An underestimated problem: dentin hypersensitivity [Vol I]

25 Sep 2017 - 14054

Dentin hypersensitivity (DHS), what on earth is it?

It is a problem, a real one; a problem for the patient, and for the clinician.

DHS is defined as a “short, sharp pain derived from exposed dentin in response to chemical, thermal, tactile or osmotic stimuli which cannot be attributed to any other dental defect or disease”. So, it is painful!

It often happens that both patients and dentists underestimate this pain; we all may think that it’s not so important. Patients can be shy about complaining for this hypersensitivity, so they just change their lifestyle, avoiding any behavior that could cause pain to arise. So – maybe – our patient is just avoiding eating an ice cream with friends, because he’s afraid about having pain!


Fig. 1

Maybe we just need to talk to our patients, and to listen to them! We, as clinicians, should be able to understand patients’ problems even if there is something they are not telling us. Pain occurs when an external stimulus (hot, cold, evaporative or osmotic) contacts exposed dentin and triggers a change in the flow of the dentinal fluid. The fluid motion stimulates a baroreceptor and leads to neural discharge causing pain. DHS prevalence is varying from 4.5% to 57% depending upon the population and the criteria used to assess sensitivity, but what is sure is that it will keep increasing, because more and more adults will (hopefully) keep their teeth in advanced age, so inevitably, there will be an increasing number of exposed dentin surfaces. Symptoms may affect patients of every age, especially those between 20 and 40 years old, with a higher incidence on female subjects, and it’s spread all over the world. Patients react to cold (75%), tactile (25%) and osmotic (16%) stimuli, and the pain can affect every tooth with this distribution: premolars (38%), incisors (26%), canines (25%) and molars (12%).

According to the hydrodynamic theory, dentin hypersensitivity occurs when an external stimulus contacts exposed dentine and triggers a change in the flow of dentinal fluid. The motion of the fluid stimulates a baroreceptor and leads to neural discharge causing pain. What about the etiology? DHS is caused by exposed dentin and open tubules and this can be linked to gingival recession, loss of enamel, loss of cementum, smear layer removal or bleaching treatment. Of course the main cause for dentinal exposure is gingival recession, that can be caused by a lot of factors, such as a wrong brushing technique, periodontal disease, aging, chronic trauma or even a lot of periodontal treatment; just think about a surgical crown lengthening technique, that of course will cause dentin exposure.

We MUST consider DHS in every branch of dentistry! Periodontal disease and some treatment procedures involve a remodeling of tooth support tissues, with an apical shift of gingival margins often associated with root sensitivity (about half of patients undergoing scaling and root planning procedures according to Von Troil B, J Clin Perio 2002). Always remember to talk to your patients BEFORE treatments! If you tell them that they might suffer from DHS, you are just explaining some side effects, if you tell it after the symptoms appear, you are apologizing!

Another great reason of DHS is the loss of hard tissues, and we can find different patterns:

Attrition: tooth to tooth contact.

Abrasion: by mechanical forces from a foreign element.

Erosion: chemical dissolution by acids not of bacterial origin.

Abfractions: concentration of stress and flexion on the CEJ area.

Multifactorial etiology with possible attrition, abrasion and erosion. Erosion can be caused by extrinsic factors (acid food, soft drinks, energy drinks) or by intrinsic factors (exposure of teeth to gastric juices for G.E.R.D., hiatal hernia, chronic alcoholism or eating disorders). Trying to understand the nature of the lesion is really important. If you see sharp and shiny margins you’re facing a mechanical abrasion situation. If you find smooth, dull and concave lesions, they’re probably due t0 erosion; always try to imagine the cause of the erosion. If you see it on palatal surfaces of upper frontal teeth, you should think about eating disorders. If you have small “vulcano shaped” lesions on the occlusal surface of molars and premolars, think about gastro esophageal reflux. It’s always important to ask yourself  “why?”, because then you can find a solution!

G.E.R.D. (gastroesophageal reflux disease) is a very common disease, and it can often be asymptomatic; it can cause erosion on palatal surfaces of all the upper teeth and on occlusal surfaces of lower molars (in frontal area same damage on upper and lower teeth). From 5% to 50% of patients with GERD may have no other symptoms beyond teeth wear, and we always have to keep in our mind that it’s a potential precursor of Barrett’s esophagus, which might lead to esophagus cancer. In patients affected by bulimia we often see deep erosions on palatal surfaces of all upper teeth, wear on upper teeth is significantly higher than in lower.

Also with DSH the first step is DIAGNOSIS: we always have just one true diagnosis, and then we can have several different treatment options. Differential diagnosis is really crucial dealing with DHS; we always have to remember the definition of a “short, sharp pain […] which cannot be ascribed to any other dental defect or disease”. So, if the patient complains about pain following a cold stimulus (or maybe the patient is silent, but you realize he feels pain when you use cold water or the air spray), always ask the magic question: “how long did it last?”. If the pain quickly disappeared, start thinking about DHS! Running tests for DHS is really easy, and you can use a VAS scale to give a value to the pain.

Fig. 2

Air blast stimulation

Fig. 3

Cold water stimulation

Fig. 4

Tactile stimulation

Fig. 5

An overview on the stimuli can cause DHS

Fig. 6

Differences between attrition and erosion

Fig. 7

Typical erosion pattern in a patient with eating disorders

Fig. 8

Abfraction lesions

Fig. 9

Diffused erosions and attrition

Fig. 10

Gingival recessions



This is the end of our first issue on DHS. In the next article we will try to understand how to relieve pain in a quick and predictable way, so stay in the loop!


Cummins D. J Clin Dent. 2009; 20 (spec iss): 1–9. Zapera. YouGov, 2009.

Brannstrom M, Astrom A. Int Dent J. 1972; 22: 219-27.

Canadian Advisory Board on Dentin Hypersensitivity. J Can Dent Assoc. 2003; 69: 221-6.

Susin C, Haas AN, Oppermann RV, Haugejorden O, Albandar JM. J Periodontol. 2004; 75: 1377–1386

Von Troil B, Needlemen I, Sanz M. J Clin Periodontol. 2002; 29 (supplement 3) :173-7.

Addy M. Int J Dent . 2002; 52: 367 – 375.

Van Haywood B. Inter Dent J. 2002; 52: 7–10.

Dowell P, Addy M. J Clin Periodontol. 1983; 4: 341-50.

Kleinberg I. Dent Today 2002; 21: 42-7.

Chesters R. J Clin Periodontol. 1992; 19: 256–261.

Vasconcelos A. Acta Odontologica Scandinavica. 2012; 70: 337–34.

NathooS J. Clin Dent 2009, 20 special issue: 123-130

Ayad F et al. J Clin Dent 2009. 20 special issue: 10-16