Dentin hypersensitivity (DH) or dentin sensitivity (DS) is ‘pain derived from exposed dentin in response to chemical, thermal, tactile or osmotic stimuli which cannot be explained as arising from any other dental defect or disease’ (Canadian Consensus Document 2003). The pain is rapid in onset, sharp in character and transient in nature: the sharp pain lasts only as long as the stimulus is present. DH can present at any age, and is particularly common in patients who have had periodontal disease or tooth surface loss.
Dentin hypersensitivity affects 10–20% of adults and has a substantial impact on lifestyle and quality of life (QoL) (Cunha-Cruz & Wataha 2014). Unfortunately, it is neither routinely identified nor effectively managed by the general dental profession. Furthermore, whilst there is a plethora of products available for both professionally applied (in-office) and at-home [over-the-counter (OTC)] products, general dental practitioners lack confidence in managing DH effectively.
Prevalence
Dentin hypersensitivity is a common condition with a prevalence reported to be up to 57% (Irwin & McCusker 1997, Taha 2015), although a more reasonable estimate is 10–20% of the population (Cunha-Cruz & Wataha 2014). One of the problems in determining prevalence is that screening for DH is not routinely conducted, except when prompted by patients. This difficulty is exacerbated by differences in the populations investigated in different studies and in the settings and the clinical methodologies employed to assess DH, as well as variations in patients’ perception of pain. A further consideration is the apparent differences in perception between the patient who self-reports DH and the clinician who diagnoses and treats it.
The following discussion of three of these issues shows that it is reasonable to conclude DH is under-estimated in general dental practice and is not effectively managed by clinicians.
Impact of methodology on prevalence data
An example of these difficulties is the way prevalence data are usually dependent on the methodology employed in the various studies:
- In general terms, the results from questionnaire studies rely on the patients’ perception of the condition, which tends to overestimate the problem. Overestimation of DH is due, in part, to the patient's difficulty in remembering the type of dental pain they have experienced when asked to complete a questionnaire on dental pain
- This disparity creates some confusion as to whether the condition is under- or overestimated, and as such needs to be investigated in well-conducted studies
Patients’ perception of dentin hypersensitivity
Published questionnaire studies have highlighted that most patients do not perceive DH as a severe dental problem and, consequently, fail to seek treatment from their dentist or self-treat with recognized over-the-counter products. This conclusion is supported by studies that suggest most individuals do not seek desensitizing treatment because they do not perceive DH as a severe oral health problem (Table 1.1). For example, in a study by Dhaliwal et al. (2012), out of the 650 patients who complained of DH only 15.1% (n = 98) received treatment from the dentist; most patients (84.9%, n = 552) did not attempt to seek treatment from their dentist, preferring instead to self-treat with a desensitizing toothpaste.
Clinicians’ perception of dentin hypersensitivity
It is also apparent that most clinicians do not perceive DH as a severe problem for most of their patients, as demonstrated by a selection of studies shown in Table 1.2. For example, in the Benoist et al. (2014) study only 18% of dentists considered routinely screening for DH, and 66% did not consider it necessary to undertake a differential diagnosis. The latter is somewhat surprising given that DH is a diagnosis of exclusion and therefore, requires consideration of the other conditions with pain characteristics similar to those of DH.
Impact on quality of life
Dentin hypersensitivity is a painful, unpleasant experience and initiates changes in sufferers’ behavior, to adapt to and often modify their lifestyle for DH (Bekes et al. 2009, Bekes & Hirsch 2013). For example, many patients guard the sensitive tooth with the tongue, drink on the opposite side of the mouth, or even avoid cold food and drinks completely, as did the patient shown in Figure 1.1. Additionally, patients with a localized DH problem deliberately avoid brushing the sensitive areas, which may increase the risk of periodontal diseases and their sequelae in a susceptible patient.
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Figure 1.1: Gingival recession as seen on the upper teeth in this photo leads to the exposure of dentin. The enamel dentin junction can clearly be seen on the exposed teeth. The patient reported dentin hypersensitivity with cold and sweet stimuli.
Dentin hypersensitivity is also provoked by some routine dental procedures such as scaling and polishing, thereby making regular dental visits both unpleasant and painful for the patient (Dhaliwal et al. 2012, Lin & Gillam 2012). This discomfort adds a sense of anxiety to an already stressful experience. Preventive treatment for DH – 6such as applying a desensitizing polishing paste before carrying out any potentially painful, stress-provoking dental procedure – is recommended for such patients, to create 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 anesthetic.
Relatively few investigators have addressed the impact of DH on the patient's quality of life using QoL questionnaires such as the Dentin Hypersensitivity Experience Questionnaire (DHEQ). In the studies that have been done (Boiko et al. 2010, Gibson et al. 2010, Baker et al. 2014, Machuca et al. 2014), DH was shown to have had a major impact on patients’ quality of life. For example, in the study by Gibson et al. (2010), 28.2% of participants were unable to drink cold water without some form of discomfort, and 26.5% could not eat ice cream without discomfort. Interestingly, only 8.7% of participants claimed that they were unable to brush their teeth without some form of discomfort.
