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   Table of Contents    
Year : 2022  |  Volume : 26  |  Issue : 4  |  Page : 307-333  

ISP good clinical practice recommendations for the management of dentin hypersensitivity

1 Department of Periodontology, Dr. H. S. J. Institute of Dental Sciences, Panjab University, Chandigarh, India
2 Department of Periodontology, Dental College, Regional Institute of Medical Sciences, Imphal, Manipur, India
3 Department of Periodontology, Dental Institute, Regional Institute of Medical Sciences, Ranchi, Jharkhand, India
4 Department of Periodontology, Renupriya Dental Health Care, Bengaluru, Karnataka, India
5 Department of Periodontology, Dr. Grover's Dental Clinic, New Delhi, India
6 Department of Periodontology, D. A. V Dental College and Hospital, Yamunanagar, Haryana, India
7 Department of Periodontics and Oral Implantology, Institute of Dental Sciences, Siksha “O” Anusandhan (Deemed to be University), Bhubaneswar, Odisha, India
8 Department of Periodontology, Government Dental College, Kottayam, Kerala, India
9 Department of Periodontics, Mahe Institute of Dental Sciences and Hospital, Mahe, Puducherry, India
10 Department of Periodontology, Teerthanker Mahaveer Dental College and Research Centre, Teerthanker Mahaveer University, Moradabad, Uttar Pradesh, India
11 Department of Periodontics, Saraswati Dhanvantari Dental College and Hospital, Parbhani, India
12 Department of Periodontology, Dental College and Hospital, Bharati Vidyapeeth (Deemed to be) University, Navi Mumbai, India
13 Department of Periodontology, K. M. Shah Dental College, Sumandeep Vidyapeeth Deemed to be University, Vadodara, Gujarat, India
14 Department of Periodontology, Kalka Dental College, Meerut, Uttar Pradesh, India
15 Department of Periodontology, Ragas Dental College and Hospitals, Chennai, Tamil Nadu, India
16 Department of Periodontics, GSL Dental College, Rajahmundry, India
17 Department of Periodontics, Sri Sai College of Dental Surgery, Kaloji Narayana Rao University of Health Sciences, Vikarabad, Telangana, India
18 Department of Periodontics, Sudha Rustagi Dental College, Faridabad, Haryana, India
19 Department of Periodontology, Buddha Institute of Dental Sciences and Hospital, Patna, Bihar, India
20 Department of Periodontology, Government Dental College and Hospital, Mumbai, India
21 AFMC, Pune, India
22 Department of Periodontology, G. Pulla Reddy Dental College and Hospital, Dr. NTR University of Health Sciences, Kurnool, Andhra Pradesh, India
23 Department of Periodontology, Government Dental College and Hospital, Guntur, Andhra Pradesh, India
24 Department of Periodontology, Sibar Institute of Dental Sciences, Dr. NTR University of Health Sciences, Guntur, Andhra Pradesh, India
25 VSPM Dental College and Research Centre, Nagpur, Maharashtra, India
26 Department of Periodontics and Implantology, VSPM Dental College and Research Centre, Nagpur, Maharashtra, India
27 Department of Periodontics, Sibar Institute of Dental Sciences, Dr. NTR University of Health Sciences, Guntur, Andhra Pradesh, India
28 Department of Periodontics, AECS Maaruti Dental College and Research Center, Bengaluru, Karnataka, India

Date of Submission08-May-2022
Date of Decision11-May-2022
Date of Acceptance11-May-2022
Date of Web Publication02-Jul-2022

Correspondence Address:
Ashish Jain
Dental Institute, Regional Institute of Medical Sciences, Bariatu, Ranchi - 834 009, Jharkhand
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jisp.jisp_233_22

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Dentin hypersensitivity (DH) is a rising concern in clinical dentistry that causes pain and discomfort and negatively affects the quality of life of patients. Indian Society of Periodontology conducted a nationwide survey, involving 3000 dentists in December 2020, which revealed significant knowledge gaps regarding DH, viz., under-diagnosis, incorrect differential diagnosis, and treatment strategies/recommendations for the management of DH patients in daily clinical practice. The current paper has been envisioned and conceptualized to update the practicing Indian dentists regarding the so-called enigma of dentistry “Dentin Hypersensitivity,” based on the best available contemporary evidence. An expert panel was constituted comprising 30 subject experts from across the country, which after extensive literature review and group discussions formulated these recommendations. The panel advocated routine screening of all dentate patients for exposed dentin areas and DH to avoid under-diagnosis of the condition and suggested an early preventive management. Consensus guidelines/recommendations for the use of desensitizing agents (DAs) at home, including the use of herbal agents, are also provided within the backdrop of the Indian context. The guidelines recommend that active management of DH shall be accomplished by a combination of at home and in-office therapies, starting with the simplest and cost-effective home use of desensitizing toothpastes. A diagnostic decision tree and a flowchart for application in daily practice are designed to manage the patients suffering from DH or presenting with exposed dentin areas in dentition. Various treatment methods to manage DH have been discussed in the paper, including the insights from previously published treatment guidelines. Further, a novel system of classification of DH patients based on specific case definitions has been developed for the first time. Explicit charts regarding the available treatment options and the chronology of institution of the agent, for the management in different case categories of DH, have been provided for quick reference. The management strategy takes into account a decision algorithm based on hierarchy of complexity of treatment options and intends to improve the quality of life of the patient by long-term maintenance with an innovatively defined triple C's or 3Cs approach.

Keywords: Classification, dentin hypersensitivity, DAs, diagnosis, differential diagnosis, management

How to cite this article:
Grover V, Kumar A, Jain A, Chatterjee A, Grover HS, Pandit N, Satpathy A, Madhavan Pillai BR, Melath A, Dhruvakumar D, Thakur R, Joshi NV, Deshpande N, Dadlani H, Meenakshi A A, Ashok K P, Reddy K V, Bhasin MT, Salaria SK, Verma A, Gaikwad RP, Darekar H, Amirisetty R, Phadnaik M, Karemore V, Dhulipalla R, Mody D, Rao TS, Chakarpani S, Ranganath V. ISP good clinical practice recommendations for the management of dentin hypersensitivity. J Indian Soc Periodontol 2022;26:307-33

How to cite this URL:
Grover V, Kumar A, Jain A, Chatterjee A, Grover HS, Pandit N, Satpathy A, Madhavan Pillai BR, Melath A, Dhruvakumar D, Thakur R, Joshi NV, Deshpande N, Dadlani H, Meenakshi A A, Ashok K P, Reddy K V, Bhasin MT, Salaria SK, Verma A, Gaikwad RP, Darekar H, Amirisetty R, Phadnaik M, Karemore V, Dhulipalla R, Mody D, Rao TS, Chakarpani S, Ranganath V. ISP good clinical practice recommendations for the management of dentin hypersensitivity. J Indian Soc Periodontol [serial online] 2022 [cited 2022 Aug 9];26:307-33. Available from:

   Dentin Hypersensitivity Top

Dentin/dentinal hypersensitivity (DH), or cervical dentinal sensitivity, is a common clinical issue. It is defined as pain arising from exposed dentin typically in response to thermal, chemical, tactile, or osmotic stimuli.[1]

The definition was modified by the Canadian Advisory Board on DH in June 2002, and DH was further defined as: short sharp pain arising from exposed dentin in response to stimuli, typically thermal, evaporative, tactile, osmotic, or chemical, and which cannot be ascribed to any other form of dental defect or pathology.[2],[3]

This definition applies the principle of exclusion to clinically describe DH. The principle of exclusion means that for DH to be diagnosed as a distinct dental condition, it needs to be distinguished from other etiologies of dental pain.

Although the terminology of DH has been in use for long time, it is not without its share of controversy. Long-term usage of the term DH does not answer the argument over the accurateness of the usage of the term “hypersensitivity” as many authors believe that exposed dentin is purely sensitive, and therefore, conditions should be called as dentin sensitivity (DS) and not hypersensitivity.[4]

One of the foremost researchers on DH, Addy put forward his explanation for calling it as DH and not DS.[4] His argument in favor of DH is based on the available histological evidence from studies of DH. Evidence from the histological evaluation of lesions of DH have shown more and wider dentinal tubules open at the dentin surface and are patent to the pulp than nonsensitive dentin.[4],[5],[6] More and wider open dentinal tubules lead to increased probability for fluid flow.[4] This condition of dentinal tubules leads to the exposed dentin to be hyperreactive to and thereby “hypersensitive.”

Earlier DH and root sensitivity (RS) were considered as the same condition till the definition of DH was published. RS also causes dentinal pain and sensitivity. In a consensus report of The European Federation of Periodontology, it was recommended that the term RS should be used to describe short sharp pain from exposed dentin of periodontally involved teeth or following periodontal treatments.[4],[7]

The reason for differentiating between DH and RS is that periodontally involved teeth do not fit the definition of DH. Furthermore, dentinal tubules in RS, because of periodontal involvement, have been found to have bacterial invasion which has not been seen in DH.[4],[8] Furthermore, the prevalence of DH is far less than the prevalence of RS.[4],[9]

Understanding the physiology of dentin is important to understand DH.

It has been known for long the enamel does not respond to any stimuli. When the stimulus is near the dentinoenamel junction (DEJ), a sharp pain is felt which indicates the difference between enamel and dentin because of the responsiveness of tissue. This responsiveness could have been attributed to nerve tissue in the dentinal tubules. However, in reality, there is no histological evidence of any nerve tissue at DEJ.

Byers in 1984 stated that nerves are restricted to the inner half of the dentin tissue, adjacent to the pulp.[10] The odontoblasts are present at the junction of pulp and dentin and have a process that extends into dentin to one-third of the distance from pulp to the DEJ.[11]

The sensitivity of dentin was due to stimulus-evoked fluid shifts in the dentin tubule, which was first reported in 1900 by Gysi.[12],[13] In a series of in vitro studies conducted by Brännström, fluid movement in dentin in response to tactile, osmotic, thermal, and evaporative stimuli was studied.[14],[15],[16],[17],[18],[19] The result of these experiments was the Brännström's concept which was called as hydrodynamic hypothesis.

The pain can be elicited not only by mechanoreceptors which respond to fluid flow, but intradental nerves can also respond to pain-producing stimuli regardless of the dentin fluid shift.[20] Cold eatables stimulate nerves directly by activating thermal receptors located on intradental nerve endings.[21]

The movement of dentinal fluid can be explained on the basis of difference between capillary hydrostatic pressure exceeding the oncotic pressure of plasma proteins and the small amount of lymph drainage of the pulp, resulting in positive pulpal tissue pressure.[22],[23] The intrapulpal tissue positive pressure of 14–16 mmHg[23] is responsible for the slow outward movement of dentin fluid whenever the enamel or cementum is lost.[24] Without any stimulation, this outward fluid flow cannot activate sensory nerves in the pulp.[25]

There is an increase in the fluid flow in response to stimuli such as probing, air blasts, or thermal changes, owing to fluid convection or due to the fact that the direction of the flow is reversed.[26] The intradental nerves have been shown to be less sensitive to inward fluid displacements than to outward flow.[27]

Intradental nerve responds to both tactile stimulation and air blasts which are generally used stimuli in DH. Presence of smear layer reduces or obliterates the response of the nerves to these stimuli.[28] The reduction in response to hydraulic conductance is approximately 10–30 times.[29],[30] Dissolution of smear layer by organic acids or acids produced by microorganisms exposes the dentin and results in sensitivity.[31]

Pressing the dentin with a sharp explorer induces sufficient inward fluid shift to exceed the pain threshold. When the pressure is removed, an outward fluid shift occurs due to the elastic recoil of the dentin surface that also activates the intradental nerves.[32]

Air blasting vaporizes fluid from dentin tubules and is a very efficient method to initiate sensitivity pain by encouraging swift outward fluid movement.[26],[33] The outward movement of fluid due to air blasts occurs by cooling of the dentin and resultant capillary action. Evaporative fluid movement may occur through small or incompletely occluded tubules.

