© Springer International Publishing Switzerland 2015
David G. Gillam (ed.)Dentine Hypersensitivity10.1007/978-3-319-14577-8_5
5. Advances in the Diagnosis of Dentine Hypersensitivity
Periodontology, Clinical Trials Unit, Bristol Dental School and Hospital, Lower Maudlin St, Bristol, BS1 2LY, UK
Dentine hypersensitivityOral painDiagnosisDentine
The diagnosis of dentine hypersensitivity (DH) is not a straightforward one, as the pain and clinical presentation of the condition is similar to that resulting from other oral conditions that result in tooth-related pain (Addy 2000). For example, following the bleaching of vital teeth, many individuals experience sharp, shooting pain of short duration (Tam 1999; Dahl and Pallesen 2003) which exhibits the characteristics of pain from DH. However, the aetiology of vital tooth bleaching is the result of direct irritation of the vital pulpal tissue by hydrogen peroxide, which from in vitro studies has been shown to penetrate enamel and dentine (Patri et al. 2013; Cooper et al. 1992). This is in contrast to the currently accepted hydrodynamic theory of DH working on the concept that sensitive dentine is based on the stimulus-induced fluid flow in the dentine tubules and consequent nociceptor activation in the pulp/dentine border area (Matthews et al. 2000). Similarly, both DH and pulpitis illicit a sharp pain response following the application of a thermal stimulus (Bender 2000; West et al. 2013a), and other conditions such as caries, marginal leakage of restorations, composite contraction and chipped, cracked, grooved or fractured teeth result in similar pain responses (Porto et al. 2009; Gernhardt 2013; Gillam 2013). These conditions can be differentiated from DH with clinical observation, for example, a cracked cusp will give pain upon release of biting.
Certain clinical features and patient practices, such as exposed dentine as a result of gingival recession or enamel tooth wear, a diet high in acid intake smoking and excessive brushing, are associated with DH (Addy and West 2013), and their presence or history might suggest that DH is the cause of the pain reported. Sufferers from xerostomia not only have a higher risk of erosion and potentially DH but also of caries as a result of reduced saliva flow (Grisius 2001). The effect of overzealous brushing can lead to the exposure of radicular dentine and, when in combination with erosion, coronal dentine exposure, which can result in DH (West et al. 2012), especially in the cervical region.
However, not all individuals with exposed dentine suffer from DH. Often the dentine tubules are occluded, most often due to surface coverage with oral debris creating a smear layer or toothpaste ingredients such as silica or stannous particles (Banfield and Addy 2004; Claydon et al. 2009; White et al. 2007). Alternatively, age-related changes such as the deposition of secondary dentine and fibrosis of the pulpal tissue result in reduced DH (West et al. 2013b).
Although the term DH is familiar to the dental profession (Addy and West 2013), there is little evidence to indicate that hypersensitive dentine differs in any way from normal dentine and the pain mechanisms are probably the same, sensitive dentine looking clinically the same as nonsensitive dentine. The status of the pulp in DH is not known although symptoms would suggest it unlikely that there is an acute or chronic inflammation due to the length of time symptoms persist. Most investigations report no correlation between pathology and symptoms (Seltzer et al. 1963; Tydesley and Mumford 1970); however, ethically, studies are fraught with difficulty. The term ‘dentine hypersensitivity’ can be questioned, with perhaps ‘dentine sensitivity’ being a more accurate description although not used as often (see Chapter 1). Thus, while helpful in diagnosis, the presence of features indicative of DH, such as exposed dentine, alone can only suggest that this might be the cause of a patient’s pain.
DH is known to be an episodic condition (Addy 2002), often more prevalent in cold weather and in practicing certain habits, e.g. frequent highly acidic diet. This observation may be as a result of a dynamic equilibrium between the opening and closing of the dentine tubules during daily activity and toothbrushing (Adams et al. 1992). Hence the twice-daily instruction to patients for the use of occluding toothpaste formulations with potential acid-resistant properties (Mason et al. 2010), which may maintain tubule occlusion and reduce or negate any pain symptoms associated with DH (West et al. 2012).
