Epidemiology of dentin hypersensitivity

As in early caries epidemiology, the literature on dentin hypersensitivity presents various puzzle pieces, and different studies seem to be partly contradictory. Cross-sectional surveys in dental offices which reveal prevalence rates of 3–5 % seem to indicate that dentin hypersensitivity might be a minor or even irrelevant problem [13, 14]. On the other hand, with a prevalence of 84.5 %, almost all patients experience hypersensitivity after periodontal treatment [8] and most practitioners in a UK sample (72 %) stated that dentin hypersensitivity is a severe problem for at least 10 % of their patients [15]. In addition, they expressed a need for appropriate scientific information on prevention and treatment.

Most review articles conclude that the prevalence of dentin hypersensitivity ranges from 3 to 57 % [16, 17] depending on the study sample. Regarding gender, women tend to be more frequently affected than men, although these differences often do not reach a statistically significant level [18‐22].

Early research found that all age groups are affected [22], but also an age peak from 30 to 40 years has been reported [18, 21, 23]. A reduction in seniors could be plausible due to the development of secondary or reparative dentin and subsequent sclerosis of the dentinal tubules accompanied by reduced sensitivity. In contrast to this, prevalence rates from 22 to 30 % in adults without clear age pattern were found in a representative Canadian sample [17].

Regarding the intraoral distribution, dentin hypersensitivity is mostly associated with exposed buccal dentin in permanent teeth [18, 24]. Addy and Pearce [25] connected that to vigorous tooth brushing. This gives a clear hint to an etiological factor for dentin hypersensitivity and was also confirmed by a recent review [26]. Supposedly, the left side is more affected due to mostly right-handed brushing.

Other potential causes of dentin hypersensitivity are erosion, gingival recessions, or abfractions per se or in combination with vigorous tooth brushing. They are thought to result in exposed cervical dentin, open dentin tubules, and painful sensations to thermal, tactile, or other stimuli [24, 27‐30]. Thus, the etiological factors clearly explain the intraoral distribution with a high preference for the buccal surfaces.

In general, maxillary teeth seem to be more affected than the mandibular [25], but this often fails to reach a statistically significant level [18]. The distribution among teeth favors premolars, for instance, in Gillam et al. [31] with 30.6 % being affected compared to canines with only 14.9 %. On the other hand, there is only one canine for two premolars, and dividing the premolar rate by two gives almost identical values for premolars and canines. The very detailed recording in a recent Australian study reveals that the first and second premolars, the first molars, and canines are all affected at very similar rates ranging from 8 to 11 % in the maxilla and 4 to 9 % in the mandible [18]. This is also plausible, when erosion, abfractions, and/or vigorous tooth brushing are considered as etiological factors [27, 28]. As a direct result, these teeth are all in line and exposed to similar conditions.

In a survey, UK dentists were asked about their perception and knowledge on dentin hypersensitivity [15]. They stated that about 25 % of their patients suffered from dentin hypersensitivity. Furthermore, the vast majority of dentists (72 %) considered it to be a severe problem in at least 10 % of their patients. In spite of various treatment approaches such as careful brushing instructions, desensitizing toothpaste, fluoride applications, or dentin bonding agents, the dentists highlighted that certain aspects of this topic were lacking such as appropriate scientific information including prevention and treatment.

These uncertainties among dentists were also detected in a Canadian survey where fewer than half of them considered a differential diagnosis, although dentin hypersensitivity is, by definition, a diagnosis of exclusion [17]. The majority of the dentists and dental hygienists identified bruxism and malocclusion as triggers of dentin hypersensitivity even though neither has been identified as a major causative factor. In addition, 17 % of the dentists and 48 % of dental hygienists failed to identify the hydrodynamic theory as underlying mechanism. In conclusion, dentin hypersensitivity is a relevant problem for patients and dentists, but scientifically and in dental education, it has not been examined to the same extent as other oral problems.

In a very recent study, Australian dentists were a little bit more relaxed about dentin hypersensitivity: Most dentists rated the occurrence below 20 %, and the overwhelming majority clearly identified the underlying pathological mechanism, potential etiological factors as well as the appropriate hierarchy of treatment options [32].

