Treatment Approaches for Dentin Hypersensitivity

Abstract

The aim of this chapter is to review the various treatment approaches used by clinicians to treat dentin hypersensitivity and evaluate their efficacy in reducing dentin hypersensitivity. Evidence from both in vitro and in vivo studies will be assessed to determine whether there is any support for these treatment products and procedures based on their proposed underlying mechanism of action.

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5.1 Introduction

The hydrodynamic theory promotes two basic approaches based on in vitro, in situ, animal and human studies for treating dentin hypersensitivity (DH) (Ling and Gillam 1996; Orchardson and Gillam 2006) (Fig. 5.1):

Fig. 5.1

Outline of the hydrodynamic mechanism by which (a) stimuli activate intradental nerves to cause pain and (b) subsequent resolution following natural desensitisation and treatment (Acknowledgement Orchardson and Gillam 2006)

• 1. Dentin blocking agents that occlude patent (open) tubules (fluoride, strontium salts, oxalate, calcium phosphate, restorative materials, etc.) and as a consequence reduce any stimulus-evoked fluid movements within the dentin tubule

• 2. Nerve desensitisation agents that reduce intradental nerve excitability (e.g. potassium ions, guanethidine) in order to prevent a response from intradental nerves to the stimulus-evoked fluid movements within the dentin tubules

It should be acknowledged that in vitro results demonstrating superiority of the various products under examination should not be extrapolated into making claims on the efficacy of these products without first undergoing extensive clinical evaluation. There are however a vast array of products currently out on the commercial market with various claims of clinical efficacy in reducing DH, although currently there does not appear to be a gold standard product or therapy universally accepted by clinicians to treat the condition (see Chap. 6).

Application of these successfully tested products may either involve ‘in-office’ procedures by a clinician using a restorative approach (for example, restorative materials in the form of dentin bonding agents, glass ionomer cements (GIC), and periodontal surgical techniques) or by a clinician recommending an over-the-counter (OTC) approach (involving toothpastes, gels, mouthwashes).

5.2 Dentin Blocking Agents

Currently the hydrodynamic theory (Brännström 1963) is generally considered to be the mechanism of choice although other alternative mechanisms of stimulus transmission cannot be ruled out, since some clinical phenomena cannot be explained solely by this theory (Gillam 1992; Orchardson and Gillam 2006) (Fig. 5.1).

There are a number of products commercially available for the treatment of DH these include both in-office applied and over-the-counter products. The proposed mode of action for most of these products has been established using in vitro, animal, in situ and in vivo studies (Orchardson and Gillam 2006 Tables 5.1a and 5.1b).

Table 5.1a Characteristics of selected occluding toothpastes

Table 5.1b Characteristics of selected dentin blocking toothpastes

5.2.1 Strontium-Containing Toothpastes

Strontium chloride has been claimed to act as both a protein precipitant and a tubule-occluding agent (Cohen 1961; Skurnik 1963; Blitzer 1967; Gedalia et al. 1978; Uchida et al. 1980). Gutentag (1965) however also demonstrated that strontium may stabilise excitable neural membranes by modifying their permeability to sodium and potassium. Several investigators have shown that strontium ions may be deposited as an insoluble barrier, possibly a calcium strontium–hydroxyapatite complex, at the dentin tubule openings (Pawlowska 1956; Ross 1961; Blitzer 1967; Gedalia et al. 1978). Kun (1976) however demonstrated in vitro that a topical application of concentrated strontium chloride solution produced a continuous deposit on the dentin surface as well as a degree of penetration into the dentin tubules. Furthermore he proposed as a result of evidence from the electron probe microanalysis and X-ray diffraction studies that the fundamental mechanism of the formation of strontium deposits was an exchange with the calcium of the dentin, resulting in recrystallisation in the form of strontium apatite. Evidence from other in vitro studies (Greenhill and Pashley 1981; Mostafa et al. 1983; Pashley et al. 1984; Addy et al. 1991), however, would appear to suggest that these results were attributable not to active ingredient per se but to the abrasive component(s) of a toothpaste which may contribute to the formation of a smear layer and to some degree occlude or block the exposed dentin tubule opening (Mordan et al. 2002) (Fig. 5.2a, b).

Fig. 5.2

(a) Coverage of the exposed dentin following a 2 min application of a fluoride toothpaste (Mordan et al. 2002). (b) Evidence of tubular occlusion of dentin tubules by toothpaste ingredients (e.g., silica) following a 2 min application of a fluoride toothpaste (Mordan et al. 2002)

5.2.2 Selected Calcium Compounds

5.2.2.1 Casein Phosphopeptide–Amorphous Calcium Phosphate (CPP–ACP)

Toothpastes containing Casein Phosphopeptide–Amorphous Calcium Phosphate (CPP–ACP) were primarily developed for anticaries and remineralisation strategies rather than for the treatment of DH per se. According to Reynolds (1998), the CPP component binds to surfaces in the oral environment such as plaque, bacteria and soft tissue providing a bioavailable Ca and PO₄ at the surface of the tooth (e.g. enamel) without any precipitation. The ACP is subsequently released from the dental plaque during acidic challenges. The stabilisation of ACP component by the CPP ensures the delivery of both Ca and PO₄ ions onto the enamel surface for remineralisation. Both in vitro and in vivo studies have demonstrated that calcium phosphate preparations deposit a mineral precipitate on to the dentin surface, block dentin tubules and reduce dentin permeability in the dentin disc model and DH in patients (Ebisu 2002; Suge et al. 2002; Cherng et al. 2004; Geiger et al. 2003; Azarpazhooh and Limeback 2008; Charig et al. 2009; Gandolfi et al. 2010; Walsh 2010) (Table 5.1a).

5.2.2.2 Calcium Carbonate and Arginine (Colgate Pro-Argin™)

Kleinberg (2002) suggested at physiological pH the positively charged arginine in the arginine/insoluble calcium carbonate compound combination binds to the negatively charged dentin surface enabling a calcium-rich mineral layer into the open (exposed) dentin tubule to act as an effective plug or tubular occludent. Initial laboratory (in vitro) evidence appears to support this in that the product does occlude the dentin tubules and effectively block fluid flow and is resistant to an acid challenge (Petrou et al. 2009), and subsequent clinical studies evidence appears to support its efficacy as a desensitiser (Ayad et al. 2009; Docimo et al. 2009; Hamlin et al. 2009; Nathoo et al. 2009; Schiff et al. 2009a, b, 2011; Que et al. 2010; Cummins 2011) (Table 5.1a). Recent systematic reviews by Sharif et al. (2013) and Yan et al. (2013) have also indicated that there are clinical benefits for using Pro-Argin™ toothpastes in reducing DH; however both these investigators raised concerns regarding the quality of the conducted studies and recommended that further well-designed studies should be conducted to determine the efficacy of the product in reducing DH.

