Quintessence Journals

pyri ORIGINALBamiseC o andARTICLE Esangh Not for Publicationt

b y Q

Mechanisms and Treatment Approaches of Dentine N

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t t r f e o Hypersensitivity: A Literature Review ssence

Cornelius Tokunbo Bamisea/Temitope Ayodeji Esana

Purpose: To review major mechanisms of dentine hypersensitivity and the treatment approaches offered.

Materials and Methods: Medline was used to find relevant literature published up to December 2006. Based on ab- stracts and full articles, studies (in human and in animals) were identified describing mechanisms and management of dentine hypersensitivity. Additional information was also obtained by using manual library search for relevant topics in standard texts and journals of dentistry.

Results: Discussion about the sensitivity of dentine started over a century ago, but it was not until sixty years later that a possible theory was posited. The so-called hydrodynamic theory became popular and was applied to understand the mechanism responsible for hypersensitive dentine. Nevertheless, because of the discrepancies in the pattern by which the dentine responds to various stimuli, several theories of dentine hypersensitivity were proposed which include the hydrodynamic theory, odontoblast transducer mechanism and direct innervation theory. None of these mechanisms was said to fully explain dentine hypersensitivity, thus indicating that as-yet unexplained mechanisms were possibly responsible. A multitude of products were tried and reported to be effective. The efficacy of many was not clearly established and their mechanisms of action were inadequately elucidated. The potential of gene therapy to reduce the burden of dentine hypersensitivity in the future is being examined.

Conclusions: Considerable effort has been made to precisely explain dentine hypersensitivity, but doubt still exists whether any one theory can be applied to understanding this condition. This has led to a constant increase in therapeutic approaches worldwide, but with no conclusive evidence of reliable, successful treatment regimens.

Key words: dentine hypersensitivity, mechanisms, review, treatments

Oral Health Prev Dent 2011; 9: 353-367. Submitted for publication: 17.04.07; accepted for publication: 15.08.07

entine hypersensitivity is characterised by Dentine desensitisation may occur spontaneous- Dshort, sharp pain arising from the exposed den- ly in some patients, but in most cases treatment is tine in response to thermal, evaporative, tactile, necessary. An array of tried and suggested treat- osmotic or chemical stimuli, which cannot be ment regimens has been offered to relieve the pain ascrib ed to any other form of dental defect or path- of dentine hypersensitivity. Some workers (Morris ology (Holland et al, 1997). There is a wide vari- et al, 1999) expressed concern about the efficacy ation in prevalence values reported for this condi- of most of these treatments, which seem unrelia- tion, as illustrated in Table 1. ble and not well established, while others (Schuurs Dentine exposure may result from enamel loss et al, 1995) call into question the longevity of their by attrition, abrasion, erosion, abfraction and root desensitising effect. The conventional conservative surface stripping from gingival recession or perio- approach is based on using topically applied de- dontal treatment. Most hard tissue loss probably sensitising agents which can be applied either pro- occurs from a combination of these factors. fessionally or prescribed for home use.

a Senior Lecturer, Department of Restorative Dentistry, Obafemi Awolowo University, University Campus, Ile-Ife, Nigeria. PULP–DENTINE COMPLEX Correspondence: Cornelius Tokunbo Bamise, Department of Restorative Dentistry, Obafemi Awolowo University, University The dentine is permeated throughout by minute Campus, Ile-Ife, 22005 Nigeria. Tel: +234-803-711-5388. tubes, the dentinal tubules, which contain the pro- Email: [email protected]

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b y The pulp tissue is innervated by theQ fibres of the Table 1 Prevalence of dentine hypersensitivity as re-

sensory divisions of the trigeminal ganglion andN

ported by various authors i

those of autonomic (principally nsympathetic)o

t t r f e o Prevalence (%) References branches of the superior cervical ganglion.ss Theen cprin-e 25 Abel (1958) cipal function of the sensory nerves is to detect stimuli and to conduct that to the central nervous 30 Jensen (1964) system, while the function of the autonomic system 14.5 Graf and Galasse (1977) is to keep the internal state of the organism con- 8.7 (probing), 18.0 (cold water) Flynn et al (1985) stant and maintain homoeostasis. These basic functions operate in the pulp (Torabinejad and Wal- 17 Fischer et al (1992) ton, 1989). 57.2 Irwin and McCusker (1997)

