January 2018
Volume 39, Issue 1

Comparative Evaluation of Fluoridated Mouthwash and Sodium Bicarbonate in Management of Dentin Hypersensitivity: An In Vitro SEM Study

Vasundhara Rikame, BDS; Yogesh Doshi, MDS; Robert A. Horowitz, DDS; Vidhi Kevadia-Shah, MDS; and Mona Shah, MDS


Sodium bicarbonate (ie, baking soda) can be used as an adjunct to surgical periodontal therapy to reduce dentin hypersensitivity (DH). Sodium bicarbonate mouthwash has numerous appealing attributes, including high availability, low cost, low abrasivity, water solubility, buffering capability, and, in high concentrations, antimicrobial properties. It is also safe to use. The primary underlying cause of DH is open dentinal tubules from loss of either cementum or enamel. The aim of this in vitro study was to evaluate, through scanning electron microscopic examination, the effect of sodium bicarbonate on dentinal tubule occlusion and compare it with that of fluoridated mouthwash.

Due to an increased awareness of the benefits of oral healthcare among the current generation, the incidence of tooth loss has been decreasing as people seem to have a greater interest in preserving their natural teeth rather than replacing them with a prosthesis. Periodontal treatments aimed at saving teeth have been given a high priority. A greater number of retained teeth in the mouth, however, can lead to various hard-tissue problems.1 Dentin hypersensitivity (DH) is one such common complaint that prompts patients to visit their dentist. DH can be a complex clinical condition to diagnose, because there may be no obvious signs present in the mouth that would provide a precise diagnosis. Dentists have to rely on both the patient's history and a thorough clinical examination, often using thermal or tactile stimuli.

Dentin receptors have a unique feature of eliciting pain as a response to any environmental stimulus. The sensory response in the pulp cannot differentiate between heat, touch, pressure, or chemicals. This is because the receptors in the pulp organs lack specificity.2 Whatever the provocation may be, the patient perceives it as pain.3 Hence, careful examination should be performed to rule out other conditions that may present in a manner similar to DH.

According to Holland et al, “Dentin hypersensitivity is defined as short, sharp, well-localized pain arising from exposed dentin in response to stimuli, typically thermal, evaporative, tactile, osmotic, or chemical and which cannot be ascribed to any other dental defect or pathology.”4 Various theories have been proposed to explain the mechanism behind DH, including the direct innervation theory, odontoblastic transduction theory, and hydrodynamic theory.5 In the direct innervation theory, the belief was that direct communication exists between nerve fibers of the pulp and dentinal tubules.6 Hence, the stimulus applied to the dentin would trigger the pain response from the pulp tissue. Now, however, it has been proven by scanning electron microscopic (SEM) examination that nerve fibers do not pass across the dentinal tubules and travel only for a short distance in the predentin, mainly near the pulp horns.6 The odontoblastic transduction theory stated that there is a synaptic junction between odontoblastic processes and nerve fibers7; however, no release of neurotransmitter has ever been detected by odontoblasts, which is required for nerve conduction. Finally, Brannstrom's hydrodynamic theory8 considers the fluid movement in the dentinal tubules when an impulse is applied. The nerve endings from the pulp sense this movement, resulting in the production of pain response. This latter concept is the most widely accepted theory for the cause of DH.

DH may present on several teeth or on one specific tooth. It is most commonly noted on facial surfaces of teeth in the cervical region.9 While any tooth in the dentition can be affected, increased prevalence is seen with canines and premolars of both arches, followed by incisors and molars.10 The primary underlying cause of DH is open dentinal tubules from loss of either cementum or enamel. The most common cause of DH is dentinal tubule exposure due to gingival recession.11,12 Exposed cementum is more susceptible to chemical and mechanical insults, because it has less mineral content than enamel and dentin. Cementum is very thin in cervical regions (0.1 mm to 0.05 mm thickness), and it is absent in around 10% of people due to it not meeting the enamel at the cementoenamel junction.13 Therefore, root dentinal tubules become exposed easily as a result of abrasion, abfraction, and erosion.14