5.2.2.3 Bioactive Glasses

Bioactive glasses (calcium sodium phosphosilicate), for example, NovaMin® (developed by NovaMin Technology Inc., Alachua, FL, USA) based on the original 45S5 Bioglass® formulation by Larry Hench (US Biomaterials Corp., Jacksonville, FL, USA, now GSK) (Hench 2006), have been incorporated into toothpastes for the treatment of DH. The proposed mode of action is by the precipitating of hydroxycarbonate apatite (HCA) onto the dentin surface and subsequently occluding the dentin tubules (Litkowski et al. 1998; Gillam et al. 2002; Tai et al. 2006; Vollenweider et al. 2007; Burwell 2006; Burwell et al. 2009; Wang et al. 2010; Pradeep and Sharma 2010; Mneimne et al. 2011) (Table 5.1a).

One advantage of the precipitated HCA layer is that it is chemically and structurally similar to natural enamel and dentin (Burwell 2006). A recent randomised double-blind controlled trial, by Orsini et al. (2010), compared the clinical efficacy of a new toothpaste containing (HCA) nanocrystals and a sodium fluoride/potassium nitrate toothpaste and concluded that a new novel toothpaste formulation containing zinc-HCA nanocrystals significantly reduced DH after 4 and 8 weeks. There have however been concerns over the long-term durability of HCA in the oral environment, and it has been postulated that the formation of fluorapatite (FAp) rather than HCA is preferable, since this layer may be more resistant to acid attack and would therefore dissolve less readily when teeth are exposed to acidic conditions (e.g. during consumption of fruit juice and carbonated beverages). It has been recently demonstrated that fluoride-containing bioactive glasses form FAp rather than HCA in physiological solutions (Brauer et al. 2010).

5.2.2.4 Hydroxyapatite-Based Toothpastes

According to Hill et al. (2012), hydroxyapatite-based toothpastes have been widely used in China and the Far East (Park et al. 2005; Kang et al. 2009; Kim et al. 2009; Yuan et al. 2012). The published literature on hydroxyapatite toothpastes however is mainly in non-English journals and may, therefore, not be readily available in an English translation format (Park et al. 2005; Kang et al. 2009; Kim et al. 2009; Yuan et al. 2012). More recently, the commercial emphasis has focused on the use of nanocrystalline hydroxyapatite in toothpastes for desensitising and remineralising strategies (Rimondini et al. 2007; Orsini et al. 2010; Tschoppe et al. 2011). The proposed mechanism of action for hydroxyapatite-containing toothpastes is blocking the dentin tubules (Rimondini et al. 2007; Hill et al. 2012; Yuan et al. 2012) (Table 5.1a).

5.2.3 Selected Fluoride Formulations

Fluoride was first proposed as a desensitising agent in 1941 by Lukomsky (1941) and has subsequently used in toothpastes, gels, mouth rinses and varnishes (Orchardson and Gillam 2006). Sodium fluoride and stannous fluoride have been shown to reduce DH (Morris et al. 1999), and amine fluoride has also been incorporated into dentifrices although there is currently limited published data to support its use. Stannous fluoride (SnF₂) in a 0.4 % glycerin gel has also been reported to be effective in reducing DH (Miller et al. 1969) although this formulation and the use of SnF₂ may be problematic for a number of reasons, for example, (1) when placed in an aqueous environment, it appears to undergo hydrolysis and precipitates out of solution (Miller et al. 1969) hence the incorporation into a gel and (2) poor taste and staining characteristics. More recently investigators have demonstrated that a reformulated toothpaste containing stannous fluoride with a novel 0.454 % stabilised stannous fluoride formulation containing sodium hexametaphosphate (SHMP) was effective in reducing DH during an 8-week treatment compared to a sodium fluoride toothpaste as a control (Schiff et al. 2005, 2006; Day et al. 2010; Einwag et al. 2010; cited by Ni et al. 2010). According to Greenhill and Pashley (1981), fluorides decrease the permeability of dentine in vitro possibly by the precipitation of insoluble calcium fluoride within the tubules. However the exact mechanism whereby fluoride reduces DH is unknown. Fluoride incorporation increases the resistance of dentin to decalcification (Furseth 1970) and reduces its solubility (Sandoval and Shannon 1969) as fluorapatite is more resistant to acid attack(s) than hydroxyapatite. Sodium monofluorophosphate has also been previously investigated as a toothpaste ingredient with desensitising effects by Hazen et al. (1968) and by Addy et al. (1987) who reported on its clinical effectiveness in combination with strontium acetate. Recently several investigators have reported on the clinical efficacy of a combined sodium monofluorophosphate/strontium acetate formulation for the treatment of DH (Mason et al. 2010; Hughes et al. 2010) (Table 5.1b). Higher fluoride concentration toothpastes containing 2,800/5,000 ppm sodium fluoride (Colgate Duraphat) have also been advocated for prevention of dental caries and as such may be of potential benefit in the treatment of root caries and DH.

One however should not ignore that natural desensitisation of dentin (both internally and externally) may occur irrespective of whatever treatment is provided by the clinician to the patient. For example, Orchardson and Gillam (2006) have suggested that there may be natural desensitising of dentin through precipitation of salivary proteins, toothpaste ingredients, etc., forming a smear layer which may occlude the dentin tubules or remineralisation (Pashley 1992a; Kawasaki et al. 2001) as well as the formation of both intra-tubular dentin and secondary/tertiary dentin over time (Addy and Dowell 1983) (Fig. 5.1).

5.3 Nerve Desensitisation and Noci0ception

As indicated earlier, the hydrodynamic theory (Brännström 1963) is generally considered to be the mechanism of choice, and as with dentin blocking agents, this theory appears to explain how nerve desensitisation may occur following the application of potassium-containing products (e.g. toothpastes gels, mouth rinses).

Several investigators (Greenhill and Pashley 1981; Pashley et al. 1984) however failed to observe any effect of potassium nitrate (either as a 30 % solution or 5 % toothpaste) in terms of a reduction in dentin fluid flow (dentin permeability) in the in vitro dentin disc model. In other words, these investigators were unable to demonstrate whether potassium nitrate reduced DH by blocking the dentin tubules and were therefore unable to determine the exact mechanism of action of potassium-containing toothpastes which were reported to be clinically effective when treating DH. These investigators however did not rule out the possibility that these agents may desensitise dentin via neural effects unrelated to hydrodynamic mechanisms.

In order to ascertain the precise mechanism for action for potassium, several investigators utilised a neurophysiological animal (cat) model which involved deep-cut cavity preparations with a very thin slice of dentin between the exposed dentin surface and the pulp (Kim 1986; Markowitz and Kim 1985, 1990; Markowitz et al. 1991). These investigators subsequently demonstrated that when using large molar concentrations of various divalent cation solutions (including potassium) applied to the dentin surface, both intradental nerve activity and sensory nerve activity were reduced. It was also evident from these studies that the important chemical moiety of potassium nitrate was the potassium salt and not the nitrate anion as previously believed. Furthermore potassium appeared to be the more effective desensitising agent compared to the other solutions tested irrespective of which combination of anion was used. On the basis of these observations, these investigators proposed that the mode of potassium desensitisation was through raising the intra-tubular potassium (K⁺) concentration which would render the intradental nerves less excitable to any further stimulation by depolarisation of the nerve fibre membrane. Initially this increase in the potassium ion content elicits an increased number of action potentials, after the initial depolarisation; however the nerve fibre(s) cannot depolarise due to the maintained high levels of extracellular potassium ion content and as a consequence a sustained depolarised state occurs (axonal accommodation).