25 Liu et al (1998) TRANSMISSION OF DENTINE 8.0–57.0 Dababneh et al (1999) HYPERSENSITIVITY PAIN 4.1 Rees and Addy (2002) Odontogenic pain transmission is mediated primar- 67.7 Rees et al (2003) ily by peripheral sensory neurons of the trigeminal 1.34 Bamise et al (2007) nerve. The peripheral terminals of these nerves innervate the dental pulp and other oral tissues, whereas the central terminals release neurotrans- mitters that are involved in the initiation of pain. There are myelinated and unmyelinated nerve fibres toplasmic processes of the odontoblasts. The den- within the nerve bundles. The myelinated fibres, tinal tubules run parallel to each other and in one called the A-fibres, are grouped according to their direction, from the outer surface of the dentine to diameter and conduction velocities. Predominantly, the pulp cavity. The dentinal tubules are more A-fibres innervate the dentine (Ahlquist and Franzen, closely packed towards the pulp than in the outer 1999). The unmyelinated fibres, known as C-fibres, part of the dentine; the amount of intertubular ma- innervate the body of the pulp and its blood ves- trix, therefore, varies considerably at different lev- sels. Differences between the two sensory fibres els in the dentine. This is a result of the greater enable the patient to discriminate and characterise area of the external surface of the dentine com- the quality, intensity and duration of the pain re- pared with its inner or pulpal surface. At the pulpal sponse. Although due to the short distance be- surface of the dentine, there are 30,000–70,000 tween the site of stimulation and the brain, the two tubules per mm2 and it has been calculated that sensations might not be as clearly separated as in halfway between the pulpal surface and the amelo- stimulation of, for example, the extremities. dentinal junction, the total cross-sectional area of the tubules is equal to a 0.3-mm-diameter tube for each square millimetre of dentine. Such a degree of PROCESSING OF IMPULSES porosity could permit a considerable amount of fluid movement through the dentine (Scott and Sy- The cell bodies of the trigeminal nerve are located mons, 1977). in the Gasserian ganglion; the primary neuron syn- The pulp is composed of cells and intercellular apses with the second-order neuron in the subnu- substance. The intercellular tissue consists of fi- cleus caudalis region of the trigeminal spinal tract bres and an amorphous ground substance of a ge- nucleus. Once the second order receives the input, latinous consistency. The principal cells present in it is carried to the thalamus. The second order the dental pulp are odontoblasts, fibroblasts, undif- crosses the brain stem to the opposite side of the ferentiated cells and defence cells. In addition, brain and ascends to the higher centres. A-delta-fi- there are blood vessels, lymphatics and nerves. bres from the pulp synapse in the lamina I area of Odontoblasts are highly differentiated mesenchy- the subnucleus caudalis, and C-fibres synapse in mal cells of the pulp with cell processes that ex- the lamina II and III areas. The A-delta neurons tend into the dentinal tubules. pass to the thalamus directly, by way of the neo-

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i N

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Fig 1 Schematic representation of fluid moving away from Fig 2 Schematic representation of fluid moving away from the odontoblast in response to cold stimulus (Drisko, 2002). the odontoblast in response to hot stimulus (Drisko, 2002).

spinothalamic tract and are said to carry fast pain. would prove the presence of nerves deep in dentine The second-order C-fibre neuron carries impulses have indicated otherwise because application of via the palaeospinothalamic tract, which pass pain-inducing substances, such as histamine, ace- through the reticular formation where they are influ- tylcholine and potassium chloride, to the dentine enced by modulating interneurons before they reach fails to produce pain. Furthermore, the application the thalamus. Because these impulses take longer of local anaesthetics to exposed dentine does not to reach the thalamus, it is said to carry slow pain. prevent dentine hypersensitivity. Finally, application Fast pain tends to be sharp and easy to localise; of hypertonic fluids to dentine does produce pain. whereas slow pain tends to be dull and aching. Because of these discrepancies in the pattern by A comparison of the response characteristics of which the dentine responds to various stimuli, sev- the pulp nerve fibres and the sensations induced eral hypotheses for dentine hypersensitivity have from human teeth indicates that: been proposed (Torabinejad and Walton, 1989). r A-fibres are responsible for the sensitivity of dentine and thus for the mediation of the sharp pain induced by dentinal stimulation. Hydrodynamic theory r Pre-pain sensations induced by electrical stimulation result from the activation of the lowest Of the several theories proposed, the most widely threshold A-fibres, some of which can be classi- accepted is the hydrodynamic theory of sensitivity. fied as A-beta-fibres according to their conduction This theory postulates that rapid shifts, in either velocities. A comparison of the responses of the direction, of the fluids within the dentinal tubules A-beta- and A-delta-fibres indicates that they be- following stimulus application result in the activa- long to the same functional group. tion of sensory nerves in the pulp/inner dentine re- r Intradental C-fibres are activated only if the exter- gion of the tooth (Gysi, 1900; Brännström, 1972). nal stimuli reach the pulp proper. Their activation The hydrodynamic hypothesis for dentine hypersen- may contribute to the dull pain induced by in- sitivity was proposed over a century ago by Gysi tense thermal stimulation of the tooth and to (1900) with confirmatory evidence produced in the that associated with pulpal inflammation (Narhi 1950s and the 1960s (Brännström, 1972). Essen- et al, 1992). tially, certain stimuli create a pressure change across the dentine that can excite individual intradental nerves (Narhi and Hirvonen, 1987). In vivo THEORIES OF DENTINE HYPERSENSITIVITY studies revealed that the response of the pulpal nerves was proportional to the pressure and there- Elicitation of pain by scraping of dentine, applica- fore the rate of fluid flow. Cold stimuli that cause tion of cold, heat and hypertonic solutions supports fluid to flow away from the pulp produce more rapid the presence of a classic pathway for pain conduc- and greater pulp nerve responses than those, such tion through extension of the nerve fibres to the as heat, that cause inward flow. Heat expands the dentino-enamel junction. However, experiments that fluid within the tubules, causing it to flow towards

