INTRODUCTION

Dentin sensitivity could be defined as “pain arising from exposed dentin, typically in response to either a chemical, thermal, tactile or osmotic stimuli that cannot be explained by other dental defect or pathology.”¹ There are other dental conditions such as caries, tooth and/or restoration fracture, and cracked-tooth syndrome that may produce the same short, sharp tooth pain. Thus, a careful dental history and precise clinical and radiographic examinations are necessary to establish a differential diagnosis of the clinical condition.^1,2

The highly subjective nature of dentin sensitivity and the large variability among individual responses makes it difficult for an accurate assessment of this disorder.³ Indeed, studies show extreme variations in the prevalence of this condition, ranging from 3% to 57% of dentin sensitivity in individuals with no previous dental diagnosis to as much as 72% to 98% of patients affected by periodontal conditions.²

According to Brännstrom, the mechanism of dentin sensitivity is considered to be related to a hydrodynamic theory in which fluid moves, within or through the dentinal tubules, at a rate that activates mechanoreceptor nerves in the dental pulp, causing pain.^4-6 The unit of measurement for the movement of fluids through the dentinal tubules is called dentin hydraulic conductance.⁵ The occlusion of the dentinal tubules prevents fluid movement and therefore avoids dentinal sensitivity.^4-6 Agents such as oxalates, which promote the occlusion of the dentinal tubules, aim to cause the precipitation of crystals, thereby reducing the movement of the dentinal fluids. Ideally, these agents must be resistant to pH variations that take place in the oral environment, such as variations in diet and saliva quality and quantity.⁷ Dentin desensitizers, based on oxalates, effectively reduce the dentin hydraulic conductance^6,8 by forming calcium oxalate crystals that precipitate over the dentin surface, occluding dentinal tubules. These desensitizers are available in gels or solutions that contain a low concentration of oxalic acid at low pH (Table 1).^8-10

Table 1 Examples of Oxalate-Based Dentin Desensitizers

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Gillam and others¹¹ evaluated in vivo the effects of ferric oxalate solution on the reduction of dentin sensitivity during a four-week time period. They reported a significant reduction in sensitivity five minutes after the solution was applied. However, the dentin sensitivity came back to its baseline level four weeks later. Another study demonstrated that the application of potassium oxalate has a relatively low life span for occlusion of dentinal tubules, as a significant loss of the oxalate precipitate was observed only one week after its application.¹²

Different authors have associated oxalate-based desensitizing agents and adhesive restorations, in in vitro studies, with improving the long-term occlusion of the dentinal tubules, and therefore reduction of dentin sensitivity, in teeth with cervical loss of tissue.^7,8,11-13 This treatment combines the occlusion of dentin tubules with the oxalate-based compounds and the use of an adhesive system.¹³

The aim of this randomized controlled clinical trial was to determine the performance of oxalic acid as a desensitizer when used under adhesive restorations during a four-month period. The hypothesis to be tested was that oxalic acid, placed under resin-based composite (RBC) restorations in cervical lesions, reduces dentin sensitivity compared with resin-only restoration.

METHODS AND MATERIALS

This double-blind randomized controlled clinical trial recruited 36 patients, aged 25 to 66 years (mean, 40.3±7 years), with 103 sensitive teeth. Dentin sensitivity was defined as having a minimum score of 1.5 on a visual analog scale (VAS), in response to air being applied directly to exposed dentin using an air syringe.

The sample size was determined a priori using G*Power 3,¹⁴ with a population effect size of 0.4, a significance level α of 0.05, and a power (1-β) of 0.8 (Figure 1).

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Inclusion criteria were as follows:

1. Patients older than 18 years having at least two sensitive teeth.

2. Teeth that have evidence of buccal cervical loss of tissue by abrasion or erosion, with the indication of resin-based restoration

3. Teeth without cavities or defective restorations in the buccal hypersensitive area

Patients presenting any of the following conditions were excluded from the study:

1. Chronic inflammatory systemic diseases

2. Chronic pain

3. Pregnancy

4. Recent periodontal surgery, orthodontic treatment, or desensitizing treatments within the past three months

All patients signed the informed consent approved by the Ethics Committee (Dental School, Chile University).

