Dentine hypersensitivity – guidelines for the management of a common oral health problem

Definition of dentine hypersensitivity

Dentine hypersensitivity has been defined as a short, sharp pain arising from exposed dentine in response to stimuli, typically thermal, evaporative, tactile, osmotic or chemical and which cannot be ascribed to any other dental defect or disease.13

Epidemiology

Dentine hypersensitivity is a commonly occurring condition with a reported prevalence varying from as little as 4% to as high as 57%.6 This wide range is thought to be because of differences in the population, the setting and the clinical methodology employed to assess DHS and also variations in patient perception. Canines and first premolars are most frequently affected, followed by incisors and second premolars, with molars being least affected.14 The sites of those teeth most commonly affected are the buccal cervical regions. In 1987, Orchardson and Collins15 reported that, in 90% of cases, the hypersensitive area was at the cervical margin. However, occlusal/buccal sites are now becoming more frequently affected in young adults, probably due to the combination of erosive and abrasive toothwear.16 DHS can present at any age, but the majority of individuals range from 20–50 years, with a peak in prevalence in the age range 30–39 years.6

Dentine may become exposed through either gingival recession or enamel loss. Experts have concluded that gingival recession, rather than cervical enamel loss, is the key pre-disposing factor for exposing the dentine surface. However, once the dentine has been exposed, it is evident that erosion is a key factor in dentine hypersensitivity initiation.13 Exposed dentine is a common clinical finding. Albandar and Kingman17 estimated that 23.8 million individuals in the USA have one or more tooth surfaces with ≥3 mm gingival recession. Kassab and Cohen also reported that 50% of those aged 18–64 years have at least one or more sites with recession and that the prevalence and extent of gingival recession was reported to increase with age.18 There are limited data, however, on the association between gingival recession and DHS. The presence of gingival recession does not mean that DHS is inevitable. For example, Kamal19 reported that only 23.6% of individuals experienced DHS in teeth with associated gingival recession. Information on the prevalence of toothwear and associated DHS is also limited and most studies appear to report mainly on the presence or absence of occlusal, buccal and cervical wear rather than any prevalence data on associated DHS per se.20^–22 These clinicans reported that most patients will have a degree of toothwear which may increase throughout life. According to a systematic review by Van't Spijker et al,22 the predicted percentage of adults presenting with severe toothwear increases from 3%, at the age of 20 years, to 17%, at the age of 70 years. It is evident from six of the studies included in this review and a recent study by Cunha-Cruz et al,23 that males have significantly more toothwear than females. However, it is also clear that some dental procedures may also be associated with an elevated incidence of tooth sensitivity. For example, several clinicians have reported that the prevalence of DHS associated with periodontal treatment was 9–23% before treatment and 54–55% following treatment, although this discomfort may be both mild/moderate and transient (up to four weeks post treatment) in nature for the majority of patients.24^–26 Overall, DHS cannot occur without exposed dentine, but the inter-relationship with recession, toothwear and erosion is complex.

Relevance

DHS is a painful experience that, for the majority of sufferers, generates a very unpleasant feeling, causing them to adapt and often modify their life styles. For example, patients may start guarding the sensitive tooth with the tongue or drinking on the opposite side of the mouth, or even avoiding ice-cold food and drinks completely. However, for some people, DHS can be so disturbing that it affects their quality of life.1^–2 Additionally, it has been reported that localized DHS can lead to sensitive areas being avoided during toothbrushing, which in turn can increase the risk of periodontal diseases and sequelae (see ‘Aetiology’ below).

DHS may also be provoked by some routine dental procedures such as scaling and polishing, thereby making a regular dental visit unpleasant and painful for the patient. This discomfort may therefore add anxiety to an already stressful experience. Preventive treatment for DHS before carrying out any potentially painful, stress-provoking dental procedure is recommended in such cases as it creates a calmer environment in subsequent treatment visits, for both the patient and the professional. In more severe cases, it may be more appropriate to complete the procedure under a local anaesthetic.

Aetiology

Currently, the most widely accepted theory to explain the aetiology of the pain sensation caused by DHS is the ‘hydrodynamic theory’ advanced by Brännström and Aström.27 According to the hydrodynamic theory, DHS occurs when an external stimulus contacts exposed dentine and triggers a change in the rate of flow of dentine fluid within the dentine tubule(s), and the resultant pressure change across the dentine activates intra-dental nerve fibres to cause immediate pain. DHS is similar to any other condition involving subjective experiences, such as pain, in that there is a difference in reported hypersensitivity of patients displaying the same exposure to aetiologic factors. Thus the clinical observations are not necessarily correlated with the degree of sensitivity reported by the patient. Such an apparent mismatch between the clinical condition and the extent of discomfort experienced by the patient complicates the management of DHS. This disparity may also raise the question ‘Why do some patients who have exposed roots suffer from dentine hypersensitivity yet others with exposed roots do not?’.