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b y the pulp, whereas cold causes the fluid to contract, 1999). However, Narhi et al (1999) pointedQ out that

u producing an outward flow (Figs 1 and 2). Research- hypersensitivity may sometimes persist despite ef-N

ers (Vongsavan and Mathews, 1992; Mathews et fective blocking of the tubules; they suggestedn thato

t t r f e o al, 1996) found that outward flow of fluid produces this may indicate that mechanisms others thansen core in a much stronger nerve response than inward move- addition to the hydrodynamic one may operate in ment. This certainly would explain the rapid and se- nerve activation. vere response to cold stimuli compared to the slow dull response to heat. The exact mechanism by which the fluid flow stimulates pulpal nerves is not Odontoblast transducer/modulation known with any certainty. However, from animal ex- hypothesis periments a mechanoreceptor response was suggested by Mathews and Vongsavan (1994). The The role of odontoblasts and the odontoblastic pro- pain-producing stimuli can be thermal, tactile, os- cesses in dentine hypersensitivity has been re- motic, chemical or evaporative (Holland et al, 1997), viewed (Pashley, 1996). Studies have shown prox- but cold stimulus appears to be the strongest and imity between odontoblastic processes and nerve causes the greatest problem to those troubled by fibre-like structures in the dentinal tubules (Frank, dentine hypersensitivity (Orchardson and Collins, 1968). Based on the proximity of odontoblastic pro- 1984; Irwin and McCusker, 1997). Not all exposed cess and nerve fibres, it has been theorised that dentine is sensitive. Evidence from scanning elec- odontoblastic processes act as receptors for con- tron microscopic and dye penetration studies dem- duction and transmission of impulses in dentine. onstrated the presence of a greater number and Lack of conclusive evidence for extension of od- wider tubules in hypersensitive dentine compared ontoblastic processes to the dentino-enamel junc- to non-sensitive dentine, as illustrated in Table 2 tion and the absence of definitive synaptic junctions (Ishikawa, 1969; Dowell and Addy, 1983; Absi et al, between odontoblastic process and nerve fibres 1987). diminish the validity of the theory (Torabinejad and Additionally, another scanning electron micro- Walton, 1989). scopic study based on replica models of hypersen- With regard to the membrane properties of od- sitive and non-sensitive dentine showed that, in ontoblasts, it has been reported that the membrane hypersensitive dentine, the smear layer was thinner, potential of odontoblasts is low (around -30 mV) different in structure and probably under-calcified and that the cell does not respond to electrical compared to that in non-sensitive dentine (Rimon- stimulation (Winter et al, 1963). dini et al, 1995). These findings are consistent with the hydrodynamic theory. The greater number of open and wider tubules at the dentine surface Direct innervation theory would enhance fluid permeability through dentine and as such increase the possibility for stimulus Light and electron microscopic studies as well as transmission and subsequent pain response. It is cytolabelling examinations of the dentine have the width of the tubules that is particularly relevant, shown the presence of nerve fibres in some den- since the fluid flow is proportional to the fourth pow- tinal tubules that extend maximally to one-third the er of the tubule radius; doubling the tubule diam- thickness of the dentine (Frank, 1959; Langeland eter results in a 16-fold increase in the flow rate. and Yagi, 1972; Byers and Dong, 1983). This is relevant for the treatment regimens that aim However, no studies exist which conclusively to narrow or occlude the tubules (Dababneh et al, show that there is an extension of nerve fibres in all types and ages of teeth to the dentino-enamel junction, which is the most sensitive area of dentine. Table 2 Differences in the number and diameter of tu- The presence of dentine hypersensitivity after the bules between hypersensitive and non-sensitive dentine application of local anaesthetic and the failure of (Absi et al, 1987) pain-inducing substances to evoke pain when ap- Tubules Hypersensitive Non-sensitive plied to dentine (Brännström, 1962) show that den- dentine dentine tine hypersensitivity does not depend solely on the Number–ratio 8 1 extension of nerve endings to its external surfaces.

Diameter (μm) 0.83 0.4

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b y Other theories mentioned in the literature are the TREATMENT APPROACHES Q

u direct ionic diffusion, ‘gate’ control and the vibra- N

tion theory (Berman, 1985; Gilam, 1995). Because Overall, there are two treatment approachesn for o

t t r f e o none of these theories fully explains dentine hyper- dentine hypersensitivity (Addy, 2002; Kimss eetn cal,e sensitivity, other mechanisms not fully elucidated 2002): to occlude dentinal tubules, thereby block- may also be involved (Winter et al, 1963). ing the hydrodynamic mechanism, and to block neural transmission at the pulp. With scientific acceptance of the hydrodynamic MANAGEMENT STRATEGY OF DENTINE theory to explain dentine hypersensitivity, many HYPERSENSITIVITY treatment strategies now focus on blocking the dentinal tubules and preventing any fluid shift. Even As with all conditions or diseases, management partial blocking of the tubules is effective in stop- strategies that include treatment are usually more ping dentine hypersensitivity because the fluid flow successful than treatment alone; therefore the fol- is proportional to the fourth power of the tubular lowing management strategy was proposed by Addy radius (Dababneh et al, 1999). (2002): Many agents and treatment modalities have been used in the treatment of dentine hypersensi- r Ensure the correct diagnosis of dentine hyper- tivity. Some are available for home use by the pa- sensitivity, which is based on a history and exam- tient, usually in the form of a dentifrice or ination and is compatible with the definition’s mouthrinse. Others are applied professionally by a clinical descriptor. dentist using a simple cotton wool pellet or a brush r Consider a differential diagnosis, as suggested to apply the agents or using very sophisticated by the definition of dentine hypersensitivity, which equipment such as laser and iontophoresis units. alone may explain the symptoms or identify the The ideal desensitising agents as listed by Gross- presence of other conditions contributing to the man (1935) should not irritate or endanger the in- pain of dentine hypersensitivity. tegrity of the pulp, should be relatively painless on r Treat any and all secondary conditions that in- application or shortly afterwards, should be easily duce symptoms similar to dentine hypersensitiv- applied, rapid in action and permanently effective ity (differential diagnosis). and should not discolour tooth structure. To date, r Identify aetiological and predisposing factors, no such agent has been discovered and there is no particularly with respect to erosion and abrasion. ‘gold standard’ for assessing new treatment Consider detailed, written dietary histories and (Dababneh et al, 1999). oral hygiene habits (frequency, duration and tim- Topical desensitising agents have been classi- ing of brushing, brushing technique, estimation fied (Scherman and Jacobsen, 1992) on the basis of brushing force, frequency of brush change and of their chemical and physical properties as inva- appearance of brush at change). Some of these sive and non-invasive, fluoride- and non-fluoride-con- aspects of tooth brushing behaviour are best ap- taining. praised by observing the patient brushing in the dental practice. r Remove or modify identified aetiological or pre- TREATMENT REGIMENS FOR DENTINE disposing factors. Offer dietary advice to min- HYPERSENSITIVITY imise erosion and oral hygiene instruction to minimise abrasion and to distinguish abrasion Strontium chloride from erosion. r Recommend or provide treatments appropriate A topical varnish containing 10% strontium chloride to the individual needs of the sufferer. The num- has been shown to significantly reduce the pain of ber of teeth involved and the severity of the pain patients who present with dentine hypersensitivity are important variables and should influence the (dall’ Orologico et al, 1999; Kishore et al, 2002). In treatment options. a study carried out by Mazor et al (1991) to assess the effect of topical application of a sustained-release device in the form of a varnish containing strontium chloride, they found a marked decrease