Routine assessment of impact
For many clinicians, formal QoL questionnaires are too time consuming for use in general practice; it is more practical to use a simple questionnaire asking a series of questions relating to a patient's daily activity, to achieve a similar level of understanding of the impact of DH. For example:
Which of these activities do you find you can/cannot do during your daily routine?
- Brush your teeth?
- Use a mouthwash?
- Eat/drink hot/cold food and drink?
Beyond the above questions, the dentist should also expand questioning to identify any lifestyle factors that impact on the patient's quality of life. For example, the patient should be advised not to consume orange juice before brushing his or her teeth to reduce any further damage to the tooth surface and pain associated with DH (see section on management).
Pathophysiology
Three physiological mechanisms have been proposed to explain DH:
- Direct innervation: It is thought that nerve endings extend from the pulp chamber through the dentin structure and reach the dentin-enamel junction (DEJ) (Irvine, 1988). When the dentin surface comes into contact with some outside stimuli, i.e. fluid or changes in temperature, these nerves initiate an action protentional. The drawback of this theory is that there is not enough evidence to support the presence of nerve endings in the outer surface of dentin.7
- Odontoblast receptor: It is possible that odontoblasts in dentin act as receptors and can relay pain stimuli to a nerve terminal in the pulp. However, odontoblasts are matrix forming cells and do not have the ability to transmit signals between odontoblasts and nerve terminals (Pashley et al. 1996).
- Fluid movement/hydrodynamic theories: Gingival recession exposes the underlying dentin surface, resulting in open dentin tubules, which enables external stimuli such as cold air to affect the dentinal fluid within the dentin tubules (Figure 1.2). The movement of fluid within these dentin tubules stimulates the mechanoreceptors, which activates nerve endings within the pulp–dentin complex. This in turn elicits a pain response.
The currently held view is that the process is mediated through a hydrodynamic mechanism as proposed by Brännström & AstrÓm (1972). Dentinal tubules, which are microscopic channels that extend from the enamel surface through dentin to the pulp chamber, have a major role in this theory. Within the tubules, there is an odontoblast process, which is an extension of an odontoblast, and dentinal fluid. This makes dentin a permeable structure. Molecules present within the dentinal tubules such as albumin, fibrinogen, and IgG have been shown to decrease fluid flow through dentin in vitro (Pashley et al. 1982, Hahn & Overton 1997). It is therefore likely that dentinal fluid components are involved in host defence, by both interacting directly with bacteria and products, and by reducing the permeability of dentin.
The hydrodynamic theory hypothesizes that the sensation of pain within the dentin is due to fluid movement from the pulp toward the outer dentin within the dentin tubules, causing nociceptor activation in the pulp–dentin border area. This theory is now widely accepted as the cause of DH. An open dentin tubule is exposed to the oral environment and in contact with different stimuli. Open dentin tubules are considered to be the cause of increased fluid movement that results in DH, supported by the observation that severity of DH directly correlates with the number of open dentin tubules.
Nerve fibers (A-β and A-δ) are the intradental nerve fibers associated with DH. Intradental myelinated A-β and some A-δ fibers are thought to respond to stimuli that displace the fluid in the dentinal tubules resulting in the characteristic short, sharp pain of DH.
Dentin hypersensitivity is differentiated from other types of tooth pain because A-δ fibers are mainly stimulated by the application of a cold stimulus, producing sharp pain, compared to the stimulation of C fibers which produce a dull aching pain.
However, not all stimulus transmission across dentin can be explained by the hydrodynamic theory, and alternative mechanisms may be involved. For example, cold foods and beverages may stimulate nerves directly by activating thermal receptors located on the intradental nerve endings, irrespective of the dentin fluid shifts evoked by those stimuli.
Implications for therapy
The key to understanding the hydrodynamic theory is understanding the role of fluid dynamics through an open tubule. The rate of fluid flow in a capillary tube is dependent on its radius and as a result increasing the tubule diameter by half results in a 16-fold increase in potential fluid flow. Conversely a desensitizing agent reducing the tubular diameter by half will result in the fluid flow within the tubules decreasing to 1/16th of its original rate. There are two treatment approaches for DH based on the principle(s) underpinning hydrodynamic theory:
- Tubule occlusion, which reduces fluid flow through the dentin tubules. This is achieved by either the deposition of an occluding layer on top of the dentin or the introduction of occluding material into dentin tubules
- Increasing potassium ion concentration, resulting in reduced pulpal sensory nerve activity (Talioti et al. 2014)
Etiology and predisposing factors
Several etiological and predisposing factors relating to the exposure of dentin have been implicated in the initiation of DH (Addy 1990, 2000, Addy & Pearce 1994, Chabanski & Gillam 1997):
- Gingival recession resulting from over excessive, inappropriate tooth brushing in plaque free mouths, nonsurgical and surgical periodontal treatment, and restorative treatment
- Anatomical recession. This is caused by the presence of a thin or absent buccal alveolar bone plate causing bone loss and gingival recession and hence, exposure of the dentin. Malpositioned teeth are also prone to buccal or lingual alveolar bone fenestrations and hence exposure of dentin
- Patients’ habits, e.g. stripping of the gingiva with finger nails
Additionally, plaque (as a cause of periodontal disease) and tooth wear have been proposed as predisposing factors, but these factors are more controversial as discussed below.