For an epidemiologist, it is puzzling to find a range in prevalence studies from 3 to 98 % in one country for the same disorder [14, 33]. Apart from real differences, a possible explanation lies in various biases. The most obvious one is a selection bias in the recruitment of the study sample. In contrast to many caries studies with representatively selected samples, most studies on dentin hypersensitivity are restricted to highly selected populations such as patients at periodontal offices [8, 33], students [28], or hospitalized patients [34]. This explains already a lot about the variation in prevalence rate. But also “representative” studies concerning patients in general practice vary considerably. First of all, the pattern in general dentistry can also differ: In some countries and practices, the focus is on prevention, and most patients turn up for regular recall visits. In other settings, patients are mostly scheduled for restorative or periodontal treatment which shifts the study sample towards higher disease categories. This was confirmed by a national representative survey on oral health in Germany [35] where the DMFT data in adults were slightly lower than the data from a national survey in patients from dental offices in the same year [36]. In addition, it is questionable if individuals with dentin hypersensitivity automatically seek professional help, especially when dentists themselves are lacking appropriate scientific information including prevention and treatment of hypersensitivity [15].

There is also conflicting evidence for the gender distribution in dentin hypersensitivity: The numbers of affected females tend to be higher than those of males, though often failing to reach the level of statistical significance [8, 18]. A possible explanation could be that women tend to brush more intensively than men [37, 38] and that they eat more healthy fruity food items which are also erosive [39]. This combination of erosion and abrasion presents an ideal mixture of etiological risk factors for dentin hypersensitivity. Furthermore, women tend to visit the dentist more frequently [40] which results in an overrepresentation and, therefore, classical selection bias if the study sample is recruited in dental practices. In addition, women articulate health problems more willingly than men [41], which leads to further detection bias for women.

Another reason for the varying prevalence data could be that different diagnostic criteria are used in the studies. Even within the same study, prevalences differ when tactile or thermal tests are applied [42]. Thus, it is very likely that clinical tests [31], self-reporting by patients [13, 43], or the dentists’ assessment [15] result in different prevalence values for the same sample.

Another interesting point of discussion is the age distribution. Almost all studies report a reduction in prevalence for seniors, but also the number of dentate individuals, who exhibit teeth at risk, decreases with age. A similar epidemiological problem can be observed in root caries (Fig. 1). With tooth loss and edentulism, the number of teeth and individuals at risk is constantly reduced in a “classical” population. The distribution of exposed cervical dentin in Fig. 1 reflects the age distribution of dentin hypersensitivity assessed in Australian dental offices [18]. Therefore, it is important to calculate the relative risk for root caries which increases with age, meaning that the proportion of retained teeth affected by root caries grows continuously [29].

As far as dentin hypersensitivity is concerned, the relative risk could be constant, and the clear peak that is observed in patients around 40 years of age presenting with dentin hypersensitivity in dental practices might be explained by the high rate of exposed root surfaces at that age. In seniors, the lower number could simply be based on the reduced number of teeth present. In the near future, this question will be of growing importance, as the number of retained teeth increases in adults. This means a marked increase in the number of teeth and individuals at risk for exposed cervical dentin and dentin hypersensitivity will be observed in the senior population. The rise will be especially prominent if it is accompanied by improved and prolonged toothbrushing and/or erosive food components which are considered as major etiological risk factors for dentin hypersensitivity [27, 28, 44]. In countries with a long-standing history of prevention and, therefore, a high number of dentate seniors, such as Canada [45], the prevalence of dentin hypersensitivity is independent of age, at a rate of about 25–30 % [17].

Longitudinal epidemiological studies on dentin hypersensitivity hardly exist at all, but several clinical studies examine development over a few weeks, mostly in the context of the effectiveness of desensitizing agents or following dental treatment. Hypersensitivity due to procedures such as adhesive restorations, periodontal surgery, or bleaching has been examined under the term of “sensitivity,” which does not exactly reflect the situation as far as exposed cervical dentin is concerned [46]. Still, 54 % of the randomly selected control group in a study on bleaching reported mild sensitivity which decreased to 6 % after 4 weeks using a placebo gel [47]. In addition, the presence of gingival recessions increased the probability of tooth (hyper)sensitivity significantly, but this also decreased as the treatment progressed.

As mentioned above, periodontal treatment almost automatically leads to dentin hypersensitivity [48]. In a recent American study [42], the prevalence of 30 % preoperative tactile and thermal hypersensitivity increased to 67 and 76 % 1 week after periodontal surgery, depending on the diagnostic stimulus used. Including the subjective patient statement, the combined prevalence even reached 79 %. After 6 weeks, dentin hypersensitivity had decreased dramatically to almost preoperative values, even—as the authors state—without the use of desensitizing therapy. Thus, iatrogenic dentin hypersensitivity exhibits a high rate of spontaneous remission without professional treatment. There are probably some patients who apply desensitizing toothpastes on their own accord [49], but it can be speculated that dentin hypersensitivity shows the same fluctuating patterns as other kinds of somatic pain [50]. This is most likely, as in randomized clinical trials, even patients of the placebo control group experience a remission of their dentin hypersensitivity, although the reduction has been more pronounced in the test group with the therapeutic dentifrice [51‐53].