|Year : 2022 | Volume
| Issue : 3 | Page : 786-791
Dentinal hypersensitivity: A clinical dilemma
Deepa Sara John, Nina Shenoy, Rahul Bhandary
Department of Periodontics, AB Shetty Memorial Institute of Dental Sciences, Nitte (Deemed to be University), Mangalore, Karnataka, India
|Date of Submission||12-Sep-2021|
|Date of Decision||20-Sep-2022|
|Date of Acceptance||21-Sep-2022|
|Date of Web Publication||2-Nov-2022|
Dr. Nina Shenoy
Department of Periodontics, AB Shetty Memorial Institute of Dental Sciences, Nitte (Deemed to be University), Mangalore, Karnataka
Source of Support: None, Conflict of Interest: None
The increase in lifespan and decrease in the prevalence of edentulism have increased the overall risk of tooth wear. This in turn has caused dentinal hypersensitivity (DHS) to be one of the most frequently encountered oral health problems. DHS, commonly referred to as the “common cold” of dentistry, is associated with pain due to exposure of dentine following loss of the enamel. The discomfort caused due to DHS is highly subjective and can lead to deterioration of their quality of life. The most crucial but often neglected phase of the management of DHS is the elimination of its etiology. Identifying the etiology enables the clinician to include prevention in the treatment plan. There is a wide range of treatment modalities ranging from those that can be self-administered by the patient at home or those that can be applied by clinicians in a dental clinic. However, one of the main limitations is that there is no universally accepted, gold-standard treatment for DHS, which gives a long-term pain relief. Different agents have been suggested with varying degrees of efficacy when studied scientifically. An electronic literature search was conducted through PubMed, and dental associations of different countries' website and full-text articles in the English language were selected. This article concisely reviews the prevalence and distribution, etiological factors, and the management of DHS.
Keywords: Assessment, desensitizing agents, gingival recession, hydrodynamic theory, prevalence
|How to cite this article:|
John DS, Shenoy N, Bhandary R. Dentinal hypersensitivity: A clinical dilemma. J Datta Meghe Inst Med Sci Univ 2022;17:786-91
| Introduction|| |
Dentinal hypersensitivity (DHS) is a commonly occurring dental condition that was initially reported by Blum in 1530. However, until 1700, it was not widely investigated. Patients experiencing DHS was observed to have sharp ,discontinuos pain for a short period. This could interfere with the day-to-day activities such as eating, drinking, and brushing. Despite its frequent occurrence, this condition was poorly understood and thus in 1982, DHS was described as an “enigma.”
A computerized search of the PubMed database was performed to select relevant articles from 1990 to November 2021. Primary subject headings such as DHS, dentinal tubules, dentinal permeability, and desensitizing agents were combined using “and” with secondary terms such as prevalence, incidence, theories, predisposing factors, and resulting in various Boolean searches. The search included screening of original reports, review articles, and references of retrieved articles. All searches were focused on the reports published in English, discussing the etiology and clinical management of DHS, and studies analyzing the potency of various desensitizing agents.
The first half of this review focuses on the prevalence, pain mechanisms, and clinical features of DHS, followed by the second half which discusses the diagnosis, and management of DHS.
| Definition|| |
Holland et al. defined DHS as a “short, sharp pain arising from exposed dentine in response to stimuli, typically thermal, evaporative, tactile, osmotic, or chemical, which cannot be ascribed to any other form of dental defect or pathology.” A modification to this definition was proposed in 2003, where the term “pathology” was replaced with “disease.” This definition encourages the clinician to contemplate the other possible causes associated with DHS pain.