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b y ride and 40% formalin solutions wereQ found to sig-

nificantly reduce dentine hypersensitivity, whereasN

5% solution of potassium nitrate did not.n o

t t r f e o ssence

Calcium hydroxide

Calcium hydroxide has been variously used in clinical practice. Its use in the treatment of dentine hypersensitivity was investigated by Landry and Voyer (1990). Two types of agents were used, sodium fluoride (Duraflor, Medicom; Augusta, GA, USA) and calcium hydroxide (Dycal catalyst, Dentsply; York, Fig 3 Scanning electron micrograph showing open dentinal PA, USA), and were found to be effective in the treat- tubules before treatment with strontium chloride varnish. ment of dentine hypersensitivity. After 6 months, 94% of the subjects treated with calcium hydroxide and 87% of those treated with sodium fluoride were still desensitised, thus showing a slight advantage in using calcium hydroxide.

Potassium nitrate

The most common, professionally endorsed, self- applied approach to treating sensitive teeth is the use of desensitising dentifrices (Addy, 2002) which contain potassium salts (nitrate or chloride). Potas- sium ions pass easily through the enamel and dentine to the pulp in a matter of minutes (Hodosh, dentinal tubule 1974; Markowitz, 1993). An attempt to evaluate the role of potassium ions as a desensitising agent Fig 4 Scanning electron micrograph of obliterated dentinal was described by McCormack and Davis (1996); tubule after treatment with strontium chloride varnish. the experimental paradigms of the Nernst equation demonstrate a direct inhibitory effect of potassium ions upon nerve conduction. Most potassium-based desensitising dentifrices in hypersensitivity as compared to the placebo and also contain fluoride for cavity protection, and some untreated group. The SEM images shown in Figures offer an array of flavour and whitening, tartar-control 3 and 4 depict open dentinal tubules before and and the abrasive benefits of baking soda found in closed dentinal tubules after the application of most regular dentifrices, e.g. the Sensodyne range strontium chloride, resp. (Glaxo Smithkline; Brentford, Middlesex, UK), Crest Sensitivity Protection (Proctor and Gamble; Cincin- nati, OH, USA) or Colgate Sensitive (Colgate Palmo- Formaldehyde live; New York, NY, USA) (Addy, 2002). In clinical trials, the desensitising effect of anti- Formaldehyde has been used to precipitate pro- sensitive dentifrice generally takes about 2 weeks teins in the dentinal tubules (dall’ Orologico et al, of application twice a day to show reductions in 1999). In a study carried out by Kishore et al sensitivity, and greater effect develops with contin- (2002), the efficacy of desensitising agents for the ued use (Silverman et al, 1996). However, desensi- treatment of dentine hypersensitivity was evaluated tising dentifrices have been applied in a variety of using four agents and triple distilled water as con- formats. Jerome (1995) published a case study de- trol. About 10% strontium chloride, 2% sodium fluo- scribing a technique for treating tooth sensitivity in

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b y post-periodontal surgery patients. Instead of having Q

u the patient brush with a dentifrice containing potas- N

sium nitrate, he placed the desensitising dentifrice n o

t t r f e o in a custom-made soft tray. By increasing medica- ssence tion/tooth contact time, the tray delivery system increased the efficiency of the potassium nitrate dentifrice. Haywood et al (2001) published a paper describing the use of 5% potassium nitrate in bleaching trays to reduce the sensitivity triggered during bleaching. A significant reduction in sensitivity and pain was achieved by burnishing saturated potassium nitrate onto exposed dentine at the cervical margins of teeth (Touyz and Stern, 1999). Desensitisation of Fig 5 Scanning electron micrograph showing open dentinal tubules before treatment with stannous fluoride. hypersensitive teeth has also been achieved by the combination of dimethyl isosorbide (DMI) and potassium nitrate (KNO3), which were claimed to be more effective than when potassium nitrate is used alone. KNO3 and DMI work together to quickly desensitise hypersensitive teeth at a higher, more pro- found and lasting level (Hodosh, 2001). In a review published by Poulsen et al (2001), the effectiveness of dentifrices containing potassium nitrate and placebo dentifrices in reducing dentine hypersensitivity was compared; they revealed that no strong evidence was available supporting the efficacy of potassium nitrate dentifrice in reducing dentine hypersensitivity.