Molecular weight of solutes will determine whether outward movements would be initiated or not. The large molecular weight solutes cannot diffuse into dentin. Low molecular weight solutes applied to the dentin surface also initiate outward osmotic water movements.[34]

A sharp well localized pain from the exposed dentin in otherwise healthy human teeth, which lasts as long as the stimulus is applied, reflects the pain response elicitation from A-fibers.[35],[36],[37] The identity of the nerve fiber type responding to dentin stimulation was confirmed in several experiments and the findings revealed that A fibers responded to air blasts, probing, and other stimuli applied to etched dentin also. These transmission of impulses are characterized by low electrical thresholds and rapid conduction rate.[38],[39] A fibers are generally myelinated throughout their course in the dentin but may lose the myelin sheath as they reach the superficial pulp and dentin.

As is evident from the anatomy and morphology of dentin, dentinal tubules need to be exposed for hypersensitivity to occur. Open dentinal tubules are the common feature of hypersensitivity, irrespective of the etiology of dentin exposure. The open tubules expose the internal structure of tooth to the external environment. It has been stated that hypersensitivity will not occur if tubules are not exposed.

Absi et al. while studying the differences between sensitive and nonsensitive teeth found not only that nonsensitive teeth had very few exposed tubules, whereas the number of open tubules in the sensitive teeth per unit area was 8 times more, but also the diameter of tubules in nonsensitive teeth was half the diameter in sensitive teeth (0.83 μm vs. 0.4 μm).[6] Poiseuille's law when can be applied to explain the difference of the diameter of tubules will cause in the fluid movement. As per the law, fluid flow is proportional to the fourth power of the radius. This would mean that the difference in tubule size will result in dentinal fluid flow to be 16 (i.e., 24) times greater in sensitive teeth than in nonsensitive teeth. Hence, open tubules with increased rate of fluid flow could result in hypersensitivity. The number of tubules increases near the pulp, thereby increasing the symptoms of hypersensitivity, as tooth wear nears the pulp.

   Etiopathogenesis of Dentinal Hypersensitivity Top

Two processes are indispensable for the development of DH: Lesion localization and lesion initiation.[40],[41] Lesion localization means that dentin must become exposed either because of loss of enamel or gingival recession while lesion initiation means that the dentin tubules must be open to both the oral cavity and the pulp.[3]

Three hypotheses (theories) have been proposed to explain the sensitivity of dentin: nerves extending to the outer end of the dentin tubules, odontoblast transducer mechanism, and hydrodynamic mechanism.

Odontoblastic transduction theory

Exposed odontoblastic processes on the dentin surface can be excited by diverse chemical and mechanical stimuli.[42],[43] It is hypothesized that on stimulation, neurotransmitters are released and impulses are transmitted toward the nerve endings, although no neurotransmitters produced or released by odontoblastic processes have been discovered.

Neural theory

This theory states that nerve endings within the dentinal tubules which have direct communication with pulpal nerve fibers are directly stimulated (mechanical or thermal stimulation). Unmyelinated nerve fibers have been shown to be present in root dentin in some of the observations,[44] which supports the concept of this theory however, as such innervations is not seen in all cases, thus this theory remained more of as a theoretical concept.

Hydrodynamic theory

This theory of DH is the most widely accepted theory and was proposed by Brännström and Aström.[45],[46] The fluids within the open dentinal tubules in the oral cavity move in response to either by temperature, physical changes, or osmotic changes, and these movements activate a baroreceptor which leads to neural discharge.

Lesion localization which means dentin exposure can arise by loss of enamel and/or gingival recession (with loss of cementum).

DH can be related to many etiologies such as

  1. Nonsurgical and postsurgical treatment of periodontal disease (recession resulting from periodontal treatment)
  2. Tooth wear and gingival recession (erosion, abrasion, and abfraction)
  3. Tooth bleaching
  4. Developmental lesions (rare conditions which lead to alteration in surface morphology of teeth)
  5. Oral hygiene and recession.

Nonsurgical and postsurgical treatment of periodontal disease (recession resulting from periodontal treatment)

Dentin exposure by gingival recession can be classified as “healthy” or “unhealthy.” Healthy gingival recession can be caused by chronic trauma, particularly tooth brushing, as the major etiological factor.[47],[48] However, there are insufficient data to quantify the role of tooth brushing or toothpaste in gingival damage and recession. The dentin exposure observed in the cervical areas of teeth on buccal surfaces, is attributed to either gingival recession or loss of enamel of teeth. Although gingival recession has been implicated in most of the cases, it may be difficult to differentiate between the underlying associated factors on clinical examination.

Iatrogenic induction of DH has been reported after scaling and root planing.[49] The dentinal tubules are exposed after root surface debridement due to removal of smear layer. The smear layer which is formed by collagen and glycosaminoglycans and forms an adherent matrix over mineralized tissue is thought to occlude the dentin tubules.[16],[50] Pashley et al. in 1978 stated that, in health, the smear layer reforms and prevents 86% of dentinal fluid movement.[51]

Periodontal disease or treatment may expose dentin. It has been hypothesized that bacteria may colonize and break down the smear layer and penetrate into the root dentin.[52]

This penetration of bacteria or bacterial products might initiate inflammation in the pulp. Although many authors accept this mechanism associated with DH,[40],[53] the reason for differentiating between DH and RS is that periodontally involved teeth do not fit the definition of DH. The dentinal exposure through unhealthy gingival recession cannot be included as DH and is associated with RS.

Tooth wear and gingival recession (erosion, abrasion, and abfraction)

Tooth wear can be physiologic as a part of aging or may be pathologic.[54] It can be defined as irreversible, nontraumatic loss of dental hard tissues due to etiological processes classified as erosion, attrition, abrasion,[55],[56] and abfraction.[57] In comparison to physiologic tooth wear, pathological tooth wear has faster rate of progression and appears in younger patients. Normally, in the physiological tooth wear, pulp lays down reparative dentin (as it is a slow process), within the dentin tubules, and may also reduce the incidence of DH.[58] Due to faster tooth wear in the pathological variety, DH is reported more commonly.[6],[40],[41],[54],[59]

As tooth wears near pulp, the radius of dentinal tubules becomes larger and also the fluid movement increases. Increase in the fluid movement leads to intensification in symptoms associated with DH.[60] However, exposure of dentin (as a result of tooth wear or gingival recession) will not necessarily lead to the presence of DH.[6],[41],[61] Hence, the measurement of tooth wear by tools alone may not essentially reflect the presence of DH.

To understand etiology, lesion localization and lesion initiation have to be understood. Lesion localization is the area of dentin exposure as a result of tooth wear or gingival recession. Lesion initiation, which is the second step, means that exposed dentinal tubules in the area of dentinal exposure (lesion localization) have to patent for fluid movement to occur and symptoms of DH to appear. The symptoms, as mentioned earlier, in such cases of patent dentinal tubules, appear subsequent to the loss of the smear layer.

Patency of dentinal tubules is an important aspect in lesion initiation. Presence of exposed dentinal tubules necessarily does not lead to DH if the tubules are blocked by peritubular and reparative dentin. This blockage affects the fluid movement within the dentin tubules.[61]

Erosion and dentin hypersensitivity

Erosion is superficial demineralization by chemical dissolution of the apatite crystals in enamel by an acid that is not produced by the oral microorganisms.[62] Acid production can be from intrinsic or extrinsic sources,[63] both of which are strongly associated with DH.[64] Erosion is the most common and important etiological factor for tooth wear in Europe.[65],[66],[67],[68],[69]

Regurgitated acid (hydrochloric acid [HCL]) due to vomiting or gastroesophageal reflux is the most common intrinsic source.[70]

The extrinsic sources which can cause erosion are:[69],[71]

  1. Drinks and eatables (e.g., acidic citrus fruits, carbonated beverages, beers and herbal teas, vinegars and pickles, and candies)
  2. Medicines (e.g., aspirin, Vitamin C tablets, iron tablets, nonencapsulated HCL replacement, and salivary stimulants)
  3. Occupation (e.g., exposure to acidic industrial vapors and wine tasters)
  4. Sports (e.g., swimmers using incorrectly chlorinated swimming pools).

One of the most important extrinsic sources which causes erosion is acidic food products. The erosive potential of any acidic food product depends on titratability rather than pH.[72] Titratability means how much volume of alkali needs to added to a standardized volume of beverage (25 ml) to raise the pH to 7.[73] Higher titratability and lower pH mean more erosive potential. In addition to higher titratability, the erosive effect also depends on duration and frequency of the acid challenge, presence of chelating agents, ion concentration, and temperature.[74],[75]

Chelating agents have the calcium-binding properties. Acids such as citric, malic, and tartaric acid are chelating agents. Their chemical structure permits binding of multiple soluble calcium ion complexes at high pH.[76] Loss of calcium from saliva due to binding may lead to more dissolution to compensate for salivary calcium.[77] Thus, buffering action of these chelating agents can cause additional erosion of the surface.[72] Citric acid was described at the time as the most detrimental to human enamel.[76]

The Cola drinks have low pH but contain phosphates.[72] The phosphates in Cola drinks increase the saturation of the solution to calcium and phosphate. Hence, popular erosive beverages (Cola and lemonade drinks) cause less demineralization than fruit juices as they contain phosphates.[72]

Recent studies have established that the salivary pellicle forms a protective layer against erosion and DH.[78]

Abrasion and dentin hypersensitivity

Abrasion is a pathological mechanical wear of teeth due to extrinsic reasons, e.g., tooth brushing and use of toothpastes.[67],[79] Abrasion caused by tooth brush has been considered to be one of the common etiologies of DH.[67],[79],[80] Toothbrush abrasion is influenced by type of brush and brushing habits, which include force, duration, and frequency of brushing.[81] Use of medium or hard bristle[82] and application of more force during brushing can increase dentinal wear. Manual brushes cause more dentinal wear than electric brushes.[83],[84] It has also been reported that normal tooth brushing does not cause any significant wear on enamel alone.[85]

Toothpaste also has an abrasive effect. Toothpaste abrasivity is a numeric value measured using the relative dentin abrasivity (RDA). The abrasivity of tooth paste for dentin should not exceed 2.5 times the reference abrasive, and pH of the paste should be above a pH which can cause demineralization (pH 5.5 for enamel and pH 6.5 for dentin) according to the International Organization for Standardization guidelines (ISO).[86] Toothpaste containing fluoride encourages remineralization due to their buffering capacity, and consequently, abrasion is less.[87]

Tooth brushing with toothpastes (with the exception of nonhydrated alumina) not containing acid produces little or no wear of enamel and dentin.[85],[86]

The normal toothpastes alone cannot cause DH lesion localization, but toothpastes of higher abrasivity or abnormal brushing or use of a toothpaste may cause lesion localization and initialization by dentin wear and by removal of the smear layer and establishment of patent dentin tubules.[67]

Toothpastes containing silica may have a beneficial effect in preventing DH by partially occluding the dentin tubules.[88],[89] Abrasion can be caused by occupational hazards also such as holding nails in the mouth by carpenters and needles between the teeth by tailors.

