Skip to main content
International Dental Journal logoLink to International Dental Journal
. 2020 Oct 30;66(1):49–57. doi: 10.1111/idj.12206

Prevalence of dentinal hypersensitivity and study of associated factors: a cross-sectional study based on the general dental population of Davangere, Karnataka, India

Ryana Kour Haneet 1, Laxman Kharidi Vandana 1,*
PMCID: PMC9376521  PMID: 26582076

Abstract

Background: Dentin hypersensitivity (DH) is a common clinical finding with a wide variation in prevalence and aetiological factors. The aim of this cross-sectional study was to determine the prevalence and examine some associated aetiological factors of DH in a study of an Indian population residing in and around Davangere district of Karnataka. Material and methods: A total of 404 patients (3,859 teeth) were examined for the presence of DH by means of a questionnaire and intraoral tests (air and tactile stimuli). Plaque, gingival recession, abrasion/erosion, labioversion and toothbrushing habits were noted. Results: A total of 795 teeth, in 404 patients, were diagnosed as having DH, giving an overall prevalence figure for DH of 20.6%. The chi-square test and the Z-test values for proportions were used to evaluate statistical correlations. The 36–45 years’ age group was the cohort with the highest number of subjects with DH, and female subjects had greater predilection for DH compared with male subjects. Incisors were the tooth type most affected. DH was significantly correlated with gingival recession, labioversion and abrasion/erosion (P < 0.05). Both gingival recession and abrasion/erosion were significantly correlated with brushing once daily in a horizontal direction and use of a toothbrush with medium-hardness bristles (P < 0.05). Conclusion: The prevalence of DH in the Indian population is 20.6%, with a higher predilection for DH in the age cohort 36–45 years and in female subjects. DH is a multifactorial entity with several aetiological factors, making its diagnosis and treatment a challenge for the clinician.

Key words: Dentin sensitivity, prevalence, cross-sectional studies, gingival recession, toothbrushing, dental plaque

INTRODUCTION

Apart from carious destruction resulting in pulpitis or postoperative hypersensitivity, dental pain can be attributed to dentin hypersensitivity (DH), which is characterised by a short, sharp pain originating from exposed dentin in response to stimuli, typically thermal, evaporative, tactile, osmotic or chemical, and which cannot be ascribed to any other form of dental defect or pathology1.

Dentin may become exposed via several means (lesion localisation)2. Regardless of the aetiology of dentin exposure, one feature appears to be common and that is open dentinal tubules (lesion initiation), which provide a direct link between the external environment and the internal pulp of the tooth3. When the exposed dentin comes into contact with externally introduced tactile, thermal or chemical stimuli, painful sensations can arise4.

From the literature it is apparent that other terms are used to describe this clinical condition, for example, cervical dentine sensitivity (CDS), cervical dentine hypersensitivity (CDH), dentine sensitivity (DS) or root dentine sensitivity (RDS)/root dentine hypersensitivity (RDH), which describes sensitivity arising from periodontal disease and its treatment. However, the sensitivity that occurs following periodontal therapy may be distinct from the DH that occurs after hydrodynamic stimulation5. To date, the term ‘dentin hypersensitivity’ has been preferred in the published literature, partly because of its historical significance.

The widely accepted hydrodynamic theory6 explains the mechanism of dentinal sensitivity and suggests that shifts in fluid in response to hydrodynamic stimuli occur across exposed dentine with open tubules, which, in turn, mechanically activates the nerves situated at the inner ends of the dentine tubules or in the outer layers of the pulp, leading to DH6. DH, although neither life threatening nor a serious dental problem, can be a particularly uncomfortable and unpleasant sensation for patients. It dictates the types of food and drinks ingested by the patients7. Prevalence rates range from 3% to 98%, a heterogeneity that can be explained by the difference in the selection criteria used for each study sample and the diagnostic approaches8.

The risk factors leading to the exposure of dentine tubular openings and subsequent pain (e.g. gingival recession associated with overzealous oral hygiene practices and non-carious cervical lesions) are also controversial; although many have been identified, the main key factors have not been established7., 8..

A MEDLINE search using the key words ‘Dentin hypersensitivity’, ‘prevalence’ and ‘Indian population’ revealed only one cross-sectional study carried out in rural Punjabi Indians. There is a paucity of data on the prevalence of DH and the factors relating to this condition amongst the Indian population. Therefore, the purpose of this study was to determine the prevalence of DH in the Indian population and to identify the factors associated with this condition.

MATERIAL AND METHODS

The research protocol for the present study was initially submitted to the Institutional Ethical Committee and Review Board of the College of Dental Sciences, Davangere, Karnataka, India. After ethical approval, all subjects initially selected to take part in the study, and the guardians of subjects below 18 years of age, were verbally informed of the aims of the study and verbal informed consent was obtained before participation. The verbal consent procedure was approved by the Institutional Ethical Committee and Review Board, and the study was conducted in full accordance with the World Medical Association Declaration of Helsinki. A total of 404 subjects with no attachment loss, were included in the study. Exclusion criteria were: a known history of any disease requiring drugs such as analgesics, tranquilisers or mood-altering medications; periodontal therapy in the 6 months before the examination in the current study; use of desensitising toothpaste or mouthrinse in the 6 weeks before the examination in the current study; having teeth with cracks or fractures in the enamel, caries or restorations of any type; or having endodontic problems, abutment teeth and third molars. The recruitment method is explained in the flow chart (Figure 1).