The interpretation based on the investigation by Kim and co-workers (1985, 1986, 1990, 1991 see above) has however been criticised by Sena (1990) who suggested that as a result of the deep-cut cavity preparations in the cat, the applied potassium ion only had a short distance to traverse the length of the dentin tubule to exert its effect to desensitise the nerve. In the normal clinical situation (in intact human teeth), however, the incoming potassium ion (e.g. if applied in a toothpaste product on the exposed cervical dentin) would have to overcome the opposing pulpal pressure that produces an outward flow of dentin fluid. Such an outward flow may therefore prevent the inward diffusion of substances from the oral cavity. Currently it is important to note that this proposed mechanism was based on animals and has not been confirmed for human dentin (Orchardson and Gillam 2000) (Table 5.2). For example if the desensitising effects of potassium are due to action potential inactivation, one might expect as Orchardson and Gillam (2000) suggested that the patient would experience a transient pain when a potassium-containing toothpaste is applied to the exposed dentin surface. This phenomenon has not been reported for toothpastes in humans. It may also be of note in this context, however, to reconsider the work by Anderson and co-workers (1958, 1962a, b) who postulated that if dentin was directly innervated, then chemical stimuli to the exposed dentin surface should cause a patient discomfort. Application of algogenic (pain-inducing) substances such as potassium chloride, acetylcholine and histamine, however, failed to elicit a response. By way of contrast when these substances were applied directly to exposed pulpal tissue, an immediate response was elicited (Anderson and Naylor 1962; Anderson 1968, 1972). This observation may therefore be of interest when ascertaining the precise mode of action of potassium-containing preparations.

Table 5.2 Characteristics of selected nerve depolarising toothpastes

Several investigators have however attempted to explain the role of potassium diffusion across dentin (Stead et al. 1996; McCormack and Davies 1996).

• (a) Mathematical Model of Potassium Ion Diffusion

  In order to ascertain whether the potassium ion could diffuse down the dentin tubule, Stead et al. (1996) proposed a mathematical model of potassium ion diffusion which incorporated a number of variables, for example, dentin thickness, tubule diameter, time, diffusion gradient, outward fluid flow, the constituents of dentin fluid (molecule size), permeability of the odontoblast layer and the concentration of potassium (based on 5 % potassium in toothpastes).

  According to these investigators, the application of potassium-containing preparations to the exposed dentin may increase potassium ions at the inner ends of the dentinal tubules to levels sufficient to inactivate intradental nerves; however, the localised increase in potassium ions may only be transient, and the concentration change will also be reduced by conditions that increase the tubular fluid flow velocity or the permeability of the barrier between the tubule and the pulp. The prediction from this model regarding nature of the transient effect of the potassium ion on nerve inactivation may be of interest particularly in the light of the results from the clinical studies by Ajcharanukul et al. (2007, 2011, 2012). These investigators utilised a cut cavity preparation approach based on the animal model in human subjects and demonstrated that potassium salts had a transient desensitising effect as predicted by Stead et al. (1996). However one of the conclusions from these studies was that the hydrodynamic mechanism responsible for responses to stimulation of dentin in humans has different properties from those demonstrated in the cat and may not necessarily be mediated by a hydrodynamic mechanism.

• (b) The Role of Nitric Oxide as a Secondary Messenger

  One of the problems with the mathematical model of potassium diffusion as proposed by Stead et al. (1996) was the various constraints to the diffusion of the potassium ion along the entire length of the dentin tubule (Orchardson and Gillam 2000). An alternative mechanism for potassium ion-mediated desensitisation was proposed by McCormack and Davies (1996). These investigators suggested that the potassium ion could evoke a novel synthesis of a mobile secondary messenger (nitric oxide) within dentin and the dental pulp. The proposed hypothesis is that the potassium ion may act on the odontoblast process to release nitric oxide (in the dental pulp) which in turn produces an analgesic effect by modulating nociceptive input through downregulation of sensitised nociceptors. Although this hypothesis may provide a plausible explanation for the role of the potassium ion in the treatment of DH there does not appear to be any supporting evidence from the published literature (Orchardson and Gillam 2000; Jackson 2000).

  According to Orchardson and Gillam (2000), there appears to be no convincing evidence that desensitising preparations based on potassium chloride, nitrate and citrate act in the manner proposed. It is possible that any desensitising effects may be due to constituents other than the potassium salts. Although there is some evidence that toothpastes containing potassium ions are more effective than minus-active preparations in reducing dentin hypersensitivity, the potassium-containing preparations are not always superior to controls such as sodium monofluorophosphate. Furthermore while a number of studies included in the Orchardson and Gillam (2000) review reported that potassium-containing salts were significantly better than the inactive (placebo) controls, a number of these studies did report an appreciable reduction in dentin hypersensitivity with the supposedly ‘inactive’ controls. One of the problems, in evaluating the various studies was the reported variation(s) in the extent of the ‘control/placebo’ response which may have accounted for most of the disparities between trial outcomes (Jackson 2000; Cummins 2009, 2010). A previous published systematic review by Poulsen et al. (2006) included six studies in the meta-analysis and concluded that there was no clear evidence available in the published literature for the support of potassium-containing toothpastes for the relief of DH. More recent reviews by Pol et al. (2010) and Karim and Gillam (2013) also highlighted the lack of data on the efficacy of potassium salts in reducing dentin hypersensitivity.

  The use of topical guanethidine (1 % guanethidine solution (Ismelin, Ciba-Geigy, UK)) as a desensitiser has also been advocated although there are only two published studies by Hannington-Kiff and Dunne (1993) and Dunne and Hannington-Kiff (1993). These investigators proposed that topically applied guanethidine affects the anti-noradrenergic mechanisms in the teeth.

5.4 Placebo Effect

Both placebo and nocebo effects have been documented in the published literature and may impact on the results from studies evaluating the efficacy of a drug. The term ‘nocebo’ comes from the Latin ‘noceo’, to harm, and means ‘I shall harm’, whereas the term ‘placebo’ means ‘I shall please’ (Definition of placebo 2013: http://www.medterms.com). A negative placebo effect may occur during a clinical study where patients participating in the study experience adverse side effects unrelated to the specific pharmacological action of the drug that they are taking. The nocebo effect may be associated with a subject’s prior expectations of adverse effects from treatment as well as with conditioning in which the subject learns from prior experiences to associate a medication with certain somatic symptoms (Definition of nocebo effect 2013: http://www.medterms.com). The placebo or placebo effect has been defined in the following manner:

• (a) A substance containing no medication and prescribed or given to reinforce a patient’s expectation to get well.