Attrition and dentin hypersensitivity

Attrition is considered to be physiologic process of wear of hard tissues of teeth due to tooth-to-tooth contact (incisal, proximal, or occlusal). The contact time of teeth during normal functioning is momentary and generally cannot cause DH. DH is seen with attrition in individuals with parafunctional habits. The contact time and force between maxillary and mandibular teeth are substantially increased. This increased force and the time of contact could lead to excessive attrition and subsequently DH.

Abfraction and dentin hypersensitivity

Abfractions were the lesions seen in the cervical regions and suspected etiology was occlusal stress. The new classification of periodontal diseases has termed them as theoretical phenomenon as evidence to back the relationship between occlusal stress and abfraction is very limited. Hence, the etiology of DH in cases of Non carious cervical lesions(NCCL) would probably be erosion and abrasion.[80],[82]

It is highly unlikely that attrition, abrasion, or erosion would affect the teeth individually. These processes can occur simultaneously with oral hygiene habits, dietary habits, stress, and their effects on the occlusion.[80],[81],[82],[83],[84],[85],[86],[87],[88],[89],[90],[91] Smith and Robb in a prevalence study on dental hospital patients in 1996 concluded main etiologies of DH as erosion and abrasion.[92] Hence, multiple factors especially erosion and abrasion together have been implicated in the etiology of DH, even though one factor may be dominant in the process.

Developmental lesions (rare conditions where surface morphology of teeth changes)

Any developmental lesions which affect enamel and dentin (amelogenesis and dentinogenesis imperfecta) cause hypoplasia and hypomineralization and put the teeth at risk of DH.

Tooth bleaching

DH has been frequently reported after tooth bleaching procedures, although the symptoms exist for the duration of treatment and, therefore, can be called temporary.[93] The dehydration caused within the tooth by bleaching agent carbamide peroxide, because of its breakdown into hydrogen peroxide, results in the symptoms of DH. As the mechanism of causation of DH in bleaching is different,[94] so it cannot be considered an etiology factor and also necessitates different treatment modalities.[95]

Oral hygiene, gingival recession, and dentin hypersensitivity

People with good oral hygiene and lower plaque scores may have symptoms of DH. The symptoms of DH are generally more pronounced on the opposite side of the oral cavity with respect to the dominant hand of the individual e.g., upper left quadrant in case of the right handed patients and vice versa are more likely to have DH.[96],[97] Indeed, tooth surfaces with healthy gingiva, good oral hygiene, and absence of gingival bleeding are more likely to exhibit DH.[98]

Abnormal brushing techniques in terms of excessive times, duration, and pressure can result in gingival recession. Gingival recession can in turn cause dentin exposure and lesion localization.[67],[81],[82] Hence, a relationship between oral hygiene habits, recession of gingiva, and scores of DH exists.[96],[98]

   Clinical Presentation of Dentin Hypersensitivity Top

The definition of DH itself describes the clinical features of DH. Various definitions have been proposed over a period of time[2],[99] and Canadian Advisory Board on DH in 2003 defined DH as “is characterized by short sharp pain arising from exposed dentin in response to stimuli typically thermal, evaporative, tactile, osmotic, or chemical and which cannot be ascribed to any other form of defect or disease.”[3]

The definition explains the clinical features of DH in the initial part of this definition. Moreover, latter part of definition eliminates all the clinical conditions that may have identical symptoms but not treatment options.[100] The diseases that could mimic DH in clinical symptoms include dental caries, postnonsurgical/postsurgical periodontal sensitivity, sensitivity after restoration or fractured restorations, cracked tooth, and palatogingival grooves.

   The Prevalence of Dentin Hypersensitivity Top

Self-reported questionnaires and clinical examination are the two most common methods employed to study the prevalence of DH. Self-reported questionnaires report higher prevalence rates (because of inclusion of other diseases which also cause hypersensitivity) than clinical studies or questionnaires combined with clinical examination.[101]

The results of surveys are also dependent on types of questions asked. The clinical examination studies have generally used air blast or probe to identify DH with more prevalence reported with air blast method. The lower prevalence reported with probe may be ascribed to the chances of missing out the sensitive area of the exposed dentin by tine of probe.[101]

There are a lot of factors that need to be considered in the prevalence of DH. There are inconsistencies in reports of intraoral locations affected with DH.[102]

The tooth surfaces affected by DH in the descending order are buccal surface followed by labial, occlusal, distal, and lingual surfaces, and the incisal and palatal surfaces are the least affected.[103],[104]

The teeth most commonly involved with DH are canines and first premolars, followed by incisors, second premolars, and molars.[40]

Age is another factor that seems to have relationship with the prevalence of DH. People in in the third and fourth decades have higher prevalence of DH. The reasons could be attributed to increased oral hygiene maintenance and food habits which could include higher intake of acidic food or drinks.[9],[105]

Effect of gender on the prevalence is not clear, and different results reported in various studies could be due to difference in study populations. Many studies have reported higher prevalence in females[101],[106] due to their better oral hygiene awareness[40] and their dietary habits.[107] Furthermore, the females tend to visit the dentist more frequently, thus resulting in more detection of DH in females than males.[104]

Prevalence of DH has been reported to increase after periodontal therapy. The prevalence of DH 1 day after nonsurgical treatment was stated to be between 62.5% and 90%, which declined to 52.6%–55% after 1 week. Similarly, 1 day after surgical treatment, the prevalence of DH has been reported between 76.8% and 80.4% and decreased in subsequent weeks to 36.8% after 1 week, 33.4% after 2 weeks, 29.6% after 4 weeks, and 21.7% after 8 weeks.[108]

Various cervical lesions such as abrasion, erosion, and attrition have been associated with DH as predisposing factors and varied percentage of prevalence have been reported with these lesions. The difficulty in diagnosing these cervical lesions may be the reason for difference in reportage of prevalence of DH.

   Diagnosis and Differential Diagnosis Top

As the definition of DH applies the principle of exclusion to clinically describe DH, for DH to be diagnosed as a distinct dental condition, it needs to be distinguished from other etiologies of dental pain. Diagnosis of DH can only be confirmed after all other etiologies have been ruled out.

Exclusion would include all those conditions that elicit similar clinical presentation of short, sharp tooth pain that is typically observed in DH. Great caution needs to be exercised while diagnosing DH to eliminate all other conditions which may present like DH clinically but require treatment much different for similar symptoms. Many conditions enumerated in may produce clinical symptoms similar to DH and be considered for differential diagnosis [Table 1].[3],[109],[110],[111],[112]
Table 1: Conditions presenting similar/overlapping symptoms as associated with dentin hypersensitivity

Click here to view

To eliminate the conditions in the differential diagnosis of DHS, a proper include examination is required. The examination should start with recording of chief complaint, symptoms, history of present illness, clinical examination, and diagnostic testing.

Chief complaint and illness history

If a patient complains about sensitive teeth, allow the patient to describe the condition in his/her own words. The chief complaint provides primary subjective information for the diagnosis of DH.

DH is characterized with transient sharp pain following various stimuli, and it disappears immediately after removal of the external stimulus. After description of pain characteristics by the patient, the examiner can ask specific questions about the persistence of pain after the stimulus has been removed. DH pain may be minor or major issue with the patient depending on the intensity of pain and amount of dentin exposure to the patients, but its stimulation-dependent initiation and transient properties do not change.

If pain persists after the removal of stimulus, that is either continuous or spontaneous, other differential diagnoses should be considered. The dull throbbing continuous or spontaneous dental pain is commonly a sign of inflammation associated with dental pulp and/or periodontal tissues.[41] This inflammation could be due to many of the reasons stated in [Table 1]: caries, tooth fracture, restorative reasons, pulp exposure, and periodontal or periapical conditions.

It is important to enquire about the patient's dental and medical history. History about oral hygiene habits, bruxism, acidic diet habits (e.g., citrus juices and fruits, carbonated drinks, wines), gastric reflux and bulimia, and tooth bleaching procedures should be assessed as all these factors predispose individuals to DH.

Clinical examination

The clinical examination should identify all sensitive teeth. The clinical oral examination should identify the defects that could be potential reasons for the pain and undertake tests to corroborate or reject probable causes.[112]

The exposed dentin can be identified by visual/tactile examination of the teeth and recorded. Different triggers[94],[113],[114] which can elicit response can be used:

  1. Mechanical/tactile stimuli, e.g., walking a sharp explorer over exposed dentin in a mesio-distal direction. The test may be accomplished by a conventional or pressure-sensitive sharp dental probe, although pressure-sensitive probe enables a quantifiable repetitive force.[115] The force at which the elicitation of pain occurs can be measured by use of pressure-sensitive probe, e.g., Yeaple probe in which the operator can increase the force by 5 g up to a force of 70 g and easily measure at what force did the patient feel pain.[116]

  2. The probe is moved over the area of exposed dentin in incremental horizontal lines. It is quite possible that a very tiny area of dentin might respond to this movement of probe. This method is considered less invasive than thermal stimuli (cold air blast).[117] Though this stimulus does not evoke response from all hypersensitive teeth, yet it still finds an important place in the assessment protocols of DH in the clinical settings.[113],[118],[119],[120]

  3. Osmotic stimuli, e.g., hypertonic solution as sodium chloride, glucose, or sucrose. The sugar diffuses into dentinal fluid and may elicit a hypersensitivity response. Because of the diffusion of sugar, the response cannot be controlled and repeat assessment is very difficult instantly as there is reduction in difference in osmotic pressure between the inside and outside of the tubule
  4. Electrical stimulation with electrical pulp testers. The advantage of using electric stimulation lies in its measurability to elicit response. Studies have not reported any correlation between the electrical current threshold and air blasts.[121],[122] These findings question the relevance of use of electric stimulation as a diagnostic tool. The use of electrical stimulation as diagnostic tool for DH is not recommended[2],[117]
  5. Thermal and evaporative stimuli such as cold air blast from three-way syringe, ice, ethyl chloride, or cold water are also commonly used to assess DH.[113],[119] Use of air blast is a preferred method to check DH in clinical diagnostic examination as well as in clinical studies of DH.[64],[120],[123] An evaporative stimulus is applied perpendicular to the area of exposed dentin from a distance of 10 mm in a short burst of 1 s, at nearly 20°C.[64],[124]

The stimulus should result in a short sharp pain that lasts as long as the stimulus prevails. The use of similar stimulus, as reported by patient, to elicit a response from affected tooth would help in confirmation of the patient's chief pain complaint.

