Review of dentin hypersensitivity: Etiology, diagnosis, & non-invasive management

Abstract

Dentin hypersensitivity (DH) is a condition characterized by a short, sharp pain from exposed dentin in response to various stimuli which cannot be ascribed to any other dental conditions.¹ The prevalence of DH varies widely, with estimates ranging from 1% to 92%.² Most importantly, DH impacts patients’ quality of life by affecting daily activities such as eating, drinking, and tooth brushing. Despite the many treatment options, gaps remain in the routine screening and management of DH, highlighting the need for ongoing education and research to improve patient outcomes. This article provides an overview of DH and its diagnosis, etiology, and non-invasive management strategies, including lifestyle modification approaches and treatments ranging from over-the-counter desensitizing toothpastes to professional in-office options. The aim is to help dental professionals have a deeper understanding of DH, enable informed decision-making, and minimize patient discomfort associated with this condition.

Dentin Hypersensitivity (DH) is characterized as ‘a short sharp pain arising from exposed dentin in response to a stimulus typically thermal, evaporative, tactile, osmotic, or chemical and which cannot be ascribed to any other form of dental defect or disease’.¹ The Canadian Advisory Board on DH agreed on this definition in 2002 following a comprehensive review of the literature.¹ The prevalence cited at that time was 30%, based on a nationally representative sample of adults aged 18-64.¹ A more recent global 2018 systematic review and meta-analysis on the prevalence of DH concluded the best estimate of prevalence is 11.5% with the average from all studies being 33.5%.² The study noted that the prevalence ranged from 1% to 92% and that this wide range could be partly explained by the high risk of bias in the included studies.²

DH may disrupt a patient’s ability to eat, drink, brush their teeth, breathe comfortably, and speak, affecting their overall quality of life.^3-5 While some questionnaire studies suggest that patients do not view DH as a severe dental problem, it has been reported that day-to-day activities are impacted.⁶ For example, 28.2% of patients experienced discomfort when drinking cold water, 26.5% while eating ice cream, and 8.7% while brushing their teeth.⁶ However, it should also be noted that only 48% of patients with DH mentioned it to their dentist, and only half of them received treatment.⁶ In severe cases, DH can last more than 6 months, becoming a source of irritation that may impact a patient’s psychological and emotional well-being.³

Etiology of DH

Over the years, several theories have been proposed to explain DH. While these theories have been explored, the Hydrodynamic Theory remains the most widely accepted explanation.^7-9 Table 1^7-9 outlines the different theories and their respective mechanisms.

Table 1

Theory	Mechanism
Neural Theory	The Neural Theory suggests that dentin contains nerve fibers that are directly activated by stimuli, leading to pain. However, it was later discovered that nerve fibers do not penetrate the dentinal tubules but are near the pulpal horns.
The Dentinal Receptor Mechanism Theory	The Dentinal Receptor Mechanism Theory suggests that nerve endings are present within the dentin, and when external stimuli come into contact with the dentin, they stimulate these nerve endings, causing pain. However, it is unlikely that neural cells are present in the outer dentin.
Odontoblastic Transduction Theory	The Odontoblastic Transduction Theory suggests that odontoblasts act as sensory receptors. When a stimuli reaches the dentin, odontoblasts transmit a signal to the nerve fibers. This theory is less supported compared to the hydrodynamic theory, but it provides an alternative explanation for how stimuli might be transmitted to the nerves.
Hydrodynamic Theory	The Hydrodynamic Theory suggests DH is caused by fluid movement within the dentinal tubules. When stimuli such as touch, cold, air, or osmotic changes are applied to exposed dentin, they cause the fluid inside the tubules to move. This movement stimulates the nerve endings in the pulp, resulting in a painful sensation. The theory is supported by evidence showing that blocking the tubules can reduce sensitivity, further validating the role of fluid dynamics in this condition.

