Dentin hypersensitivity: pain mechanisms and aetiology of exposed cervical dentin

The first part of this paper will focus on pain mechanisms of dentin hypersensitivity, suggesting hypotheses in explanation. Human dentin tubules taper from a diameter of about 2 μm at their pulpal end to about 0.5 μm or less peripherally and dependent on age of the individual [1‐3]. It is also well known that the pulp is richly innervated with sensory afferents, mostly involved in pain mediation [4‐6] and that the dentin has limited innervation, yet appears highly sensitive with patency of the dentin tubules [7]. What is less well known, however, is whether the movement of the tubule contents excites the nerve endings directly, either in the inner ends of the tubules or in the superficial pulp, or whether the odontoblasts play a role in the transduction mechanism [7].

The second part of this paper will review the aetiology and risk factors associated with dentin hypersensitivity. The incidence of the condition is thought to be rising year on year due to increased longevity of life accompanied by retention of teeth and maintenance of a healthy dentition [8, 9]. Dentin must be exposed for pain to exist and dentin tubules patent. The area of dentin thus needs to be localised and the condition initiated by opening the tubules [10]. Individuals suffering periodontal disease frequently have exposed radicular dentin as do the healthy individuals from for example overzealous toothbrushing and trauma to the gingival marginal tissues, with subsequent wear of dentin. Hard tissue wear processes of the coronal tooth area are also frequently seen clinically at the cervical margin [10]. Recent changes in lifestyle, notably diet, have been shown to promote dental hard tissue loss by erosion, exacerbating the condition. Both exposed coronal and radicular dentin can be sensitive, but in the majority of cases, this condition preferentially occurs in the buccal, cervical region of the tooth or in the coronal radicular area [11].

Although much has been learnt about dentin hypersensitivity since it was first documented by Blum [12], clinical evidence-based research, particularly in respect of the pain mechanisms, is lacking and not well understood. Dentin hypersensitivity has been defined as the pain arising from exposed dentin, typically in response to chemical, thermal, tactile or osmotic stimuli that cannot be explained as arising from any other form of dental defect or pathology [13]. Tooth hypersensitivity can fit the criteria of several pain terms as described by Merskey [14] for the International Association for the Study of Pain. Pain being described as an unpleasant sensory emotional experience, associated with actual or potential tissue damage or described in terms of such damage. Perception of pain emanating from the oral cavity is also perceived as disproportionately large regarding the actual physical cause, compared with the rest of the body [15]. The pain of dentin hypersensitivity is classically, short, sharp, of rapid onset in character and of the duration of the applied suitability [16]. The question of how an appropriate stimulus applied to exposed dentin could evoke an essentially instantaneous painful response has been the subject of debate for many decades.

There has been much discussion concerning the pulpal changes, if any, associated with sensitivity pain. Much of the current opinion on dentin hypersensitivity is based on logical and sensible supposition rather than scientific evidence [10]. The status of the pulp in dentin hypersensitivity 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 [17, 18]; however, studies are fraught with difficulty due to ethical consideration. At a clinical level, even with magnification, sensitive dentin looks the same as non-sensitive dentin. There is little to indicate that hypersensitive dentin differs in any way from normal dentin and the pain mechanisms are probably the same [13]. The term “dentin hypersensitivity” can be questioned, with perhaps “dentin sensitivity” being a more accurate description. However, historically, dentin hypersensitivity has been a useful term as it has described a distinct clinical entity familiar to the dental profession [13]. Some individuals also experience a vague dull, throbbing ache, persisting for variable periods of time after the stimulus has been removed [19]. Whilst this pain sensation could be part of the condition, it does not fit the definition, utilises C fibres in the innervation process and is highly likely to be due to pulpal inflammation, needing endodontic or exdontia management [10].

In an attempt to explain dentin hypersensitivity, a number of theories have been put forward. One of the early, and most obvious hypotheses, was that dentin was innervated and therefore nerves were directly triggered by the stimulus. Histological stain techniques later proved not to be totally specific for nerve fibres [19]. Later evidence from electron microscopy revealed that nerve fibres do penetrate the dentinal tubules but only for a very short distance into the inner dentin, and mainly over the pulpal horns [20].

