Understanding Dentin Hypersensitivity
Effective treatment depends on appropriate diagnosis, which encompasses a myriad of factors from the etiology of the condition to recognizing predisposing factors.
DIFFICULT to diagnose and treat, dentin hypersensitivity is a controversial topic as there is no consensus on what causes it or how best to manage it. The dentin hypersensitivity literature reveals unanswered questions and many oral health care providers profess little confidence in treating this condition.
The perception of pain and people’s reaction to it are both physiological and psychological. A variety of emotional elements affect pain coping mechanisms of different individuals. These pain parameters are especially relevant in dealing with hypersensitivity as they help explain the pervasive placebo effect seen with hypersensitivity treatment. Understanding what is known about the etiology of dentin hypersensitivity and knowing how to recognize predisposing factors are critical for oral health professionals involved in the prevention and treatment of hypersensitivity.
Photos courtesy of David H. Pashley, DMD, PhD, and reprinted with permission from Seltzer and Bender¹s Dental Pulp, Quintessance Publishing Co Inc.
What Is Dentin Hypersensitivity?
Hypersensitivity is a unique entity apart from other sources of dental pain, such as a fractured or leaking restoration, cracked or fractured tooth, caries, pulpitis, sinusitis, periodontal ligament inflammation, and occlusal trauma. Differentiating among these conditions is challenging because symptomology is often described similarly by patients.
Dentin hypersensitivity is often described 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.”1
Ruling out other possible causes of tooth pain is essential before making a diagnosis of dentin hypersensitivity. The short, sharp pain of hypersensitivity generally disappears when the stimulus is removed and can be differentiated from the other sources of pain described as severe, intermittent, throbbing, elicited by chewing, or occurring without provocation. A thorough assessment of symptoms and clinical findings assisted by diagnostic aids and tests can, by ruling out the presence of other conditions, confirm a diagnosis of hypersensitivity.
There is great variation in published studies concerning the prevalence of hypersensitivity. This may be due to variability in the methods of experimentally eliciting hypersensitivity and whether the data are based on self-reports or more objective assessment methods. Self-reported sensitivity data may be elevated since patients may include other conditions. One recent review describes the prevalence as ranging from less than 5% to more than 50%, suggesting that there is not an accurate prevalence figure.2 The often reported prevalence based on the average from a variety of studies is 25% of the population.3 A higher percentage is seen in periodontal practices, where the prevalence can be as high as 80% of patients.4
Which Teeth Are Affected?
Most oral health professionals know intuitively which teeth are most often sensitive. Canines and first premolars seem to exhibit sensitivity most frequently, followed by incisors, second premolars, and then by molar teeth.2,3 The area affected most often is the buccal aspect of the tooth.5 Recession is primarily a buccal phenomenon since brushing is usually more vigorous at buccal gingival surfaces.6 Recession, hypersensitivity, and toothbrushing are linked, although the relationship is still not clearly established. Recession and the often accompanying hypersensitivity are not always distributed bilaterally. This may be explained by right-handed brushers exerting more pressure on the left side, although the converse does not apply for left-handed brushers.
The Gender and Age Factors
Studies are inconsistent in demonstrating a gender-related statistical difference in incidence. However, women may report hypersensitivity more frequently than men and may be more likely to develop recession-associated hypersensitivity due to more diligent oral hygiene practices.6 Studies have demonstrated that patients do not seem to consider hypersensitivity very serious since only 32% had tried a self-help dentifrice and only 20% sought professional help.3,7 People between the ages of 30 and 40 experience and report dentin hypersensitivity most frequently, although the condition is often reported within 10 years of this age range.8 The logical reason is that prior to the second decade of life, the contributing factors of recession and dentin exposure are not as pervasive, and after the fourth decade, the benefits of natural desensitization mechanisms have begun to take effect.
Why Does Pain Occur?