The weight of evidence suggests that this may occur not only because of the subjective nature of pain, but also because of the natural process of tubule occlusion. Blocking of the dentine tubule can occur over extended time periods as a result of precipitation of calcium phosphate complexes triggered by proteins in saliva.6 For a number of years it has been known that both calcium and phosphate ions in saliva can remineralize tooth defects, such as early carious lesions. Research into the mechanism of natural desensitization suggests that calcium and phosphate ions, associated with salivary glycoproteins, can also facilitate tubule plugging.6 The role of plaque in the aetiology of DHS is controversial.28 Some clinicians25^,29 report that plaque is not a significant factor in DHS. However, other clinicians9 proposed that plaque played an important role, possibly due to the production of acids, which may affect the patency of the dentine tubules by the dissolution of the smear layer. It may also be possible that the importance of plaque as a factor in DHS depends upon the patient type. For example, it is recognized that DHS is generally associated with good oral hygiene practices in periodontally healthy patients.25 Regardless of whether plaque is a significant cause of lesion initiation, the importance of good plaque control is beyond dispute. However, there is also the possibility that a patient's oral dental hygiene may be affected by the discomfort arising from DHS and this may, in turn, increase the risk for both caries and periodontal diseases. There is therefore a compelling clinical reason for dental professionals not only to recognize, assess and manage DHS, but to address a patient's comfort and quality of life during the management of the condition.

Management of dentine hypersensitivity and underlying conditions

From the literature, it is evident that a number of different therapeutic approaches have been used for the treatment of DHS. Currently, these therapeutic approaches include:

Monitoring is essential in any management strategy and this may be the most important component of the management strategy when implemented in dental practices. The Expert Forum considered a number of published management paradigms, including Schuurs et al.30, Addy and Urquhart31, Gillam et al4, Drisko32, Orchardson and Gillam33, Drisko34, West35, Porto et al.36 It was decided that, while there was considerable merit in terms of content, there was a need for a simplified management scheme, which should be easier to incorporate into clinical practice for the general dental setting. After careful consideration, the Forum proposed a simplified management scheme (Figure 1). This scheme is elaborated in the following sections starting with a section on patient screening.

Screening

As suggested in the recommendations of the Canadian Advisory Board of Dentin Hypersensitivity,13 all dentate patients should be actively screened for dentine hypersensitivity by dental professionals at both the initial and subsequent check-ups (dental examinations), because DHS is frequently unreported by the patient. A simple but effective strategy is to ask patients whether they have, or have had, any problems with sensitive teeth (discomfort) recently or since their last visit. This simple strategy should ’capture’ the vast majority of dentine hypersensitivity sufferers, thus enabling the dental professional to manage the problem more thoroughly.

History

Once the dental professional has identified that the patient has a problem with sensitive teeth, it is essential to let the patient use his/her own words to describe both the symptoms and stimuli that trigger pain. At this stage, dental professionals should avoid putting words in the patient's mouth (leading the patient to a diagnosis). Once the pain characteristics have been described by the patient, the dental professional can use ‘closed questions’ in order to confirm the diagnosis, for example: ‘Does the pain persist when you drink cold drinks?’ or ‘Does the pain linger once you have stopped drinking your drink?’

It is important therefore to obtain and record the patient's dental and medical history. It is also advisable to check for any history of an excessive intake of acid food and drink (eg citrus juices and fruits, carbonated drinks, wines or ciders) in the diet, as well as to consider evidence of gastric reflux and eating disorders prior to considering a management strategy. This is because, once gingival recession occurs, the cementum covering the dentine surface can be removed easily, thereby exposing the vulnerable underlying dentine (lesion localization). This may subsequently be followed by the removal of the smear layer through acid erosion from dietary acids opening the dentine tubules (lesion initiation).9

Clinical examination

The clinical examination should ideally include an assessment to identify all sensitive teeth. This examination could involve triggers such as thermal and evaporative stimuli (eg a short blast of cold air from the 3-in-1 syringe), or mechanical/tactile stimuli (eg running a sharp explorer over the area of exposed dentine).25 The application of a controlled stimulus would be expected to result in a short sharp pain that generally lasts just for the duration of the stimulus. However, pain/discomfort may sometimes continue for a short time post stimulation, particularly if the patient has severe dentine hypersensitivity. This assessment can also be used to assess the severity of the patient's DHS (see ‘Assessment of DHS severity’).