Internal and external factors

DH is a multifactorial condition influenced by both internal and external factors. It often involves the loss of hard tissues, such as cementum or enamel, or soft tissues, such as gingival recession, all leading to dentin exposure.^9-11

Clinically, both sensitive and non-sensitive dentin appear similar.⁹ Exposure of the dentin alone does not cause hypersensitivity. For DH to occur, the dentin tubules must be open to allow fluid movement and sensitive teeth will have a greater number of open tubules per unit area of exposed dentin compared to non-sensitive teeth.^8,12 The diameter, patency, and number of open tubules are key factors that differentiate teeth affected by DH from those not affected. ^8,10

Hard tissue loss: Loss of enamel can result from several factors, including attrition, abfraction, abrasion, and erosion. Attrition is enamel wear from direct tooth-to-tooth contact or grinding.^10,11 Abfraction is physical wear resulting from tensile or shear stress in the cemento-enamel region, causing microfractures in the enamel and dentin (bruxism).^9,11 Abrasion is enamel wear from objects, such as toothbrushes and certain toothpaste ingredients.¹⁰ Finally, erosion is the loss of tooth structure due to non-bacterial acids.^9,11

There is uncertainty around the impact of toothbrushing and toothpaste on enamel wear.¹¹ Generally, brushing with toothpaste is unlikely to abrade the enamel since most abrasives in toothpaste are softer than the enamel, making it less likely to cause significant wear.^9-11 However, there are exceptions, such as when the enamel is exposed to acids.^10-11 Acid-softened enamel is highly susceptible to abrasion, and brushing can remove this softened enamel, making the tooth surface more vulnerable to further erosion.¹¹ Another patient-specific factor to consider is the combination of toothbrush filament stiffness and brushing force, as aggressive toothbrushing along with a higher abrasive toothpaste may lead to abrasion.^9,11,13

Dentin is more susceptible to abrasion than enamel; therefore, both abrasive and erosive components must be considered when dentin is exposed.⁹ Abrasives in toothpaste, combined with detergents, can remove the smear layer and open the tubules.¹ In addition, when dentin is exposed, the presence of dietary acids, along with toothbrushing with toothpastes, can exacerbate erosive loss of dentin.¹¹ For these individuals, lower abrasive toothpastes should be recommended, along with preventative measures.⁹

Erosion can be caused by both intrinsic and extrinsic acids. Intrinsic acids originate from gastric acid exposure, such as regurgitation caused by gastroesophageal reflux disease (GERD), eating disorders, chronic alcoholism, and pregnancy.⁹ Extrinsic acids come from dietary sources such as acidic foods, beverages, medications, and oral hygiene products, as well as environmental factors such as swimming pool water with low pH.^9,14-15 Competitive swimmers, in particular, are at a higher risk of erosive enamel loss due to prolonged exposure to low pH chlorinated pool water and extensive years of practice.^14-15 Erosion leads to tooth dissolution because a low pH oral environment causes demineralization and calcium chelation.⁹ This process begins by the softening of the tooth surface and can progress to permanent tooth volume loss.⁹

Soft tissue loss: Soft tissue loss, such as gingival recession, can result from various factors including trauma, oral piercing, aggressive brushing, and periodontitis.⁹ Smoking is associated with periodontitis and can increase the likelihood of gingival recession.⁹ Gingival recession, which exposes the cementum and can lead to dentin exposure on the root surfaces over time, is not age-related and can occur in both healthy and diseased periodontium.⁹ On diseased periodontium, periodontal treatment is essential for eliminating inflammation, regenerating missing periodontium, and halting disease progression.¹⁰ However, patients undergoing such treatment may experience DH since scaling and root planing procedures can remove 20 to 50 µm of cementum, exposing dentinal tubules to various stimuli.¹⁰ In healthy periodontium, toothbrushing can scratch the gingival tissue to some degree, causing recession.⁹ Additionally, excessive brushing and brushing for extended periods can further contribute to gingival recession.⁹

Bleaching: Sensitivity can also occur following bleaching procedures, including in-office treatments, over-the-counter products, and bleaching trays.¹⁰ While sensitivity from bleaching is typically temporary, it can be more severe and prolonged in individuals who already have sensitive teeth.⁹ It is important to note that bleaching sensitivity differs from DH. Bleaching sensitivity is proposed to occur because hydrogen peroxide molecules penetrate the enamel and dentin, reaching the pulp and causing inflammation.⁹

Diagnosis

Proactive screening is considered essential to avoid underdiagnosing the condition. When patients report symptoms, the clinician should conduct a thorough history of the complaint to elicit information regarding the character, site, onset, duration, periodicity, and intensity of the symptom.^1,6,16-17 Potential questions include:

1. Ask the patient to describe the pain (looking for characteristic description of ‘short, sharp pain’)¹
2. Ask the patient for inciting stimuli (looking for thermal, tactile, evaporative, osmotic, chemical)¹
3. Ask the patient regarding severity and if they desire treatment¹
4. Investigate for intrinsic (gastric reflux, excessive vomiting) or extrinsic (dietary) sources of acids¹

Pain arising from DH is subjective and will vary between patients from mild to severe.^6,16,18 While there are a variety of methodologies for the chairside clinician to evaluate DH, such as the visual analog scale or a rating from 0-10, it is important that the clinician adopts a systematic approach and records their findings.^6-8,16,18

DH is a diagnosis of exclusion and it is important to complete a thorough clinical exam and eliminate other conditions that present with sensitivity as a symptom prior to proceeding with treatment.¹ While caries is usually asymptomatic until the lesion begins to encroach on the pulp, DH-like symptoms are often present in the early stages of carious pulp involvement; thus, caries must be ruled out.³ Furthermore, DH rarely presents as spontaneous or continuous pain, so if these symptoms are present, other diagnoses should be considered.³ A lingering, non-transient pain is more typically associated with inflammation of the dental pulp or periodontal tissues.³

Diagnostic tools and tests can be used depending on the patient history and they include:¹

• Air jet, cold water jet, thermal tests, dental explorer, perio probe
• Radiographs (if indicated)
• Percussion testing
• Assessment of occlusion
• Bite stress tests
• Selective anaesthesia
• Transillumination

Hot and cold response can sometimes help distinguish DH from reversible or irreversible pulpitis where the discomfort response will usually linger.³ DH is usually not provoked by occlusal or percussive forces which might suggest occlusal trauma, dental trauma, periodontal or apical problems, or a cracked tooth.³ Asking the patient to roll their bite over a cotton roll, a tooth sleuth, and transillumination can help identify or rule out cracks.³ Finally, radiographs may help rule out caries, overt fractures, defective restorations, or other lesions that could cause pain.³

Once other potential causes of the pain such as cracked teeth, chipped teeth, dental caries, gingival inflammation, post-operative sensitivity, marginal leakage, restorations left in traumatic occlusion, fractured restorations, pulpitis, and palatogingival grooves are eliminated, symptoms are consistent with the definition, and can be reproduced by the healthcare practitioner, then the diagnosis of DH can be confirmed.^1,3,7,16-17 At this point, initial preventive counselling and removal of potential risk factors can be initiated.^1,16-17 A number of diagnostic algorithms have been suggested, such as the one by the Canadian Advisory Board, which clinicians can consult.^{1,3,6-7,16-17}

Management

Lifestyle modifications: Preventative counselling can help manage and prevent DH. For example, it is essential to educate patients on proper dental hygiene techniques such as avoiding aggressive or frequent brushing, using a soft-bristled toothbrush, regularly brushing twice daily with a fluoride toothpaste, using a less abrasive toothpaste, modifying brushing techniques to avoid causing trauma to the gingival tissues, and spitting excess toothpaste instead of rinsing with water immediately after brushing.^9,19 To prevent enamel erosion and subsequent dentin exposure, patients should be advised to reduce the intake of acidic food and drinks and to wait 30 minutes after meals before brushing to avoid enamel loss.¹⁹ Smoking cessation should be encouraged since it can contribute to gum recession.⁹ Lastly, patients who experience bruxism, or teeth grinding, should consider having this condition managed since it can also cause significant enamel wear.⁹ Providing education with these helpful tips can help patients manage and reduce the symptoms of DH.