dentinal tubule Fluorides Fig 6 Scanning electron micrograph showing sealed den- Fluorides have long been used in the treatment of tinal tubules after treatment with stannous fluoride hypersensitivity, particularly in combination with other agents to enhance treatment. The mechanisms by which fluoride is beneficial are not fully understood, but it is thought to increase the stabil- 2002), rinsing with 0.05% sodium fluoride solution ity of the dentine surface. By reducing the solubility (Addy and Urquhart, 1992) and 0.2% sodium fluor- of dentine, for example, fluoride can shift the equi- ide/3% potassium nitrate mouthwash were found librium at the dentine surface in favour of non-sen- to have therapeutic potential and significantly re- sitivity (Addy and Urquhart, 1992). Fluorides have duced hypersensitivity when compared with 0.2% also been said to decrease sensitivity peripherally sodium fluoride alone (Pereira and Chava, 2001). by occluding the dentine tubules through crystalli- Stannous fluoride has also been variously used sation and reducing the fluid flow to the pulp (Gaf- in the therapeutic approach to dentine hypersensi- far, 1998). Ellingsen and Rolla (1987) described tivity. The SEM image in Fig 5 shows open dentinal this as precipitation of particles on the dentine sur- tubules before the application of stannous fluoride, face. but closed tubules after stannous fluoride applica- Thrash et al (1992) found that a 0.7% fluoride tion (Fig 6). An in vitro scanning electron microscop- solution significantly decreased dentine sensitivity ic study demonstrated the presence of a homoge- after two one-minute applications. Various concen- neous smear layer after treatment with stannous trations have been claimed to reduce dentine sen- fluoride gel and was said to confirm its capacity to sitivity: 2% sodium fluoride solution (Kishore et al, modify dentine permeability of sensitive dentine

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b y (Lucchese et al, 1997). Miller et al (1994) conclud- Iontophoresis with 2% sodium ﬂuorideQ

u ed that when properly formulated, stannous fluoride Iontophoresis is the use of an electric current toN

preparations could provide multiple oral therapeutic drive relative concentrations of ionic drugsn into hardo

t t r f e o benefits; 0.4% has been used (Addy and Urquhart, or soft tissue, as described by Nelson (1994).ssenc Ion-e 1992; Thrash et al, 1994) and a long-term effect tophoretic therapy is based on the simple principle was achieved when used at home after 0.717% that similar electromagnetic charges repel each fluoride solution application in the office (Thrash et other. When sodium fluoride dissolves in solution, al, 1994). the fluoride molecules form anions with an extra Fluoride varnish has also been used to relieve electron. In other words, the fluoride ions are nega- dentine hypersensitivity. It is said to form a protec- tively charged. A direct current is established in the tive layer of calcium fluoride that prevents the fluid patient’s mouth and a drop or two of fluoride solu- flow in open dentinal tubules, thereby reducing dention (negative ion) is put on the cathode (the nega- tine sensitivity (Gaffar, 1999). Duraphat is a varnish tive electrode) and placed on the tooth. Since simi- with high fluoride ion content. It is used in caries lar charges repel, the negative electrode will literally prevention and to relieve dentine hypersensitivity push the fluoride ion into the tooth surface. The (Komatsu et al, 1990). higher the current, the greater the electrical pres- Prescription dentifrices with a higher concentra- sure. The fluoride ions react with calcium in the hy- tion of fluoride (5000 ppm) have been given to pa- droxyapatite to form fluoroapatite. The CaF2 precipi- tients (Haywood, 2002). Sowinski et al (2000) con- tates, leaving the tubules blocked with the insoluble firmed the efficacy of an anti-hypersensitivity compound (Gangarosa and Park, 1978). By plug- dentifrice and provision of superior control of tactile ging the tubules and restricting fluid movement, ion- and airblast sensitivity by Colgate Sensitive max- tophoresis reduces the hydraulic transmission of imum strength dentifrice containing 5% potassium stimuli to the odontoblasts and the neurons below nitrate and 0.455% stannous fluoride in a silica them. The result is immediate, significant and pro- base, vs the clinically tested, commercially availa- vides many patients with a permanent reduction in ble anti-hypersensitivity dentifrice, Sensodyne, hypersensitivity (Nelson, 1994). which contains 5% potassium nitrate and 0.76% so- Most researchers studying iontophoresis, except dium monofluorophosphate in a dicalcium phos- Minkov et al (1975), have found significant improve- phate base. ment in 70%–80% of the patients they examined Marini et al (2000) described the effectiveness (Lutins et al, 1984). Not all patients responded to of an intraoral fluoride-releasing device (IFRD) in re- the same degree. Mild cases required only a single ducing the level of pain in patients with primary or treatment, while severe hypersensitivity required a post-surgical dentine sensitivity. The IFRD consists second treatment one week later (Carlo et al, of sodium fluoride encased in an acrylic polymer, 1982). Czukor (1993) claimed that additional ionto- which releases fluoride at a rate of approximately phoretic treatment with Pikomed-Dention equip- 0.04 mg/day. They described the method as fast, ment was found to be more effective than topical painless and inexpensive, and it appears to be suit- sodium fluoride alone. McBride et al (1991) demon- able as a routine treatment. strated a 97.9% response with reduced levels of In a study by Suge et al (2006), ammonium hex- sensitivity when they investigated the use of ionto- afluorosilicate (SiF) and diamine silver fluoride (AgF) phoresis in altering the sensitivity level of teeth that were applied to dentine disks from extracted teeth; displayed thermal and tactile hypersensitivity. Two scanning electron micrographs demonstrated that percent sodium fluoride iontophoresis as an alter- the dentine tubules were completely occluded by native to lining in Class I cavity preparations was the precipitate, and dentine permeability was re- investigated in an in vivo study with positive results duced to 10.3% after SiF treatment, while they re- (Reddy and Mathew, 1994). mained open after AgF treatment. A significantly greater reduction in hypersensitivity response has been obtained by sequential chlorhexidine and sodium fluoride rinses when compared to chlorhexidine alone or sodium fluoride alone (Lawson et al, 1991).

