© Springer International Publishing Switzerland 2015
David G. Gillam (ed.)Dentine Hypersensitivity10.1007/978-3-319-14577-8_1
1. Introduction and Overview: Statement of the Problem
School of Oral and Dental Science, University of Bristol, Bristol, UK
Aim and Objective
It is more than three decades since dentine hypersensitivity (DH) was described as “an enigma being frequently encountered but ill-understood” (Johnson et al. 1982). Since this time, the “three Rs” of research, writing and review have, considerably but not completely, improved the understanding of DH. A number of surveys in several countries would appear to conclude that DH remains ill-understood by a considerable proportion of dental healthcare professionals (Canadian Advisory Board on Dentine Hypersensitivity 2003; Rao et al. 2010). With respect, it would not seem unreasonable or derogatory to suggest that the topic of DH has received limited attention in both dental undergraduate and postgraduate curricula. Also it would appear that the plethora of literature on the subject, which has grown enormously over relatively recent years, has been read by a minority of dental professionals. The overall aim of this book must be, therefore, to address this imbalance in the understanding of the problem. Specifically using question-based section headings, the aim of this first chapter is to provide a brief overview of DH including current concepts of the condition and possible future innovations in diagnosis, management and treatment. The objective of this chapter, therefore is to provide a basis for the Authors in the subsequent chapters to detail the specific aspects of the diagnosis, management and treatment of DH.
How Common Is Dentine Hypersensitivity?
There have been a number of surveys of the prevalence and distribution of DH in a variety of subject groups (for reviews, see Addy 2000, 2002; West 2006) (Chap. 3), but whether these surveys used selection protocols based on classical population epidemiological studies is open to question. Indeed, some of these surveys were only from patients attending dental practices or hospitals, some were based on question and answer surveys only and several predated the now agreed definition of the condition and may have included subjects that would be excluded by the said definition. One frequently quoted study was published only as an abstract (Graf and Galasse 1977). However, the average percentage prevalence across studies spanning nearly 35 years that used a dental inspection would suggest that 15 % of adults suffer from DH from one or more teeth at any one time, although much lower, 3 %, and much higher, >50 %, prevalence figures have also been published (for review, see West 2006). A recent review on the burden of DH by Cunhan-Cruz and Wataha (2014) from the published studies would appear to suggest that the best estimate of the prevalence of DH is 10 % with an average of 33 % across the studies. Despite the fact that DH can be diagnosed in individuals at the extremes of age, teenagers to octogenarians, most commonly it appears to afflict young people between 20 and 40 years old. Females have been reported to be more commonly affected than males and at a younger mean age but not all data reached statistical significance. Available distribution data mostly indicate four features of DH: Canines and first premolars, then incisors and second premolars and finally molars is the order of teeth most commonly affected; left-sided teeth are more frequently afflicted than their right-sided, contralateral counterparts; the site of predilection by far is the buccal cervical region; lesions show little or no plaque (Addy et al. 1987; Fischer et al. 1992).
What is largely missing from the prevalence and distribution data are the numbers of teeth affected and the range of pain scores experienced per individual. This lack of information makes difficult an accurate judgement of how DH impacts on the quality of life of sufferers (see Chap. 9). Thus, although DH is stated to be a common painful condition of the teeth, do 15 % of all populations in developed countries visit the dentist at any one time to report suffering from the condition? Unlikely! Indeed, do 15 % of adults who regularly attend the dentist report voluntarily as suffering from DH? Also, most unlikely! Furthermore, over many years, authors have reported DH to be cyclical, which suggests that lesions “self-heal” through tubule occlusion and then restart by tubule exposure: Is this really the case? Possibly, but other explanations are available, including seasonal variation in aetiological factors and stimuli, stimuli avoidance tactics by sufferers and periodic self-medication with home use desensitising products. All of these would preclude the need for professional intervention. At this early stage of the present chapter, it is apparent that there are important gaps in our knowledge of DH. In summary, prevalence and distribution data associates DH more commonly with younger adults, specific teeth, tooth sides and sites, good oral hygiene and possibly females. Such information must beg the question: Are these associations indicative and even supportive of present-day thoughts on the aetiology of DH? Probably!
Definition and Terminology: Hypersensitivity or Sensitivity?