One of the problems when examining patients with DH is that the clinical observations with respect to these features do not necessarily correlate with the degree of sensitivity and discomfort reported by the patient. For example, some patients who have exposed root surfaces complain of DH whereas others with similar exposure do not complain of any sensitivity. This mismatch between clinical features and the extent of discomfort does makes it hard to research the causes of DH (and also complicates the planning of appropriate management decisions; see Chapter 3).
Exposure of the underlying dentin
For DH to occur dentin must be exposed. Exposure results from either gingival recession or cervical enamel loss, but initially it is gingival recession rather than cervical enamel loss that is the key predisposing factor (West et al. 2013a).
Once the dentin has been exposed, through toothbrush trauma or the effect of periodontal disease and/or its treatment (lesion localization), then the dentin tubules become exposed and subsequently open (lesion initiation). The key factor in lesion initiation is erosion. This is due mainly to erosive agents (intrinsic and extrinsic factors) such as consuming acidic drinks and intrinsic factors such as acidic gastric reflux. But it can be potentiated by abrasion (Dababneh et al. 1999), e.g. as a result of traumatic tooth brushing and/or the presence of tongue jewellery rubbing on the tooth surfaces. Gingival recession is relatively common and increases with age, e.g. it has been estimated that 23.8 million adults in the USA have one or more tooth surfaces with ≥3 mm gingival recession (Albandar & Kingman 1999). Other investigators have also reported that 50% of individuals aged 18–64 years have at least one site with gingival recession (Albandar & Kingman 1999).
A difficulty in examining the association between gingival recession and DH is that the data are limited. Nevertheless, it has been reported in one study that 23.6% of individuals with gingival recession had associated DH (Kamal et al. 2014 see also West et al. 2013b). Other investigators have also reported that the prevalence of DH associated with periodontal treatment increases following treatment (periodontal10 disease causes bone loss and increased gingival enlargement. When periodontal disease is treated, the inflamed tissues shrink to normal size, revealing the newly exposed dentin), although this discomfort may be both mild/moderate and transient (up to 4 weeks post-treatment) in nature for most of the patients (Chabanski et al. 1996, 1997, von Troil et al. 2002, Lin & Gillam 2012).
Role of plaque
The role of plaque in the etiology of DH is controversial. Several investigators have reported that it is not a significant factor. Others, however, have suggested that plaque does play a role due to its ability produce acids which subsequently affect the patency of the exposed dentin tubules (West et al. 2013a, Gillam 2015).
In general, true DH is associated with good oral hygiene practices in periodontally healthy patients. However, tooth sensitivity does arise in periodontal disease and as a result of plaque control measures, and surgical and non-surgical procedures. For this latter problem, and to distinguish it from DH, the term root sensitivity (RS) has been introduced by the European Federation of Periodontology (Sanz & Addy 2002), although prevalence data published to date do not support a distinction between the two conditions.
Regardless of whether plaque is a significant etiological factor in the initiation of DH, it is prudent to maintain the patient's oral hygiene status to prevent any further discomfort arising from DH (and to reduce the risk of caries and periodontal disease).
Role of tooth wear
More recently, several investigators have suggested that DH results from tooth wear, a phenomenon characterized predominantly by erosion which eventually exposes the dentin surface and initiates tooth wear lesions (Addy 2000, 2005). Information on the prevalence of tooth wear associated with DH appears to be limited. However, one recent study reported that approximately 29% of young people aged 18–35 years had erosive tooth wear and 42% of this subset experienced pain associated with DH; 28% of those with DH reported that this pain had a significant effect on their QoL (West et al. 2013b). An acidic (erosive) diet and heartburn were identified as risk factors for tooth surface loss.
Tooth surface loss is caused by one or more factors, including traumatic tooth brushing, consumption of acidic drinks, parafunctional habits, and acid regurgitation, therefore the history should cover medical problems. If the medical and lifestyle factors implicated in the etiology of DH are not modified during the counseling, prevention and maintenance phase of the treatment offered by the clinician, it is likely that both hard and soft tissue damage will continue, and pain arising from the condition will persist.11
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