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b y Oxalate salts Sodium phosphate/calcium chlorideQ

i N

Another group of materials used are the oxalate Imai and Akimoto (1990) tried to block nthe tubules o

t t r f e o salts, such as potassium oxalate, ferric oxalate, al- by in situ precipitation of insoluble calciumss ephos-nce uminium oxalate and oxalic acid. These materials, phate. Calcium phosphate crystals precipitated in that are generally applied in a rubbing or burnishing situ on patients’ dentine surfaces and formed in motion, act by occluding the tubules and reducing the tubules immediately upon serial application of the fluid flow in either direction (Hodosh et al, 1994; sodium phosphate and calcium chloride solutions, Burke et al, 2000; Haywood, 2002). Gillam et al thus occluding the tubules. The size of the crystals, (2001) investigated four commercially available ox- their degree of coverage and the thickness of the alate-containing products – Tenure Quik (aluminium precipitate depended on the method of application oxalate; DenMat; Santa Maria, CA, USA), Senso- and concentration of the solutions. The application dyne Sealant (ferric oxalate), Butler Protect (potas- of 5% disodium phosphate solution followed by rub- sium oxalate; Sunstar Americas; Chicago, IL, USA) bing with 10% calcium chloride solution resulted in and MS Coat (oxalic acid; Sun Medical; Tokyo, Ja- immediate relief from dentine hypersensitivity in pan) – applied to etched dentine disks, and ob- 84% of patients treated. served the extent of tubule occlusion by scanning electron microscopy. It was shown that all the applied desensitising agents covered the dentine sur- Guanethidine face and produced some occlusion of the tubules. However, potassium oxalate (active ingredient of Guanethidine has been recently indicated to be of Butler Protect) did not cover the surface to any great value in the treatment of dentine hypersensitivity. extent. The topical application of guanethidine solution to the affected teeth successfully relieved natural and clinically induced dentinal pain and hypersensitivity Magnesium sulphate in 13 of 14 dental patients in a pilot study carried out by Hannington-Kiff and Dunne (1994). The Liu and Morimoto (1991) introduced magnesium mechanism of this analgesia was unclear but prob- sulphate as a new type of desensitising agent when ably involved an anti-noradrenergic block, as there 4% magnesium sulphate was applied iontophoreti- was no evidence of local anaesthesia. These inves- cally at 2 mA for 3 min. These optimal conditions of tigators also examined whether guanethidine was time and current were determined by animal experi- more effective than a distilled water control in alle- ments, but only a minor effect on dentinal tissues viating dentinal pain, and found that guanethidine was observed within 4 weeks after treatment. When reduced dentine hypersensitivity more effectively this desensitising agent was used to treat dentine than distilled water (Dunne and Hannington-Kiff, hypersensitivity, the cure rate of 62.4% remained 1993). steady within the 25-week observation period, while some effect was achieved in all the subjects who participated in the study. Potassium chloride

Krahwinkel et al (2001) assessed the clinical effec- Aluminium lactate tiveness of a chewing gum containing potassium chloride in the treatment of hypersensitive teeth. The effectiveness of a dental rinse containing alu- The results of this study showed that the daily use minium lactate, which was used as a daily home of chewing gum containing potassium chloride is a treatment for dentinal hypersensitivity, was evalu- useful non-invasive method of reducing dentine hy- ated in a 6-week double-blind study by Higuchi et al persensitivity over an extended period of time. (1996). A concentration of 2.18% was used. Find- ings suggested that daily home use of a dental rinse containing aluminium lactate was effective in the treatment of dentine hypersensitivity.

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b y Hydroxyapatite gel al (1994), non-carious dental lesionsQ were catego-

rised as abrasions, attritions, erosions or abfrac-N

Hydroxyapatite gel application to hypersensitive tions. From these destructive processes,n hypersen-o

t t r f e o teeth has been shown to be effective as one of the sitive dentine was a common consequencessence therapeutic approaches to dentine hypersensitivity experienced by the dental patient. Treatment meas- management. Barone and Malpassi (1991) demon- ures for hypersensitive dentine from these lesions strated its effectiveness when they used 15% hy- include restoring them with composite resin or droxyapatite gel. They found that this product gave glass-ionomer material. Glass ionomers provide a immediate relief of pain caused by dentine hyper- longer-lasting benefit than do resins or varnishes, sensitivity. which are often immediately effective but rapidly re- moved by tooth brushing (Addy and Urquhart, 1992). Corticosteroids

