A Scanning Electron Microscopic Study to Compare the Effect of Different Application Time of Desensitizing Agent on Dentinal Tubules

Abstract

Background: Dentin hypersensitivity is a common clinical condition caused by exposed dentinal tubules, leading to sharp, transient pain in response to external stimuli. Management involves tubule occlusion or neural modulation using agents like potassium salts, fluorides, oxalates, adhesives, and resin materials; hence, this study assessed the effect of different application times of desensitizing agents on dentinal tubules.

Materials & methods: This study evaluated the tubule-occluding ability and durability of Vivasens using 60 dentin specimens prepared from 30 extracted maxillary first premolars. After standardized cavity preparation, EDTA treatment, and SEM confirmation of open dentinal tubules, specimens were randomly allocated into four groups (Immediate, 5 min, 15 min, and 30 min) and treated per manufacturer’s instructions. All samples underwent simulated brushing for one week and one month, followed by SEM analysis, with tubule occlusion graded by blinded observers to assess efficacy and longterm stability.

Results: The Immediate group demonstrated the highest mean score (10.32 ± 3.25), indicating maximum response at baseline. The 5 minutes group showed a reduced mean value of 5.99 ± 2.45, reflecting a significant decline compared to the immediate response. The 15 minutes group exhibited a further decrease with a mean of 2.36 ± 2.08, while the 30 minutes group recorded the lowest mean (0.89 ± 1.13), suggesting the greatest reduction over time. Overall, the findings indicate a progressive decline across groups, with the response diminishing steadily from the immediate period to 30 minutes.

Conclusion: Longer time is beneficial because the agents continue to act on the dentinal tubules with time, either by further precipitating within the tubules or forming a more stable barrier. This reduction in permeability translates into less fluid movement in the tubules, which reduces stimulation of nerve endings in the pulp — the key mechanism behind decreased sensitivity.