An air blast from a cold air syringe and an explorer, along with a subjective response from the patient' regarding pain score, are most useful for clinical diagnosis of DH. During clinical examination, evaporative stimulus such as a blast of can be used first to identify the sensitive tooth, and after a suitable time interval, tactile stimulation method may be used to identify specific areas of sensitivity.

The use of these stimuli in diagnosis of DH in clinical trials should be in the order of pain evoked. It has been recommended to use two stimuli[2],[3] with appropriate time interval (about 5 min) between the two stimuli. The reason for this time gap is to avoid overlap of symptoms elicited by each response and the pulp has time to recover. The use of least invasive stimulus always precedes the use of more invasive. In contrast to clinical examination in practice, stimuli first used in clinical trials are a mechanical stimulus such as an explorer probe, moved in the mesiodistal direction on the area of dentinal exposure,[125],[126] followed by an evaporative stimulus such as an air blast.[117],[120],[124],[127]

Diagnostic tests such as percussion, palpitation, vitality test, transillumination, and radiographic examination are used for diagnosis to exclude other etiologies for dental pain, many of which are enumerated in [Table 1], e.g., pulpitis, pain due to restorative reasons, cracked tooth syndrome, and periodontal involvement.[99],[107],[112],[113]

A useful guide for distinguishing the different types of dental pain which may lead to a correct diagnosis of DH is suggested in [Table 2].[107],[128] A diagnostic flowchart is also presented herewith as [Figure 1]. The extent and severity of DH are assessed generally by inciting the potential sensitive teeth by appropriate stimuli as discussed earlier. While interpreting the pain response, individual's pain perceptions and their anxiety in anticipation of pain also must be kept in mind. The information so collected shall guide in localization of the offending tooth/teeth as well as the intensity of the pain reaction which in turn shall pave the path for case treatment planning.[113]
Table 2: Differential diagnosis of dentin hypersensitivity based on the characteristics of associated pain

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Figure 1: Diagnostic work flow for dentin hypersensitivity during dental examination

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Further, it is suggested that based on the concept of lesion localization and lesion initiation for DH, it is important to identify individuals with DH lesions at the stage of localization as susceptible individuals for the development of DH over a period of time. Such individuals may not need an active management of DH as no active symptoms/signs of DH are there, but they essentially are candidates for education and behavior modification as needed on case-to-case basis for the prevention of development of DH. This group shall be periodically evaluated and educated at the time of their regular dental maintenance visit for early diagnosis and management of DH.

   Dentin Hypersensitivity Management Top

Adequate diagnosis and prophylactic measures are essential for successful outcomes of the treatment of DH and need to be supplemented with a long-term follow-up for the special needs of these patients. Based on the existing knowledge of etiopathogenesis of DH such as the concept of lesion localization and initiation, it is important to identify the risk factors conducive to these aspects of the disease. An individual risk profile for each patient may be categorized. Many factors such as composition and flow and saliva, dental plaque, acid production in the biofilm, morphology and structure of teeth and gingiva, self-cleansing, and demineralizing potential of the oral cavity can impact the chances of occurrence of DH; further, the oral hygiene and the dietary habits of the patient have a strong and large bearing on the prevalence and incidence of DH in individual cases.[66] Most significant is to eliminate or modify the identified individual risk factors and behaviors so as to prevent and manage DH on case-to-case basis.

To determine when and whether we need to institute the DH treatment, certain recommendations from the previously published literature are available which suggest the necessity of DH treatment in case of patients who self-report the pain. Such patients should be subjected to pain provocation test. If they exhibit a positive response, exclusion of other pathologies and treatment for DH should be initiated and in case of negative response to pain provocation, a comprehensive differential diagnosis and careful evaluation is advised. Provocation tests are recommended during routine dental scaling even in the absence if hypersensitive episodes. A prophylactic treatment for DH is sorted for sensitive and exposed cervical areas. There is evidence suggesting that preventive aspects of DH are often overlooked by professionals[109],[111],[131] and since not all patients report the hypersensitivity routine screening for DH by the dentists is advised at the time of oral examination visits.[132] Further, it has been demonstrated the value of preventive approach as the treatment efficacy of the active agent used for occlusive treatment for DH, i.e., laser desensitizing treatment increased when associated predisposing etiologic factors were eliminated.

Major strategies for the management of DH include: (1) patient education and behavior modification; (2) noninvasive treatments for occluding dentin tubules and relieving pain associated with DH; and (3) restorative or surgical treatments for the management of DH along with restoration of associated tooth structure and soft tissue loss.[133]

Patient education and behavior modification

A careful history-taking from the patient, clinical examination, and a dedicated counseling session for patient education and motivation is a vital step as a prophylactic management strategy for DH and shall be considered as an essential phase for DH management. Patients suffering from DH have been reported to have a significantly impaired Oral health related quality of life(OHRQoL); this may be improved following different treatment methods as an apt for a specific case scenario. However it is of the utmost importance to reduce the incidence by carefully identifying and modifying the various risk factors associated with the causal chain. Generally, faulty toothbrushes, periodontal-treated patients, patients with aberrant dietary habits such as bulimia, older individuals, and smokers are considered at a higher susceptibility for DH. The etiologic factors can be improper/overzealous tooth brushing, high tooth contacts, gingival recession, and the presence of excessive citrus/acidic (exogenous and endogenous) substances in dietary intake.[134]

Patients should be educated and counseled for behavioral modifications as follows:

  1. Patient should be instructed regarding the use of correct tooth brushing technique including selection of soft bristle brush and nonabrasive tooth pastes (details of tooth pastes provided in subsequent section on the use of dentifrices for DH management), using vertical sweeping motion to minimize damage to dental hard and soft tissue
  2. Further, the patient should be advised to brush their teeth before the consumption of acidic food substances or at least 1 h after the intake as they may accentuate the loss of tooth substance by brushing in a susceptible individual
  3. For avoiding excessive pressure during brushing, the patient may opt for pressure-sensitive brush. Moreover, a careful selection of the use of interdental aid such as dental floss or interdental brush should be made to avoid inadvertent tooth wear associated with their use
  4. In patients with parafunctional habits such as bruxism, the use of an occlusal splint night guard may be advised; sometimes, the premature contacts in such dentitions can be resolved by selective correction of the occlusion
  5. The patients should be encouraged to monitor his/her diet for accessing the quality and consumption of acidic foods and recommendations for the use of alkaline foods such as milk or even rinsing with water after the intake of acidic food should be given
  6. Use of straw for the intake of citrus and acidic substances should be suggested
  7. Patients suffering from systemic eating disorders such as bulimia should be referred for medical consultations
  8. As gingivitis, periodontitis, and associated management have been identified as predisposing factors for DH due to the exposure of dentin, regular maintenance of good oral hygiene to avoid this situation is warranted. Periodic dental examination and professional plaque control as and when needed shall be carried out.[133],[134],[135]

Active dentin hypersensitivity management

The primary objective of cause-related therapy is to reduce the fluid flow across the dentinal tubules or to suppress the nerve stimulation associated with intratubular fluid movements. There are multiple treatment options based on abovementioned two mechanisms, yet there is no defined therapeutic gold standard which can be considered highly predictable to eliminate the pain perception in the long-term management of DH.

The task of classifying treatments for DH is daunting as there is limited knowledge regarding the mechanisms of actions; however, these are generally classified based on the mode of administration for a simplified understanding. Treatments can be self-administered by the patient at home (simple, cost-effective, targeted to multiple teeth at one point in time) or be applied by a dental professional in the dental office complex, expensive generally limited to one or a few teeth.[111] Generally, the complexity of the treatments increases with the increase in the severity, extent, and persistence or recurrence of DH. Conceptually, minimally invasive and reversible approaches should be instituted at the outset, and in case of persistence of the complaint at reevaluation, more complicated and irreversible treatment options may be opted for patient management.[132]

Noninvasive treatments for pain relief

The use of DAs is the most widely used treatment option for the management of DH, particularly in the cases with limited or minimal tooth structure loss. These agents work by either occlusion of the patent dentin tubules by mechanical or chemical means or by directly halting the nociceptive responses in the nerve terminals.

Ideal dentin-DA must act fast, produce long-lasting effect, must not cause harm to dental pulp, shall be convenient to use and pain-free, and does not cause staining.[136]

   Classification of Desensitizing Agents Top

Contemporary DAs are classified primarily on two criteria given as follows [Figure 2]: [109],[125]
Figure 2: Classification of desensitizing agents

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Dentin hypersensitivity management at home

Currently, home care management of DH involves the use of the following:

  1. Desensitizing toothpastes
  2. Desensitizing mouthwashes
  3. Herbal agents in dentifrices and mouth rinses.

Use of desensitizing toothpastes

Toothpaste or dentifrices is a noninvasive treatment option available for the treatment of DH. Toothpastes are the simplest, cost-effective, and efficacious first-line treatment for DH.[137]

Toothpastes are easily available over-the-counter medications. Most of the desensitizing toothpastes contain ionic salts such as fluoride, strontium, and potassium.

Desensitizing toothpastes work on the same principle of blocking the open tubules by chemical or physical modes and have the potential to provide adjunctive benefits in terms of reducing the sensitivity scores for the patient. Over the decades, toothpaste formulations have been modified to provide benefits in control of dental plaque, dental caries, as well as treatment of DH. A dental practitioner should make recommendations regarding use of any particular toothpaste based on the diagnosis of the disease.

As is the case with any treatment modality, excessive tooth brushing can lead to tooth wear leading to DH. The reason for this is the abrasive content in the toothpaste.[85]

The abrasivity of the toothpastes is expressed in terms of RDA value. In 1976, ADA published the RDA method to measure the abrasivity of toothpastes. In 1995, ISO adopted these methods as an international standard for measuring toothpaste abrasivity. According to these guidelines, toothpastes should not exceed RDA value of 250. The clinical investigations conducted to comparatively evaluate the toothpastes with RDA levels below 250 failed to reveal any significant differences in the wear of teeth or dentition.[138]

To date, no gold standard exists for the treatment of DH, and all treatment strategies revolve around tubule occlusion and decreasing nerve conduction.

In many toothpastes, more than one active ingredient is present. The earlier formulations of toothpastes contained formaldehyde which was found to be harmful to pulp; hence, it was removed later.[134]

Most of the toothpastes contain potassium salts, strontium salts, and fluorides. Potassium salts are now most commonly used agents incorporated in toothpastes for the treatment of DH. Most of the studies have shown that potassium-containing toothpastes demonstrated improvement in patients' perceived symptoms of DH and the effectiveness increased with time. Toothpastes containing potassium salts penetrate into dentinal tubules and depolarize the nerve synapse, thereby reducing sensitivity by preventing conduction of pain impulses.[85]

Other toothpastes contain either physical or chemical agents which occlude exposed dentinal tubules, thereby reducing sensitivity.

Most of the dentifrices based on strontium salts work on the principle of tubular occlusion. On the other hand, fluoride indifferent formulation is also one of the most widely applied and an effective strategy for sensitivity management at home, and similar to strontium salts, these compounds also block the dentinal tubules and tend to reduce the sensitivity.