Figure 1.

Figure 1.

Flowchart for enrollment of patients in the study. DH, dentin hypersensitivity; OPD, out patient department.

The questionnaire

A questionnaire and clinical examination data sheets were designed for data collection. The questionnaire included questions about the participant’s name, age, gender, occupation and medical history and on oral hygiene habits, such as the type, method and frequency of toothbrushing. Participants were also questioned about the presence of sensitivity in their teeth. A verbal rating scale (VRS) was used to record the degree of DH. Subjects who responded positively to tooth sensitivity were asked to quantify their sensitivity levels on the VRS9., 10.. In total, 3,859 teeth were stated to have DH by the patients.

Clinical examination

Subjects who reported sensitivity were tested clinically to confirm the presence of DH. The sensitivity levels of the teeth were evaluated using tactile and cold air stimuli. Tactile sensitivity was assessed using a Shepherd’s hook explorer, which was applied perpendicular to the cervical third of each tooth and the tip of the explorer was used to scratch the surface in a horizontal direction. Ten minutes after the tactile stimulus (TS), the patient’s response to cold air stimulus (AS) was assessed using a blast of cold air from dental unit triple syringe for 1 second, which was applied approximately 2 mm from and perpendicular to the tooth surface, isolating the tooth concerned from neighbouring teeth using cotton rolls11. Of the 3,859 teeth, 795 were confirmed clinically to have DH.

DH measurement using the VRS

Immediately after application of TS or AS to a tooth, the patients were asked to quantify the tooth’s sensitivity using the VRS. The VRS is a 5-point scale consisting of a list of phrases that describe increasing levels of pain intensity. Respondents select the single phrase that best characterises their pain intensity9., 10.. The phrases selected by the subjects who responded positively to DH were recorded as TS-VRS and AS-VRS, respectively, for each tooth.

For each tooth that was sensitive to either of the stimuli, plaque was measured by application of disclosing solution and quantified using the Turesky modification of the Quigley–Hein plaque index12. Gingival recession13, attrition, abrasion, abfraction and erosion14 and labioversion were recorded.

Statistical analysis

Statistical analysis was performed using SPSS version 17 (IBM, SPSS, Chicago, IL, USA). Data comparison was carried out by applying specific statistical tests, and the statistical significance of the results was measured. Categorical data were analysed using the chi-square test. The Z-test for proportions was used to analyse whether the sample average was statistically consistent with a hypothesised population average. The independent t-test was used for intergroup comparisons.

RESULTS

A total of 3,859 teeth were examined in 404 patients; 795 teeth were diagnosed clinically as positive for DH, giving an overall prevalence of 20.6%. The age distribution within subjects is shown in Table 1. Among the four age groups, the 36–45 years’ age group had the highest prevalence of DH, of 59.3% (P= non-significant among groups). The 404 study subjects were matched according to gender: 51.2% were male and 48.7% were female. The percentage of female subjects with clinically diagnosed DH was 50.3%, and that of male subjects was 36.7%. The chi-square test demonstrated a significant association between gender and DH (P < 0.05) (Table 2). The presence of DH, when assessed utilising the AS method (15.3%), was highly significant (P < 0.001) compared with the TS method (5.3%) (Table 3). The prevalence of DH according to tooth type was as follows (from most-affected to least-affected tooth type): incisor (35.6%) > premolar (29.2%) > molar (23.2%) > canine (12.1%) (Table 4). Table 5 shows a highly significant relationship between the absence of plaque and DH (P < 0.001). A role of plaque in the prevalence of DH was observed in 638 teeth. Irrespective of the toothbrushing frequency, method and toothbrush bristle-type used, the prevalence of DH was similar (Table 6). The amount of gingival recession associated with sensitive teeth showed that, overall, 56.8% of teeth with gingival recession had DH, which was a highly significant association (P < 0.001) (Table 7). The presence of DH in teeth with labioversion was 29.7%, which was highly significant (P < 0.001 (Table 8). DH was present in 7.5% of teeth with attrition, in 71.9% of teeth with abrasion and in one abfraction site, which was highly significant (P < 0.001). Amongst these conditions, the most common cause of DH was abrasion (71.9%), followed by attrition (7.5%) (Table 9). Gingival recession was significantly associated with brushing once daily (85.1%), horizontal toothbrushing (66.7%) and use of a toothbrush with medium-hardness bristles (86.2%) (Table 10). Similarly, abrasion/erosion was significantly associated with brushing once daily (81.4%), horizontal toothbrushing (64.5%) and use of a toothbrush with medium-hardness bristles (80%) (Table 11).

Table 1.