The current accepted theory to explain the pain of dentin hypersensitivity has not been unequivocally proven, but has stood the test of time. The hypothesized mechanism is based on fluid dynamics, hence the name hydrodynamic theory.9,10 When a stimulus is applied to the tooth surface, there is a disturbance of the fluid within the dentinal tubule, which in turn, signals the nerve endings located near the pulp. Consequently, the nerve membrane depolarizes, inducing pain. Key to this process is that the dentin tubules must be open or patent at the extreme tooth surface end of the tubule (see Figure 1).
A sequential cascade of events leads to hypersensitivity. There are two conditions that precede open or patent tubules: 1) the protective positioning of the gingiva must be altered to expose enamel and/or cementum and 2) enamel or cementum must be lost to expose dentin. Subsequently, if the exposed dentinal tubules remain patent, sensitivity is likely to develop. When hypersensitive dentin is examined with scanning electron microscopy, a pattern of open dentin tubules is a consistent finding. This explains why some areas with recession are not hypersensitive—they do not exhibit open tubules.
Efforts to decrease or prevent loss of gingival and tooth structure are preventive. Once hypersensitivity is diagnosed, treatment consists either of blocking the tubules to inhibit fluid disturbance or blocking the nerve response.
What Are the Risk Factors?
Recession is the initiating event that leads to exposure of the dentin layer and the development of hypersensitivity. Recession is often initiated by damaging oral hygiene practices. Other factors that predispose an individual to recession include oral surgery procedures; treatment for periodontal disease; effects of periodontal diseases, such as necrotizing ulcerative gingivitis; crown preparation procedures; anatomic thin buccal plate of bone or tissue; or narrow zone of attached gingiva.
Recession becomes more prevalent throughout life. It is not a natural sequela of the aging process, but likely results from the additive effects of various insults to the soft tissue. A direct correlation between recession and hypersensitivity does not exist since recession increases with age while hypersensitivity diminishes.
- SELF-APPLIED TREATMENT OF DENTIN HYPERSENSIVITY
- PROFESSIONALLY APPLIED TREATMENT OF DENTIN HYPERSENSITIVITY
Following gingival recession, the loss of enamel or cementum presents a major risk factor for the development of hypersensitivity as the underlying dentin becomes exposed. Cementum is more easily lost than enamel because it is thinner and less mineralized. Although there are a variety of risk factors that can lead to the loss of tooth structure, the singular or combined effects of abrasion, attrition, erosion, and possibly abfraction are important considerations.
The contact between the tooth and an object like a toothbrush, abrasive particles in a dentifrice, prophylaxis paste, or a coarse diet, can contribute to abrasion under certain conditions.
Generally, the texture of the toothbrush bristles combined with the aggressiveness of the brushing lead to abrasion. Commercially available dentifrices used in a reasonable amount and with an appropriate brushing technique do not cause loss of tooth structure on their own. However, dentifrice, in combination with aggressive brushing and especially when used in an acidic oral environment favoring erosion, is a risk factor for tooth structure loss. Patients should be questioned to rule out use of self-prepared, coarse mixes of abrasive agents such as baking soda and salt.
Although the abrasion of a damaging oral hygiene regimen may be correlated with both recession and tooth loss, there is less connection between abrasion and hypersensitivity. This is because abrasion also stimulates natural desensitization mechanisms.
The tooth-to-tooth wear that can result in the loss of enamel or cementum to expose the underlying dentin is called attrition. Bruxism, initiated by occlusion or habit, is often responsible for attrition. Wear facets created by occlusal forces during chewing excursions are another example of attrition. Although these types of tooth structure loss can lead to hypersensitivity, the gradual nature of such wear stimulates natural desensitization.