There are two aspects to the definition – The first is that it provides a clinical description of the disorder; second, probably more critically, it distinguishes DHS as a separate clinical entity, prompting the clinician to explore a differential diagnosis, given that other illnesses may have similar symptoms but require different therapeutic strategies.
| Prevalence and Distribution|| |
Prevalence of dentinal hypersensitivity
The reported prevalence of DHS varies globally and it is also called the “common cold” of dentistry. According to various reports, DHS affects approximately 15% of the adult population and its prevalence varies from 1.34% to 98%,. The disparity in prevalence data could be due to different methods of assessment, ranging from questionnaires to clinical detection, as well as study location. Furthermore, the majority of DH research have focused on very specific populations, such as periodontal office patients, students, or hospitalized patients. Several studies show that though a large number of the population may report having sensitive teeth, only a small fraction of those with DHS is diagnosed based on clinical diagnostic criteria. The subjective character of pain may also contribute to the wide range of prevalence.
| Gender Difference|| |
DHS is more common in women than in men, which is mainly attributed to the influence of hormones and dietary habits., It is also thought to be due to the increased oral health awareness in women and their higher health concern that makes them more conscious about the condition. In addition, women are more sensitive to pain than men and this physiological phenomenon could also be a reason for the gender differences in the prevalence of DHS.
| Age|| |
It commonly affects individuals between the ages of 20 and 50 years. However, a peak is observed between 30 and 40 years. However, after the 4th decade, the prevalence of DHS reduces which can be due to the formation of secondary or reparative dentine and the subsequent sclerosis of dentinal tubules. It is now presumed that the prevalence of DHS will increase with increasing life expectancy and the greater incidence of development of periodontitis and its treatment, recession, and tooth wear, all of which can exposed dentine to external stimuli.
| Intraoral Distribution|| |
DHS is reported to occur more frequently in the buccal cervical zones of the permanent dentition. Canines are the most affected of all teeth, followed by the first premolars, incisors, second premolars and molars. Individuals with periodontal disorders are also affected more often and prevalence ranges from 72% to 98%. Lower plaque scores are associated with DHS, implying a relationship between overzealous toothbrushing and the initiation of tooth sensitivity.
| Clinical Features|| |
A sharp pain of short duration occurs when exposed dentine comes in contact with any external stimuli. The most common stimuli that cause pain in patients with DHS is cold beverage followed by hot drinks, brushing, and sour substances. One of the main characteristics of DHS is the subjective nature of its pain, which means that it can vary from person to person based on their pain tolerance and also physical and emotional factors.
However, all exposed dentine is not sensitive. For DHS to occur the protective smear layer covering the dentine should be lost, leading to exposure of tubules to the external environment. The “hypersensitive dentine” is characterized by increased number of widely open tubules and a thin smear layer. The fluid movement is increased by the wider tubules, and so the pain response is increased.
Practitioners should also differentiate between patients who complain of DHS with a healthy oral cavity and those who complain of DHS due to periodontal disease and its treatment. Recently, to describe sensitivity resulting from the latter, the terms “root sensitivity, or root dentine sensitivity (RDS) or root dentine hypersensitivity” has been used. Following nonsurgical periodontal therapy, RDS tends to increase during a few weeks, and declines thereafter.
| Etiology and Predisposing Factors|| |
An interaction between the stimuli and predisposing factors tends to initiate DHS. By definition, DHS occurs as a result of wearing of enamel, and further exposure of dentin. Loss of enamel could be due to the regressive alterations of the teeth, namely attrition, abrasion, and erosion. However, gingival recession is considered the most common cause of DHS. There is exposure of the cementum when the gingival margin shifts apically. Due to various factors such as aggressive toothbrushing, poor oral hygiene, and periodontitis, this thin layer of cementum is easily lost and the underlying tubules are exposed [Figure 1].
|Figure 1: Etiology of DHS and their prevention. DHS: Dentinal hypersensitivity|
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In short, DHS develops in two phases: “Lesion Localization” and “Lesion Initiation”. Lesion localization occurs by exposure to dentine which mainly results due to abrasion and erosion of the enamel. Furthermore, the opening of the dentinal tubules causes lesion initiation. This occurs when cemental layer is removed by erosive or abrasive agents. From the evidence available, it is said that erosion is the predominant factor. Nonetheless, abrasion can also potentiate the effect.
| Theories of Dentinal Hypersensitivity|| |
Since the time of its first documentation by Blum, various researches have been conducted on DHS and many new findings have been recorded. However, the mechanism by which the pain is induced in DHS is still poorly understood. One of the earliest theories, named as “Direct Innervation Theory,” states that dentine has a nerve supply which is triggered on the application of stimulus. However, it was proved wrong with the electron microscopy findings.