Prevalence of dentin hypersensitivity (DH) based on age

Age(years) DH
Total n(%) χ2* P value
Present n (%) Absent n (%)
16–25 102 (39.2) 158 (60.8) 260 (100) 6.05 0.10, NS
26–35 54 (49.1) 56 (50.9) 110 (100)
36–45 16 (59.3) 11 (40.7) 27 (100)
46–55 3 (42.9) 4 (57.1) 7 (100)
Total 175 (43.3) 229 (56.7) 404 (100)
*

Chi-square test. NS, non-significant.

Table 2.

Distribution of dentin hypersensitivity (DH) based on gender

Gender DH
Total n (%) χ2* P value
Present n (%) Absent n (%)
Male 76 (36.7) 131 (63.3) 207 (100) 7.53 0.007, S
Female 99 (50.3) 98 (49.7) 197 (100)
Total 175 (43.4) 229 (56.6) 404 (100)
*

Chi-square test. S, significant.

Table 3.

Distribution of dentin hypersensitivity (DH) following application of tactile stimulus (TS) and cold air stimulus (AS) methods

Method DH
Total n Z* P
Present n (%) Absent n (%)
TS 206 (5.3) 3,653 (94.6) 3,859 14.65 <0.001, HS
AS 589 (15.3) 3,270 (84.7) 3,859
*

Z-test for proportions. HS, highly significant.

Table 4.

Distribution of type of tooth according to dentin hypersensitivity (DH)

Tooth type DH
χ2* P value
Present n (%) Absent n (%)
Incisor 227 (35.6) 1,021 (31. 2) 7.10 0. 06, NS
Canine 77 (12.1) 504 (15.6)
Premolar 186 (29.2) 930 (28.9)
Molar 148 (23.2) 766 (23.8)
Total 638 (100.0) 3,221 (100.0)
*

Chi-square test. NS, non-significant.

Table 5.

Correlation between plaque and dentin hypersensitivity (DH)

Plaque score DH
t* P value
Present Absent
n 638 3,221 15.40 <0.001, HS
Mean ± SD 1.47 ± 0.71 1.05 ± 0.62
*

Independent t-test. HS, highly significant; SD, standard deviation.

Table 6.

Correlation between toothbrushing habits and dentin hypersensitivity (DH)

Toothbrushinghabits DH
Total n (%) χ2* P value
Absent n (%) Present n (%)
Frequency
Once daily 161 (56.5) 124 (43.5) 285 (100) 0.015 0.91, NS
Twice daily 68 (57.1) 51 (42.9) 119 (100)
Total 229 (56.6) 175 (43.7) 404 (100)
Method
H 120 (54.3) 101 (45.7) 221 (100) 3.69 0.15, NS
H + V 84 (63.2) 49 (36.8) 133 (100)
V 25 (50.0) 25 (50.0) 50 (100)
Total 229 (56.6) 175 (43.7) 404 (100)
Bristle type
Soft 34 (64.2) 19 (35.8) 53 (100) 1.95 0.37, NS
Medium 185 (56.1) 145 (43.9) 330 (100)
Hard 10 (47.6) 11 (52.4) 21 (100)
Total 229 (56.6) 175 (43.7) 404 (100)
*

Chi-square test. H, horizontal; H + V, horizontal + vertical; V, vertical; NS, non-significant.

Table 7.

Correlation of gingival recession (GR) and dentin hypersensitivity (DH)

GR DH
Total n χ2* P value
Present n (%) Absent n (%)
Present 109 (56.8) 83 (43.2) 638 237.1 <0.001, HS
Absent 529 (14.4) 3,138 (85.6) 3,221
Total 192 3,667 3,859
*

Chi-square test. HS, highly significant.

Table 8.

Correlation of labioversion and dentin hypersensitivity (DH)

Labioversion DH
Total n (%) χ2* P value
Present n (%) Absent n (%)
Present 68 (29.7) 161 (70.3) 3,221 (100) 30.5 <0.001, HS
Absent 570 (15.7) 3,060 (84.3) 638 (100)
Total 229 3,630 3,859 (100)
*

Chi-square test. HS, highly significant.

Table 9.

Correlation of abrasion/erosion and dentin hypersensitivity (DH)

Wasting diseases DH
Total n (%) χ2* P value
Present n (%) Absent n (%)
Absent 513 (15.5) 2,792 (84.5) 3,305 (100) 30.5 <0.001, HS
Attrition 32 (7.5) 393 (92.5) 425 (100)
Abrasion 92 (71.9) 36 (28.1) 128 (100)
Erosion 0 (0.0) 0 (0.0) 0 (100)
Abfraction 1 (100) 0 (0.0) 1 (100)
Total 229 3,630 3,859 (100)
*

Chi-square test. HS, highly significant.

Table 10.

Correlation of toothbrushing with gingival recession (GR)

GR Toothbrushing
Frequency
Total n (%) Method
Total n (%) Bristle type
Total n (%)
Once daily n (%) Twice daily n (%) H n (%) H + V n (%) V n (%) Soft n (%) Medium n (%) Hard n (%)
Present 74 (85.1) 13 (14.9) 87 (100) 58 (66.7) 21 (24.1) 8 (9.2) 87 (100) 7 (8.0) 75 (86.2) 5 (5.7) 87 (100)
Absent 211 (66.6) 106 (33.4) 317 (100) 163 (51.4) 112 (35.3) 42 (13.2) 317 (100) 46 (14.5) 255 (80.4) 16 (5.0) 317 (100)
Total 285 (70.4) 119 (29.4) 404 (100) 221 (54.6) 133 (32.1) 50 (12.3) 404 (100) 53 (13.1) 330 (81.5) 21 (5.2) 404 (100)
χ2* 416.2 411.4 407
P <0.001, HS 0.002, S 0.01, S
*

Chi-square test. H, horizontal; H + V, horizontal + vertical; V, vertical; HS, highly significant; S, significant.