Topical application of corticosteroids in the form of Resins (dentine bonding systems) gel has been indicated in the therapeutic approach to relieve the pain of dentine hypersensitivity. The Within the past two decades, the use of dentine effectiveness was probably due to their anti-inflam- bonding systems has been suggested in the treat- matory effects (dall’ Orologico et al, 1999). ment of dentinal hypersensitivity (Burke et al, 2000). Watanabe et al (1991) reported the effective use of a 35% aqueous solution of hydroxyethyl Silver nitrate methacrylate (HEMA) to desensitise rabbit teeth, especially when a bonding agent was also applied. Silver nitrate has been used in the treatment of Among the first bonding agents to be used, dall’ dentine hypersensitivity and it is said to work by Orologico and Malferrari (1993) found that single precipitating proteins in the dentinal tubules (dall’ applications of Gluma Primer and Gluma 2000 Orologico et al, 1999). (Bayer Dental; Dormagen, Germany) successfully eliminated or reduced dentine hypersensitivity over a 6-month period. Since Gluma contains glutaralde- DP-bioglass hyde, a biological fixative, it may be anticipated that the glutaraldehyde reacts with the proteins in the DP-bioglass paste was suggested by Lee et al dentinal tubules, resulting in a partial or total occlu- (2005) to produce considerable sealing depth in sion of the tubules (Burke et al, 2000). Dall’ Oro- dentinal tubules with the potential of efficaciously logico et al (1999) evaluated the use of Gluma Al- prolonging the therapy. DP-bioglass paste was pre- ternate (an experimental version of Gluma pared by mixing 20%–60% phosphoric acid and DP- Desensitizer [Bayer Dental] with reduced glutaralde- bioglass to treat dentine surfaces. CO2 laser irradi- hyde and HEMA), Gluma Desensitiser and Scotch- ation was used to melt the DP-bioglass paste. The bond Multipurpose (3M; St Paul, MN, USA), with the results demonstrated that 30% phosphoric acid results indicating that each of these materials was was the optimum concentration to produce homo- effective in reducing sensitivity for the 6-month ob- geneous occlusion of exposed dentinal tubules and servation period. 60 μm of sealing depth. CO2 laser irradiation was Scotchbond 1, also known as Single Bond (3M), able to melt the DP-bioglass paste and create about has been introduced as a one-bottle alternative to 10 μm of sealing depth. Scotchbond Multipurpose (3M). This system uses some of the components from Scotchbond Multi- purpose and lists treatment of dentine hypersensi- Glass-ionomer cement and resin composites tivity among its indications for use (Scotchbond I, Product Profile, 1997). This is the direct application of glass ionomer and/ Clinical evidence of effective desensitisation of or resin composite to sensitive areas (Kelleher and Gluma desensitiser has been found by different au- Bishop, 1999) to achieve resolution. In the review thors. In a clinical comparison of the effectiveness of non-carious dental cervical lesions by Gallien et and longevity between Gluma Primer and two direct-

362 Oral Health & Preventive Dentistry pyri BamiseC oand Esangh Not for Publicationt

b y application oxalate systems in reducing root sur- Lasers Q

u face hypersensitivity (Cochran, 2011), the oxalate N

products became completely ineffective after only 5 Maiman developed the ruby laser in 1960.n In their o

t t r f e o months, whereas the effectiveness of Gluma Prim- review of laser applications for the treatmentssen cofe er diminished slightly only after one year and for a dentine hypersensitivity, effects of laser on pulp tis- few patients. Gluma Primer was found to be an ef- sue and problems in treatment, Kimura et al (2000) fective desensitising agent for dentine hypersensi- noted that four kinds of lasers have been used for tivity and had no adverse effects on the pulp during the treatment of dentine hypersensitivity, and the or after treatment; thus, it can be considered safe effectiveness ranged from 5.2% to 100%, depend- for clinical use (Inone et al, 1996). ing on the laser type and the parameters used. They concluded that it is necessary to consider the severity of dentine hypersensitivity before laser Resins as protective layer against tooth wear use. and hypersensitivity Gelskey et al (1993) studied the effectiveness of laser therapy in the reduction of dentine hypersen- In an in situ study by Azzopardi et al (2004) to de- sitivity and its effects on pulp vitality. They noted termine whether covering dentine with adhesive that He:Ne and He:Ne+ Nd:YAG laser treatment can resins protects against acid erosion, it was found be used to reduce dentine hypersensitivity without that Optibond Solo and Seal and Protect protected detrimental pulpal effects. The desensitising ef- dentine against a vigorous wear regime. Optibond fects of an Er:YAG laser (Key 11, KaVo; Biberach, Solo deteriorated faster than Seal and Protect. Germany) vs Dentine Protector (Ivoclar Vivadent) on They concluded that both materials could potential- cervically exposed hypersensitive dentine were ly be used to protect dentine, but it appears that compared, showing that desensitising of hypersen- Seal and Protect is more useful. For patients with sitive dentine with Er:YAG laser was effective and uncontrolled erosion or toothwear, applying a den- the positive result more prolonged than with Den- tine bonding agent to the exposed dentine is a prac- tine Protector (Schwarz et al, 2002). Other authors tical option to prevent further damage. noted the combined occluding effect of Fluor Pro- tector and Nd:YAG laser irradiation on human dentinal tubules (Zhang et al, 2001). Another effective Varnishes laser treatment for dentine hypersensitivity is the use of GaAlAs laser. Gershman et al (1994) demon- Varnishes are valuable means of protecting the strated that thermal sensitivity decreased by 67% pulp when cementing crowns or inlays, especially with laser vs 17% with a placebo, and tactile sensi- when phosphate cement is to be used. Messing tivity decreased by 65% with laser vs 21% with a and Ray (1982) noted that the application of Tresio- placebo at 8 weeks. In addition, those authors lan (ESPE; Seefeld, Germany), or Copal-ether var- found no adverse reactions or instances of oral ir- nish (Bosworth; Skokie, IL, USA) would help desen- ritation occurring with GaAlAs laser use. sitise hypersensitive dentine. Although employed The mechanism involved in laser treatment of mainly in caries prevention, varnishes (Duraphat dentine hypersensitivity is relatively unknown (Kimu- [Colgate], Fluor Protector [Ivoclar Vivadent; Schaan, ra et al, 2000), but in a study done by Stabholz et Liechtenstein] and Cervitec [Ivoclar Vivadent]) can al (1993) using scanning electron microscopy, the give immediate relief of pain of dentine hypersensi- results indicate that the application of XeCl excimer tivity. laser at a specific fluence on exposed dentinal tu- Arends et al (1997) studied the penetration of bules of human extracted teeth can cause melting varnishes into demineralised root dentine in vitro of dentine and closure of exposed dentinal tubules. and concluded that the drying procedure in pretreat- Melting of the surface and closure of exposed den- ment of the dentine influences the penetration into tinal tubule orifices was also confirmed by Lan and the tissue and presumably ‘seals’ the tubules com- Liu (1996) after irradiating the dentine surface with pletely or partly. This is valuable with respect to car- Nd:YAG laser at an energy output of 30 mJ, 10 ies prevention and relieving pain of dentine hyper- pulses/s (pps), for 2 min. In a subsequent study to sensitivity. evaluate the sealing depth of Nd:YAG laser on human dentinal tubules, the sealing depth of