Calcium phosphate is another product available for treating hypersensitivity. Free calcium and phosphate ions are leached out in the saliva from amorphous form of calcium phosphate compounds and help remineralize the surface layer of teeth bathing in the saliva. Products containing casein phosphopeptide-amorphous calcium phosphate can be used to partially occlude dentinal tubules.

Another additional compound silica which is present in some of the dentifrices can serve as the initiator for the precipitation of calcium and phosphate. In the contemporary, calcium phosphate technology in addition of tricalcium phosphate has been the latest, which aids to a slow release of calcium, designed to enhance the remineralizing effects of formulations when coupled up with fluoride.[139]

8% arginine is used along with other combinations in the treatment of DH. It is available in toothpaste form. It also works on the principal of tubule occlusion. Saliva transports calcium and phosphate ions near to dentinal tubules, and along with the salivary glycoproteins, they form a layer which occludes the dentinal tubules.[140] Arginine/calcium carbonate-containing toothpastes have shown better results in decreasing DH compared to strontium acetate-containing toothpastes.[141]

In fact, in addition to the primary original research studies, a lot of systematic reviews comparing the different DAs have been carried out in the last two decades.[109],[111],[134],[142],[143],[144] The availability of published evidence has essentially improved; yet, based on the volume of scientific data available, there is no one stop solution or any gold standard toothpaste that can be recommended for the treatment of DH. Bae et al. in 2015 conducted a systematic review and meta-analysis found sufficient evidence to support the use of potassium-, stannous fluoride-, potassium and stannous fluoride-, calcium sodium phosphosilicate-, and arginine-containing desensitizing toothpastes for DH management. The author suggested lack of evidence regarding the use of strontium-containing desensitizing toothpaste.[142] Based on 53 randomized clinical trials (RCTs) with 4796 patients, Hu ML et al. in 2018 reported in a meta-analysis that the toothpastes with active ingredients targeted for DH showed a greater reduction in the sensitivity scores compared to the negative control, except in case of dentifrices containing strontium and amorphous calcium phosphate components. The authors suggested the premise that commonly used active agents such as potassium, stannous fluoride, potassium and strontium, calcium sodium phosphosilicate, arginine, and nanohydroxyapatite relieve the symptoms of DH however did not recommend the use strontium- and amorphous calcium phosphate-based tooth pastes.[143] Further, findings from a network meta-analysis revealed that the most toothpaste formulations showed evidence of better effectiveness against placebo or fluorides. There were observed variable outcome effectiveness in terms of the DH associated with diverse stimuli, e.g., Calcium sodium phosphosilicate (CSP) was most beneficial for all stimuli with high-to-moderate certainty. Stannous fluoride (SnF2) alone and even in combination with other salts were better effective against tactile and air stimulus with high-to-moderate certainty. Arginine worked well for air stimulus, whereas strontium and potassium were beneficial for moderate tactile stimulus.[144] A very recent systematic review on the use of bioactive DAs in toothpastes has concluded that these compounds at low concentrations (2.5%–7.5%) can be used as the treatment of DH both at-home and in-office.[145] Major mechanisms of action of various desensitizing toothpastes are summarized in [Table 3].[125]
Table 3: Major mechanisms of action of various desensitizing toothpastes

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  1. Use soft tooth bristled tooth brush, patients are advised to use minimum amount of water so that the toothpastes would have their maximum positive effects[125]
  2. The effectiveness of these homecare toothpastes for the management of DH depends upon the lifestyle of patients. Consumption of acidic foods may soften the dentin and remove deposits on the dentin surface. Hence, dietary counseling to reduce the acidic food contents will improve the effectiveness of toothpastes[146]
  3. In cases where acidic food is the primary cause for DH, the patient is advised to brush teeth before meals so that remineralization of dentin can take place and the effect of dietary acids will be less[146]
  4. It is advised to change toothbrush after every 3–4 months or at the first sign of bristle fraying.

Efficacy of desensitizing mouthwashes for the treatment of dentin hypersensitivity

The literature has been analyzed to evaluate the reported efficacy of the home use of desensitizing mouthwashes, compared to placebo rinses and desensitizing toothpastes, in DH or RS patients. The outcomes of interest were reduction in pain symptoms to clinical stimuli, or patients' subjective reports following the product use. Focused PICO question answered the comparative clinical effects of the home use of desensitizing mouthwashes on self-reported or stimuli elicited hypersensitivity compared to placebo. Only randomized controlled trials (RCTs) either parallel, double blinded or placebo controlled, of at least 6 weeks duration with daily home use of desensitizing mouthwashes versus control mouthwashes were included. Patients' response had to be registered by means of a verbal rating scale, a numerical rating scale, or a visual analog scale (VAS). Observations based on the RCT studies include the following:

  1. Gillam et al., 1996 observed significant improvement in DH scores at 2- and 6-week follow-ups compared to the baseline data, irrespective of the patients being a part of test or control group. Test group utilized an active ingredient-based desensitizing dentifrice (potassium nitrate). However, they failed to perceive any statistical differences between groups at any point of observation, except for the thermal stimuli (cold air blast), which showed highly significant difference in the improvement of DH in the patients using potassium nitrate[147]
  2. Pereira and Chava, 2001 registered a significant improvement in DH scores for both groups, throughout the study duration for all stimuli used to check the sensitivity response. Potassium nitrate group revealed slightly better outcomes, which reached statistical significance detected at 6 weeks for patient's subjective daily life perception and air blast (thermal/evaporative stimuli). However, patient witnessed no significant difference for DH scores evaluated at early periods such as 2 weeks[148]
  3. Yates et al., 1998, 2004 reported improvements in both study groups over time, with short differences in favor of the test mouthwash (potassium nitrate and sodium fluoride). Control group of the investigation did not reveal any statistically significant differences at any point of the trial[106],[149]
  4. Higuchi et al., 1996 observed a decrease in sensitivity scores at 4 and 6 weeks in both groups: test (aluminum lactate) and control. Statistically significant differences between groups were observed in favor of test group, in response to tactile stimulus at 4 and 6 weeks. Statistically significant DH improvement in the test group at 4 weeks for cold water stimulus and at 6 weeks for cold air evaluation was also witnessed[150]
  5. Sicilia et al., 1996 detected an improvement in the sensitivity scores in both treatment groups over time, but statistical differences between groups were only found at 2 weeks, favoring test group containing potassium nitrate[151]
  6. Oteo et al., 1998 reported the effects of a desensitizing mouthwash containing potassium nitrate in periodontal patients after pocket reduction surgery in terms of significant reduction in sensitivity with placebo group, showing a much slower decrease in the DH symptoms. The findings suggested statistically significant differences between groups throughout the study period, favoring test group.[152]

The results from another meta-analysis demonstrated statistically significant reductions in sensitivity scores, favoring the test groups, for patients' self-reported pain experience.[153] Such findings have been replicated in the meta-regression analysis also, limited to show a continually improving efficacy of the DA, only when assessed in terms of patients' subjective perception. However, the same trend was not observed for rest two evaluation methods (up to 8 weeks).

Other studies

  1. Elias-Boneta et al. in 2013 in a randomized, double-blinded, parallel single-center clinical study concluded that mouth rinse containing arginine provided a superior reduction in DH compared to potassium nitrate and a negative control mouthwash after 2 weeks[154]
  2. Sharda et al., 2018 compared effectiveness of a desensitizing dentifrice and mouthwash containing calcium sodium phosphosilicate on DH and found the mouthwash to be as effective as the toothpaste in reducing DH and with a fair remineralization potential[155]
  3. Sen et al., 2018 also compared effectiveness of a desensitizing dentifrice and mouthwash containing potassium nitrate on DH and found the mouthwash to be as effective as the toothpaste in reducing DH[156]
  4. Sharma et al. determined the efficacy in relieving dentinal sensitivity of 4 weeks' treatment with an alcohol-free mouth rinse comprising 1.4% potassium oxalate compared with negative and positive controls. The findings revealed a decreased sensitivity by 110% in the positive-control subjects versus negative-control subjects (P < 0.001), and no serious treatment-related oral adverse events were seen in any of the study subjects.

Mechanism of action of desensitizing mouthwashes is summarized in [Table 4].[147],[154],[155],[156],[157] Based on the above-mentioned studies, the following patient-related instructions and recommendations to the clinicians have been devised:
Table 4: Major mechanisms of action of various desensitizing mouthwashes

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Instructions to be given to the patient for using the desensitizing mouthwash:

  1. To rinse twice daily with 10 ml or 15 ml of the assigned mouthwash for 30 or 60 s
  2. Patients to be instructed to brush their teeth before using the mouthwash assigned. It has to be done minimum ½ h after brushing or placed in between 2 brushing timings, e.g., before a meal
  3. Patients to avoid consuming anything for ½ h after the use of the mouthwash
  4. Use of the mouthwash recommended for a period of 4–6 weeks followed by a recall to assess and advise further
  5. Maximum period for which mouthwash could be used 8 weeks
  6. Patients to avoid consuming anything for ½ h after the use of the mouthwash.
  7. In case of combined approach, i.e., simultaneous use of the desensitizing toothpaste and mouthwash for 4–6 weeks should be followed by a recall visit and the patient may be instructed to continue using the desensitizing mouthwash for another 4 weeks, as assessed for the specific case situation and the clinical improvement observed.


In 2002, the World Workshop of the European Federation of Periodontology suggested the term RS making reference to a peculiar case condition type of DH, which is the consequence of the gingival recession caused by periodontal disease or by its treatment.[4],[7] This group of patients would be subsidiary of bacterial invasion into the open tubules of dentin on exposed root surfaces of teeth affected by periodontal disease. Such patients might present pain in the interdental areas also concurrently to the presence of gingival recession. RS and DH would be, therefore, two conditions with different etiologies, but with a similar clinical presentation in terms of pain in teeth.

As a consequence of the periodontal treatment, both nonsurgical and surgical recession of the soft tissues and/or exposure of the root surfaces after periodontal pocket reduction can happen. The root dentin so exposed becomes devoid of cementum, may be impacted by oral fluids, and becomes susceptible to hypersensitivity. This condition may lead to an erroneous impression on the patient, i.e., pain in teeth which were probably asymptomatic before the periodontist's intervention, thus leading to a misinterpretation of the successful results obtained in terms of periodontal stability. On the other hand, the discomfort caused by the hypersensitivity also may deter the patient from a proper plaque control.

  1. The group recommends that mouthwashes will allow the agent for a better access to all tooth areas, in comparison to the limited accessibility of a dentifrice, especially in the interproximal spaces, thus may enhance the adjunctive benefits in improving the efficacy of the desensitizing treatment
  2. Further, the use is far more convenient during the immediate postsurgery phase, when the use of toothpastes and brushing should be avoided
  3. Reducing hypersensitivity symptoms would make easier the reestablishment of an adequate oral hygiene, thus contributing to the proper healing and success of the therapy
  4. As use of chlorhexidine digluconate remains the gold standard antimicrobial mouth rinse postperiodontal surgeries; in view of certain cases experiencing extreme hypersensitivity postnonsurgical or surgical periodontal therapy, a desensitizing mouthwash would remain a useful adjunct to the standard antimicrobial regimen

There seems a need for further well-designed and structured clinical studies, especially RCTs to minimize the bias allowing for comparison/pooling in of multicenter homogenous data to enhance the quantity, quality, reliability, and validity of the generated evidence which shall serve as a guide for the best treatment strategies for our patients.