Table 11.

Correlation of toothbrushing habit with abrasion/erosion

Toothbrushing habits
Frequency
Total n (%) Method
Total n (%) Bristle type
Total n (%)
Once daily n (%) Twice daily n (%) H n (%) H + V n (%) V n (%) Soft n (%) Medium n (%) Hard n (%)
Present 57 (81.4) 13 (18.6) 70 (100) 45 (64.5) 19 (27.1) 6 (8.6) 70 (100) 4 (5.7) 56 (80.0) 10 (14.3) 70 (100)
Absent 228 (68.3) 106 (31.7) 334 (100) 176 (52.7) 114 (34.1) 44 (13.2) 334 (100) 49 (14.7) 274 (82.0) 11 (3.3) 334 (1,000
Total 285 (70.4) 119 (29.6) 404 (100) 221 (54.6) 133 (32.8) 50 (12.3) 404 (100) 53 (13.1) 330 (81.5) 21 (5.2) 404 (100)
χ2* 409.8 408.2 422.0
P 0.001, S 0.008, S <0.001, HS
*

Chi-square test. H, horizontal; H + V, horizontal + vertical; V, vertical; HS, highly significant; S, significant.

DISCUSSION

The exclusion criteria for the current study were use of analgesics, tranquilisers or mood-altering medications, use of desensitising toothpaste or mouthrinses and the presence of a restoration of any type, all of which can alter the patient’s sensation and reception of pain. Periodontal therapy can itself result in DH, which can act as a confounder whilst measuring the effects of other risk factors. Teeth having cracks, fractures in the enamel or endodontic problems can give rise to pain, which the patient may perceive as DH.

The prevalence of DH was highest in the 36–45 years age cohort (Table 1). Several investigators have also reported a high prevalence of DH in the 40-49 years age group15., 16., 17., 18.. Furthermore, a high prevalence of DH has also been reported in other age groups of 50–59 years19, 20–39 years20, 20 years and 25 years21. The differences in distribution of DH, according to age, in different studies could arise from the age compositions of the study populations. The increased exposure of cervical dentine with age peaked at 40–50 years and was followed by a decrease with age11. The age-related changes in the pulp–dentine complex, such as dentinal sclerosis and laying down of secondary and tertiary dentine, may be responsible for the decrease in DH17.

The study subjects were sex matched. The matching performed in this study minimises the error of gender bias, similarly to that in Al-Wahadni & Linden22. In the present study, the prevalence of DH was significantly higher in female subjects than in male subjects (Table 2). A number of studies have reported a higher prevalence of DH in female subjects than in male subjects in the general population15., 18., 23.. In contrast, a recent study reported that the ratio of female subjects with hypersensitivity to male subjects with hypersensitivity was 1.3:1, which was not statistically significant20. The possible reasons for the generally higher prevalence of DH in female subjects are heightened oral hygiene awareness and the difference in diet. Consequently, patterns of abrasion and erosion of dentine may differ between sexes15. The lower threshold of pain in female subjects is another reason quoted for the higher prevalence of DH in women24.

The presence of DH, assessed utilising the AS method, was highly significant (<0.001) compared with the TS method (Table 3). In the current study, a simple explorer was used for assessment of tactile sensitivity25. Teeth can show sensitivity to one stimulus but not to another. For this reason, more than one method is usually needed in a study. As there may be carryover from one method to another, the order of administration of stimuli was tactile followed by air26. It has been suggested that a minimum rest period of 10 min between each test stimulus must be applied to each tooth in order to reduce the possibility of one method having an influence on the other27. De Assis et al.28 reported mean VRS scores of 1.7 ± 0.9 and 1.5 ± 0.8 in the placebo group with AS and TS, respectively. Torwane et al.29 reported 16% of teeth with mild pain and 56% with moderate pain after AS in their Group A (treated with 30% ethenolic extract of Indian Propolis), whereas in the same group 32% of teeth had mild pain and 36% had moderate pain after TS; the authors stated that moderate DH was more prevalent than severe or mild DH.

The most common tooth type showing DH was the incisor and the least common tooth type with DH was the canine (Table 4). Several investigators have found that the teeth most commonly affected in the general adult dentate population were premolars followed by first molars11., 15., 30., 31.. However, other investigators reported mandibular anteriors to be the most common teeth affected19., 20.. There is increasing evidence31 to suggest that DH may be a tooth-wear phenomenon. Also, the most common location of recession is on the facial aspect of canines, premolars and molars32, which could explain why these teeth are the most sensitive.