At an international meeting, DH was defined as: 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 form of dental defect or pathology (‘pathology’ was subsequently changed to ‘disease’) (Holland et al. 1997, Canadian Consensus Document 2003). Essentially, the definition is a clinical descriptor of DH as a specific dental condition which needs to be distinguished from other causes of dental pain and calls out for a diagnosis of DH by exclusion (for reviews, see West 2006; Addy and Smith 2010). Moreover, the definition is recommending the continued use of the term DH, perhaps if only because of long-time common usage. This, however, does not end the long-running debate over the accuracy of the term and the conclusion of many authors that the exposed dentine is merely sensitive and therefore lesions should be termed dentine sensitivity. Whilst for many years being sympathetic even supportive of this view, the present author, clearly playing with the semantics of the definition, would like to put forward a counterargument in favour of the term DH. Available evidence indicates that lesions of DH have many more and wider dentine tubules open at the dentine surface and patent to the pulp than nonsensitive dentine (Ishikawa 1969; Absi et al. 1987). According to Poiseuille’s law, the potential for fluid flow is therefore increased exponentially in DH lesions. Thus, the affected tooth may be “sensitive” but the exposed dentine is hyper-reactive to appropriate stimuli and thereby “hypersensitive”. One condition, within the spectrum of those causing dentine pain, that should be discussed separately is root sensitivity (RS), not least because, until the publication of the definition of DH, it was considered to be the same as DH. The European Federation of Periodontology recommended the term RS to describe short sharp pain from exposed dentine of periodontally involved teeth or following periodontal treatments (Sanz and Addy 2002). Three points need to be made in support of the term: Periodontally involved teeth do not fit the definition of DH; available figures put the prevalence of RS very much higher than DH (Chabanski et al. 1996); and deep bacterial invasion of the dentine tubules has been reported in periodontally involved teeth (Adriaens et al. 1988) and thus far not in true DH.
Mechanism of Dentine Sensitivity: Does It Apply to Dentine Hypersensitivity?
Three hypotheses have been proposed to explain the sensitivity of dentine: nerves extending to the outer end of the dentine tubules, odontoblast transducer mechanism, and hydrodynamic mechanism. Significant evidence against the first two hypotheses is available but will not be propounded upon further (for reviews, see Pashley 1990; Addy and Smith 2010) (see Chap. 2). Based upon the knowledge that fluid flows outward from the pulp along dentine tubules, Gysi in 1900 proposed the hypothesis of a hydrodynamic mechanism explaining dentine sensitivity. Unfortunately, there was a wait of more than 60 years before the eloquent experiments of Brannstrom and co-workers provided evidence to turn the hypothesis into a theory (for review, see Brannstrom 1963, 1966). Essentially, the hydrodynamic theory of dentine sensitivity postulated that stimuli applied to exposed dentine, such as those listed in the definition of DH, caused an increase in fluid flow in the dentine tubules, the resulting pressure change triggering a mechanoreceptor response in A-beta and A-delta nerve fibres in and around the pulp dentine border. All stimuli applied to dentine were reported to cause an increased outward flow of fluid except heat where there was inward flow. Interestingly, when fluid flow in tubes is increased, a pressure-related streaming potential is triggered suggesting that stimulation of pulp nerves could also be electrical (Anderson and Matthews 1967; Griffiths et al. 1993). For the hydrodynamic theory to apply to DH, lesions would have to exhibit open tubules at the dentine surface and patent to the pulp. Evidence, alluded to already, indeed supports that this is the case. Furthermore, the extensive work of Pashley and co-workers into dentine permeability, including the development and use of the dentine fluid flow cell, provided strong support for a hydrodynamic mechanism explaining the pain mechanism in DH (for reviews, see Pashley 1990, 1992) (Chap. 2). Of note and over the last two to three decades, the flow cell model demonstrated that some DH treatments reduced fluid flow across dentine (Greenhill and Pashley 1981). More recently, albeit indirectly, treatments known to block the dentine tubules in vitro and in situ have been proven to be effective in DH (for review, see Addy and West 2013) (Chaps. 6 and 8).
Aetiology of Dentine Hypersensitivity: Are Lesion Localisation and Initiation Tooth (and Gingival) Wear Phenomena?
The preceding sections indicate that for DH to occur, at any site on a tooth, dentine has to be exposed (lesion localisation) and the tubule system opened (lesion initiation). Evidence concerning the aetiology of these two distinct but interrelated processes unfortunately has been drawn at best from studies in vitro and in situ and epidemiologically derived associations and at worst case reports and clinical anecdote. As no classical randomised controlled trials (RCTs) exist, proving cause and effect, available data are circumstantial albeit quite compelling. Chapter 4 will consider the aetiology in detail and a list of relevant reviews can be found in Addy and Smith (2010), so here, only the salient points will be discussed.