At-home management: DH can be treated with the use of a desensitizing toothpaste, a simple, convenient, and non-invasive solution.²⁰ They work by either nerve desensitization (potassium salts) or physical occlusion (stannous fluoride, arginine and calcium carbonate, calcium sodium phosphosilicate (CSPS), and nano-hydroxyapatite).¹⁸ Products that are available off the shelf in the Canadian market are detailed in Table 2,^{8,10,12,18,21-25} along with their proposed mechanisms. Strontium salts precipitate insoluble metal compounds which occlude open dentin tubules but these are no longer available in Canada.⁸

Table 2: Available Dentifrices on the Shelf for Dentin Hypersensitivity in Canada

	Ingredient	Mechanism
Remineralization	Sodium Fluoride	Fluoride ions bind to calcium and phosphate, forming calcium phosphorous precipitates, calcium fluoride, and fluorapatite. These compounds create a stronger enamel structure and obstructs the dentin tubules, reducing the fluid movement that triggers DH.
Remineralization	Tricalcium Phosphate with Sodium Fluoride (TCP)	TCP releases calcium and phosphate ions which are essential for enamel remineralization. When combined with fluoride, it enhances fluorapatite formation. TCP and fluoride work independently to promote enamel remineralization of subsurface lesions.
Nerve Desensitization	Potassium Nitrate	Potassium ions depolarize the nerve terminals, preventing repolarization; thereby, decreasing the excitability of a fibers surrounding the odontoblasts and thus preventing pain signal transmissions. Increasing the concentration of potassium ions around peripheral dental afferent neurons reduces the perception of pain.
Physical Occlusion	Stannous Fluoride	Stannous fluoride reacts with hydroxyapatite and forms stannous fluorophosphate and calcium fluoride products which occlude the dentin tubules. Concurrently, the oxidation of Sn (II) to Sn (IV) leads to the formation of stannous oxides which also occlude the dentin tubules.
Physical Occlusion	Arginine-Calcium Carbonate	Arginine and calcium carbonate react with saliva to create a plug composed of arginine, calcium, phosphate, and carbonate that occludes the open dentin tubules. It also creates an alkaline environment which drives calcium and phosphate ions to deposit and occlude open dentin tubules.
Physical Occlusion	Calcium Sodium Phosphosilicate (CSPS)	Upon contact with saliva, calcium and phosphate ions are released and undergo a chemical reaction to form hydroxycarbonate apatite crystals resulting in the formation of a mineralized layer which is similar to biological apatite. This layer occludes the dentin tubules.
Physical Occlusion	Nano-hydroxyapatite	Mimicking natural tooth mineral composition, these synthetic biomimetic nanocrystals remineralize enamel surfaces, closing dentin tubules and reducing sensitivity.

A recent 2023 systematic review and network meta-analysis of thirty-two randomized controlled trials (RCTs) involving 4,638 subjects concluded that formulations with stannous, potassium, and arginine provided short- and long-term DH relief as measured with air blast and tactile stimuli, when compared to negative controls.²⁶ In a 2020 systematic review and network meta-analysis of 125 RCTs involving 12,541 subjects, the authors concluded that CSPS demonstrated beneficial effects for DH caused by tactile, cold, and air blast stimuli, stannous fluoride was effective for tactile and air blast stimuli, arginine was effective for DH caused by air blast stimulus, and potassium was effective for DH caused by tactile stimulus.²⁷ All interventions were shown to be beneficial compared to fluoride or placebo.²⁷ Furthermore, a 2019 network meta-analysis of thirty RCTs, which evaluated studies using air blast stimulus only, concluded that stannous fluoride was significantly superior to fluoride toothpaste; arginine was significantly superior to potassium, fluoride toothpaste, and placebo at 2, 4, and 8 weeks.²⁰ Nanohydroxyapatite was also shown to be significantly superior to potassium, fluoride toothpaste, and placebo at 2 and 4 weeks; potassium was significantly superior to fluoride toothpaste at 4 and 8 weeks, and CSPS was significantly superior to fluoride toothpaste at 4 weeks.²⁰ Overall, some limitations of these systematic reviews include small sample sizes, short follow-up periods, publication bias, and heterogeneity due to the different design methodologies and differences in the concentration of desensitizing toothpastes in the included RCTs. ^20,26,27

Non-invasive in office management: Non-invasive in office therapies for DH include methods such as occluding and sealing dentin tubules, as well as laser therapy. Professional fluoride varnish has been extensively used to provide significant and immediate pain relief, lasting several weeks.¹² Adhesives and resins offer longer-lasting desensitization compared to many topical agents which do not adhere well to the dentin surface thus providing only temporary relief.¹ Laser treatment is another option recommended for DH, but its effects are often temporary, with sensitivity returning over time.¹⁰ Table 3^7-8,10,12,21 provides a summary of non-invasive in office therapies to consider for DH.