The absence of plaque and the occurrence of DH was highly significant (Table 5). Plaque accumulation on tooth surfaces may lead to demineralisation of tooth structures, which could be associated with patency of dentinal tubule orifices33. It has been reported that patients who maintain good levels of plaque control are less likely to report DH34. On the other hand, patients who have significant proportions of their root surfaces covered with dental plaque report higher DH35., 36.. Plaque accumulation results in the subsequent production of acids within plaque in response to glucose exposure. This process of acid production is widely accepted to result in the demineralisation of tooth structure (enamel and dentin), as seen in caries, which can lead to the opening of dentinal tubules and thus to DH37. Despite these findings, the influence of plaque on DH remains controversial.

The role of toothbrushing as an aetiology of DH is discussed as follows. Traumatic toothbrushing in an otherwise healthy dentition is often undiagnosed in adolescents and young adults. Subclinical soft- and hard-tissue abrasion lesions are probably a precursor of gingival recession and tooth wear, and thus DH38. Chrysanthakopoulos39 reported that the horizontal brushing method, performed once daily with a toothbrush with medium-hardness bristles, is associated with gingival recession, one of the aetiological factors for DH. Addy supported the evidence of a probable link between toothbrushing (with or without toothpaste and with or without an acidic diet) and both tooth wear and DH, and also suggested that DH is a tooth-wear phenomenon31. It seems reasonable to assume that a significant degree of subclinical gingival inflammation, abrasion and early exposure of cervical dentin after toothbrushing frequently occurs, which can lead to DH40. The most brushed teeth with the lowest plaque scores exhibit the most gingival recession. This has led to the description of gingival recession/DH as ‘toothbrush disease’38. Various reviews have concluded that toothbrushing is implicated in gingival recession, but the evidence available is circumstantial rather than factual41, emphasising that oral-hygiene habits play an important role in the aetiology of DH. There is inadequate oral-health awareness in the Indian population because of various socio-economic, cultural and geopolitical reasons. Irrespective of the toothbrushing frequency, toothbrushing method and type of toothbrush used, the occurrence of DH was similar (Table 6).

The presence of DH in teeth with gingival recession (56.8%) was highly significant (Table 7). Perhaps the most important factor in the aetiology of DH is gingival recession because it results in the exposure of root surfaces. The causes of gingival recession have been reviewed42. Once gingival recession has exposed root surfaces, the cementum is rapidly lost by brushing with toothpaste and/or professional cleaning38. There is general consensus that gingival recession usually precedes DH and is perhaps the most significant predisposing condition for DH2., 43., 44..

DH was observed in 29.7% of teeth with labioversion, which was highly significant (Table 8). Tooth malpositioning, such as crowding, or orthodontic tooth movement that inadvertently repositions teeth outside the buccal plate, increase the risk of gingival recession, which, in turn, can lead to DH38. Such teeth are difficult to clean by the patient, increasing plaque accumulation, which leads to further attachment loss and recession. However, there are no data in the literature reporting the frequency of DH in such teeth.

DH was present in 7.5% of teeth with attrition, in 71.9% of teeth with abrasion and in one abfraction site, which was highly significant. Amongst these conditions, abrasion was the most common cause of DH, followed by attrition (Table 9). Peripheral dentin is covered by cementum on root surfaces and by enamel on coronal surfaces. Thus, loss of enamel can expose dentin, placing it at risk of developing DH. The loss of enamel is usually a result of the combined action of attrition, abrasion and erosion. Evidence currently available suggests that lesion initiation in DH can be induced by abrasive and erosive agents, and erosion alone is probably the most dominant factor, in synergy with abrasion, resulting in dentine wear and tubule opening2. There is increasing evidence to suggest that DH may be a tooth-wear phenomenon31. It is now considered that erosion is a more important factor than abrasion in removing the smear layer or dentinal plugs, thereby causing DH. In addition, once erosion has occurred, patients become more susceptible to subsequent abrasion, further exacerbating the loss of tooth structure and risk of DH. Attrition can also be accelerated by the presence of softened tooth surfaces following erosion2.

Gingival recession was present in subjects who brushed once daily using a toothbrush with medium-hardness bristles and brushed in a horizontal direction (Table 10). Chrysanthakopoulos39 showed that patients who applied the horizontal method of toothbrushing had more gingival recession than those who applied either the Bass technique or circular methods. The same finding was recorded for patients who used a toothbrush with medium-hardness bristles and brushed their teeth once daily. Similar findings in previous studies reported that excessively vigorous, forceful and excessive use of a toothbrush with medium-hardness bristles in a horizontal direction could cause abrasion of the gingiva. These studies reported that the frequency of brushing and the hardness of the toothbrush44., 45., 46., the duration and technique of toothbrushing (especially using the horizontal scrub technique)47., 48. and trauma from toothbrushing45., 46. were associated with gingival recession. In other studies, the use of excessive brushing force has been shown to be a major cause of gingival abrasion, and the frequency of toothbrush changing had a significant influence on the number of sites with gingival recession46. A systematic review reported that only two of 17 studies concluded that there appeared to be no relationship between toothbrushing frequency and gingival recession, whereas eight studies reported a positive association between toothbrushing frequency and gingival recession49. Other potential risk factors were duration of toothbrushing, brushing force, frequency of changing the toothbrush and brush hardness. The horizontal scrub technique of brushing using a toothbrush with medium-hardness bristles has been reported to cause gingival recession39.