Later, Rapp et al. proposed the Odontoblastic Transducer Theory, in which he suggested that the odontoblasts acted as receptors that transmit signals to the pulpal nerves. Hoever, it was proven from the direct microscopic studies that odontoblast lacks the capacity of excitation and production of impulses. Hence, this theory was also rejected.,
During the 1960s Brännström developed the “Hydrodynamic theory”, and it is considered the most widely accepted theory of DHS. Gysi, in the 19th century, had proposed a hypothesis that on the application of stimulus there was increased fluid flow along the dentinal tubules which in turn activated the pulpal nerves. This idea was further developed and studied by Brännström and his co-workers. According to this theory, the pain associated with DHS is coupled with the rate of dentinal fluid flow within the tubules. The changes in fluid flow can stimulate the mechanoreceptors and initiate pain. Furthermore, A-delta fibers are anticipated to play an important role in this response.
| Assessment of Dentinal Hypersensitivity|| |
In order to provide accurate treatment, a proper diagnosis must be made initially. The clinician must be aware of other conditions which mimic DHS. As with every other disease, the assessment of DHS begins with a comprehensive personal and medical history. The patient should be enquired about the onset, duration, intensity, and aggravating and relieving factors of the disease.
In general, DHS is assessed in terms of patient's response to application of stimuli. These responses are recorded either using questionnaires or verbally or through Visual Analogue Scales., Various stimuli used for the assessment of DHS are listed in [Table 1].
|Table 1: Assessment of dentinal hypersensitivity comprising subjective and objective evaluation|
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| Patient Reported Outcome (PRO) Measures in Dentinal Hypersensitivity|| |
Patient reported outcome represents the psychological aspects of pain, discomfort, and quality of life (QoL), and they are used to supplement the clinical signs. Since DHS does not have unique clinical signs and is a diagnosis of exclusion, the evaluation of subjective experience is important. Emphasizing on the subjective symptoms not only aids in diagnosis, but also helps in evaluating the treatment. Oral health-related QoL (OHQoL) is a formal technique used to assess such subjective experience of oral problems. Previous research has shown that DHS has a negative impact on everyday activities, resulting in low OHRQoL. A OHRQoL measure specific for DHS was developed, which is called the DHS Experience Questionnaire.
This questionnaire contains a 34-item main scale that recorded the impact in five subscales: functional limitations, coping techniques, emotions such as stress and anxiety, identity, and social impact. Participants were asked to rate their experience on a scale of 17, with 1 indicating strong disagreement and 7 indicating strong agreement. The questionnaire was found to be a reliable and valid measure of DHS experience.
| Differential Diagnosis of Dentinal Hypersensitivity|| |
DHS is considered to be a diagnosis of exclusion. One of the major challenges faced by the clinician is to rule out the other conditions which has a similar clinical presentation to DHS [Table 2]. The characteristics of the pain experienced by patients with DHS are that it is rapid in onset, sharp in nature, and short in duration (seconds to minutes). If the pain does not subside even after the withdrawal of the stimulus, it is suggestive of inflammatory changes of the pulp.. Identification of other conditions requires prolonged examination using various diagnostic tests such as pulp vitality tests, percussion, radiographs, and transillumination (for cracked tooth syndrome). The type of presented is different for different conditions, for example, pulpitis presents with a sharp, stabbing pain which is evoked on stimulation whereas a periodontitis pain is deep and continuous in nature.
| Management|| |
The two main approaches to managing DHS are:
- Occlusion of dentinal tubules, thereby blocking the hydrodynamic mechanism
- Blocking the neural transmission.