Table 3: Non-Invasive in office Therapies for Dentin Hypersensitivity

	Type	Mechanism
Occlude Dentin Tubules	Professional Fluoride Treatment	Professional fluoride treatments, such as fluoride varnish, gel applications in trays, and fluoride rinsing solutions, help reduce and block fluid movement in dentinal tubules. This is accomplished by forming calcium-phosphorus deposits, calcium fluoride, and fluorapatite.
Occlude Dentin Tubules	Casein Phosphopeptide-amorphous calcium phosphate (CPP-ACP):	Peptides in CPP-ACP promote mineral deposit formation on the dentin surface, reducing the opening of dentinal tubules. When combined with fluoride, CPP-ACP offers the added benefit of aiding remineralization and tubule occlusion.
Occlude Dentin Tubules	Oxalates	Oxalates have been used to precipitate and block dentinal tubules, but their effectiveness in treating dentin hypersensitivity is not universally supported by all studies.
Occlude Dentin Tubules	Glutaraldehyde	Glutaraldehyde blocks dentin tubules by reacting with serum albumin in dentinal fluid, leading to precipitate formation that narrows or blocks the tubules. This process decreases dentin permeability and counteracts the hydrodynamic mechanism responsible for dentin hypersensitivity.
Dentin Bonding	Adhesives, Glass Ionomers, Resins	Although dentin bonding products were not originally designed to manage dentin hypersensitivity, they have proven effective in reducing sensitivity. Resins and adhesives seal dentin tubules, preventing the transmission of hydrodynamic stimuli to the pulpal nerve complex. These materials, along with dentin-bonding agents, create an artificial smear layer to seal exposed tubules.
Lasers	Low intensity lasers	The exact mechanism of laser treatment for DH is not fully understood, but studies suggest that low-output lasers may reduce pain by decreasing nerve signal transmission.
Lasers	High intensity lasers	Higher output lasers work by blocking or narrowing dentinal tubules. There is potential for using lasers to manage DH, but more research is needed to address issues like the recurrence of DH.

Post-treatment follow-up is indicated to assess the effectiveness of interventions.^1,17 If symptoms persist, a review of the diagnosis is recommended, with periodontal pain, referred pain, neuropathic pain, and chronic pain syndrome as conditions to consider.¹

Conclusion

An educational needs assessment was conducted as part of the Canadian Advisory Board review where a questionnaire was mailed out to 5000 dentists and 3000 dental hygienists across Canada. Some of the knowledge gaps identified from the random sample include:¹

1. The prevalence was underestimated, particularly in young adult patients.¹
2. Some dental professionals were not screening for DH except when prompted by patients.¹
3. Fewer than half of dental professionals considered a differential diagnosis.¹
4. About half of the respondents reported they lacked confidence in managing the condition.¹

An updated needs assessment should be considered for future research to evaluate whether the identified gaps two decades ago have changed and are still relevant in Canada. Furthermore, a standard methodology to assess the efficacy of treatments could help further guide decision-making.

In summary, the multifactorial etiology of DH includes gingival recession and enamel loss and the most widely accepted Hydrodynamic Theory attributes that DH is caused by the movement of fluid within patent dentin tubules resulting in pain signals.

DH is a prevalent condition that may impact a patient’s quality of life. Dentists can identify patients with DH through a thorough clinical examination including patient history gathering and the use of diagnostic tools to exclude other conditions. Management strategies include proper brushing and dental hygiene, dietary adjustments, at home treatments with desensitizing toothpastes, and non-invasive in office treatments, which can be chosen based on patients’ needs and priorities, while also balancing risk versus benefits of the proposed treatment. 

Oral Health welcomes this original article.

Disclosure: Authors Carmen Cheung, Ian Willette, and Sashi Prasad are employees of Haleon. This article received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.

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About the authors

Ian Willette is an Oral Care Field Consultant at Haleon in Mississauga, Ontario, Canada. 

Sashi Prasad is the Expert Partnerships Manager at Haleon in Mississauga, Ontario, Canada. 

Carmen Cheung is a Medical & Scientific Affairs Senior Scientist at Haleon in Mississauga, Ontario, Canada.