Abrasion/erosion was significantly associated with once daily brushing, horizontal toothbrushing and use of a toothbrush with medium-hardness bristles (Table 11). It has been reported that the horizontal brushing technique is strongly correlated to abrasion and toothbrushing factors related to the individual (brushing frequency and brushing technique) and exerts a greater influence than material-oriented toothbrushing factors, such as dentifrice abrasivity and bristle stiffness49.

Toothbrushing plays an important role in maintaining oral health and fluoride exposure by dentifrices, providing not only protection against caries, but also some protection against dental erosion. On the other hand, abrasive wear of sound, and especially of eroded, dental hard tissues, is considered a potential adverse side effect of toothbrushing, leading to DH50. The abrasion of enamel and dentin increases with increasing abrasivity of the dentifrice51; thus, dentifrices with high abrasivity, such as whitening dentifrices, should not be used on a frequent basis.

CONCLUSION

DH is usually treated on the basis of providing symptomatic relief using various DH agents. However, the current study results suggest that the multifactorial causes of DH need to be ascertained and evaluated. It is important to identify the factors causing DH. The treatment of DH should be approached by minimising or eliminating the cause of DH and by the use of DH agents, via professional and personal (patient based) approaches, to relieve discomfort.

The prevalence of DH peaked in subjects between 36 and 45 years of age. DH was significantly correlated with gender, gingival recession, labioversion and abrasion/erosion. The AS method was three times more efficient than the TS method for detecting DH. A role of plaque in the occurrence of DH was observed. Irrespective of the toothbrushing frequency, method and type of toothbrush used, the occurrence of DH was similar. Gingival recession and abrasion/erosion were correlated with brushing once daily in a horizontal direction and with the use of a toothbrush with medium-hardness bristles. Hence, DH is multifactorial, wherein more than one causative factor always plays a role, either directly or indirectly. Therefore, it is important to identify the aetiology behind DH, and minimise these contributory factors before formulating treatment strategies.

Acknowledgement

The study was self-funded. No funding to declare.

Conflict of interest

All authors have no conflict of interest to report.