Efficacy of herbal agents for the treatment of dentin hypersensitivity

  1. India with its ancient and rich heritage in regarding the use of herbal agents in our daily lives is essentially the most suitable candidate to explore and adopt these resources for the management of this dental condition. A variety of herbal resources have been explored as DAs for the management of DH and are available in the form of toothpastes or gels, which are used for treating dentin hypersensitivity. Major mechanisms of action of various desensitizing toothpastes are as given.[158],[159],[160],[161],[162],[163] Major mechanisms of action of various herbal agents used for the management of DH are summarized in [Table 5].
Table 5: Major mechanisms of action of various herbal agents used for the management of dentin hypersensitivity

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Although this specific area seems promising based on the available published evidence, it yet needs extensive body of concerted research effort to materialize the home-grown benefits of herbal remedies available for the management of DH.

Efficacy of chewing gums for the treatment of dentin hypersensitivity

Regarding the use of chewing gums, not much work has been carried out and only a limited scientific literature is available as published research. Few studies have been conducted to explore this option for home management, primarily utilizing potassium chloride. However, the findings from the studies cannot be considered much reliable.[109],[134] There is another investigation pointing to the effectiveness of the potassium chloride-containing chewing gum.[164] However, there is clearly a lack of supportive evidence in terms of recommending the use of chewing gum for the management of DH, and this area needs a great deal of primary research to explore the use of chewing gums as a delivery vehicle for DAs for DH management.

Dentin hypersensitivity management in office

Nonsurgical periodontal therapy for the management of dentin hypersensitivity

Patients with periodontitis have a much higher prevalence of DH ranging between 60% and 98% as compared 45%–57% observed in general population.[104],[165],[166] DH is far more commonly observed in patients of periodontal disease, but the role of dental plaque in the causation or association of DH is very controversial. Patients with DH usually have a good plaque control in the oral cavity.[104],[127],[167] Addy et al. in a landmark investigation suggests that the intraoral distribution of recession, sensitivity, and plaque in this selected population is complex and tooth cleaning is one of several major factors that influence the occurrence and distribution of DH.[168]

In contrast, many other authors have suggested the association of dental plaque and microbial contamination of dentinal tubules of exposed surfaces in cases of DH.[168],[169] High inflammatory and plaque scores have been observed in sights of gingival recession.[170] Tooth brushing behavior was thought to be responsible for the distribution of gingival recession, whereas plaque was thought to be the cause of sensitivity by inducing resolution of the smear layer and concomitant penetration of bacteria into the dentinal tubules.[8],[40] Transient hypersensitivity may occur after periodontal procedures such as deep scaling, root planing, or gingival surgery. Therefore, appropriate measures should be taken before, during, and after treatment of gingival diseases for the successful management of DH.[133],[171],[172],[173]

Suggestions for dentists/caregivers

  1. Avoid over instrumenting the root surfaces during scaling (cervical area)
  2. Avoid over polishing exposed dentin during stain removal
  3. Avoid burning the gingival tissues during in-office bleaching
  4. Advise patients to be careful during home-bleaching
  5. Avoid harmful instruments and materials.[135]

Supportive evidence

de Oliveira et al. in 2020[174] carried out a meta-analysis to analyze the efficacy of the use of the DAs on DH after scaling and root planing. The authors included only randomized control clinical trials that were focused to check the clinical effectiveness of the DH controlling agents with the use of placebo or other toothpastes in adult patients. The findings revealed a high prevalence of DH approximately affecting 46% of the people in age group of 18–77 years, in which approximately 42% were included from below 35 years of age. Further, it was seen that the patients with periodontal disease had higher prevalence of DH as they had tooth root surfaces exposed either owing to destruction of the periodontal tissues or due to the treatments offered to combat periodontitis. The proportion of DH was evident in the study population with an increase to 54% from 9% at the outset, with approximately sixfold increase in by 1 week after nonsurgical management of the patients.

The present review suggested that despite the transient duration of DH after nonsurgical periodontal therapy, desensitizers are important to offer pain relief to patients. The desensitizing materials available also have another mechanism of action, i.e., obliterating of neuronal action mechanism, and this study provided an insight that obliterating DAs has greater potential for relieving DH. When evaluating the efficacy of DA under mechanical stimuli, they found that patients who were treated with DA presented a lower mean of DH pain reduction when compared to the control group. However, under other stimuli, e.g., water and evaporative stimuli, patients using DA reported a greater mean of DH pain reduction when compared to the control group.

   Occlusive Approach – Aiming at Dentinal Tubular Blocking/Plugging Top

There is a plethora of agents, materials, and products commercially for in-office use and the management of DH. There is mounting evidence in the form of systemic reviews and meta-analysis showing efficacy of occlusive agents which is statistically significant when compared against placebos in the management of DH.[172],[173] However, retention of physical or chemical occluding agents is controversial and the long-term effects of these agents remain unclear.[133] Classification of occlusive agents used in the management of dentin hypersensitivity is given in [Figure 3].
Figure 3: Classification of occlusive agents used in management of dentin hypersensitivity

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Occlusive approach – Aiming at dentinal tubular blocking/plugging for the management of dentin hypersensitivity

Chemical occlusion of dentinal tubules


Early used Copal varnishes were known to make a layer over the dentin tubules and block the passage of other compounds, thus reducing sensitivity. However, a short time of effectiveness was the major hurdle to use as it required a very frequent reapplication of the agent. As improvised delivery system, new versions of varnishes are preferred for its ease of use, prolonged fluoride exposure time, and relative safety. A concern with other carrier modalities is that there is an increased risk of ingestion, as well as decreased contact time with the teeth. In spite of having a very high concentration of fluoride, the varnishes are generally considered safe for use because the varnish sets so fast that it causes a minimal chance for the ingestion of free fluoride. Apart from this, the long duration of contact between the tooth enamel and the varnish; usually, there is observed a very slow release of the fluoride in the vicinity. Most varnishes on the market contain 5% Sodium Fluoride (NaF) with an alcohol- and resin-based solution. The evaporation of the alcohol makes the system fast drying, and the resin functions to allow the fluoride to adhere to the teeth. The most common resin additive is colophony, a rosin derived from pine tree sap. The carrier is the cause of the main complaint about varnish, in that it is “sticky” and leaves a noticeable film on the teeth.[175],[176]

Conventional procedure

The varnish is generally applied after thorough cleaning of the tooth surfaces. The quadrant to be treated is isolated using cotton rolls; however, as the presence of moisture is helpful for the adherence of the agent, excessive drying of the teeth is not recommended. The product is dispensed according to the manufacturers' instruction and applied to the selected teeth or surfaces using a disposal brush or cotton applicator with specific care to apply on the exposed area of the root/tooth and soft tissue contact should be avoided. The varnish may set in few seconds leaving an active ingredient-rich layer on to the surface of tooth with application usually taking up to 5 min. On the day of application, the patient is advised for not eating for 2 h immediately after the application and the brushing is avoided for the full day of varnish application. Some of the products may transiently alter the tooth color and appearance, so the patient needs to be informed regarding the same, as it will vanish once the tooth brushing is resumed the next day.

The most popular in-office treatment is fluoride varnish which normally contains a resin-based fluoride. Fluoride varnish is primarily intended to reduce the incidence of dental caries as it strengthens the tooth enamel surface biologically with the formation of fluorapatite.[175],[176] The fluoridated tooth surface becomes less susceptible to acidic bouts of demineralization. Fluoride varnishes are used after subtle priming with acid also to increase the effectiveness by penetration of ions. Fluoride varnish prevents new cavities from forming and slows down or stops decay from progressing. In fact, very early hypomineralized areas get remineralized with the application of these varnishes. These are convenient to use, cost-effective, and generally safe options to use in the mouth, except in case of an allergic tendency to one of the ingredients in the varnish. Various types of products are available with distinctive features to allow a great deal of choice as appropriate from patient to patient.[177],[178]


Oxalates are plant-based organic substances that have an important place in the management of DH, as these compounds tend to block the opened tubules and reduce the fluid flow across the tubules.[179] Many in vitro and in vivo studies have established that oxalates delivered by any of the technique, for example, mouth rinsing, brushing, or tray systems; there occurs a deposition of oxalate crystals in the patent tubules which translate as a decreased sensitivity scores.[157],[180] A very salient feature describing this class of compounds is that these are relatively insoluble in the acids.[181] This makes them a particularly appealing option from the wide variety of available agents, since acidic challenge is a very common situation in the oral cavity, where a lot of physiologic and biochemical influences and dietary influences are a routine feature. Oxalates stand to perform affectively in the management of DH.[182] In a systematic review by Cunha-Cruz et al.,[183] evidence supported only the use of 3% monohydrogen monopotassium oxalate, for the treatment of DH treatment with oxalates.

A patented technology of antisensitivity strips coated with a 1.5% oxalate gel is commercially available. This particular strip took cue from the tooth-whitening strip system which had been utilize to deliver hydrogen peroxide in the 2000s. The system contains a flexible thin polythylene strip which contains a dipotassium oxalate gel on one of the surfaces and can be extended as a unique delivery system for the active agent across the gingival margin. The strip enables the release of oxalate and keeps it in contact with the open dentin tubules for approximately 10 min. The strip has been known to provide instantaneous relief from the DH with 1–3 strip applications providing a respite for almost 1 month or longer duration of time. The patient may himself/herself also apply the strip as a home care system following daily oral hygiene. Separate strips can be applied for different sensitive areas in the oral cavity. The patients, however, have been instructed to consult their dentist in case the DH persists after the application of consecutive three strips. These are considered safe to be used for adult patients over 18 years who suffer from sensitivity to hot, cold, acid, or sweet stimuli. The system has been contraindicated to be used in people suffering from periodontal disease, renal disease, pregnant or breastfeeding mothers, or people suffering from allergy tendency to oxalate or any of the other ingredients of the strip.

Glutaraldehyde-based agents

It is an aqueous solution of 5% glutaraldehyde (GA) and 35% 2-hydroxyethyl methacrylate (HEMA). Its application effectively inhibits the discharge of serum albumin from freshly cut dentin cavities[184] and causes tubular blockage by means of coagulation of plasma proteins due to fixative nature of GA. It has been shown to penetrate exposed dentinal tubules up to 200 ml,[185] leading to the formation of multilayered protein walls to prevent an osmotic fluid exchange with tubular contents.[186]

Physical occlusion of dentinal tubules


Composite resins, as the name indicates, are composed of a mixture of organic and inorganic components put together and from an important class of dental restorative materials. The resin coupling agent and the initiator are the three main organic constituents, whereas filler makes up the inorganic part. Usually, the materials are prepared by polymerization reaction based on free radical interactions and are initiated by a high-energy stimulus, for example, visible light, and has much better mechanical properties for clinical applicability. The properties of a composite can be impacted by manipulating various components and addition of new constituents also, for example, barium silicate glasses are an improvised version of the conventional composite. Many organic salts, for example, fluorides can be incorporated which impart the capacity of fluoride release from the finished surface of the composite material in the mouth, thus making the area lesser susceptible to acid attack and ensuing dental caries.