Differential diagnosis

DHS can only be diagnosed by exclusion of other potential causes for the patient's sensitivity. Hence the information provided by the screening questions, patient history and clinical examination is essential in order to exclude dental diseases and dental defects, such as dental caries, pulpitis, cracked tooth syndrome, fractured restorations, gingival inflammation, chipped teeth, fractured restoration and TMJ disorders.13^,33^,36

Other pain symptoms, such as dull and throbbing pain, pain that persists after the stimulus has been removed, pain that may keep the patient awake at night, the need for pain relief (medication), pain irradiating from other sites in the mouth (referred pain), pain occurring at the chewing/biting surfaces, may be an indication of other dental diseases or defects that would warrant further investigation (for example, pulp vitality [sensibility] testing, diagnostic radiographs, etc).

Once the dental professional has excluded other potential causes of pain symptoms, typically associated with DHS, a more definitive diagnosis of DHS can be reached. This will enable the dental professional to manage the condition effectively.13^,33^,35^–36

Assessment of dentine hypersensitivity severity

It is advisable to record the severity of DHS, even though such measurements are notoriously problematic owing to the subjective nature of pain. Assessments provide the dental professional with a way of monitoring the effectiveness of any management plan. These assessments also have the added advantage of increasing the involvement of the patient in the management of his/her condition. Since all assessment methods are likely to cause pain or discomfort, only one measure should usually be used (for example, an air blast from a triple syringe). If, however, the patient's DHS is seriously impacting a patient's quality of life, then multiple assessments may be justifiable, provided this provides essential additional information to manage the condition.

In general, the use of a well-controlled stimulus should help obtain a more reproducible assessment. Whatever approach for monitoring sensitivity is used, this should be addressed from the patient's perspective. Such an approach could be as simple as asking the patients whether they think that the pain/discomfort has ‘diminished’, ‘stayed the same’ or ‘increased since the last visit’. This can then be broadened to encompass questions aimed at whether any improvements have allowed them to discontinue any of their avoidance strategies. More complex scales and Visual Analogue Scales (VAS) have been extensively used in clinical trials, however, these require the patient to be trained in their use.37

Treatment planning

As DHS is not a disease per se, but rather a symptom of one or more underlying causes, it is essential that all possible conditions potentially mimicking the symptoms of DHS should be identified and eliminated prior to deciding upon a management strategy. The management of DHS should identify and aim to eliminate any underlying and predisposing factors, which could lead to lesion localization (exposure of dentine) and/or to lesion initiation (opening of tubules). By identifying and treating the underlying causes, it should be possible to reduce both the frequency and intensity of DHS episodes.

In the following sections, the most common predisposing factors have been reviewed and management strategies presented as guidance on how to manage dentine hypersensitivity and any related underlying conditions.

Dentine hypersensitivity management strategies

Gingival recession from mechanical trauma

Gingival recession is a multi-factorial condition rendered more complex by predisposing and precipitating factors.18^,38 Over-zealous toothbrushing and improper toothbrushing techniques have been associated with gingival damage and loss of gingival tissue through mechanical trauma. Once gingival recession occurs, the cementum covering the dentine surface can be removed easily, thereby exposing the vulnerable underlying dentine, which is at increased risk of DHS.9

A treatment strategy for patients where mechanical trauma is primarily responsible for the gingival recession is summarized in Figure 2, based on the DHS Management Scheme (Figure 1). This group of patients normally exhibits good plaque control with minimal gingivitis and no evidence of periodontitis.

Initiate the patient's education by showing him/her the sites with gingival recession and check what type of toothbrush (soft, medium, hard texture) the patient normally uses. If possible, assess the patient's toothbrushing technique to see if this is likely to be responsible for the gingival recession or whether there are anatomical features, such as prominent canines or premolars or thin gingival tissue biotypes38 which predispose the patient to gingival trauma. Where there is an indication to modify the patient's manual or powered toothbrushing technique, this should be implemented at this stage, together with a discussion on the importance of the role of any supplemental hygiene measures (eg floss, interdental brushes) with the patient (Figure 2).

Explain the cause of sensitive teeth and check that the patient understands what can trigger episodes of DHS. In particular, explain that frequent consumption of acidic food and/or drink may remove the protective smear layer and hence cause teeth to become more sensitive.

The use of a professional desensitizing treatment to provide instant relief for any sensitive site is recommended, as this may not only reduce the stress associated with the dental check-up, but can also improve overall patient satisfaction. Check the patient's periodontal health, if this has not been previously been checked, and then work with the patient to agree an effective oral hygiene regimen. Keep in mind that this group of patients usually exhibits a good standard of plaque control. However, it may be useful to point out to the patient that good brushing technique rather than use of excessive force is critical to good plaque control. It is often useful to demonstrate the ideal brushing force (pressure) required. Finally, record the essential details on the patient's records and check at follow-up appointments about DHS and compliance with the previously agreed oral hygiene regimen.