At baseline, a clinical evaluation was made by thermal/evaporation test with an air syringe. The test was carried out using an air syringe with direct air pressure for one second (Siemens, Sirona, at 60 psi, from 19°C to 24°C and with an air flow of about 2 mm diameter) applied perpendicularly, 1 cm from the tooth's surface.^11,15–17 Dentin sensitivity was scored using a VAS. Patients quantified responses to the air stimulus by placing a mark on a 100-mm-length line anchored by word descriptors at each end: no pain at the left end and very severe pain at the right end. The VAS score was determined by measuring in millimeters from the left-hand end of the line to the point indicated by the patient.^18,19 All assessments were done by the same evaluator (G.X.).

Patients were recruited continuously over the course of five months, the period at which the desired sample size was reached. Once teeth were evaluated for sensitivity, they were assigned to one of the groups using a coin-toss method to randomly assign one tooth to either the experimental or control group. The next tooth was automatically assigned to the other group, and if a third tooth was involved, the coin was used again (Pocock Method).^18,20

• Group A: Experimental group, n=52 teeth (13 molars, 39 premolars) treated with BisBlock (Bisco Inc, 1100 W Irving Park Rd, Schaumburg, IL 60193, USA)

• Group B: Control group, n=51 teeth (15 molars, 36 premolars) treated with distilled water

Each patient participated in both groups (experimental and control) with at least one tooth in each category, so both groups were composed of patients of identical age and gender: 24 women (66.66%) and 12 men (33.33%).

The exposed dentin of the teeth of both groups was etched with Uni-Etch (Bisco Inc) 32% orthophosphoric acid for 15 seconds, rinsed with water, and air dried to remove the excess water while retaining slight moisture on the surface. Teeth in group A were treated with BisBlock, over the dentin surface, for one minute and then rinsed with water for 15 seconds. Teeth in group B were treated with distilled water, over the dentin surface, for one minute and then rinsed with water for 15 seconds. To ensure the double-blind aspect of the trial, a different operator applied the experimental/control treatment prior to the adhesive/restoration placement. The dentin surface was left slightly moist before applying two layers of one-step dentin adhesive (biphenyl dimethacrylate >10%, hydroxyethyl methacrylate >10%, acetone >40%)²¹ according to the manufacturer's instructions (Bisco Inc). After the adhesive application, the surface was polymerized for 15 seconds. The area was then restored with Aelite Composite (Bisco Inc) by applying the material in two small increments. The material was polymerized after each application for 40 seconds. During all procedures, moisture control was accomplished by using cotton roll isolation, gingival cord, and low- and high-power suction. All treatments, other than the desensitizing step, were done by the same operator (C.B.).

Four months after treatment, a visual clinical examination of the restorations confirmed that they remained intact during the period of the study, and another evaluation using the thermal/evaporation test and the original rater (G.X.) was performed.

Two-way analysis of variance (ANOVA) test was applied with dentin sensitivity as the dependant variable and treatments and time as factors (SPSS 14.0, Chicago, IL, USA).

RESULTS

Mean VAS scores, standard deviation (SD), and comparison between the initial and final VAS score of each group (represented as mean sensitivity reduction) for dentin sensitivity at baseline and four months after treatment are presented in Table 2 and Figure 2.

Table 2 Dentin Sensitivity Expressed in VAS Score and SD at Baseline and Four Months After Treatment, Separated by Group

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Sensitivity reduction for each sample (each tooth) was obtained using the following formula:

Mean sensitivity reduction and SD were obtained by averaging the data obtained by each tooth.

At baseline, both groups presented similar scores for sensitivity (p=0.289).

Four months after treatment, group A showed an 88.99% ± 23.42% reduction in dentin sensitivity, whereas the dentin sensitivity reduction in group B was 61.01% ± 35.71%.

Two-way ANOVA showed significant sensitivity reduction associated with the following variables: time (p=0.0001), oxalate application (p=0.003), and when the two variables were combined (p=0.0001; Table 3).