References

  • 1.Holland GR, Narhi MN, Addy M, et al. Guidelines for the design and conduct of clinical trials on dentine hypersensitivity. J Clin Periodontol. 1997;24:808–813. doi: 10.1111/j.1600-051x.1997.tb01194.x. [DOI] [PubMed] [Google Scholar]
  • 2.Addy M. Dentine hypersensitivity: new perspectives on an old problem. Int Dent J. 2002;52:367–375. [Google Scholar]
  • 3.Bartold PM. Dentinal hypersensitivity: a review. Aust Dent J. 2006;51:212–218. [PubMed] [Google Scholar]
  • 4.Chasen SA, Kaslick R, editors. Mechanisms of Pain and Sensitivity in the Teeth and Supporting Tissues: Proceedings of a Symposium. Hackensack. Farleigh Dickinson University; New Jersey: 1973. [Google Scholar]
  • 5.Lin YH, Gillam DG. The prevalence of root sensitivity following periodontal therapy: a systematic review. Int J Dent. 2012;2012:407023. doi: 10.1155/2012/407023. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 6.Brannstrom M, Astrom A. The hydrodynamics of the dentine, its possible relationship to dentinal pain. Int Dent J. 1972;22:219–227. [PubMed] [Google Scholar]
  • 7.Gillam DG, Seo HS, Bulman JS, et al. Perceptions of dentine hypersensitivity in a general practice population. J Oral Rehabil. 1999;26:710–714. doi: 10.1046/j.1365-2842.1999.00436.x. [DOI] [PubMed] [Google Scholar]
  • 8.West NX, Sanz M, Lussi A, et al. Prevalence of dentine hypersensitivity and study of associated factors: a European population-based cross-sectional study. J Dent. 2013;41:841–851. doi: 10.1016/j.jdent.2013.07.017. [DOI] [PubMed] [Google Scholar]
  • 9.Tarbet WJ, Silverman G, Stolman JM. An evaluation of two methods for quantization of dentinal hypersensitivity. J Am Dent Assoc. 1979;98:914–918. doi: 10.14219/jada.archive.1979.0182. [DOI] [PubMed] [Google Scholar]
  • 10.Ferreira-Valente MA, Pais-Ribeiro JL, Jensen MP. Validity of four pain intensity rating scales. Pain. 2011;152:2399–2404. doi: 10.1016/j.pain.2011.07.005. [DOI] [PubMed] [Google Scholar]
  • 11.Rees JS, Jin LJ, Lam S, et al. The prevalence of dentin hypersensitivity in a hospital clinic population in Hong Kong. J Dent. 2003;31:453–461. doi: 10.1016/s0300-5712(03)00092-7. [DOI] [PubMed] [Google Scholar]
  • 12.Turesky S, Gilmore ND, Glickman I. Reduced plaque formation by the chloromethyl analogue of Victamine C. J Periodontol. 1970;41:41–43. doi: 10.1902/jop.1970.41.41.41. [DOI] [PubMed] [Google Scholar]
  • 13.Sullivan HC, Atkins JH. Free autogenous gingival grafts. 3. Utilization of grafts in the treatment of gingival recession. Periodontics. 1968;6:152–160. [PubMed] [Google Scholar]
  • 14.Grippo JO, Simring M, Schreiner S. Attrition, abrasion, corrosion and abfraction revisited: a new perspective on tooth surface lesions. J Am Dent Assoc. 2004;135:1109–1118. doi: 10.14219/jada.archive.2004.0369. [DOI] [PubMed] [Google Scholar]
  • 15.Bahşi E, Dalli M, Uzgur R, et al. An analysis of the aetiology, prevalence and clinical features of dentine hypersensitivity in a general dental population. Eur Rev Med Pharmacol Sci. 2012;16:1107–1116. [PubMed] [Google Scholar]
  • 16.Rees JS, Addy M. A cross-sectional study of buccal cervical sensitivity in UK general dental practice and a summary review of prevalence studies. Int J Dent Hyg. 2004;2:64–69. doi: 10.1111/j.1601-5029.2004.00068.x. [DOI] [PubMed] [Google Scholar]
  • 17.Chabanski MB, Gillam DG, Bulman JS, et al. Clinical evaluation of cervical dentine sensitivity in a population of patients referred to a specialist periodontology department: a pilot study. J Oral Rehabil. 1997;24:666–672. doi: 10.1046/j.1365-2842.1997.00552.x. [DOI] [PubMed] [Google Scholar]
  • 18.Ye W, Feng XP, Li R. The prevalence of dentine hypersensitivity in Chinese adults. J Oral Rehabil. 2012;39:182–187. doi: 10.1111/j.1365-2842.2011.02248.x. [DOI] [PubMed] [Google Scholar]
  • 19.Dhaliwal JS, Palwankar P, Khinda PK, et al. Prevalence of dentine hypersensitivity: a cross-sectional study in rural Punjabi Indians. J Indian Soc Periodontol. 2012;16:426–429. doi: 10.4103/0972-124X.100924. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 20.Al-Khafaji H. Observations on dentine hypersensitivity in general dental practices in the United Arab Emirates. Eur J Dent. 2013;7:389–394. doi: 10.4103/1305-7456.120634. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 21.Orchardson R, Collins WJN. Clinical features of “hypersensitive” (HS) dentine. J Dent Res. 1984;63:521. [Google Scholar]
  • 22.Al-Wahadni A, Linden GJ. Dentine hypersensitivity in Jordanian dental attenders. A case control study. J Clin Periodontol. 2002;29:688–693. doi: 10.1034/j.1600-051x.2002.290804.x. [DOI] [PubMed] [Google Scholar]
  • 23.Rees JS, Addy M. A cross-sectional study of dentine hypersensitivity. J Clin Periodontol. 2002;29:997–1003. doi: 10.1034/j.1600-051x.2002.291104.x. [DOI] [PubMed] [Google Scholar]
  • 24.Wiesenfeld-Hallin Z. Sex differences in pain perception. Gend Med. 2005;2:137–145. doi: 10.1016/s1550-8579(05)80042-7. [DOI] [PubMed] [Google Scholar]
  • 25.Klienberg I, Kaufman HW, Confessore F. Methods of measuring tooth hypersensitivity. Dent Clin North Am. 1990;34:515–529. [PubMed] [Google Scholar]
  • 26.Orchardson R, Gangarosa LP, Sr, Holland GR, et al. Towards a standard code of practice for evaluating the effectiveness of treatments for hypersensitive dentine. Arch Oral Biol. 1994;39:S121–S124. doi: 10.1016/0003-9969(94)90198-8. [DOI] [PubMed] [Google Scholar]