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b y Nd:YAG laser on human dentinal tubules was re- FUTURE THERAPIES FOR DENTINEQ HYPER-

u vealed to be approximately 4 μm (Liu et al, 1997). SENSITIVITY N

In summary, clinical effectiveness of lasers in n o

t t r f e o the treatment of dentine hypersensitivity has been In the future, gene therapy may include treatmentssence of confirmed, depending on the type of laser and the the sensory nerves in dental restorative procedures severity of the hypersensitivity. Their effects can be as well as in surgical and non-surgical debridement greatly enhanced or improved when combined with that elicits dentine hypersensitivity. One such other modalities, i.e. the application of varnish (Lan method may include blocking the increased produc- et al, 1999; Zhang et al, 2001). tion of nerve growth factors by pulpal fibroblasts near the lesion, which are thought to contribute to tooth hypersensitivity after restorative procedures Electro-analgesia (Byers et al, 1992).

Dental pain propagation has been said to be due to the triggering of the action potential from the rest- CONCLUSIONS ing potential. Vachey (2000) suggested that this could be reduced by the reversible process of an Attempts to explain dentine hypersensitivity have electrotonus in electro-analgesia. been made for more than a century, but because of the discrepancies in the pattern by which the dentine responds to various stimuli, several theories of Gingival grafts dentine hypersensitivity have been proposed. The most widely accepted of these is the hydrodynamic Surgical corrections for dentine hypersensitivity in- theory of sensitivity. clude root coverage with connective tissue grafts An array of tried and suggested desensitising (Drisko, 2002) where there is severe recession and agents used in vitro on dentine disks or on patients sensitivity. A flap is reflected to expose the reces- have been broadly grouped into physical and chem- sion defect, a connective tissue graft is placed and ical agents and reviewed. Despite a multitude of a coronally repositioned flap is closed over it. products available for treatment, as West (2006) For patients complaining of sensitive teeth from recently concluded, the results show that conclu- exposed dentine secondary to gingival recession, sive evidence of successful treatment regimens is Thompson et al (2000) described a semilunar coro- still elusive. nally positioned flap to cover the denuded root sur- Prior to that, Morris et al (1999) expressed con- face. One of the three principal treatment strate- cern about the longevity of the desensitising effect gies suggested by Jacobsen and Bruce (2001) for of fluoride and oxalate precipitates, which are some dentine hypersensitivity is covering the exposed of the commonly used treatment regimens, while dentinal tubules by gingival grafts. In some cases, Schuurs et al (1995) stated that the efficacy of guided tissue regeneration for the treatment of lo- most of the available therapies seems unpredicta- calised gingival recessions using bioresorbable ble and not well established. It therefore behoves membrane (Vanden and Esposito, 1997; Drisko, clinicians to determine appropriate, acceptable and 2002;) may represent an effective alternative to tra- effective treatment strategies for this relatively ditional mucogingival therapy (Vanden and Esposi- common dental problem in their own milieu. to, 1997). The use of the bioresorbable membrane (Guidor; Sunstar) has made re-entry surgery for membrane removal unnecessary, and the guided REFERENCES tissue regeneration technique is likely to result in a greater number of new connective attachment for- 1. Abel I. Study of hypersensitive teeth and a new therapeutic aid. Oral Surg 1958;11:491–495. mation (Vanden and Esposito, 1997). 2. Absi EG, Addy M, Adams D. Dentine hypersensitivity: a study of the patency of dentinal tubules in sensitive and non-sensitive cervical dentine. J Clin Periodontol 1987;14:280–284. 3. Addy M. Dentine hypersensitivity: new perspective on an old problem. Int Dent J 2002;52:367–375.

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