Approximately half of patients experience DH after either surgical or nonsurgical periodontal therapy.15 Scaling and root planing exposes freshly cleaned tooth surfaces in the oral cavity that were previously covered by calculus and extrinsic deposits, resulting in hypersensitivity. Periodontal treatments are aimed at removing the local etiologic factors and reducing inflammation. As inflammation is lessened, tissues undergo shrinkage, which leads to apical migration of the gingival margin.16 Root planing removes diseased cementum and some volume of dentin, thereby causing exposure of underlying dentin. Dentin permeability is increased for fluids and bacteria, leading to sensitive dentin.17 Patients, in turn, prefer not to brush these hypersensitive tooth surfaces, which makes them prone to plaque accumulation. This can predispose these areas to caries and periodontal inflammation and result in increased sensitivity, thus creating a destructive cycle.18-20 Additionally, isolated gingival recession can occur as a result of past orthodontic treatment and oral piercing.21

Numerous methods have been developed for the treatment of DH that have claimed to reduce pain by occluding dentinal tubules.22 Sodium bicarbonate (NaHCO3, ie, baking soda) is one such agent that can be used as an adjunct to surgical periodontal therapy to reduce hypersensitivity. Its usage can greatly enhance a patient's oral hygiene and motivation postoperatively. Sodium bicarbonate mouthwash is appealing to patients because of its safety attributes, availability, low cost, low abrasivity, water solubility, buffering ability, and, in high concentrations, antimicrobial properties.23,24

The aim of this in vitro study was to evaluate, through SEM examination, the effect of sodium bicarbonate on dentinal tubule occlusion and compare it with that of fluoridated mouthwash.

Materials and Methods

Specimen Preparation

Thirty human single-rooted teeth freshly extracted for orthodontic purposes and having a hopeless prognosis for periodontal treatment were used in this study (Figure 1). The teeth, which were stored in regular saline, were intact with no cervical caries, restorations, erosions, or fractures. They were cleaned of blood, saliva, plaque, and calculus using an ultrasonic scaler (DTE D3, Guilin Woodpecker Medical Instrument Co., glwoodpecker.com).

The anatomical crown, including 1 mm of root portion below the cementoenamel junction, was sectioned transversely. These decoronated root specimens were sliced horizontally using a diamond disc to obtain dentin discs of 1 mm to 2 mm thickness (Figure 2).

Chemical Treatment

All of the specimens were treated by using 37% phosphoric acid for 2 minutes. They were washed using distilled water and air-dried. This removed any surface debris without changing the superficial topography. These etched sections were scanned under scanning electron microscope to obtain images of opened dentinal tubules prior to treatment with sodium bicarbonate and fluoridated mouthwash.

SEM Preparation

The specimens were divided into two groups with 15 specimens in each group. One group was treated with a sodium bicarbonate aqueous solution, which was prepared by dissolving a half-teaspoon (ie, approximately 2.5 grams) of sodium bicarbonate (ie, baking soda) in a half glass (ie, 100 ml) of room-temperature water by mixing for 2 minutes. The other group was treated with fluoridated mouthwash (Orogard, Alkem Laboratories Ltd., alkemlabs.com). Each group was treated for 60 seconds. Five specimens from each group were air-dried and the remaining samples were washed with regular saline. The specimens were scanned under SEM. (SEM specifications [ICON Analytical Equipment Pvt. Ltd., iconanalytical.com] = specimens scanned at 20.00 kV under 65 Pa pressure and photographed at 2000X and 4000X)


The use of a diamond disc to prepare samples from the teeth led to the deposition of a smear layer on the specimens. If the hydrodynamic theory is to be accepted, it is necessary for the dentinal tubules to be open to cause DH.15 Pretreating the specimens with 37% phosphoric acid for 2 minutes removed the entire smear layer from all the samples (Figure 3). A homogenous surface with patent tubular openings of various sizes and shapes was observed. Dentinal tubule orifices were uniformly round or oval in shape with well-defined borders (Figure 4).

