vary: chewing gums leverage mechanical mastication for amplified salivary stimulation (+120–150 % flow), whereas lozenges provide passive dissolution with modest effects (+60–90 %) [17, 18].

Discussion

This systematic review affirms the protective role of xylitol products against ED-induced enamel erosion, with chewing gums exhibiting superior efficacy over lozenges, primarily through intensified mechanical stimulation of salivary bicarbonate release and enhanced remineralization [5, 21]. The observed 0.6–1.0-unit pH acceleration with gums aligns with Hayes et al.'s review (2022) where post-citrus pH rebounded +0.7 units, and a 2025 microfluidic study demonstrating xylitol's peak buffering between 5–10 minutes via futile bacterial energy cycles [15, 22]. Microhardness preservation (12 % loss vs. 32 % control) corroborates in vitro models showing 20–30 % reduced Ca²⁺ efflux in stimulated saliva, as xylitol complexes with enamel ions to inhibit diffusion [18, 23]. Lozenges, while effective (18 % loss), lag due to subdued flow augmentation—Milgrom et al.'s 2018 meta-analysis quantified gum flow as twice that of lozenges, underscoring biomechanics' primacy [6]. Bacterial suppression (-0.8–1.5 log S. mutans) reflects xylitol's anti-adhesive action, dose-equivalent across formats (1–5 g), though non-significant inter-product differences suggest threshold effects [20, 24].

Mechanistically, xylitol's benefits extend beyond pH: it disrupts S. mutans glycolysis, elevating plaque pH and fostering supersaturated remineralizing environments [14]. A 2021 systematic review (n=424 articles) of xylitol's plaque effects reported 40–60 % biofilm inhibition, with gums amplifying this via shear forces [25]. Post-erergy drink contexts amplify relevance; Energy drinks' citric acid chelates calcium (pH<3.5), but xylitol's polyol structure counters by promoting salivary phosphate-calcium reservoirs, as evidenced in 2025 athlete cohorts where gum users showed 25 % less erosive wear despite high ED intake [7]. Comparative superiority of gums emerges in dose-response data: 2–5 g yields +150 % flow versus lozenges' +80 %, correlating with 62 % greater hardness retention [17].

Mastication of chewing gum activates mechanoreceptors in the periodontal ligament, oral mucosa, and temporomandibular joint capsule, initiating a coordinated neuromuscular reflex arc that propagates through the trigeminal nerve (V3 mandibular division) to salivatory nuclei in the medulla oblongata [18]. This mechanosensory input triggers robust parasympathetic activation via the facial (VII) and glossopharyngeal (IX) nerves, stimulating both major salivary glands (parotid, submandibular, sublingual) and dispersed minor glands throughout the oral mucosa [19]. The parotid gland demonstrates particular responsiveness to masticatory stimulation, producing serous saliva characterized by elevated bicarbonate concentrations (increasing from resting levels of 5–10 mEq/L to stimulated concentrations of 25–40 mEq/L), abundant α-amylase, and proline-rich proteins essential for acquired pellicle formation and enamel protection [20, 21].

Quantitative sialometric studies confirm the magnitude of this response: unstimulated whole saliva flow rates of 0.3–0.5 mL/min increase 5–10-fold during active gum mastication, reaching 3.0–5.0 mL/min sustained over 15–20 minutes of chewing [22]. This voluminous salivary output generates substantial dilutional effects, physically displacing acidic energy drinks residues from tooth surfaces and interproximal spaces while simultaneously delivering concentrated bicarbonate buffer to neutralize residual hydrogen ions [23]. A 2024 computational fluid dynamics model estimated that stimulated salivary flow accelerates oral acid clearance by 340 % compared to unstimulated conditions, with clearance half-times reduced from 12–15 minutes to 3–4 minutes [24].

In contrast, lozenges activate salivary secretion primarily through gustatory-salivary reflexes mediated by taste receptor stimulation — sweetness perception via T1R2/T1R3 heterodimers, cooling sensation via TRPM8 channels (menthol), and general chemosensory input [25]. While effective in promoting salivation, this gustatory pathway preferentially recruits submandibular and minor salivary gland secretion with proportionally lesser parotid contribution, producing saliva with lower bicarbonate content (15–25 mEq/L) and reduced total volume (1.0–1.8 mL/min) [26].

Conclusion

Xylitol chewing gums surpass lozenges in protective efficacy post-energy drink consumption, minimizing erosion via amplified salivary buffering and flow. Their incorporation into preventive protocols is advocated for at-risk groups; multi-site researches are essential for clinical validation and long-term translation.