Before initiating the treatment for DHS, the potential etiological factors must be addressed and eliminated. A wide variety of treatment options are available and can be classified as in-office management and at-home management. The majority of treatments, whether used at home or applied in-office, are formulated such a way that they occlude tubules.
| At-Home Desensitizing Therapy|| |
Patients are often prescribed over-the-counter desensitizing agents. They are available for use in the form of mouthwashes, dentifrices, and chewing gums. They mainly contain potassium salts, fluorides, dibasic sodium citrate, etc. A toothbrush with soft bristles should be used with the desensitizing toothpastes. To avoid dilution of the active ingredient, patients should be instructed to use only a small amount of water. Every 34 weeks, the effects of “at-home” desensitizing therapy should be assessed. If DHS does not improve, “in-office” therapy should be started.
| In-Office Desensitizing Therapy|| |
Theoretically, it is expected to give a spontaneous pain relief. It is advised to start with noninvasive procedure and then gradually progress to invasive (grafting, laser) procedures by reviewing the treatment.
Various treatment options available for the management of DHS and their mechanism of action are listed in [Table 3].
|Table 3: Various treatment options available for dentinal hypersensitivity and their mechanism of action|
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| Conclusion|| |
DHS meets all the criteria to be regarded as a true “pain syndrome.” The degree of pain experienced differs from individual to individual. DHS is also associated with a complex interplay of the etiological factors. Hence, identifying the proper causative factor is important in the management of DHS. Reversible procedures should be employed before nonreversible procedures, depending on the degree and extent of the disease.
The management of DHS begins with a thorough history taking and diagnosis. Differential diagnosis of the condition is crucial since there are a variety of other diseases that mimic DHS. This is followed by the elimination of all local factors that trigger the condition, especially those pertaining to habits that cause abrasion and erosion. Preventive measures should be implemented through dietary advice and oral hygiene instructions. Finally, a tailor-made treatment plan has to be designed which incorporates the patient's needs. A summary of the steps to be followed while diagnosing and managing DHS is given in [Figure 2].
|Figure 2: Flowchart depicting the diagnosis and management of DHS. DHS: Dentinal hypersensitivity|
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Conflicts of interest
There are no conflicts of interest.
| References|| |
Holland GR, Narhi MN, Addy M, Gangarosa L, Orchardson R. Guidelines for the design and conduct of clinical trials on dentine hypersensitivity. J Clin Periodontol 1997;24:808-13.
Canadian Advisory Board on Dentin Hypersensitivity. Consensus-based recommendations for the diagnosis and management of dentin hypersensitivity. J Can Dent Assoc 2003;69:221-6.
Bekes K. Clinical presentation and physiological mechanisms of dentine hypersensitivity. InDentine Hypersensitivity Elsevier 2015. p. 21-32. Academic Press.
Mohammed AS, Ofuonye IL. Dentine hypersensitivity: Review of a common oral health problem. J Dent Craniofac Res 2017;2:16.
Bubteina N, Garoushi S. Dentine hypersensitivity: A review. Dentistry 2015;5:2161-1122.
Leye Benoist F, Niang SO, Faye B, Sarr M, Seck A. Treatment of dentin hypersensitivity: A systematic review of randomized clinical trials. J Dent Oral Care Med 2016;2:204.
Dababneh RH, Khouri AT, Addy M. Dentine hypersensitivity – An enigma? A review of terminology, mechanisms, aetiology and management. Br Dent J 1999;187:606-11.
Addy M. Dentine hypersensitivity: New perspectives on an old problem. Int Dent J 2002;52:367-75.
Miglani S, Aggarwal V, Ahuja B. Dentin hypersensitivity: Recent trends in management. J Conserv Dent 2010;13:218-24.