  • 27.Ide M, Morel AD, Wilson RF, et al. The role of dentine bonding agent in reducing cervical dentine sensitivity. J Clin Periodontol. 1998;25:286–290. doi: 10.1111/j.1600-051x.1998.tb02442.x. [DOI] [PubMed] [Google Scholar]
  • 28.De Assis JS, Azevedo Rodrigues LK, Fonteles CSR, et al. Dentin hypersensitivity after treatment with desensitizing agents: a randomized, double-blind, split-mouth clinical trial. Braz Dent J. 2011;22:157–161. doi: 10.1590/s0103-64402011000200012. [DOI] [PubMed] [Google Scholar]
  • 29.Torwane NA, Hongal S, Goel P, et al. Effect of two desensitizing agents in reducing dentin hypersensitivity: an in-vivo comparative clinical trial. J Clin Diagn Res. 2013;7:2042–2046. doi: 10.7860/JCDR/2013/6005.3401. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 30.Irwin CR, Mccusker P. Prevalence of dentine hypersensitivity in a general dental population. J Ir Dent Assoc. 1997;43:7–9. [PubMed] [Google Scholar]
  • 31.Addy M. Tooth brushing, tooth wear and dentine hypersensitivity–are they associated? Int Dent J. 2005;55:S261–S267. doi: 10.1111/j.1875-595x.2005.tb00063.x. [DOI] [PubMed] [Google Scholar]
  • 32.Orchardson R, Collins WJ. Clinical features of hypersensitive teeth. Brit Dent J. 1987;162:253–256. doi: 10.1038/sj.bdj.4806096. [DOI] [PubMed] [Google Scholar]
  • 33.Kawasaki A, Ishikawa K, Suge T, et al. Effects of plaque control on the patency and occlusion of dentine tubules in situ. J Oral Rehabil. 2001;28:439–449. doi: 10.1046/j.1365-2842.2001.00682.x. [DOI] [PubMed] [Google Scholar]
  • 34.Manochehr-Pour M. Clinical evaluation of two potassium nitrate toothpastes for the treatment of dental hypersensitivity. Periodontal Case Rep. 1984;6:25–30. [PubMed] [Google Scholar]
  • 35.Trowbridge HO, Silver DR. A review of current approaches to in-office management of tooth hypersensitivity. Dent Clin North Am. 1990;34:561–581. [PubMed] [Google Scholar]
  • 36.Cox CF. Etiology and treatment of root hypersensitivity. Am J Dent. 1994;7:266–270. [PubMed] [Google Scholar]
  • 37.Wolff MS. Dentin hypersensitivity, the biofilm and remineralization: what is the connection? Adv Dent Res. 2009;21:21–24. doi: 10.1177/0895937409335618. [DOI] [PubMed] [Google Scholar]
  • 38.Pashley DH. Consensus-based recommendations for the diagnosis and management of dentin hypersensitivity. Dentin Hypersensitivity. 2008;4:1–5. [Google Scholar]
  • 39.Chrysanthakopoulos NA. Aetiology and severity of gingival recession in an adult population sample in Greece. Dent Res J (Isfahan) 2011;8:64–70. [PMC free article] [PubMed] [Google Scholar]
  • 40.Bevenius J, Lindskog S, Hultenby K. The micromorphology in vivo of the buccocervical region of premolar teeth in young adults. A replica study by scanning electron microscopy. Acta Odontol Scand. 1994;52:323–334. doi: 10.3109/00016359409029030. [DOI] [PubMed] [Google Scholar]
  • 41.Smith RG. Gingival recession. Reappraisal of an enigmatic condition and a new index for monitoring. J Clin Periodontol. 1997;24:201–205. doi: 10.1111/j.1600-051x.1997.tb00492.x. [DOI] [PubMed] [Google Scholar]
  • 42.Addy M. In: Tooth Wear and Sensitivity: Clinical Advances in Restorative Dentistry. 1st ed. Addy M, Embery G, Edgar WM, Orchardson R, editors. Martin Dunitz; London: 2000. Dentine hypersensitivity: definition, prevalence, distribution and etiology; pp. 239–248. [Google Scholar]
  • 43.Drisko C. Dentine hypersensitivity—dental hygiene and periodontal considerations. Int Dent J. 2002;52:385–393. [Google Scholar]
  • 44.Drisko C. Oral hygiene and periodontal considerations in preventing and managing dentine hypersensitivity. Int Dent J. 2007;57:S399–S410. [Google Scholar]
  • 45.Kassab MM, Cohen RE. The etiology and prevalence of gingival recession. J Am Dent Assoc. 2003;134:220–225. doi: 10.14219/jada.archive.2003.0137. [DOI] [PubMed] [Google Scholar]
  • 46.Toker H, Ozdemir H. Gingival recession: epidemiology and risk indicators in a university dental hospital in Turkey. Int J Dent Hyg. 2009;7:115–120. doi: 10.1111/j.1601-5037.2008.00348.x. [DOI] [PubMed] [Google Scholar]
  • 47.Tezel A, Canakci V, Cicek Y, et al. Evaluation of gingival recession in left- and right-handed adults. Int J Neurosci. 2001;110:135–146. doi: 10.3109/00207450108986541. [DOI] [PubMed] [Google Scholar]
  • 48.Rajapakse PS, McCracken GI, Gwynnett E, et al. Does tooth brushing influence the development and progression of non-inflammatory gingival recession? A Systematic Review. J Clin Periodontol. 2007;34:1046–1061. doi: 10.1111/j.1600-051X.2007.01149.x. [DOI] [PubMed] [Google Scholar]
  • 49.Bergström J, Lavstedt S. An epidemiologic approach to toothbrushing and dental abrasion. Community Dent Oral Epidemiol. 1979;7:57–64. doi: 10.1111/j.1600-0528.1979.tb01186.x. [DOI] [PubMed] [Google Scholar]
  • 50.Addy M, Hunter ML. Can tooth brushing damage your health? Effects on oral and dental tissues. Int Dent J. 2003;53(Spec Iss 3):177–186. doi: 10.1111/j.1875-595x.2003.tb00768.x. [DOI] [PubMed] [Google Scholar]
  • 51.Wiegand A, Kuhn M, Sener B, et al. Abrasion of eroded dentin caused by toothpaste slurries of different abrasivity and toothbrushes of different filament diameter. J Dent. 2009;37:480–484. doi: 10.1016/j.jdent.2009.03.005. [DOI] [PubMed] [Google Scholar]

Articles from International Dental Journal are provided here courtesy of Elsevier

RESOURCES