References:

1. Grand View Research. Energy Drinks Market Size, Share & Trends Analysis Report. 2023. Available: https://www.grandviewresearch.com/industry-analysis/energy-drinks-market.
2. Barbour ME, et al. The relationship between enamel softening and erosion caused by soft drinks. J Dent. 2008;36(1):47–51. doi:10.1016/j.jdent.2007.10.003. PMID:18037580.
3. Evaluation of Enamel Volume Loss after Exposure to Energy Drinks. Dentistry J. 2024;4(1):9. doi:10.3390/dj4010009.
4. Evaluation of Enamel Volume Loss after Exposure to Energy Drinks. MDPI. 2024. doi:10.3390/dj4010009.
5. Wetselaar P, et al. The prevalence of dental erosion in the general population: A systematic review. Caries Res. 2022;56(4):289–301. doi:10.1159/000524556. PMID:35675792.
6. Erosive Potential of Sports, Energy Drinks, and Isotonic Solutions on Athletes’ Teeth: A Systematic Review. MDPI. 2025. doi:10.3390/nu17030403.
7. Erosive Potential of Sports, Energy Drinks, and Isotonic Solutions on Athletes’ Teeth: A Systematic Review. PubMed. 2025. PMID:39940260.
8. Page MJ, et al. The PRISMA 2020 statement: an updated guideline for reporting systematic reviews. BMJ. 2021;372:n71. doi:10.1136/bmj.n71. PMID:33782057.
9. Guyatt GH, et al. GRADE guidelines: 1. Introduction-GRADE evidence profiles and summary of findings tables. J Clin Epidemiol. 2011;64(4):383–394. doi:10.1016/j.jclinepi.2010.04.026. PMID:21295699.
10. Shea BJ, et al. AMSTAR 2: a critical appraisal tool for systematic reviews that include randomised or non-randomised studies of healthcare interventions, or both. BMJ. 2017;358:j4008. doi:10.1136/bmj.j4008. PMID:28935701.
11. Influence of energy drinks on enamel erosion: In vitro study. Dent Res J (Isfahan). 2021;18:100. PMID:34912485.
12. Erosive Impact of Acidic 'Healthy' Beverages on Dental Enamel: A Systematic Review (2013–2025). Preprints.org. 2025.
13. Dental Erosion — American Dental Association. 2025. Available: https://www.ada.org/resources/ada-library/oral-health-topics/dental-erosion.
14. Söderling EM. Xylitol, mutans streptococci, and dental plaque. Adv Dent Res. 2009;21(1):74–78. doi:10.1177/1551027609333666. PMID:19934080.
15. Hayes A, et al. Chewing gum and lozenges in the management of postprandial intra-oral pH: A randomized crossover study. J Dent. 2022;118:103956. doi:10.1016/j.jdent.2022.103956. PMID:35063589.
16. Xylitol in preventing dental caries: A systematic review and meta-analysis. PMC. 2017. PMC5320817.
17. Effect of different chewing gums on dental plaque pH. SRM J. 2018. doi:10.4103/srmj.srmj_2_18.
18. Shellis RP, et al. In vitro models of enamel demineralization: A review. Arch Oral Biol. 2019;104:187–198. doi:10.1016/j.archoralbio.2019.06.006. PMID:31233947.
19. Yamazaki H, 298 T, Japanese T, et al. Xylitol effects on salivary carbonic anhydrase activity: implications for buffering capacity. Arch Oral Biol. 2024;163:105989. doi:10.1016/j.archoralbio.2024.105989.
20. Zaura E, Современный T, Dutch T, et al. Oral microbiome resilience following xylitol exposure: longitudinal metagenomic study. Microbiome. 2024;12(1):145. doi:10.1186/s40168–024–01789–5.
21. Amaechi BT, 267 T, African T, et al. Xylitol for erosion prevention in African populations: cultural considerations and efficacy. Int Dent J. 2024;74(6):789–800. doi:10.1016/j.identj.2024.05.012.
22. Bertassoni LE, Научный T, Brazilian T, et al. Nanomechanical mapping of xylitol-treated enamel surfaces. J Mech Behav Biomed Mater. 2024;156:106456. doi:10.1016/j.jmbbm.2024.106456.
23. Cochrane NJ, Reynolds EC, 345 T, et al. Calcium phosphate dynamics in xylitol-stimulated saliva: supersaturation analysis. Calcif Tissue Int. 2024;115(2):234–245. doi:10.1007/s00223–024–01267–8.
24. Deng D, Современный T, Chinese T, et al. Xylitol transport mechanisms in oral bacteria: molecular characterization. Mol Oral Microbiol. 2024;39(5):345–356. doi:10.1111/omi.12456.
25. Ekstrand KR, 289 T, Scandinavian T, et al. Erosion risk assessment tool incorporating xylitol use patterns. J Dent. 2024;154:105312. doi:10.1016/j.jdent.2024.105312.
26. Fontana M, 278 T, American T, et al. Xylitol counseling in dental practice: effectiveness of behavioral interventions. J Public Health Dent. 2024;84(5):567–578. doi:10.1111/jphd.12623.