Dentin bonding systems

Bonding to dentin is both micromechanical and chemical. Micromechanical adhesion is through the infiltration of bonding resin into the dentin, which replaces dissolved hydroxyapatite crystals and surrounding the organic matrix (primarily collagen fibrils) and forms an interdiffusion hybrid layer.[187] The chemical bonding takes place due to the interaction of functional acidic monomers with dentinal hydroxyapatite crystals.

Dental bonding systems (DBSs) are resin blends that possess amphiphilic (both hydrophilic and hydrophobic) properties.[188] HEMA and the bisphenolglycidyl methacrylate (bis-GMA) are the most widely employed monomeric agents used in DBSs. HEMA is completely soluble in aqueous solution and hence works wonderfully wetting agent, which is amenable to polymerization. Bis-GMA, on the other hand, is a hydrophobic compound in nature and has limited wettability (incorporates only 3% of water by weight) when polymerized.[189] A combination in the right proportion blends the characteristics of both compounds well and serves as a useful adhesive for dental adhesive restorations. Many additional approaches such as the use of thinning agents, which tend to enhance the spreading and penetration of the polymerizable monomers into the dentin structure, are also employed. Ethyl/butyl alcohol and water are generally used as thinning agents; these are hydrophilic substances that may help the monomer to interact better with water; however, acetone is also sometime used but is not a very good choice for working to enhance dental adhesion by displacing water from within the tissue.

Dentin bonding systems have been classified into categories according to the number of procedural steps depending on whether the prime and bond solutions are used together from a single bottle or in two separate steps from two different bottles. Eliminating the separate etching step not only shortened working time but also prevented contamination by blood and saliva during postetch washing and drying, which made lesser step techniques a more clinically acceptable procedure[190],[191],[192] [Table 6].
Table 6: Dentin adhesive techniques based on clinical steps

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Dentin bonding agents (DBAs) have been also identified as per the number of steps involved in the process clinically and generations [Table 7].[193] The latest generation of adhesives consists of single-component, one-step, self-etch adhesives. Seventh-generation adhesives combine conditioning, priming, and application of adhesive resin; however, unlike sixth-generation adhesives, they do not require mixing.
Table 7: Classification of dental bonding systems by generations

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Significance of technique

Dentin bonding is essentially an infusion process; therefore, mere painting may not yield satisfactory results. Adhesives may differ in their ability to plug the dentinal tubules; however, a proper technique is imperative to success. The adhesives must be allowed to penetrate the etched zone to seal the dentinal tubules. This has been aided with the recent advent of hydrophilic components of the DBA.

Adhesives should be puddled and rubbed/burnished or scrubbed into all areas of the etched dentin. There is a significantly better chance of total penetration into every tubule with this strategy. The adhesive must be thinned to a stretched tight surface with no pooling after application. This means that every surface will have the correct thickness for optimal adhesion mechanics. Light curing should be done with a trusted light source. Commonly, on posterior teeth, the light that should be directed perpendicular to the working surface reaches the posterior interproximal areas where the incident light is often at an angle. The light should be delivered from as reasonably close as possible.

Glass ionomers

Because of a specific glass ionomer interaction, glass ionomers are the only truly self-adhesive materials that can bond to both enamel and dentin. Polyacrylic acid, alkenoic copolymers, glass-filler particles, and water make the constitution of glass ionomers. Resin-modified glass ionomers have the resin components added to glass ionomers in which the adhesion involves both a micromechanical hybridization and a chemical reaction. Thus, their adhesive capacity is twofold similar to self-etch adhesives and is dependent on both demineralization of enamel and dentin with subsequent penetration and mechanical interlocking, as well as a chemical bond between calcium in hydroxyapatite and polyalkenoic acid.

   Restorative Approach – Aiming at Prolonged Dentinal Tubular Blocking/Plugging and Restoring Tooth Structure Loss For The Management of Dentin Hypersensitivity Top

Restorations for the sensitive exposed dentin surfaces with structure loss provide prolonged occlusive effects compared to sealing agents as the retention of topically applied agents is unpredictable in the oral cavity environment. Generally, the sealers tend to wear off with time and need repetitive applications. The decision to restore depends upon multiple factors such as the amount of tooth structure loss, affected teeth and surfaces, and patient's complaint etc. A sound clinical judgment should be made weighing the cost–benefit ratio esthetic demands of the patients and the oral hygiene practices to restore the tooth surface defects.[194]

According to tooth wear evaluation system classification (TWES),[195] only preventive measures and monitoring should be advocated when grade 0 or 1 exists on the surfaces that are involved in occlusion/articulation and/or grade 0 or 1 exists on the nonocclusal /nonincisal surfaces. Similarly, restorative treatment is to be considered when grade 3 or 4 exists on the surfaces that are involved in occlusion/articulation and/or grade 2 exists on the nonocclusal/nonincisal surfaces that are diagnosed as well.

   Material Selection Top

Minimally invasive restorative intervention, such as restoring with composite, glass ionomer cements (GICs), resin-modified GICs (RMGICs), a GIC/RMGIC liner base laminated with a resin composite, and resin composite in combination with a DBA are all viable options for the management of DH.[194],[195],[196],[197],[198],[199],[200]

GIC is an acid–base biomaterial consisting of an acid-degradable fluoro-aluminosilicate glass powder, a polymeric acid dissolved in water and tartaric acid.[201] Owing to its ability to adhere to moist calcified structures and reactive chemistry, it is a material of choice to seal interfaces between restoration and tooth substance.

It has been documented to reduce DH with fewer incidences of immunological and allergic reactions compared to resin-modified glass monomer cements and makes a good choice cost-effective treatment for small cervical restorations.[202] However, poor esthetics workability and solubility make the use of GIC little limited. Further, fracture-induced failures of cervical GIC failures are very common. Therefore, nowadays, RMGIC and composites are more widely employed in the restoration of such lesions.

Modified GIC is convenient, more workable, and moisture-tolerant, which makes its use in rgw oral cavity quite easy, particularly for cervical restorations. In addition, RMGICs provide better esthetic properties and thus generally preferred by the patients as a choice over conventional GICs.[203],[204] However, the material has concerns with a higher cost, which is almost six times the regular GIC restorations and does not make it a pocket-friendly pick for the patients. Further, other characteristics, e.g., longevity, adherence to the tooth, maintenance of hygiene, and gingival response, also seem to be relevant in the treatment of DH and should be taken into consideration by while making a decision to use on case-to-case situation by the treating dentists.

Microfilled resin composite or a flowable resin also make a good choice as they flex with the tooth surface without compromising the retention.[205],[206],[207],[208],[209] [Figure 4] explains the techniques employed for restorative approaches used for the management of DH (adhesive versus conventional) approach.
Figure 4: Techniques employed for restorative approaches used for management of dentin hypersensitivity

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Adhesive restorations are considered minimally invasive as a dynamic restorative concept as almost no or minimal tooth preparation is needed to accomplish the retention and the mechanical resistance form as the workability of the restoration is ensured by good bonding strength with the use of an appropriate restorative material.[209],[210]


Once the restorative treatment is indicated, the dentist has to know the different causes and aspects of each situation and choose the best strategy to employ. Unfortunately, although NCCL restorations are a very common occurrence in clinics, they also represent one of the less durable types of restorations and have a high index of loss of retention, marginal excess, and secondary caries.[211] The restorations for such lesions are technically demanding as the sclerotic obliterated dentinal tubules result in minimum or no resin tag formations.

Steps of procedure

  1. Isolation
  2. Material selection
  3. Cavity cleaning
  4. Adhesion
  5. Insertion techniques
  6. Finishing and polishing.

Supportive evidence

They observed no statistically significant difference between clinician-stimulated or patient-reported sensitivity reduction in noncarious cervical lesions between the restoration and the sealant treatment.[212]

In a comparative trial of conventional GICs versus RMGICs, both materials produced satisfactory results in terms of pain reduction up to 6 months of observation and did not differ significantly.[213]

   Occlusive Approach By Laser in Dentin Hypersensitivity Management Top


Laser is light amplified by stimulated emission of radiation, and it is one of the methods to treat DH introduced in the mid-1980s. The technique got very popular because it is simple to operate, safe, and reliable and has a fast pain-relieving effect.[214]

Mechanism of action

  1. Effecting changes in neural transmission network inside the dentinal tubules by blocking the depolarization of C nerve fibers
  2. Low-power lasers such as diode imparts biostimulatory effect leading to secondary dentin formation and tubule occlusion in the long run
  3. High-power lasers such as Nd: YaG lead to coagulation of proteins in dentinal tubules and melting of dentinal walls.

Laser parameter settings

There is lack of evidence to suggest a gold standard for laser parameter settings at present. The settings adopted by several studies that demonstrated significant clinical benefits have been suggested as follows:

  1. Er Cr YSGG (2780 nm, pulsed mode, 0.25–0.5 W, application time 20–30 s)
  2. Nd: YaG (1064 nm, pulsed mode, 0.1–1 W, application time 20–40 s)
  3. GaAlAs diode laser (685–980 nm, continuous or pulsed mode, 0.25–0.5 W, application time 30 s to 1 min).

General guidelines for laser application

  1. Protective goggles to be worn by the patient and the dental team
  2. Strict compliance with dental laser biosafety rules
  3. Thorough hygienic phase before application
  4. Proper isolation and drying of the tooth/root surface
  5. Noncontact mode, but as close as possible to the surface to be treated
  6. Laser beam directed perpendicular to the surface to be treated
  7. Swiping motion to cover the desired area.

Frequency of application

Mild cases can be managed with single application. Severe cases may require multiple applications in the first session itself (with a 10 s interval between consecutive applications) followed by one or more sessions with a 1-week gap.

Limitations of laser

  1. High treatment cost
  2. Difficulty in treating in accessible proximal surfaces
  3. Potential for recurrence, if patient continues unfavorable dietary practices such as consumption of carbonated beverages or follows over brushing
  4. Potential damage to pulp due to rise in temperature.

Supportive evidence

Since 1980s, different types of lasers have been tried to manage DH. Several clinical trials have reported effectiveness of lasers in providing symptomatic relief as well as improvement of VAS scores.[215],[216],[217],[218],[219],[220] Some reports suggest effectiveness of laser at par with other topically applied desensitizing agents such as fluoride varnish or DBAs.[217],[218] Several systematic reviews and meta-analysis report inconsistent results in support of the efficacy of laser in terms of sustained relief of DS in the long term. Heterogeneity of the included studies in terms of the laser parameters employed, the method of evaluation of DH, follow-up periods, and the etiology of DH has affected the strength of evidence of those reviews.