A major risk factor contributing to loss of tooth structure is erosion. Erosion is caused by acids, from other than a bacterial source, eroding the tooth structure by dissolving the enamel, cementum, and/or dentin. The source of the acid can be either intrinsic, such as from gastroesophageal reflux disease (GERD), or acquired extrinsically from the diet. Damaging dietary beverages include carbonated drinks (both regular and diet sodas), sports drinks, fruit juices, wines, and, to a lesser degree, beer. The frequency of the consumption of carbonated and sports drinks is quite high, particularly among children and adolescents. Their consumption creates a habit that can be difficult to change. Until these beverages are eliminated, straw usage is suggested to decrease the acidic exposure of the teeth.
Following initial dentin exposure, continual bathing in dietary acid can continue to erode dentin and keep the dentinal tubules patent. Patent dentin tubules maintain the hypersensitivity reaction because a stimulus can affect the fluid within the tubule, which then signals the pulpal nerves. Open tubules may also transport bacterial elements inward from the oral cavity to the pulp. The localized inflammatory pulpal response adds additional discomfort. Microscopic views of dentin reveal more open tubules in hypersensitive than in nonsensitive teeth.
Although erosion itself can be problematic, it is most damaging when combined with abrasion from toothbrushes and toothpaste.11 The acid in food or beverages will demineralize the tooth structure, increasing susceptibility to abrasion. Patients experiencing chronic hypersensitivity may find relief from changing the daily sequence of morning orange juice immediately followed by an after-breakfast brushing.
Abfraction, a cervical stress-lesion, results from eccentric occlusal forces causing tooth flexure, which can create a wedge- or v-shaped configuration at the cemento-enamel junction. The significance of abfraction is still under investigation. The distinctive shape of the lesion is created by chipping or fracturing minute pieces of enamel rods. Although there may be an association between abfraction and hypersensitivity, this relationship is unclear.
What Is Natural Desensitization?
Many body systems have a mechanism for countering the effects of injury. In the oral cavity, the trauma or irritation of an aggressively activated toothbrush or heavy occlusal forces can stimulate the creation of secondary dentin on the floor and roof of the pulp chamber, creating a walling-off effect from the irritation. Another natural desensitizing phenomenon is the tertiary dentin that develops when already exposed dentin receives further trauma.
Sclerosis, a natural phenomenon of aging, provides mineral deposition within the tubule walls to decrease the tubule diameter, and subsequently, lessen the potential for fluid transmission. The development of secondary and tertiary dentin and the process of sclerosis explain why hypersensitivity generally diminishes over time and with aging.
Figure 3. Surface view of smear layer-covered dentin.
The presence of a smear layer plays a role in hypersensitivity, although the nature of that role is still debated (see Figure 2). The smear layer is a mixture of inorganic and organic microcrystalline debris that consists of components such as dentinal or cemental shavings, tissue debris, and microbial elements. It has the capacity to occlude dentin tubules by simply covering their open ends (see Figure 3). However, it is uncertain whether dentifrice abrasives remove the smear layer to accentuate hypersensitivity or contribute to the smear layer to diminish hypersensitivity. If the abrasive particles occlude the tubules, the detergent component may subsequently remove the smear layer. Dentifrice has been shown to remove the smear layer,12 which suggests that those with extreme sensitivity may benefit from brushing without toothpaste. Acidic food and beverages may also remove the smear layer, exposing patent tubules.13
Does Treatment Work?
A differential diagnosis is initially needed to rule out other possible sources of pain. Once hypersensitivity is diagnosed, assessing factors contributing to recession, abrasion, attrition, erosion, or any combination of these is important. Clinical examination combined with careful questioning can reveal evidence of contributing factors.
Commercial desensitization agents are intended to mimic nature’s own desensitizing defense mechanisms. They occlude, fill in the dentin tubule openings (simulates a smear layer), or create a precipitate within the tubule lumen (simulates sclerosis). Other treatment approaches include: blocking tubules by sealing with resins, using composite restorations to physically block the dentin from receiving a stimulus, and using agents to diminish nerve depolarization and the pain response.