This similarity between the pain and symptoms of DH and the pain initiated by other oral conditions, together with the fact that the oral features suggestive of DH are also common to other oral diseases and complaints, makes the diagnosis of DH problematic. The difficulties in diagnosing DH may account for the lower figures for DH detected clinically than by self-reported questionnaires observed in several studies which used both measures of assessment (Dhaliwal et al. 2012; Ye et al. 2012; Que et al. 2010) (see Chap. 3). Furthermore as it has also been reported that in some instances DH can also adversely affect the quality of life of individuals (Bekes et al. 2008; Boiko et al. 2010), an accurate diagnosis is paramount before any treatment is recommended by the clinician (see Chap. 9). This chapter (5) provides up to date guidance to help with the diagnosis of DH in general dental practice, together with methods of quantification of pain more suited to clinical trials which examine the efficacy of desensitizing products.
Current Approaches to Diagnosing Dentine Hypersensitivity
In the absence of a definitive test for DH, a differential diagnostic approach is utilised whereby other conditions are eliminated by the use of diagnostic tests for other oral conditions, together with the completion of a comprehensive medical history and in particular pain history (Porto et al. 2009; Terry 2011; Gillam 2013). Only once conditions with similar symptoms and presentation have been eliminated is it possible to arrive at a definitive diagnosis of DH.
Several studies have examined the literature and suggested guidelines for the diagnosis of DH (Canadian Advisory Board 2003; Gernhardt 2013); Gillam et al. 2013). As DH is relatively common, with recent studies in Europe, Brazil and India reporting prevalence figures of approximately 42 % in 18–35 year olds, 33 % of over 35 year olds and 42 % of patients attending a dental school, respectively (West et al. 2013a; Costa et al. 2014; Rane et al. 2013), and knowing that the condition may also negatively affect the quality of life (Bekes et al. 2008; Boiko et al. 2010) (see Chap. 9), it is therefore suggested that all patients attending routine dental appointment reviews should be asked whether they have experienced sensitivity on any of their teeth. Screening for DH has however, been reported to be uncommonly undertaken by clinicians (Canadian Advisory Board 2003; Gillam et al. 2013). If pain and sensitivity is reported, the diagnosis of DH should be determined together with a thorough medical and dental history which explores the nature of the pain, sharpness, intensity, duration, how many teeth are involved, stimulating and relieving factors that cause the pain as well as relevant information about recent tooth bleaching procedures and dietary habits, which may provide clues to the underlying cause (Terry 2011; Porto et al. 2009) (see Chap. 4). Questions should be phrased in such a way that patients are not led to the answer (Gillam et al. 2013). Classically the pain of DH is short and sharp and of limited duration (Holland et al. 1997). The dull throbbing ache type of pain of long duration is likely to be of pulpal pathology in origin and not due to DH (Addy 2002).
The medical history should be followed by a comprehensive clinical oral examination, in which the clinician looks for obvious defects that might account for the pain reported by the patient and undertakes tests to confirm or reject potential causes (Gillam et al. 2013). Most conditions which result in a pain that is similar to that caused by DH can be diagnosed through the use of diagnostic radiographs or tender tooth testing, and if these tests are negative, then DH may be considered as the potential cause. One of the commonest differential diagnoses to DH is the cracked cusp, determined by pain upon release of biting and usually affecting only one tooth, which is rare in sensitivity where a number of teeth are usually affected (see Chap. 4). It can also be more difficult to diagnose other conditions, for example, atypical odontalgia which occurs in the absence of detectable pathology (Gillam and Orchardson 2006), but if it is demonstrated that the pain is short-lived, is sharp in onset and occurs in response to stimuli known to initiate DH, then DH is indicated as the cause of the patient’s pain (Terry 2011).
Assessing the extent and severity of DH is achieved by stimulating the teeth thought to be sensitive with stimuli known to elicit a hypersensitivity response. Such stimulation will inevitably cause the patient pain and this must be taken into account when interpreting a patient’s response. People’s pain perceptions and expectation of pain also must not be underestimated. In a study by Addy et al. (2007), participants had a number of teeth which exhibited sensitivity to a cold air stimulus. When one of these teeth was stimulated, volunteers described and scored pain, although the teeth were completely shielded and the participant could not have experienced any pain.