• (b) An inactive substance or preparation used as a control in an experiment or test to determine the effectiveness of a medicinal drug.

• (c) An active placebo – a placebo used in experimental tests of a drug that has noticeable side effects; ‘an active placebo mimics the side effects of the experimental drug’ (Definition of active placebo 2013: www.thefreedictionary.com ).

According to Oken (2008), the interaction between the clinician and the subject during a clinical study may have an impact on outcomes independent of any specific treatment. For example, ‘expectancy’ may be affected by the personal history of subject–clinician interactions and shared experiences of the subject and clinician. Several investigators have also suggested that any placebo effects during a study may also be influenced by the number of subject–clinician interactions (Ilnyckyj et al. 1997; Paternak and Zimmerman 2007 cited by Oken 2008). There may also be other non-specific benefits from this interaction during a clinical study, for example, stress reduction, decreased anxiety or improvement of mood of the subject. According to Oken (2008), some clinicians are perceived to be better clinicians than others as a result of their personality or interaction style. These factors may therefore have profound effects in clinical studies, in particular pain-type studies, for example, a dentin hypersensitivity study, designed to evaluate the efficacy of various desensitising agents.

For example, a number of published studies evaluating desensitising toothpastes have demonstrated improvement in symptoms ranging from 30 to 80 % reduction in sensitivity when comparing test toothpastes to other toothpastes and placebo controls (Clark and Troullos 1990). The results from these studies are however somewhat conflicting and difficult to interpret, due in part to different methodologies and patient selection criteria. One of the main inherent problems in conducting clinical studies designed to assess the efficacy of desensitising products is the interference of placebo and/or Hawthorne effects that may introduce a degree of bias into the study (Gillam 1997, 2011; Addy et al. 2007). Several investigators have suggested that the utilisation of a double-blind placebo-controlled study is one possible way of resolving this particular bias, although such effects cannot be completely eliminated (Jeffcoat 1993; Holland et al. 1997; ADA Acceptance Program Guidelines 2012). For example, several investigators have reported that this effect can be as high as 40 % (Curro et al. 2000; West et al. 1997). Other investigators have also alluded to this effect in their published studies (Gillam et al. 1996, 1997a; Pearce et al. 1994; Chesters et al. 1992), but to what extent the placebo effect complicates the interpretation of the results of the study is difficult to predict. It should however be noted that according to Curro et al. (2000) the placebo effect observed in dentin hypersensitivity studies is not too dissimilar to those reported in other medical and dental therapeutic studies. For example, a review of 15 post-operative pain studies by Beecher (1955) cited by Curro et al. (2000) concluded that on average symptoms were satisfactorily relieved by the placebo medication in 35 % of the patients (the placebo response range of 15–58 %). According to Hróbjartsson and Gøtzsche (2001) in a systematic review detailing 27 trials involving the treatment of pain, the placebo had a beneficial effect, as indicated by a reduction in the intensity of pain of 6.5 mm on a 100-mm visual-analogue scale. If the magnitude of the placebo effect is reproduced in a clinical study, this may well confound any effects of efficacy of the active product. These and other confounding factors, for example, a random variation in patient symptoms over time (regression to the mean/mode, conditioning effects during the study, small sample size) affecting dentin hypersensitivity studies may also be complicated by the lack of universally acceptable positive and negative controls used in equivalence and superiority studies (Gillam 2011). A further problem that may confound determining the efficacy of these desensitising products is that the clinical efficacy of these products may be at the lower end of the therapeutic range (Addy et al. 2007). Curro et al. (2000) also suggested that subjects with chronic conditions such as dentin hypersensitivity typically have episodic or fluctuating symptoms and any potential change in these symptoms over time in a clinical study may be one of improvement (the so-called expectancy effect). A patient’s expectancy of improvement may therefore influence outcomes as much as some active interventions, and this effect may be greater for novel interventions and for procedures (Oken 2008). It may therefore be suggested that the clinical study duration should be of a suitable duration (e.g. at least 6 weeks) as to minimise any ‘placebo effects’.

It is important however to acknowledge that the amount of time required for a particular desensitising agent to achieve clinical effectiveness may be affected by several factors, including (a) variations in the motivation of individual patients and their ability to apply the product as intended and (b) the nature of the test agents and their likely mode of action. These factors may therefore dictate the design, nature and duration of any proposed clinical study.

5.5 Restorative Approaches

There are a number of restorative approaches for the treatment of DH that are provided for patients with localised moderate to severe DH which require immediate palliative alleviation (Orchardson and Gillam 2006). As indicated in Chap. 6, these desensitising agents may be classified on the basis of (1) whether products do not polymerise (varnishes/precipitants/primers containing HEMA), (2) whether they undergo setting or polymerisation reactions (conventional glass ionomer cements, or resin-reinforced glass [ionomers/compomers; adhesive resin primers; adhesive resin bonding systems), (3) the use of mouthguards, (4) iontophoresis combined with fluoride pastes or solutions and (5) lasers (Pashley 2000). Examples of these products are resins, varnishes, primers, dentine bonding agents and glass ionomer cements which contain fluoride, aluminium, potassium or ferric oxalates; silica or calcium-containing materials; and protein precipitants to decrease dentin permeability or block the fluid movement through dentin (Tables 5.3 and 5.4). Other miscellaneous treatment approaches have also been recommended, for example, occlusal adjustment associated with cervical abfraction lesion (Coleman et al. 2003), crown restorations, root coverage surgery, pulp extirpation, extraction (Ong and Strahan 1989), homoeopathic remedies (Plantago) (www.hpathy.com), propolis (Mahmound et al. 1999) and hypnosis (Starr et al. 1989; Eitner et al. 2010). It should however be acknowledged that some of these restorative procedures may also initiate post-operative sensitivity, for example, crown preparations, restorations, restorative materials, nonsurgical (scaling) and surgical procedures and sensitivity from bleaching or whitening procedures. One of the problems, however, when recommending or evaluating these restorative approaches for the treatment of dentin hypersensitivity is that dental professionals not only appear to be uncertain as to the most successful way in which to manage dentin hypersensitivity but also express a level of dissatisfaction with the various products and techniques available (Cunha-Cruz et al. 2010).

Table 5.3 Selected dentin desensitising solutions and products tested in clinical trials

Table 5.4 Selected professionally applied dentin desensitisers tested in clinical trials

• 1. Selected Non-polymerising Products

  These products include varnishes/precipitants/primers containing HEMA.