A further theory, termed the odontoblast transducer mechanism by Rapp et al. [21], was suggested primarily because odontoblasts are embryologically of neural crest derived mesenchymal cells. It was suggested that odontoblasts acted as receptor cells mediating changes in the odontoblasts via synaptic junctions with nerves. This could result in the sensation of pain from the nerve endings located in the pulpodentinal border. Direct microscopic techniques, as for the first theory, failed to confirm this concept with observation suggesting odontoblastic processes only extend between one third to one half of the dentinal tubule length, 0.5–1 mm from the pulpal end [22]. A space occurs between the process and the tubule wall [23], filled with dentinal fluid [24]. The reason for this phenomenon is unknown, but it is possibly involved in the pain mechanism. Further criticism of this theory stems from electrophysiological and histological studies, showing that dentin is still sensitive if irritation-induced odontoblast aspiration and nerve injury have occurred [25]. Tooth cavity preparation would destroy or disrupt the odontoblast layer and yet pain will still emanate without a local anaesthetic. Odontoblasts, however, may have a sensory function, with or without metabolic support of nerve fibres or transmission of mechanical disturbances; however, at the time, excitability was not demonstrated by intracellular electrophysiological techniques [26].

Currently, the most widely accepted theory is the hydrodynamic theory. In the nineteenth century, Gysi [27] determined that there was an outward flow of fluid along the dentinal tubules, and proposed, without research evidence, the hypothesis that appropriate stimuli applied to the dentin surface increased change of fluid flow which, in turn, triggered the pulpal nerves. Many years later, Brännström and his co-workers published over 20 years worth of studies on both human and animal models [28‐30], supporting the theory which has remained the most popular explanation to date. The theory states that sensitive dentin is based on the stimulus-induced fluid flow in the dentinal tubules and consequent nociceptor activation in the pulp/dentin border area [6]. Intradental myelinated A-β and some A-δfibres are thought to respond to stimuli that displace the fluid in the dentinal tubules resulting in the characteristic short, sharp pain of dentin hypersensitivity [7]. This type of fluid movement can be quantified by measuring the hydraulic conductance of dentin [31]. Thus, dentin with a high conductance has a low resistance, and vice versa. Human studies showed that the patency of the dentinal tubules is an important characteristic of sensitive dentin [6], with a significantly positive correlation between the density of tubules and the pain responses induced from exposed cervical dentin surfaces [32]. Further studies of extracted teeth provided compelling evidence for this requirement with sensitive teeth having many more (eight times) and wider (two times) tubules at the buccal cervical area compared to non-sensitive teeth [33]. Additionally, dye penetration to the pulp was only seen in sensitive teeth [34]. Although number and radius of tubules are relevant to fluid flow and therefore sensitivity, tubule radius is probably more important as fluid flow is proportional to the fourth power of the radius [35] hence if the diameter is doubled, the tubule fluid flow increases by 16-fold. This explains the concept of why tubular occlusion, of whatever nature, is thought to reduce the pain of dentin hypersensitivity. These features of dentin hypersensitivity lesions clearly have important implications with respect to the possible aetiological factors involved and the development of preventive and management strategies for the condition.

The definition of dentin hypersensitivity highlights a number of stimuli which can evoke a response. Evaporative stimuli such as a triple syringe air jet or cold windy weather results in desiccation of the dentin surface and is thought to increase in the outward flow of fluid in the tubules, as does a cold thermal stimulus and osmotic stimuli such as sugar or acidic fluid [36]. A thermal hot stimulus appears to result in contraction of the fluid in the tubules from in vitro research [37]. Physical stimulation is more difficult to understand, but in theory, compression of the surface such as a “stiletto heel effect” is thought to compress the surface tissue and on release cause expansion and hence increased outward fluid flow [37]. Of all the stimuli, cold is reported as most problematic and is used routinely in clinical trials as a positive stimulus [38]. Alternative interpretations of the hydrodynamic theory have been proposed including the idea that fluid movement may cause an electrical streaming potential [39, 40]. Whether this can reach proportions to electrically stimulate nerves is not known, but possible.