The information from such assessments indicates whether pain is localised or more general in nature as well as the intensity of the pain which in turn will determine the treatment planning pathway (Gillam and Orchardson 2006). Although DH can be initiated by a number of stimuli, not all are useful in assessing DH in practice. An osmotic stimulus for example, sugar may give a hypersensitivity response but is hard to control as it diffuses into the dentine fluid making accurate repeat assessments impossible in a short time period as the difference in osmotic potential between the inside and outside of the tubule reduces. The use of electrical stimulation is also not recommended (Holland et al. 1997). Although a benefit of such stimuli is that the amount of stimulus required to achieve a sensory response can be readily measured, nevertheless no correlation was reported between the electrical current threshold and pain scores obtained after stimulation with air blasts or cold (Nahri et al. 1991; Kontturi-Narhi and Narhi 1993). These findings coupled with the fact that electrical stimulation is not really clinically relevant in assessing pain associated with DH would suggest that this approach should not be recommended as a diagnostic tool for assessing DH (Gillam and Newman 1993). Furthermore it should be noted that most of these stimuli would be unsuitable for use in clinical practice apart from the use of an air blast from a cold air syringe and a explorer probe, together with a subjective assessment of the patient’s pain score (see below).
To determine the hypersensitivity response to a mechanical stimulus, a conventional or pressure-sensitive sharp dental probe can be employed. The latter provides a measurable, reproducible force (Yates et al. 1998). The Yeaple probe delivers a force which can be increased at 5 g intervals, up to a force of 70 g, stopping when pain is elicited or if no pain is experienced, the tooth being considered not sensitive (Garcia-Godoy 2013). The probe is walked over the area of exposed dentine in incremental horizontal lines. Often only a small area of dentine will respond. However, not all hypersensitive teeth respond to tactile stimulation (Flynn et al. 1985), and has been considered to be a less invasive procedure than that of a cold air blast (Gillam and Newman 1993). The Yeaple probe technology may however be problematic in that if the force is exceeded, there is no mechanism to detect or highlight this increase in force. Nevertheless, mechanical stimulation is still frequently used as part of the assessment of DH in the clinical trial setting (Gillam and Orchardson 2006; Cunha-Cruz et al. 2010; Costa et al. 2014).
Thermal and evaporative stimuli are also commonly used to assess DH (Gillam and Orchardson 2006; Cunha-Cruz et al. 2010). A short air blast is the most frequently used stimulus challenge in clinical studies seeking to determine the prevalence of DH (West et al. 2013a; Rane et al. 2013; Costa et al. 2014) and is also a practical way to identify sensitive teeth in a diagnostic exam. This stimulus can be perceived as cold if it is applied below room temperature or for a long period of time, so in most clinical studies, if an evaporative stimulus is required, it is applied in a short burst of 1 s, perpendicular to the area of exposed dentine and 10 mm away from the dentine, at approximately 20 °C (West et al. 201a3; Rahiotis et al. 2013). Of the stimuli that provoke DH, the application of cold has been shown to cause a greater pain response than other stimuli (Gillam and Newman 1993), and for this reason, it is not always appropriate to choose this as a stimulus. For clinical trials it is recommended that stimuli should be used in the order of pain evoked. Ideally two stimuli should be applied (Holland et al. 1997; Canadian Advisory Board 2003) (with the least invasive stimulus used before the more invasive stimulus), with an appropriate interval between them such that their effects do not overlap and the pulp has time to recover, about 5 min. Frequently the stimuli chosen are a mechanical stimulus such as an explorer probe, which is recommended to be moved in the mesiodistal direction on the area where dentine is exposed (Oktay et al. 2008; Miglani et al. 2010), followed by an evaporative stimulus such as an air blast (Gillam and Newman 1993; Gillam et al. 2002; Rahiotis et al. 2013; Costa et al. 2014). For a DH diagnosis in clinical practice, however, tactile stimulation of a tooth may be better employed to identify specific areas of sensitivity after an evaporative stimulus such as a blast of air has been used to identify the sensitive tooth provided a suitable time interval has been achieved (see above).
Following a diagnosis of DH an assessment of the patient’s pain may be undertaken. This is particularly important in clinical trials of DH where the efficacy of treatments is being tested. Pain assessments are difficult as pain is highly subjective in nature (Gillam et al. 2000), and the response to pain stimuli may be modified by factors such as the situation in which the pain is encountered (Dworkin and Chen 1982) and the anxiety felt by the patient (Oktay et al. 2008). In addition, in the clinical trial setting, pain scores are subject to the placebo effect (West et al. 1997), in which the expectation of receiving an effective pain relief treatment can result in reduced pain scores in all trial participants including those who have been randomised to control products. Trial participants may also temporarily alter their behaviour as a result of taking part in the trial (the Hawthorne effect) although the magnitude of the Hawthorne effect is not clear (McCambridge et al. 2014) (see Chap. 7).