  Historically varnishes and cavity liners such as Copalite have been recommended for the treatment of dentin hypersensitivity (Wycoff 1982), although most of these varnishes appear to provide inadequate insulation against thermal conduction under restorative materials (Voth et al. 1966). Varnishes such as copal varnishes (copal resin in an ether solution) were shown to be incompatible with the resin-based restorations due to their effect on the polymerisation process (Tjan and Chan 1987). As a result, a number of resin-compatible cavity varnishes, for example, Univar/Uniseal/Microjoin (Sci Pharm Duarte, Ca, USA) were introduced and evaluated on their ability to block dentin tubules (Tjan and Chan 1987; Tjan et al. 1987). Fluoride varnishes such as Duraphat® (Colgate Oral Pharmaceuticals), Dentinbloc (Colgate Oral Pharmaceuticals), Bifluorid 12 (VOCO GmbH), Isodan® (Septodont), Shellac F Cervitec® or Fluor Protector (Ivoclar Vivadent) have also been previously evaluated for the treatment of dentin hypersensitivity (Collaert et al. 1991; Thrash et al. 1992; Kielbassa et al. 1997; Gaffar 1999; Morris et al. 1999; Panduric et al. 2001; Merika et al. 2006; Ritter et al. 2006; Hoang-Dao et al. 2009; Bhandary and Hegde 2012). According to Ritter et al. (2006), the topical application of fluoride varnishes was thought to create a barrier by the precipitation of CaF₂ onto the exposed dentin surface which, in turn may occlude the dentin tubules thereby reducing dentin permeability and, as a consequence, DH. From a practical viewpoint, the application of a fluoride varnish may be useful in identifying whether a patient has DH during the diagnosis examination in order to rule out any other dental cause. The application of fluoride varnishes may also be incorporated in a stepwise management programme where non-invasive procedures are undertaken, and depending on whether the problem has been resolved or not, the clinician may either proceed to provide additional applications of the varnish or opt to provide a more invasive procedure (Orchardson and Gillam 2006). Other treatment approaches include the application of Hema-containing primers, for example, Gluma (5 % glutaraldehyde primer and 35 % hydroxyethyl methacrylate), calcium hydroxide and oxalate varnishes (Pashley 2000; Orchardson and Gillam 2006) (Tables 5.3 and 5.4). The efficacy of Hema-containing primers in treating DH has been evaluated in a number of clinical studies. For example, Felton et al. (1991) applied the primer to the facial surfaces of crown preparations in 20 patients and reported that in response to air, tactile and osmotic stimuli, DH was significantly reduced after 14 days compared to the control group. Other investigators (Dondi dall’ Orologio and Malferrari 1993, Dondi dall’ Orologio et al. 1999, 2002; Duran and Sengun 2004) reported similar successful results when using the primer on exposed dentin. However a study by de Assis et al. (2006) in periodontal patients with hypersensitive teeth failed to demonstrate any efficacy with Gluma Desensitizer® compared to the control group. A more recent study by Mehmood et al. (2011) compared Gluma Desensitizer® with Duraphat® in 196 patients with non-carious cervical lesions. They conclude that Gluma Desensitizer® significantly reduced DH compared to the Duraphat® varnish. A 6-month study by Aranha et al. (2009) evaluated Gluma Desensitizer® with four other products or therapies (Seal and Protect, OXA GEL, fluoride and low-intensity laser treatment). They concluded that although both Gluma Desensitizer® and Seal and Protect had an immediate effect in reducing DH, all therapies demonstrated lower sensitivity scores at the 6-month evaluation point. The proposed mechanism of blocking the tubules with HEMA-containing primers may be a result of the glutaraldehyde component reacting with the albumin within the dentin fluid by protein precipitation; this in turn may reduce the outward fluid flow and as a consequence reduce DH (Pashley 2000).

  The application of oxalate-containing solutions has also been evaluated for treating DH (Muzzin and Johnson 1989; Salvato et al. 1990; Kerns et al. 1991; Morris et al. 1999; Gillam et al. 1997, 2004; Pashley et al. 2001; Camps and Pashley 2003; Tay et al. 2003; Pillon et al. 2004; Pamir et al. 2007) although according to Pashley (2000) and Orchardson and Gillam (2000), the clinical evidence is somewhat inconclusive. In this context it is of interest that despite this reservation on the efficacy of these products, 40 % of practising dentists in the USA reported using oxalate preparations in order to treat DH (Cunha-Cruz et al. 2010). A systematic review by Cunha-Cruz et al. (2011) concluded that many of the oxalate products that were included for evaluation in the review were no better than the placebo controls with the possible exception of a 3 % monohydrogen monopotassium oxalate solution. These investigators concluded that the current evidence did not support recommending using oxalates for the treatment of DH. The mechanism by which oxalate products block the dentin tubules has been demonstrated by a number of investigators (Greenhill and Pashley 1981; Gillam et al. 2001; Yiu et al. 2005). According to Yiu et al. (2005) following the application of the oxalate solution on the depletion of calcium ions from the surface dentin forces the oxalate ions to diffuse further down into the dentin tubule and react to form insoluble calcium oxalate crystals. This reaction results in a subsurface tubular occlusion which will reduce fluid flow (dentin permeability) within the dentin tubules.

  According to Pashley (2000), the use of calcium hydroxide paste has been applied for the treatment of DH. For example, Green et al. (1997) applied a 5-min treatment of calcium hydroxide on hypersensitive root surfaces and reported that in response to thermal and mechanical stimuli, DH was reduced for the duration of the 3-month study. Wolfart et al. (2004) also compared a calcium hydroxide solution with a glutaraldehyde-based dentin primer in 36 patients undergoing crown preparations and evaluated over a 30-month period. Although the investigators reported that a calcium hydroxide solution may be useful in treating DH, there were no reported differences between the two products. According to Ling and Gillam (1996) citing McFall (1986), calcium hydroxide blocks the dentin tubules by a deposition of calcium ions that bind to free protein radicals and increasing the remineralisation of the exposed dentin. It was claimed that the initial application was successful for 80–90 % of the time, but this effect rapidly diminished and frequent reapplication was required. Pashley et al. (1986) applied a calcium hydroxide paste to human dentin in vitro in order to determine its effects on dentin permeability. The results indicated that although the paste reduced dentin permeability in both smear layer and non-smear layer samples, calcium hydroxide provides little protection to an acid challenge. On the basis of these studies, it would appear that the use of calcium hydroxide on exposed root surfaces may be of limited value.

• 2. Selected Products That Undergo Setting or Polymerisation Reactions

  These products include conventional glass ionomer cements, or resin-reinforced glass ionomers/compomers; adhesive resin primers; and adhesive resin bonding systems.