Dentine hypersensitivity and toothwear lesions

Toothwear refers to loss of tooth substance caused by abrasion, attrition, erosion and possibly abfraction.29 In recent years, investigators have suggested that acid erosion combined with either abrasion or attrition can significantly accelerate toothwear. Detailed in vitro and in situ studies have demonstrated that the mechanical process of brushing with a toothbrush alone has no measurable effect on enamel, and that toothbrushing with toothpaste contributes little, if anything, to the loss of enamel over a lifetime of use.39 However, studies have demonstrated that acidic foods and drinks can soften enamel, leading to significant toothwear, particularly when combined with mechanical cleaning.28 Ultimately, toothwear can lead to exposure of dentine, thus patients showing evidence of erosion/abrasion are at risk of suffering from dentine hypersensitivity.

The outline treatment strategy of DHS for patients with toothwear lesions is shown in Figure 3, following directly from the DHS Management Scheme (Figure 1). Patient education plays a critical part of the management strategy for this group of patients as it is essential to prevent, or at least reduce, the rate of toothwear and hence lesion localization. The probable cause of the toothwear should be explained to the patient as well as the location of any toothwear lesions.

The management strategy should involve pre-emptive treatment with a high fluoride professional product (eg varnish) to remineralize any softened enamel and dentine. However, this alone is unlikely to be effective, so instruction should be given to slow or prevent any subsequent future toothwear. Clearly, the measures to prevent further toothwear depend upon its probable cause. The main sources of acids are dietary (the frequency of consumption of acidic foods or drinks) or gastric (ie gastric reflux or excessive vomiting) and very rarely environmental (enamel loss caused by the patient's work environment).

Where the patient's diet is the probable cause, then the patient should be encouraged to reduce the frequency of consumption of acidic foods and drinks. In some cases, it may also be advisable to change toothbrushing practice (eg brushing before rather than after meals).28 The adjunctive use of a clinically proven desensitizing mouthwash between twice daily toothbrushing may be recommended for patients who report excessive toothbrushing frequency. Patients should also be advised to seek medical advice, where the primary cause of toothwear is either environmental or medical.

Dentine hypersensitivity and periodontal disease and treatment

Periodontal disease results in tissue damage, loss of gingival tissue and alveolar bone through biological breakdown processes and can result in gingival recession.24 Gingival recession is also a common side-effect of periodontal treatment.25 Once gingival recession occurs, the cementum covering the exposed dentine surface may be easily removed by either physical and/or chemical forces, thereby exposing the underlying dentine tubules and increasing the risk of DHS.9

Patients suffering from DHS as a result of periodontal disease or its treatment should receive a multi-phase treatment and prevention plan that addresses both periodontal health and DHS. Patient education is of paramount importance and should cover at least the points shown in Figure 4. It is vital that the patient understands the absolutely critical role played by at home oral hygiene, as well as the need to reduce periodontal risk factors by maintaining good control of systemic disease conditions such as diabetes and the need for smoking cessation.

The initial phase of management should include a periodontal assessment in order to assess what treatment, usually non-surgical, is required. Where appropriate, the possibility that the treatment may invoke temporary post-therapeutic sensitivity should be explained to the patient and consent obtained. The re-evaluation after the initial therapy phase should indicate whether there is a need to plan for a corrective phase based on the expected outcome of periodontal treatment.42 The corrective phase would typically involve the use of surgical periodontal therapy.42 Again, consideration should be given to relief of any pain associated with the treatment therapy.

Any DHS associated with exposed dentine or periodontal treatment may be managed by using a chairside desensitizing product applied by the dental professional. The application of desensitizing products, such as polishing pastes, prior to, during and after treatment, can be recommended, particularly for patients with a previous history of discomfort during such treatments. Such pre-emptive desensitization can improve patient satisfaction by making it less uncomfortable and stressful. It may also help remove a potential barrier to the patient achieving effective plaque control measures at home following periodontal treatment.

Experience has shown that an evolutionary approach to improving oral hygiene is more likely to be successful in the longer term than a revolutionary one.

Concluding remarks

After a careful review of the published literature, the DHS Expert Forum concluded that dentine hypersensitivity remains an under-reported and under-managed problem in the UK and Ireland, despite its potential to impact negatively on a patient's quality of life. The DHS Forum members therefore wish to encourage the active management of dentine hypersensitivity in ‘at risk’ patients. The DHS Expert Forum recognized the need to promote simple guidelines that can be readily applied in general practice, but also agreed that a one strategy approach would not suit all patients. This article describes a DHS Management Scheme for dental professionals covering diagnosis, prevention and treatment that is linked to management strategies targeted at three groups of patient. These patients groups include:

The DHS Expert Forum acknowledges the role of industry as well as dental professionals in a continuing role in educating the public on the topic of sensitive teeth. It is therefore important that any educational activities and materials use common terminology for both dental professionals and consumers in order to reduce the possibility for confusion.