Table 3 Two-Way ANOVA Summary Table ^a

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DISCUSSION

In this clinical study, both treatments showed reduction of dentin sensitivity as reported by participating patients after four months. However, the experimental group showed a significantly higher reduction in dentin sensitivity when compared with the control group over a four-month period. These results are in agreement with those obtained by Prati and others²² in a four-week clinical evaluation study. In that study, it was noted that an oxalate-based product applied over sensitive teeth provided a reduction in dentin sensitivity in the range of 19% to 68%. Another study showed dentin permeability reduction in the range of 65% to 95% with ferric oxalate solutions,²³ and an in vitro study showed a significant reduction of the dentin hydraulic conductance with the use of potassium oxalate.¹³ Although several of these studies reported reduction of dentin sensitivity, long-term results and permanent tooth desensitization remain a clinical problem. Later studies demonstrated that the tubular occlusion achieved by oxalate compounds lasted only a short period of time, and it was surmised that this was probably due to its solubility in the oral environment.¹²

Gillam and others,²⁴ in a scanning electron microscopy study, observed that four oxalate solutions (aluminium oxalate, potassium oxalate, ferric oxalate e, and oxalic acid) applied onto dentin discs occluded the dentin tubules to different degrees. However, radiographic diffraction techniques were unable to identify oxalate salts within the tubules. It was suggested that some oxalates appear to occlude the dentinal tubules through the formation of crystals. It is possible that the oxalate's components are important in the initial formation of those crystals.²⁴ Two possible mechanisms explaining the action of potassium oxalate have been proposed.²⁵ First, the formation of calcium oxalate crystals blocks dentinal tubules and prevents dentin fluid loss. This mechanism would be responsible for the long-term desensitizing action. The second mechanism suggests that high levels of potassium would increase the extracellular K⁺ concentration around the dentinal terminal nerves, causing depolarization and causing them to become less excitable, which would explain the temporary reduction in tooth sensitivity.²⁵

A previous in vitro study evaluated desensitizing agents and dentin bonding agents with and without placement of RBCs. That study concluded that placement of primers without etching reduced permeability more than any other treatment modality, indicating that etching a sensitive dentin area may be appropriate only if an RBC is to be placed in the area.²⁶

Some studies have reported that oxalate-based products react with the calcium ions available in the dentin surface and dentin fluid, transforming the labile cover in an acid-resistant structure by replacement of the smear layer with a layer of calcium oxalate crystals.^7,24,27 The smear layer provides a great source of calcium ions that would be available in the formation of the crystals, and an in vitro study reported a reduction in the numbers of crystals that were formed on surfaces treated with oxalate when the smear layer had been removed with chemical agents. Therefore, without the smear layer, the number of calcium ions available is decreased and so is the precipitation of crystals. The low pH of the oxalate solution causes the dissolution of the smear layer. This phenomenon gradually increases the pH because of the dissolution of the hydroxyapatite and other dentin components, which neutralize the hydrogen ions, causing the precipitation of the calcium oxalate and ferric phosphate. Although the oxalate crystals resist the acid attack, they do not completely block the tubules and therefore produce only a replacement for the smear layer.²³

The reduction of dentin permeability is obtained by a superficial tubular occlusion, which does not interfere with the adhesive technique, as demonstrated by previous studies.^7,8,11-13 The use of dentin adhesives over oxalate salts provides better tubular occlusion of the exposed dentin without affecting the adhesive resistance of the restoration.^7,8,11-13

One limitation of the study is the well-known existence of a placebo response by a subject knowingly participating in a sensitivity study.²⁸ We hope that with the double-blind randomized design of the study and the use of a control group, the placebo effect over the study was diminished.

CONCLUSIONS

The results of this randomized clinical trial show that the application of oxalate acid under RBC restorations significantly reduces dentin sensitivity, compared with resin-only restorations, over a period of four months. However, further studies are needed to evaluate the long-term stability of this technique as a permanent treatment for dentin sensitivity.