  The use of conventional glass ionomer cements (GIC) or resin-reinforced glass ionomers/compomers has been recommended for a number of clinical conditions in the oral cavity, for example, as a liner in prepared cavities (Hansen 1992; Tantbirojn et al. 2006; Burrow et al. 2009), fissure sealing (Pardi et al. 2003), cementing orthodontic brackets (Charles 1998), treatment of dentin hypersensitivity (Wycoff 1982), non-carious cervical lesions (Francisconi et al. 2009) and a combined surgical/restorative intervention of gingival recession with associated non-carious cervical lesions (Santamaria et al. 2007). It should however be acknowledged that the term ‘glass ionomer cement’ is loosely applied in the published literature and therefore may be somewhat misleading as there are differences between the original GIC product and the various resin-modified and composite resin materials that have been developed over the last 20–30 years. From a clinical point of view, it is important to note that they may bind differently to the tooth surface depending on whether they are a conventional GIC or a resin-modified GIC (Tyas and Burrows 2004). According to Mount et al. (2009), with the conventional GIC or a resin-modified GIC, there is an ion exchange adhesion with the tooth surface via a polyacid interaction even though the initiation may be different (acid–base setting/acid–base setting plus photoinitiation). There is also a sustained fluoride release from the material as well as a subsequent fluoride recharging from the oral environment over time has also been demonstrated. With both the conventional and polyacid-modified composite resin systems there does not appear to be any particular benefit apart from a minimal benefit via a polyacid reaction of the polyacid-modified composite resin system (Mount et al. 2009). Several investigators have used various GIC products to treat DH, for example, Low (1981) reported a reduction in sensitivity following the placement of the material in cervical abrasion lesions. Polderman and Frencken (2007) also reported that a low-viscosity glass ionomer (Fuji VII) was more effective in treating DH than Gluma Desensitizer after 3 months and after 24 months.

  The rationale of using adhesive restorative materials (dentin bonding agents, resins and adhesives) for the treatment of DH was based on the possibility of blocking the dentin tubules (Brännström et al. 1979; Pashley 1992b). Results from the initial studies using these materials indicated that there was an immediate and long-lasting effect in reducing DH except when the adhesive sheared off the dentin surface resulting in a return to the previous baseline values (Ling and Gillam 1996). According to Tyas and Burrows (2004), the mechanism by which these materials bond to the dentin is via a hybrid layer or resin-impregnated layer. Basically this is a micromechanical interlocking of resin around the collagen fibrils exposed by the demineralisation process during the pretreatment phase when placing the material onto the dentin surface. From a clinical viewpoint, these materials offer a challenge to the dental practitioner as they are very technique sensitive and require careful handling and manipulation. It is essential that the dental professional follow the instructions from the manufacturer very carefully when placing the material in the oral environment. Furthermore it is also important that the dental professional has an understanding of the characteristics associated with both conventional glass ionomer cements, or resin-reinforced glass ionomers/compomers, and adhesive restorative materials in order to maximise the usefulness of these materials in the oral environment.

  According to Orchardson and Gillam (2006), the dental professional should be aware of the pragmatic nature of the published clinical studies of adhesive desensitising materials. For example, many of the reported studies are single-blind studies because true double-blind conditions are difficult to achieve. A further problem when analysing results from the published literature is that there has been a major change in the available products since the original introduction of dentin bonding agents, resins and adhesives. A selection of published studies that claim to relieve DH by blocking the dentin are presented in Table 5.4 (based on Orchardson and Gillam 2006 and Pashley et al. 2008 published reviews). A recent 6-month study by Veitz-Keenan et al. (2013) reported on the use of a potassium nitrate toothpaste, sealant (one-step self-etch dentin bonding agent [Clearfil S3 Bond, Kuraray, Okayama, Japan]/Clearfil Liner Bond 2 Protect Liner F, Kuraray) or restoration (dentin bonding agent [Clearfil S3 Bond]/flowable composite resin [Premise Flowable, Kerr]) for the treatment of hypersensitive non-carious cervical lesions. The results indicated that both the sealant and the restoration treatment proved equally effective for most participants in reducing dentin hypersensitivity in non-carious cervical lesions.

  The application of both adhesive restorative materials (dentin, bonding agents, resins and adhesives) would therefore appear best suited to localised rather than generalised areas of dentin hypersensitivity and would appear to be ideal for using within the stepwise minimal intervention approach as suggested by Orchardson and Gillam (2006).

• 3. Use of Mouthguards

  According to Haywood (2000) and Tredwin et al. (2006), tooth sensitivity is a common adverse reaction of external bleaching procedures. It has also been reported in the literature that patients who have a pre-existing history of DH or with gingival recession and associated DH may be more likely to experience DH during the bleaching process (Leonard et al. 2004). For patients with pre-existing dentin hypersensitivity, the use of a desensitising product, for example, 5 % potassium nitrate (toothpaste or in a bleaching tray), prior to bleaching the teeth may alleviate further discomfort during the bleaching phase of the treatment (Haywood et al. 2001, 2005). Other products such as amorphous calcium phosphate (ACP) have also been recommended for the prevention of DH/bleaching sensitivity either as a toothpaste or as a professionally applied product (Giniger et al. 2005). According to Haywood (2002), the incidence of DH/bleaching sensitivity ranges between 55 and 75 % of subjects undergoing bleaching procedures in randomised clinical trials.

  Several investigators have suggested that bleaching sensitivity is mediated by a hydrodynamic mechanism (Croll 2003; Swift 2005; Markowitz 2010). Croll (2003) described a mechanism where oxygen bubbles from the carbamide or hydrogen peroxide form in the dentin tubules during the bleaching process and initiate dentin fluid movements that in turn may activate the intradental nerves. No evidence however has been advanced to support this interesting hypothesis although the hydrodynamic hypothesis does not appear to fully explain the mechanism of pain associated with the bleaching process.

• 4. Iontophoresis Combined with Fluoride Pastes or Solutions

  Several investigators have recommended the use and application of fluoride with or without iontophoresis (Gangarosa and Park 1978; Brough et al. 1985; Gupta et al. 2010; Aparna et al. 2010) although the clinical efficacy of this technique has been questioned (Gillam and Newman 1990; Pashley 2000).

• 5. Lasers

  The use of laser technology has been advocated by several investigators for the treatment of DH (Renton-Harper and Midda 1992; Kimura et al. 2000; Yilmaz et al. 2011a, b; Umberto et al. 2012). The evidence for the efficacy of this therapy is, however, somewhat equivocal (West 2007; He et al. 2011) (see Chap. 6). According to Kimura et al. (2000), the rationale and mechanism of how laser therapy is effective in treating DH is inadequately explained. A number of investigators have proposed that lasers may work either through a process which involves the coagulation and precipitation of plasma proteins in the dentin fluid (Pashley 2000) or by the effect of the emitted thermal energy from the laser altering intradental nerve activity (Orchardson et al. 1997, 1998). McCarthy et al. (1997) however reported that both Nd:YAG and Er:YAG lasers caused alteration of the dentin surface either by melting and re-solidification of the dentin with partially blocked tubules (Nd:YAG) or by ablation of the dentin surface leaving craters and open tubules (in the dentin discs) or blocked tubules (on the root surface) (Er:YAG), but neither lasers produced a smooth glazed impermeable surface. There are a number of different laser systems that have been recommended by investigators for the treatment of DH, for example, neodymium-doped yttrium, aluminium and garnet (Nd:YAG); erbium and chromium to yttrium, scandium and gallium (Er,Cr:YSG); erbium and chromium doped to yttrium, scandium, gallium and garnet (Er,Cr:YSGG); carbon dioxide (CO₂); and diode lasers. Several investigators have also combined various lasers with fluoride varnishes and potassium nitrate gels in order to treat DH, for example, GaAlAs (BDP 600), Co₂, Er:YAG or Nd:YAG lasers and a sodium fluoride gel or varnish (Corona et al. 2003; Ipci et al. 2009); Kara and Orbak 2009 or a 810 nm diode laser and a 10 % potassium nitrate bioadhesive gel (Sicilia et al. 2009). These investigators reported positive results with the combined application of a laser and fluoride gel or varnish; however these studies had relatively small numbers of subjects per group, and therefore further well-controlled studies are required to determine whether there would be an added benefit to the patient. Several investigators have recently undertaken reviews (systematic review/meta-analysis) on the efficacy of in-office treatments or laser therapy for the treatment of DH (Lin et al. 2013; Sgolastra et al. 2013). These investigators reported that laser therapy was efficacious in reducing DH compared to a placebo control. Lin et al. (2013) however indicated that there were no significant differences between the different treatment modalities. Although laser therapy appears to be an area of interest from a research viewpoint, there appears to be limited use of lasers in dental practice when treating DH (Cunha-Cruz et al. 2010).