Recently, new evidence has emerged again promoting the possible major role of the odontoblasts in the dentin sensitivity pain mechanism [41]. The odontoblasts are closely related to the nerve endings, and biological signals are probably transduced from them to the axons and vice versa [41]. Sensory innervation only occurs in dentinal tubules with viable odontoblasts that maintain their columnar form. This relationship, critical for odontoblast behaviour, could be similar to the role that neuregulin and its ErbB receptors play in the control of cell morphology and in hyperalgesia [42]. Much is still unknown, including which proteins mediate signals between the odontoblasts and nerves and whether cilium acts as a signal integrator. Evidence demonstrates odontoblasts express mechano- and/or thermosensitive transient receptor potential ion channels (TRPV1, TRPV2, TRPV3, TRPV4, TRPM3, KCa and TREK-1) [41]. These are likely to sense heat and/or cold or movements of dentinal fluid within tubules. This highlights that the terminal web is a pivotal zone of the pulp/dentin complex for sensing external stimuli. External stimuli causing dentinal fluid movements and or odontoblasts and/or nerve complex responses may represent a unique mechanosensory system with odontoblasts acting as sensor cells in the pain of dentin hypersensitivity [42].

The aetiology of dentin hypersensitivity is based primarily on in vitro and in situ data, case report data and epidemiological surveys, not randomised controlled clinical studies. For dentin hypersensitivity to occur, the dentin surface of a tooth must be exposed (lesion localisation) and a number of dentin tubules in close proximity to each other must be patent from the pulp to the oral environment (lesion initiation) [10]. There is no evidence that there is a differentiation between coronal and radicular dentin hypersensitivity. However, another name for the condition was coined by the 2002 Workshop of the European Federation of Periodontology [43], root sensitivity, without evidence to support a different diagnosis and management strategy. Nevertheless, there are interesting differences in the dentin of crown and root, and throughout its structure. In the crown, the tubules follow a double curved course but in the root and beneath the incisal tips, the tubules take a straighter course [44]. The circumference of the dentin at the peripheral part of the root or crown is much greater then nearer the pulp, leading to the columnar appearance of the odontoblasts as they are squashed together especially over the pulp horns [45]; the convergence of this unique structural organisation estimated at 4:1 [46] or 3:1 [47]. The number of tubules per unit area and radius of the tubules increases from enamel–cemental junction (~20,000 per mm²) to the pulp (~45,000 per mm²), as does the tubule lumina [48], resulting in the water content or wetness of the dentin increasing 20-fold from superficial to deep dentin in patent tubules [48]. This may have clinical implications. If the deeper dentin is exposed to the oral environment, it has relatively larger dentinal tubules in closer proximity to each other compared to the original surface dentin structure of the tooth. This has the potential for more rapid tubular orifice fluid flow and sensitivity, greater tubular occlusion necessary to alleviate symptoms. Conversely, the opposite appears to be the case clinical, with small, newly exposed dentin lesions, exhibiting minimal tooth wear at the buccal cervical amelocemental junction, with patent tubules in the region of about 1 μm [33], often causing excruciating sensitivity in the young individual [49]. In explanation, the tooth has excellent reparative capability with reactionary and reparative dentin deposition giving rise to considerable heterogeneity in tissue structure from regular to dysplastic atubular structure [50]. The grossly worn dentition rarely being sensitive if occurring over many years, whereas rapid wear in a young adult, is often sensitive, resulting in pain symptoms. The sensitivity of dentin correlates well with tubule patency [6]. The capability and speed of the reparative processes of the tooth and resulting tubule occlusion, as well as age of the pulp, are likely to be very important factors in the susceptibility of an individual to experience the pain of dentin hypersensitivity.

Individuals will respond differently to the same risk factors influencing outcome, while other individuals will subject themselves to a particular risk factor far more often than average. When 10 volunteers imbibed 1 l of a soft acidic drink over a period of 15 days, some volunteers showed minimal erosion of enamel and others far more erosion [156]. Identification of the cause of susceptibility is unknown but likely to be due to salivary buffering and flow rate [157], pellicle thickness and charge [158], movements of the soft tissues [159], distribution and time of acidic liquid in the oral cavity [160], tooth structure [139] and remineralising potential [161, 162]. Difference in saliva flow and composition could contribute to the development of hypersensitivity by affecting the surface layer or deposition of intratubular dentin [163]. Similarly, the biotype of the gingival margin [85], oral hygiene habits such as excessive toothbrushing and consumption of copious acidic beverage often accompanied with toothbrushing soon after consumption, will predispose the individual to dentin hypersensitivity [10].

Similar to periodontal disease and many other medical conditions, there needs to be a susceptible individual who is exposed to a one or more risk factors for dentin hypersensitivity to occur.