The ideal desensitizing agent does not exist. Study results are variable and certain agents work best in certain circumstances and with certain individuals. Consequently, clinicians must use a systematic trial and error approach based on the available evidence and professional experience. It is often necessary to use a hierarchy of products in succession until the most beneficial is identified. The strong placebo effect suggests that the combination of management strategy, treatment agents, and positive reinforcement can create a successful outcome, regardless of whether an ideal strategy or agent is utilized.
A listing of available agents, their active ingredients, and the theorized mechanism of action is provided in Table 1. With the high prevalence of sensitivity and the variety of useful products, the astute practitioner will offer hypersensitivity treatment options. There is an American Dental Association (ADA) code (09910) for “Application of Desensitizing Medicaments.” Fees are variable across the country, ranging from $20-$50 depending on the technique used, with restorative procedures priced higher.
Individuals with hypersensitive teeth should be discouraged from bleaching or directed toward treatments with lower concentration, slower acting agents, and decreased frequency of application. With bleaching products easily accessible to the general public, the potential for abuse or over-use increases the likelihood of developing sensitivity.
Some bleaching kits are marketed with concurrent use of desensitizing agents to counteract the sensitizing effects of the bleaching acids. Both potassium nitrate and fluorides are widely used in this manner.
The hypersensitivity treatment market is in constant flux as products are discontinued and others are developed in the quest for an ideally effective agent. Clinicians need to stay aware of new products on the market and to use evidence-based assessments of their efficacy.
- Addy M. Etiology and clinical implications of dentine hypersensitivity. Arch Oral Biol. 1990;34:503-514.
- Addy M. Dentine hypersensitivity: New perspectives on an old problem.Int Dent J. 2002;52:375-376.
- Fischer C, Fischer RG, Wennberg A. Prevalence and distribution of cervical dentine hypersensitivity in a population in Rio de Janeiro, Brazil. J Dent. 1992;20:272-276.
- Chabanski MB, Gillam DG, Bulman JS, Newman HN. Clinical evaluation of cervical dentine sensitivity in a population of patients referred to a specialist periodontology department: a pilot study. J Oral Rehab. 1997;24: 666-672.
- Bissada NF. Symptomatology and clinical features of hypersensitive teeth. Arch Oral Biol. 1994;39:315S-332S.
- Addy M, Mostafa P, Newcombe RG. Dentine hypersensitivity: the distribution of recession, sensitivity and plaque. J Dent. 1987;15:242-248.
- Flynn J, GallowayR, Orchardson R. The incidence of ‘hypersensitive teeth’ in the West of Scotland.Arch Oral Biol.1985;13:230-236.
- Gillam DG, Aris A, Bulman JS, Newman HN, Ley F. Dentine hypersensitivity in subjects recruited for clinical trials: clinical evaluation, prevalence and intraoral distribution. J Oral Rehabil.2002;29:226-231.
- Brannstrom M. A hydrodynamic mechanism in the transmission of pain-producing stimuli through the dentine. In:AndersonDJ, ed. Sensory Mechanisms in Dentine.London: Pergamon Press; l963:73-79.
- Brannstrom M. The hydrodynamics of the dentinal tubule of pulp fluid. Caries Res. 1967;1:310-317.
- Dababneh RH, Khouri AT, Addy M. Dentine hypersensitivity—an enigma: A review of terminology, epidemiology, mechanisms, aetiology, and management. Brit Dent J. l999;187:606-611.
- Pratti C, Venturi L, Valdre G, Mongiorgi R. Dentin morphology and permeability after brushing with different toothpastes in the presence and absence of smear layer. J Periodontol. 2002;73:183-190.
- Orchardson R, Gangarosa LP, Holland GR, et al. Dentine hypersensitivity into the 21st century. Arch Oral Biol. 1994;39:113S-119S.
From Dimensions of Dental Hygiene. October 2003;1(6):22, 24, 26, 28, 31.