• 6. Other Miscellaneous Treatment

  A large number of anecdotal reports support alternative approaches for treating DH. Although these reports are not truly evidence based, they may be applied to some clinical situations. For example, periodontal surgery involving coronally positioned flaps reportedly eliminates dentin hypersensitivity in exposed root dentin (See Sect. 5.5). If DH is associated with an abfraction lesion, occlusal adjustment may also be effective (Coleman et al. 2003). Other miscellaneous procedures for the treatment of DH were reported, for example, burnishing exposed root surfaces (Ling and Gillam 1996; Pashley 2000), crown restorations, pulp extirpation, extraction (Ong and Strahan 1989) and hypnosis (Starr et al. 1989; Eitner et al. 2010).

5.5.1 Post-operative Sensitivity from Restorative Approaches

A review of the published literature would indicate that post-operative sensitivity from restorative treatment is a commonly reported feature in dental practice. One of the problems in determining the actual prevalence of the problem however, was that some of the published studies were mainly anecdotal reports in nature and as such were prone to reporting bias when claiming the elimination of post-operative sensitivity with products which use dental adhesive liners. According to Haywood (2002), there are a number of factors associated with the placement of restorations in vivo, for example, certain amalgam materials have been shown to cause post-operative sensitivity (restorative sensitivity) of up to 48 h due to shrinkage of the material rather than the predicted expansion during setting. Other factors include the contamination of composites during placement or improper etching of the tooth during tooth preparation which may result in micro-leakage; improper technique when drying the tooth or incorrect preparation of materials such as glass ionomer or zinc phosphate cements may also be problematic. The techniques involved in cavity preparation may also affect the integrity of the pulp initiating an inflammatory response and subsequent pain as well as thermal changes due to the choice of the restorative material used to restore the tooth. Galvanic reactions due to dissimilar metals have also been reported to cause post-operative pain (Haywood 2002). Porto (2012) has also suggested that there are a number of factors that may initiate post-operative sensitivity with the placement of direct resin composite restorations (Table 5.5). As previously indicated tooth sensitivity has been reported to be associated with bleaching procedures (Haywood 2000; Tredwin et al. 2006), and a number of treatment strategies have been recommend as indicated above.

Table 5.5 Possible causes of pre- and post-operative sensitivity from direct resin composites

According to Berkowitz et al. (2009), post-operative sensitivity following the placement of posterior resin-based composites is a common concern in general dental practice although the evidence for this statement is limited.

Several investigators have however suggested that one method of relieving post-operative sensitivity is by the adjunctive use of oxalate desensitisers on acid-etched dentin prior to adhesive application (Pashley et al. 2001; Tay et al. 2003). Yiu et al. (2005) however urged caution on the use of oxalate desensitisers under certain conditions, in particular with acidic, fluoride-containing total-etch adhesives due to their incompatibility problems.

According to Gillam and Orchardson (2006), DH is a common occurrence following periodontal surgery and root scaling/debridement although with well-controlled oral hygiene procedures, this problem appears to resolve over time (Tammaro et al. 2000). Several investigators have also reported that the prevalence of DH is in the region of 9–27 % before and 54–55 % following periodontal therapy (von Troil et al. 2002; Lin and Gillam 2012). The reported intensity from DH increased up to 4 weeks following these procedures, after which the recorded values returned back to the original baseline scores (Gillam and Orchardson 2006). A number of studies have also indicated that a relatively small number of patients (1.3–7 %) complain of severe DH following treatment of infrabony defects with an enamel matrix derivative (Zetterstrom et al. 1997; Heard et al. 2000; Froum et al. 2004). It is important to note that for most patients post-operative sensitivity is of a transient nature and may be adequately managed by the clinician using the recommended materials and procedures outlined in Chaps. 5 and 6. If the post-operative sensitivity has not resolved within 6 weeks, it is recommended that further investigations be undertaken to determine the cause of the problem and treat accordingly.

5.6 Periodontal Surgical Techniques

According to Gillam and Orchardson (2006), periodontal grafts and guided tissue regeneration (GTR) procedures have been described in the published literature for the treatment of gingival recession with DH. These procedures generally have predictable outcomes and may therefore be the treatment of choice for patients since this may provide a good aesthetic as well as palliative solution to their clinical problem (Drisko 2002). Both aesthetics and pain from DH have been reported as the main concerns of patients when seeking treatment (Pagliaro et al. 2003; Zaher et al. 2005). Previously one of the problems when evaluating the efficacy of the root coverage procedures and associated DH was that there was only limited evidence-based data available on the actual extent of the problem of DH before and following the procedure(s) (Gillam and Orchardson 2006). Furthermore the results from the published clinical studies generally evaluated the success or failure of specific technique and procedures with DH as an unpleasant side effect from the surgical procedure rather than specifically evaluate patients with exposed root dentin with associated DH. For example, Al-Hamdan et al. (2003) in a meta-analysis review while acknowledging that the indications for initiating root coverage procedures included DH reported that the 40 papers included in the review provided no evidence to either determine the prevalence or extent of the problem in patients with gingival recession. This observation was also substantiated by Pagliaro et al. (2003) who reported that out of the 90 accepted papers included in the review, DH was generally identified as being either present or absent in 19 papers (21.1 %) and only nine articles (10 %) recorded any pre- and posttreatment data, with only two of these studies quantifying DH on a recognised 10-point pain scale.