A recent network meta-analysis of randomized controlled trials indicates that the four types of lasers namely Er, Cr: YSGG, Nd: YAG, Er: YAG, and GaAlAs had better desensitizing effects on DH than no treatment both immediately after application and after 1 month.[221]

On comparison of various laser types, the immediate desensitizing effect was in the order, Cr: YSGG > Nd: YAG > GaAlAs > Er: YAG.

The 1-month desensitizing effect was in the order Er, Cr: YSGG > Nd: YAG > Er: YAG > GaAlAs.

However, there was no significant difference between the four laser types.

   Surgical Periodontal Therapy For Alleviation of Dentin Hypersensitivity and Restoration of Soft Tissue Loss Top

Sensitive noncarious cervical lesions are treated with restorative options such as resin composites or RMGICs; however, to restore the original position of the gingival margin, root coverage procedures are necessary. The restorations for such lesions are technically demanding as the sclerotic obliterated dentinal tubules result in minimum or no resin tag formation. This has been documented in a number of in vitro and in vivo investigations that longer etching times also did not significantly improved the resin adhesion to sclerotic dentin.[222] Thus, such areas essentially need a soft tissue coverage particularly in instances of compromised smile and esthetic appearance due to lack of symmetry with the teeth adjacent to the recession(s).[223]

Agossa et al. in 2017 had done a study on a combined restorative surgical approach for the treatment of gingival recessions associated with noncarious cervical lesions to evaluate the outcomes such as root coverage, DH. It was a systematic review of 10 RCTs.

The combined restorative and surgical approach logically achieved better results in the reduction of DH, probably due to a complete sealing of open dentin tubules.[224]

Most common etiology of DH is gingival recession; hence, treatments to rule out the etiology should be done rather than treating the symptoms.

Santamaria et al. have done three studies in which they have used different type of restorative materials and surgical techniques such as:

  1. Connective tissue graft (CTG) alone or combined with a nanofilled resin composite restoration[225]
  2. CTG alone, or in combination with a resin-modified glass ionomer restoration (CTG1R)[226]
  3. Coronally advanced flap alone (CAF) or in combination with a resin-modified glass ionomer restoration (CAF + R) for DH and root coverage and found out that surgical therapy along with restorative therapy had given good results in reducing DH.[227]

According to Al-Sabbagh et al., root coverage procedures accomplished via reconstructive periodontal surgeries including perioplastic procedures have been documented to help alleviating the menace of DH to some extent, though intended to cover the exposed root surfaces caused gingival recession. There is a paucity of literature which could source the studies designed specifically to evaluate the effectiveness of such tissue grafting root coverage procedures as a management for DH. An extensive literature search by the authors with terms “hypersensitivity” and “graft” revealed only two citations referring to soft tissue correction of recession defects; however, none of them had an objective focused to the intervention strategy meant for cure of DH. Broader searches in the same area at best revealed postoperative sensitivity as an unwanted or negative outcome and did not focus to reduction of DH as a main outcome for analysis.[228]

Restoring the lost enamel or dentin of the tooth and soft tissue root coverage procedures can be considered as an adjunctive or alternative treatment for DH management where the indications for such procedures exist. For DH associated with tooth wear, restoring the tooth structure by resin-based composite or GIC restorations or by utilizing a crown or veneer restorations shall help manage the associated DH. On the other hand, periooplastic procedures meant for root coverage such as coronary position flaps, CTGs, or guided tissue regenerative approaches are very technique-sensitive procedures and still need more exploration and evidence in terms of their predictable and longevity of the surgical outcomes, yet utilizing these procedures in the areas, where indicated otherwise does serve as a practical perspective. In cases where a partial coverage is accomplished and there is still persistence of DH, other occlusive restorative treatment options as mentioned earlier can be utilized in combination for better management of DH in such cases.[133]

   Endodontic Therapy For the Management of Dentin Hypersensitivity Top

More invasive treatment options such as pulpectomy may be opted as a last resort in the management of DH in case of persistence or recurrence of pain perception at reevaluation. A DH patient who did not respond to the occlusive and restorative management options or any combination thereof can be considered as a candidate for root canal procedures.

The cause of concern is the practical clinical application of this management strategy in case of generalized cases of DH. Pulpectomy is an irreversible invasive time and cost-intensive procedure which further requires the restorative management of the tooth per se; thus, it remains a much limited choice for very few judiciously selected DH cases where the presence of DH significantly interferes with the normal function, and all alternative methods have failed to reduce the DH.[134],[135],[229]

   Decision Algorithms For the Management of Dentin Hypersensitivity Top

DH is a rising cause of concern in clinical dentistry that causes pain and discomfort and negatively affects the quality of life of a huge number of our patients. In fact, with increasing awareness, improved hygiene practices, and access to dental care, a greater number of patients are expected to retain their dentitions or longer periods of time in their life and as a consequence may face such issues owing to progressive soft and hard tissue loss exposing dentinal tissue of the tooth.

The current document has been conceptualized and envisioned to update the practicing Indian dentists regarding the so-called enigma of dentistry “DH,” demystifying the myths around and present the concrete information on the entity based on contemporary evidence. A nationwide survey was undertaken by ISP in December 2020 and involved approximately 3000 dentists all across India. The findings revealed significant knowledge gaps in many aspects of DH, viz., under-diagnosis, incorrect differential diagnosis, and treatment strategies/recommendations for the management of DH patients in daily clinical practice. It was observed that there is a significant need to employ criteria/methods for screening DH, emphasizing on the significance of DH case definition and identification, selection of appropriate management strategy, and adoption of long-term maintenance recommendations for these patients.

The expert panel, after extensive literature review and group discussions, recommended routine screening of all dentate patients for exposed dentin areas and DH to avoid under-diagnosis of the condition, thus inculcating and the preventive management that can be initiated early. Due to overlapping definitions and limited evidence present in the literature for differentiation of DH and RS, the panel decided to utilize DH and RS as synonyms/equivalent or interchangeable terms for all practical purposes in clinical diagnosis and management of DH. The expert panel defined distinct clinical case definitions of DH for the first time as ISP-DH case definitions, aimed at clear, concise and convenient description of the diverse clinical situations which are indicated by pertinent category code names. Four distinct case categories viz A to D has been defined based on the presence /absence of hard and soft tissue loss in an individual case scenario of DH. Category codes have been assigned to indicate the extent and severity of DH and to provide appropriate guidance for the management of DH on case to case basis [Table 8]. Further, the expert panel developed consensus guidelines/recommendations for the use of desensitizing agents at home, including the use of herbal agents within the backdrop of Indian context. A decision tree process and a flowchart for daily practice were designed which should be started up as on as a patient presents with exposed dentin areas in dentition or suffers from DH. Various treatment methods of DH have been discussed to date, based on the available literature including previously published treatment guidelines. The panel also recommended that active management of DH shall be managed by a combination of at home and in-office therapies, starting with the simplest and cost-effective home use of desensitizing toothpastes. The approach takes into account a decision algorithm based on hierarchy of complexity of treatment options and intends to improve the quality of life of the patient by long-term maintenance [Table 9], [Table 10], [Table 11], [Table 12].
Table 8: ISP-dentin hypersensitivity-case definition/classification

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Table 9: Management of Type A (no hard tissue loss + no soft tissue loss)

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Table 10: Management of Type B (hard tissue loss+no soft tissue loss)

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Table 11: Management of Type C (no hard tissue loss + soft tissue loss)

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Table 12: Management of Type D (hard tissue loss+soft tissue loss)

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   Recall/Maintenance For Dentin Hypersensitivity Management Top

Although a huge amount of scientific research has tried to unveil the etiopathogenesis to decipher the most predictable and lasting treatments for this problematic clinical entity, yet not much clarity in terms of the foreseeable future course of the DH lesion has been sorted. Since DH has been known as an enigma for dentistry from a long time, for ensuring the best effective and long-term successful patient outcomes, it is prudent to complement the active management of the patient with a strict long-term maintenance program in consistence to the specific patterns of the case scenario.

Active management of DH should involve the above-mentioned agents, options, and algorithms as applied on case-to-case basis. Once a patient has been treated with or recommended with an active treatment option, it is important to keep a recall phase for the follow-up of the patient.

A “CCC,” viz., triple C, or 3C's approach, at the recall visit of the patient after active intervention for DH, is designed by panel to aim at imparting a simplistic case planning program for the dental practitioners. This approach has essentially been conceived with an idea of giving an opportunity to the dentist to analyze the individual DH case situation, thereby making a customized treatment plan/appropriate usage of the DH treatment agent (switching to or supplementing another desensitizing agent with the same/different mode of action) or the treatment approach (at home versus use of in-office management of DH) in terms of the future course of patient care [Figure 5].
Figure 5: Triple C' approach to management of dentin hypersensitivity. DH – Dentinal hypersensitivity

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1st C - Stands for “Continue”

Recommended in case of patients with improvement in clinical condition of DH, but persisting complaint of DH at the time of recall. A reduction in sensitivity scores yet ongoing complaint of DH though, milder than before, shall be tackled by extended usage of the active desensitizing agent, until a complete remission of DH. Patient shall be asked to continue the agent along with the control of contributing and predisposing factors. A particular care should be given to the candidates with subtle hard and soft tissue loss. A through instruction regarding maintenance of good oral hygiene, and adherence to behavior pattern modification recommendations as appropriate for the patient in context should be administered.

2nd C - Stands for “Change”

This category focuses on the patients of DH who have been treated with any single or combined active therapy management agent/approaches, yet there is persistent complaint of the DH yet at the patient's end at the recall visit. Here, the dentists are suggested to recommend either an alternate desensitizing agent or supplement the ongoing agent with another based on a different mechanism to improve the effectiveness for DH management. Further, a switch over from a home care agent to a more intensive office management procedure for DH management also may be advised, if the case situation demands.

3rd C- Stands for “Cease”

It shall be adopted in case of the patient is in complete remission of DH. At the time of recall, patient shall be asked to stop using the active agent and are only recommended to continue the maintenance of good oral hygiene, and adherence to behavior modification recommendations as appropriate for the patient in context.

   Conclusion Top

DH is one of the most frequently encountered clinical conditions in general clinical practices and has a significant impact on patient's oral health and related quality of life. Thus, it is prudent for the dental clinician to be aware of the role of various etiologic factors which may potentiate/perpetuate the localization/initiation of DH lesions and enhance the prevalence of this enigmatic problem. A through patient history and clinical examination are vital for early identification of risk factors to prevent the development of DH in susceptible individuals, as many a times, DH is not reported by the patient owing to the vagueness of condition. Active management of DH shall involve adoption of a single or combinations of available agents/regimens based on the extent and severity of DH. Usually, the strategy shall aim at utilizing the simplest, easy to use, time, and cost-effective home care measures at the outset, which may be complemented by more complex, time, and cost-intensive in office treatment measures as seem appropriate on a case-to-case basis. However, periodic recalls are essential in all cases of DH to evaluate the response to active management opted and to plan further for an appropriate course of action based on triple “C” approach on an individual basis for long-term management of DH.

Financial support and sponsorship

The project was supported by an unrestricted educational grant from Dr. Reddy's Laboratories.

Conflicts of interest

There are no conflicts of interest.

   References Top

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  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8], [Table 9], [Table 10], [Table 11], [Table 12]


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