The specimens treated with sodium bicarbonate aqueous solution exhibited occluded tubules from deposition of an amorphous layer over the dentin. A thick layer of sodium bicarbonate crystals was observed on the dentin, completely obliterating the openings of the dentinal tubules (Figure 5). A number of crystals were scattered over the surface but were not plugging the tubules effectively because the crystals were larger in size than the diameter of the tubules (Figure 6). After rinsing with regular saline, weak smearing of sodium bicarbonate was noted (Figure 7).

In the case of the specimens treated with sodium fluoride mouthwash, no occlusion of tubules or smearing effect was seen. Granular deposits were observed at some places, but obliteration of dentinal tubules was not reported (Figure 8).


Dentin hypersensitivity has been a challenge for clinicians to treat because of its difficulty to diagnose, its resemblance to other dental conditions, and a lack of “gold standard” treatment options. Two primary methods of treatment are occlusion of dentinal tubules and blockage of nerve conduction. Current treatment options are not permanent, and long-term results are questionable.24

Numerous agents such as silver nitrate, zinc and strontium chloride, calcium hydroxide, sodium citrate, potassium oxalate, resins, and fluorides have been proposed for treating DH.25 Sodium bicarbonate or baking soda is one such compound that can be used to reduce DH. Over the years, it has been incorporated into mouthrinses and dentifrices to try to provide a practical approach to improving oral health. Advantages of sodium bicarbonate are that it is safe to use and low cost and has buffering ability, compatibility with fluorides, and, in high concentrations, antimicrobial properties.26,

In this in vitro SEM study, dentin specimens were treated using sodium fluoride mouthwash and an aqueous solution of sodium bicarbonate to compare the effectiveness of each agent in blocking dentinal tubules. Both agents were applied for 1 minute. Five specimens from each group were air-dried and the remaining samples were washed with regular saline. Both agents partly disappeared after spraying with saline. The SEM evaluation revealed weak smearing of the agents used on the dentin surface. Most of the crystals were washed off. Knight et al obtained similar results when they conducted a SEM study to evaluate the dentinal-tubule obliterating effect of various mechanical and chemical procedures. In the case of air-dried samples, sodium bicarbonate exhibited promising results. Complete obliteration of dentinal tubules was observed with amorphous crystalline deposition. The deposition of sodium bicarbonate crystals was not uniform. All tested samples produced almost 100% occluded tubules, but there was no plugging of dentinal tubules.27

Lumonsky was the first to suggest sodium fluoride as a desensitizing agent.28 Fluorides can be used in various formulations such as sodium fluoride, stannous fluoride, sodium monofluorophosphates, fluorosilicates, fluoride with iontophoresis, and fluoride varnishes.29 Various clinical trials to treat DH using sodium fluoride exhibited positive results. The mechanism of action can be described as precipitation of calcium fluoride crystals on open dentinal tubules occluding the tubule openings and resistance to dissolution due to increased mineralization of the tooth surface. This mechanical obliteration of dentinal tubules blocks the transmission of stimuli.30-33 SEM evaluation of teeth that were treated in vivo by single application of sodium fluoride illustrated granular deposits and reduced DH clinically.34

In the present study agents containing sodium fluoride did not result in similar precipitates. No significant SEM results were noted using sodium fluoride mouthwash. Few granular precipitates were observed under SEM examination. Neither complete obliteration of the tubules nor reduction in tubule diameter was reported with a single application. These results are in agreement with other reports in which the desensitizing agents were analyzed to assess their effect on dentin permeability and dentinal tubule occlusion.35,36 Pashley reported very small insoluble crystal formation when sodium fluoride is applied for 2 to 4 minutes.36 These crystals of calcium fluoride were unable to block the open dentinal tubules, and no reduction in DH was observed. Therefore, repeated application of fluorides for the optimal time interval is required to achieve favorable results. Periodic application of fluoride will lead to plugging of dentinal tubules with insoluble calcium fluoride salts over a period of time.36-38 Mukai et al and Arrais et al demonstrated that application of acidulated sodium fluoride on exposed dentin for 4 minutes resulted in crystalline deposition on peritubular dentin surfaces and inside dentinal tubules.37,38