Several investigators have suggested that if the root coverage of the gingival defect cannot be predictably treated by conventional surgical root coverage procedures, then the remaining exposed cervical dentin could be treated with a more invasive restorative material (Tugnait and Clerehugh 2001; Drisko 2002). This may be as a result of either patient-related factors or an extensive loss of interdental gingival and bone tissue as a result of periodontal disease. Open gingival embrasures, also called ‘black triangles’, may be produced interfering with the aesthetics of the smile (Sharma and Park 2010). A relatively simple nonsurgical approach to this problem was proposed by Greene (1998) who suggested the construction of a flexible gingival mask of silicone using a simple two-stage impression technique. Localised recession defects may also be addressed by using a partial laminate porcelain veneer technique (Capa 2007). Zalkind and Hochman (1997) also recommended the use of tooth-coloured composite as a minimally invasive adhesive restoration. The latter restorative technique may also resolve associated carious lesions and alleviate pain symptoms from DH (Zalkind and Hochman 1997). Restoration of a non-carious/carious cervical lesion with glass ionomer cements may also have the added advantage of fluoride release over a prolonged period of time (Özgünaltay and Önen 2002). A combined surgical and restorative approach has been described by Santamaria et al. (2007) in three case reports of patients with Miller’s Class I gingival margin defect with associated non-carious cervical lesions. These authors recommended a combined surgical/restorative approach using a coronally advanced flap procedure with/without a connective tissue graft together with a resin-modified glass ionomer restoration when dealing with this particular problem. However as these investigators acknowledged, further longitudinal randomised clinical trials are required to support this combined approach to correcting gingival recession defects and associated non-carious cervical lesions. If the non-carious cervical lesion is below the cementum–enamel junction, this may cause problems when adapting the gingival flap to the root surface, and modification of the root surface to eliminate the concavity of the lesion may require reshaping of the root surface using diamond finishing burs (Santamaria et al. 2007). It is however imperative that clinicians should avoid placing subgingival restorations whenever possible in order to prevent plaque retention as well as maintaining the biological width when placing crowns (Drisko 2002).

Several investigators have reported that there is an increase in DH following scaling and periodontal surgery although this effect may be transient in nature (von Troil et al. 2002; Gillam and Orchardson 2006). One possible explanation for this observation is that periodontal procedures such as scaling may initially uncover the dentin tubules (a created smear layer) exposing them to the oral environment thus causing patients transient pain when eating or drinking in the days following the procedures. It is evident however that a smear layer may be covering the dentinal tubules since the cementum would have been removed in order for the root dentine to be exposed (Pashley 1984). Natural occlusion may also occur due to the precipitation of salivary constituents onto the tooth surface (Kerns et al. 1991; Kawasaki et al. 2001). Several investigators have speculated that scaling and root planing procedures may remove 20–50 μm of cementum thus exposing the dentinal tubules to external stimuli (Nishida et al. 1976; Wallace and Bissada 1990). It has also been suggested that bacterial invasion of exposed cementum associated with periodontal disease occurs after the cementum has been altered by physiological, bacterial or environmental factors (Love and Jenkinson 2002). The implications on the integrity of the pulp as a result of bacterial invasion of the dentin tubules may therefore depend on whether the pulpo-dentin defences are able to withstand this insult. According to Love and Jenkinson (2002), it is likely that the dentin fluid components including albumin, fibrinogen and IgG are involved in host defence by interacting directly with bacteria and metabolites and by reducing the permeability of dentin. It has been speculated that any bacterial invasion of the dentin tubules would have a greater impact on outward fluid flow than with inward diffusion of noxious substances due to changes in the tubular radius rather than with diffusion characteristics of bulk fluid movements per se (Pashley 1992a, b). This speculation was however based on in vitro observations and does not appear to have been substantiated in clinical practice. Several investigators have recommended the use of a topical fluoride or a desensitising polishing paste application with a view to alleviate patient discomfort following scaling and root planing procedures (Paine et al. 1998; Hamlin et al. 2009; Schiff et al. 2009a, b; Milleman et al. 2012; Li et al. 2013; Neuhaus et al. 2013). Oxalate solutions have also been advocated for post-operative hypersensitivity, for example, Wang et al. (1993) applied a 6 % ferric oxalate solution during periodontal surgery and Pillon et al. (2004) applied a 3 % potassium oxalate application following subgingival scaling and root planing. Both investigators reported a reduction in post-operative hypersensitivity following application of the oxalate solutions.

From a treatment and management perspective, a number of classifications have been previously proposed in the published literature in order to facilitate both a diagnosis and a template for the correction of gingival margin defects. Currently the classification used in root coverage procedures is the Miller classification system ([I–IV] (Miller 1985). An example of Miller’s Class I defect may be seen in Fig. 5.3. The advantage of this classification is the ability to correlate treatment prognosis/outcome and anatomical features, whereas previous classification systems used either anatomical features or treatment prognosis only. A number of materials and techniques have been reported in the literature, and these include guided tissue regeneration (GTR), coronally advanced flap and Emdogain (CAF + EMD), connective tissue graft (CTG) and free gingival graft (acellular dermal matrix allograft/Mucograft ADM) (Table 5.6, Fig. 5.4a, b). A recent systemic review by Douglas de Oliveira et al. (2013), however, suggested that currently there is insufficient scientific evidence to conclude that surgical root coverage procedures predictably reduce DH.

Fig. 5.3

Miller Class I defect of a patient complaining of DH following completion of the orthodontic treatment. The patient was referred in order to provide root coverage of the lower central incisors (Acknowledgement KN Al Shayeb)

Table 5.6 Periodontal flap surgery/periodontal plastic surgical techniques

Fig. 5.4

(a) Clinical photograph of a Miller Class III with fenestration (Pre-operative). Patient was complaining of gingival sensitivity associated with the mandibular lower left central incisor (Acknowledgement KN Al Shayeb). (b) Clinical photograph of the Miller Class III defect 1 week post op

5.7 Conclusions

The hydrodynamic theory promotes two basic approaches based on in vitro, in situ, animal and human studies for treating DH, namely, blocking dentin tubules and nerve desensitising. There have been a number of reviews that have investigated the vast array of products and treatment approaches (both in-office or OTC) that dental professionals have used in order to treat DH, and it is evident that there is no widespread agreement as to which is the best material or procedure to treat DH (Gillam 1992; Orchardson and Gillam 2006; Cunha-Cruz et al. 2010; Lin et al. 2013). One of the problems however in evaluating the effectiveness of desensitising products is the variability in the methodology, sample size and duration used in the published clinical trials. Other factors that may influence the efficacy of the product under test in clinical studies include the impact of placebo and non-placebo effects, the random variation in patient symptoms over time (regression to the mean/mode) and the relationship between the subject and the examiner. It is also evident that patients may experience post-operative sensitivity from the various procedures in the dental office, for example, from restorative procedures, restorations, crowns, bleaching of the teeth and nonsurgical and surgical procedures. Although these effects may be of a transient nature, they may cause undue distress to the patient and their quality of life which may in turn necessitate further treatment. This may include simple reassurance and monitoring or further investigation and treatment of the particular problem. It is essential that the patient is monitored within a practical management programme, and in most situations a stepwise approach (minimally invasive) including preventive measures may be incorporated (see Chap. 6). The use of this stepwise approach as proposed by Orchardson and Gillam (2006) may enable the dental professional to use a combination of products, restorative approaches and treatment philosophies in order to successfully treat DH.