Dr.Ankita Garg
December 2025-Issue1
ABSTRACT
Background: Dentin hypersensitivity (DH) is a common dental complaint involving brief, sharp pain from exposed dentin on stimulation by various stimuli. In spite of the availability of many desensitizing agents, relative efficacy data among them, particularly in the different delivery methods are scarce.
Aim: In comparison of the short-term efficacy of three desensitizing products being GLUMA Desensitizer, Clinpro XT Fluoride Varnish, and 1.23% Acidulated Phosphate Fluoride (APF) Gel with iontophoresis to diminish DH, with two application techniques: cold air blast and explorer scratching.
Materials and Methods: This single-center, randomized clinical trial included 75 patients diagnosed with DH and divided equally among three intervention groups. Three desensitizing agents were administered to each group. Sensitivity was determined at six time points (baseline, 1 day, 14, 28, 90, and 120 days) using the Visual Analogue Scale (VAS) in response to cold air stimulation and explorer scratching. Repeated measures ANOVA and Bonferroni post hoc tests were used to compare intra- and inter-groups.
Results: All groups exhibited statistically significant decreases in VAS scores over time (p < 0.001). Group 3 (APF gel with iontophoresis) had the largest decrease, significantly more when performed under the air blast method (mean change: 63.28 ± 12.80), compared to Groups 1 and 2. Intergroup differences were not significant when using the explorer scratching method (p = 0.759).
Conclusion: All three of the desensitizing agents significantly alleviated DH. Nevertheless, 1.23% APF gel with iontophoresis offered the most prolonged and effective relief, particularly when applied using the air blast cold method. The evidence warrants its use in standard clinical practice for treatment of long-term DH.
Keywords: Dentin hypersensitivity, APF gel, iontophoresis, GLUMA, Clinpro XT, VAS score.
INTRODUCTION
Dentinal hypersensitivity (DH) is the most common dental condition and in practice still underappreciated dental condition. Since its prevalence is found at large, it is one of the important condition to be addressed.[1] It is a condition of temporary sharp pain from open dentinal surfaces to outside stimuli that are usually thermal, tactile, osmotic, evaporative, or chemical.[2] It is not only a painful but also a disabling condition because of its negative effect on oral health-related quality of life.[3,4] Dentinal hypersensitivity is not an emergent disease immediately life-threatening, but repeated discomfort which it causes can result in considerable effect on food choice, oral health habit, and on overall well-being of the patient.[4]
The DH pain has been classically described as a response which cannot be explained by another oral disease. The most widely used definition came from the Canadian Consensus Document, wherein DH was "pain resulting from exposed dentine secondary to chemical, thermal, tactile, osmotic or evaporative stimulation which cannot be attributed to any other dental flaw or pathology."[5] It requires exclusion diagnosis since the clinical situation could also be caused by other pathology like cracked tooth syndrome, broken restorations, caries, or pulpal inflammation.[6-8] Adequate diagnosis therefore forms the cornerstone for appropriate management.[8]
Dentin exposure is a mandatory prerequisite for DH to take place, and this can be initiated by a host of etiologic factors.[9] Enamel or cementum structural loss, due to abrasion, attrition, erosion, or abfraction weakens the tooth protective layer and leads to dentin exposure. Furthermore, periodontal infection-induced gingival recession exposes root surfaces to it, and one becomes more susceptible to DH.[10] Cements with a thin film over root dentin are susceptible to being removed or absent, having an open pathway for transmission of the stimulus to pulp.[11] Permeability and patency of dentinal tubules are most important for the cause and severity of DH.
Histologically, it was confirmed that hypersensitive dentin consisted of much more patent dentinal tubules with larger diameter than non-sensitive dentin. A few of the factors regulating patency of tubules are presence or absence of smear layer, extent of peritubular sclerosis of dentin, and amount of secondary or reparative dentin pulpal to it.[12,13] Physiological aging with aging leads to dentinal changes such as sclerosis and secondary dentin deposition, reducing the permeability and being involved in the decreased incidence of hypersensitivity in aged populations.[14] Epidemiologically, prevalence of dentinal hypersensitivity varies highly and ranges from 3% to as high as 57% in the literature, with considerations including research design, study population, and employed diagnostic criteria.[14]
It is found mostly in adults in the age bracket 20-40 years, but may be found in any age group. It has been noted to be more common in females and may be brought about by behavioral and physiological causes, and the greater female drive to care for their teeth through a visit to dental clinics.[15] Root sensitivity, a kind of dentinal hypersensitivity due to gingival recession has particularly been noted to increase following periodontal treatment, where incidences were reported as 9-23% pretherapy and 54-55% posttherapy.[16] The same is usually transient and subsides in 3 weeks following the treatment. Dentinal hypersensitivity has been the object of copious scientific attention towards understanding how it happens.[16,17]
Of several theories proposed, such as the neural modulation theory, gate control theory, and vibration theory, the most scientifically sound and adopted is Brännström's hydrodynamic theory. On this premise, pressure due to external stimulation forces fluid relatively quickly along dentinal tubules.[18] Fluid movement changes pressure conditions and activates mechanoreceptors that accompany Aδ fibers and produces typical instant pain. The effectiveness of this mechanism depends on the openness of dentinal tubules at both the outer dentin surface and directed away from it towards the pulp.[19] Owing to its multifactorial origin, DH is best treated using a sympathetic and individualized method. Before therapy is started, caution should be exercised to ensure diagnosis has been established and differential diagnoses for carious lesions, pulpitis, tooth chipping, or faulty restorations have been excluded.[15,18] Untreated pathology can cause not only persistent symptoms but also reduce the efficacy of therapeutic intervention intended for abolition of DH.[20]