Lesion localisation through dentine exposure can occur by loss of enamel and/or gingival recession (with loss of cementum). Loss of enamel, outside acute trauma, is a tooth wear process involving attrition, abrasion and erosion alone or more usually in combination. Abfraction (cervical tensile stress) has been hypothesised to predispose cervical enamel to abrasion and/or erosion, but opinion is divided (for review, see Grippo 1991). Numerous publications, including a conference report (Addy et al. 2000) and a monograph (Lussi 2006), have considered these wear processes and in particular the combination of abrasion and erosion acting at buccal cervical tooth surfaces (for review, see Addy and Shellis 2006). There seems to be little doubt that erosion is a major factor in enamel loss, causing dissolution and demineralisation (softening) of this tissue. The most common source of the acid being extrinsic and dietary in nature rather than from an intrinsic source; namely gastric acid. Extensive data, drawn from developed nations, also “implicate” tooth brushing with toothpaste as the main abrasive cause of enamel loss, particularly at buccal cervical areas. Given the resistance of enamel to tooth brushing abrasion, it is further theorised that enamel loss from tooth brushing arises from the abrasion of enamel softened by erosion. Data suggest additive even synergistic effects of the two wear processes (for review, see Addy and Shellis 2006).
Exposure of dentine by gingival recession can be usefully classified as “unhealthy” or “healthy”. The aetiology of the former is quite well understood, whereas the latter is poorly explained and as with DH has been described as an enigma (Smith 1997). As dentine exposure, through unhealthy gingival recession, falls outside the definition of DH and is more relevant to RS, it will not be considered further. Reviews on healthy gingival recession using clinical anecdotes, case reports and epidemiological data cite chronic trauma, particularly tooth brushing, as the major aetiological factor (Watson 1984; Smith 1997; Addy and Hunter 2003) (see Chap. 4). RCTs of tooth brushing and “gingival recession” have been conducted but have concentrated only on recording gingival damage (lacerations or excoriations) by different toothbrush characteristics and have been of insufficient duration to measure recession. Interestingly, even surprisingly, the role of toothpaste in gingival damage or recession has rarely been discussed, particularly since toothpaste rather than toothbrushes produces the most wear to dentine. It is probable that exposure of dentine at the buccal cervical area of teeth more commonly occurs through gingival recession than enamel loss, but it has not been studied; indeed, differentiating between the two processes could prove difficult.
Lesion initiation to open the dentine tubule system has mainly been investigated by studies in vitro and in situ. Scanning electron microscopic examination of extracted teeth or replicas reveals that nonsensitive dentine has few if any open tubules at the dentine surface, whereas, and alluded to already, sensitive dentine has large numbers of open tubules (Absi et al. 1987). Assuming, with some degree of caution, that tubules in nonsensitive dentine are covered by a “smear layer” made up of collagen and hydroxyapatite (Pashley 1984), to initiate DH, such a layer has to be removed. Available topographical studies reveal that artificially induced smear layers are very acid labile, thereby implicating again erosion as a major aetiological factor in DH (Absi et al. 1992). Abrasion of dentine as an initiating factor in DH, mainly but not exclusively, has been concerned with the effects of toothbrushes and toothpaste on dentine. Toothbrushes alone are very slow to remove a smear layer and therefore have been discounted as initiating factors; nevertheless brushes, used after an acid challenge, readily open tubules (Absi et al. 1992). Tooth brushing with toothpaste, considered the most common oral hygiene practice in developed countries (Frandsen 1986), has been studied extensively for abrasive effects on the dentine including the propensity to open dentine tubules. The findings are not consistent but appear to depend on the toothpaste formulation. Most toothpaste formulations appear to remove the smear layer and body dentine by an interaction of their abrasive and detergent systems (Moore and Addy 2005). With some toothpaste products however, the loss of the smear layer is followed by tubule occlusion with abrasive particles and/or specific ingredients formulated for such a purpose: Chaps. 6 and 8 will discuss such effects under treatment options for DH. As with brushes alone, erosion appears to promote abrasive effects of toothpaste and also can detach or dissolve some tubule-occluding compounds. In conclusion, is DH a tooth and gingival wear phenomenon? Almost certainly, yes (for review, see Addy 2005)!