Dental plaque is an important factor in causing DH. It has been observed that accumulation of plaque is proportional to the severity of DH. Patients who have their root surfaces covered with dental plaque reported more discomfort than those who have clean root surfaces.39-42 Accumulation of plaque on the roots leads to the development of an acidic environment with ensuing demineralization of tooth surfaces and increased patency of dentinal tubules.43 Demineralization of enamel and cementum will allow bacteria and their products to invade the dentinal tubules. Hence, there will be pulpal inflammation, which will contribute to increased DH.44 It has also been demonstrated that teeth having hypersensitivity show a significant number of larger diameter tubules with increased tubular patency.19

Periodontal pathogens are susceptible to sodium bicarbonate.45 Sodium bicarbonate-containing dentifrices exhibit greater bactericidal activity.46 Sodium bicarbonate has an abrasive consistency (relative dentin abrasivity = 7) that acts as a mechanical cleanser for teeth and gingiva. Thus, the topical application of sodium bicarbonate improves the efficacy of plaque removal. Moreover, bicarbonate in saliva can both buffer and neutralize plaque acids. Sodium bicarbonate tends to maintain a pH of 8.1 when acids, which lower pH, or bases, which raise pH, are added to the solution. By raising salivary pH that is lower than 8 (ie, increase saliva alkalinity) buffering can prevent demineralization of an exposed tooth surface.26 In the present study, sodium bicarbonate exhibited the occlusion of dentinal tubules by deposition of amorphous crystalline structures on the openings of dentinal tubules, which could lead to decreased DH over a period of time. Newer treatment modalities such as calcium sodium phosphosilicate, arginine, nanohydroxyapatite dentifrices, and potassium oxalate hydrogel have been used to reduce DH.47-49 Diode laser with a wavelength of 810 nm has been used efficiently to treat DH following periodontal surgery.50

Canines and premolars are more susceptible to hypersensitivity because of their anatomy and position in the alveolar bone.12 Canines, the cornerstones of dental arches, have large roots with prominent convexity and are buccally placed in the alveolar casing. These factors contribute to thin facial bony plate, fenestration, dehiscence, and thin biotype, making canines prone to recession, which is the leading cause of DH.51

Further clinical trials should be conducted to evaluate the desensitizing effect of sodium bicarbonate in patients. Sodium bicarbonate is a highly biocompatible substance, which makes it safe for use in humans. Patients can be advised to use sodium bicarbonate aqueous solution as a mouthwash twice a day after periodontal therapy. Hypersensitivity can be measured by a patient's response to mechanical and thermal stimuli using a visual analog scale (VAS) scale. The VAS score should be recorded at baseline and during subsequent dental visits to monitor the effect of sodium bicarbonate in reducing DH. Additionally, comparative clinical studies should be planned using fluoride mouthwashes to compare the desensitizing effect of both the agents in the long term.


This in vitro SEM study demonstrated that sodium bicarbonate can decrease DH by occluding dentinal tubules. The buffering action when in solution intraorally may increase the local pH, diminishing the effect of plaque acids on exposed root surfaces. Typically, sodium bicarbonate is a beneficial agent for obliterating the superficial openings of dentinal tubules. With its low cost and abundant availability compared with other agents, it can be an economical and easily accessible home remedy for treating DH. Clinical trials are needed to evaluate the efficacy of sodium bicarbonate as a desensitizing agent in preventing or reducing DH in human subjects.

About the Authors

Vasundhara Rikame, BDS
Post Graduate Student
First-year MDS, Periodontology and Oral Implantology
Department of Periodontics
Pandit Deendayal Upadhyay Dental College
Solapur, India

Yogesh Doshi, MDS
Department of Periodontics
Pandit Deendayal Upadhyay Dental College
Solapur, India

Robert A. Horowitz, DDS
Departments of Periodontics
Implant Dentistry
Oral Surgery
New York University College of Dentistry
New York, New York

Vidhi Kevadia-Shah, MDS
Senior Lecturer
Department of Periodontics
Pandit Deendayal Upadhyay Dental College
Solapur, India

Mona Shah, MDS
Professor and Department Head
Department of Periodontics
Pandit Deendayal Upadhyay Dental College
Solapur, India


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