] [Full text]
Gillam DG. Current diagnosis of dentin hypersensitivity in the dental office: An overview. Clin Oral Investig 2013;17 Suppl 1:S21-9.
von Troil B, Needleman I, Sanz M. A systematic review of the prevalence of root sensitivity following periodontal therapy. J Clin Periodontol 2002;29 Suppl 3:173-7.
Clark D, Levin L. Non-surgical management of tooth hypersensitivity. Int Dent J 2016;66:249-56.
West NX, Lussi A, Seong J, Hellwig E. Dentin hypersensitivity: Pain mechanisms and aetiology of exposed cervical dentin. Clin Oral Investig 2013;17 Suppl 1:S9-19.
Davari A, Ataei E, Assarzadeh H. Dentin hypersensitivity: Etiology, diagnosis and treatment; a literature review. J Dent (Shiraz) 2013;14:136-45.
Cartwright RB. Dentinal hypersensitivity: A narrative review. Community Dent Health 2014;31:15-20.
Ali S, Farooq I. Dentin hypersensitivity: A review of its etiology, mechanism, prevention strategies and recent advancements in its management. World J Dent 2013;4:188-92.
Gillam DG, Orchardson R, Närhi MVO, Kontturi-Närhi V. Present and future methods for the evaluation of pain associated with dentine hypersensitivity. Tooth wear and sensitivity. Martin Dunitz, London, 2000. p. 283-97.
Machuca C, Baker SR, Sufi F, Mason S, Barlow A, Robinson PG. Derivation of a short form of the dentine hypersensitivity experience questionnaire. J Clin Periodontol 2014;41:46-51.
Barroso NF, Alcântara PM, Botelho AM, Douglas-de-Oliveira DW, Gonçalves PF, Flecha OD. Prevalence of self-reported versus diagnosed dentinal hypersensitivity: A cross-sectional study and ROC curve analysis. Acta Odontol Scand 2019;77:219-23.
Cummins D. Dentin hypersensitivity: From diagnosis to a breakthrough therapy for everyday sensitivity relief. J Clin Dent 2009;20:1-9.
Borges A, Barcellos D, Gomes C. Dentin hypersensitivity-etiology, treatment possibilities and other related factors: A literature review. World J Dent 2012;3:60-7.
Scherman A, Jacobsen PL. Managing dentin hypersensitivity: What treatment to recommend to patients. J Am Dent Assoc 1992;123:57-61.
McFall WT Jr. A review of the active agents available for treatment of dentinal hypersensitivity. Endod Dent Traumatol 1986;2:141-9.
Yadav H, Singh H. Dentin hypersensitivity and its management: A Review. Int J Oral Care Res 2015;3.
Shiau HJ. Dentin hypersensitivity. J Evid Based Dent Pract 2012;12:220-8.
Gordan VV, Blaser PK, Watson RE, Mjör IA, McEdward DL, Sensi LG, et al
. A clinical evaluation of a giomer restorative system containing surface prereacted glass ionomer filler: Results from a 13-year recall examination. J Am Dent Assoc 2014;145:1036-43.
Douglas de Oliveira DW, Marques DP, Aguiar-Cantuária IC, Flecha OD, Gonçalves PF. Effect of surgical defect coverage on cervical dentin hypersensitivity and quality of life. J Periodontol 2013;84:768-75.
Sgolastra F, Petrucci A, Gatto R, Monaco A. Effectiveness of laser in dentinal hypersensitivity treatment: A systematic review. J Endod 2011;37:297-303.
Gandolfi MG, Silvia F, Pashley David H, Gasparotto G, Carlo P. Calcium silicate coating derived from Portland cement as treatment for hypersensitive dentine. J Dent 2008;36:565-78.
Bartold PM. Dentinal hypersensitivity: A review. Aust Dent J 2006;51:212-8.
[Figure 1], [Figure 2]
[Table 1], [Table 2], [Table 3]