Dentine Hypersensitivity
Transcription
Dentine Hypersensitivity
Dentine Hypersensitivity Recommendations for the Management of a Common Oral Health Problem AUTHORS: Editorial Dentine hypersensitivity is a common global oral health problem affecting many individuals, but despite this only a small proportion of people suffering with sensitive teeth seek advice from their dental professional (Zapera 2007). Irina Laura Chivu-Garip DDS Scientific Affairs Manager Colgate-Palmolive Europe Lone Lenes DDS Scientific Affairs Manager, Colgate-Palmolive Nordic Tanja Borch DDS, PhD Academic Affairs Advisor Colgate-Palmolive Nordic In recent years, dental professionals have grown increasingly aware that dentine hypersensitivity is an important issue that needs addressing both from a diagnostic and a management perspective. However, a survey among Danish dentists shows that only 23% of them screened their patients for dentine hypersensitivity as part of the regular dental check-up (Zapera 2009). It is therefore important that dental professionals screen their patients for this regularly. Advances in scientific understa ding have laid foundations for new approaches to the management of dentine hypersensitivity, which include control of the underlying condition, as well as management of the discomfort. This material provides an overview of dentine hypersensitivity for dental professionals, including an internationally-accepted definition of the condition, information on its epidemiology and aetiology, and its relevance for clinical practice to both patients and dental professionals. It continues by examining strategies for prevention, management and treatment, by focusing on the most common underlying conditions responsible for dentine hypersensitivity. It concludes with a concise management strategy, offering a valid option aimed at helping patients suffering (or at high risk of suffering) from dentine hypersensitivity. Katerina Solomou MSc, PhD Scientific Affairs Manager Colgate-Palmolive Greece SCIENTIFIC CONSULTANTS: Richard Chesters BSc Scientific Consultant Colgate-Palmolive Europe Diane Cummins BSc, MSc, PhD Worldwide Director Knowledge Management Oral Care, R&D Colgate-Palmolive USA Cynthia Murphy BSc, MSc, PhD Seniot Technical Associate Knowledge Management Oral Care, R&D Colgate-Palmolive USA 2 PROFESSIONALKNOWLEDGE Content Editorial.............................................................................................................2 Definition of dentine hypersensitivity.............................................................4 Epidemiology....................................................................................................4 Relevance..........................................................................................................4 Aetiology...........................................................................................................6 Treatment principles for dentine hypersensitivity..........................................9 Management of dentine hypersensitivity and underlying conditions.......18 References......................................................................................................29 3 PROFESSIONALKNOWLEDGE About Dentine Hypersensitivity Definition of dentine hypersensitivity Dentine hypersensitivity has been defined as a short, sharp pain arising from exposed dentine in response to stimuli - typically thermal, evaporative, tactile, osmotic or chemical - and which cannot be ascribed to any other dental defect or disease (Canadian Advisory Board on Dentine Hypersensitive Teeth, 2003). Epidemiology Dentine hypersensitivity is a widespread condition with a reported prevalence varying from as low as 4.5% to as high as 57% (Cummins 2009), depending upon the population and the criteria used to assess sensitivity. A Nordic countries survey of adults (Zapera 2007) shows that 79% suffer from occasional dentine hypersensitivity, with one in four people suffering from it at least once a week and 9% being affected every day. The teeth most frequently affected are the permanent premolars (38%), followed by incisors (26%) and canines (25%). Least affected are molars (12%). Premolars 38% Incisors 26% Canines 25% Molars 12% Premolars are most frequently affected by hypersensitivity The sites of those teeth most commonly affected are the buccal cervical regions. Orchardson and Collins (1987) found that in 90% of cases the hypersensitive area was at the cervical margin. Occlusal/buccal sites are also now becoming more frequently affected in young adults, probably as a result of dental wearing caused by a combination of erosion and abrasion (Jaeggi and Lussi 2006). Dentine hypersensitivity can present at any age, but the majority of individuals range in age between 20 and 50 years with a peak in prevalence in the age range 30-39 year (Cummins 2009). Relevance Dentine hypersensitivity is a painful experience which, for the majority of sufferers, generates a very unpleasant perception, causing them to adapt by developing new habits, like protecting the sensitive tooth with the tongue, drinking on the opposite side of the mouth or even avoiding ice-cold food and drinks completely. For some people, dentine hypersensitivity can be so disturbing that it affects their quality of life. 4 PROFESSIONALKNOWLEDGE 40 33,1 36,0 OHIP-G summary score 30 20 14,3 10 0 10,7 < 40 years 40+ years General population < 40 years 40+ years Patients Comparison between the OHR QoL of patients with hypersensitivity and the general population in different age groups (Bekes et al. 2009) Influence on the dental visit Dentine hypersensitivity can even be provoked by some standard in-surgery procedures, thereby making a regular dental visit unpleasant and painful for the patient. The discomfort due specifically to dentine hypersensitivity may add stress to an already stressful experience and environment for the patient. A conscientious dental professional, may tend to work more slowly, resulting in delays and an inability to complete the dental procedure within the duration of the scheduled visit. In the most severe cases, patients may even require local anaesthesia. However management options are now available to enable dental professionals to create a calmer environment for both the patient and the professional, by initiating a dentine hypersensitivity treatment before any potentially painful, stress-provoking dental procedure is performed. 5 PROFESSIONALKNOWLEDGE ABOUT DENTINE HYPERSENSISTIVTY Influence on quality of life A recent Quality of Life (QoL) study conducted in Germany (Bekes et al. 2009) shows that hypersensitive teeth affect people’s oral-health-related (OHR) quality of life as measured by the Oral Health Impact Profile-Germany (OHIP-G) score. The OHIP-G summary score is almost three times higher for patients seeking care for hypersensitivity compared with the score for the general population, and the impact is comparable with that of other oral diseases and conditions such as craniomandibular dysfunctions. Aetiology The most widely accepted theory to explain the aetiology of the pain caused by dentine hypersensitivity is the Hydrodynamic Theory advanced by Brannström (1972). Exposed dentine with open dentine tubules. Photos: www.thejcdp.com, 2007 According to the Hydrodynamic Theory, dentine hypersensitivity occurs when the external stimulus contacts exposed dentine and triggers a change in the flow of dentinal fluid. The resultant pressure change across the dentine activates intradental nerve fibres to cause immediate pain. The Hydrodynamic Theory of dentine hypersensitivity also explains that dentinal tubules are open at the dentine surface and unobstructed all the way to the pulp. Scanning electron microscopy has shown that tubules in exfoliated teeth clinically characterised as "sensitive" are eight times more numerous, twice larger in diameter and are open, whereas tubules in "non-sensitive" teeth are less numerous, smaller, and usually blocked. Non-sensitive dentine Sensitive dentine Microscopy images showing difference in structure between sensitive and non-sensitive dentine. 6 PROFESSIONALKNOWLEDGE Poiseuille’s law of fluid dynamics predicts that the flow of fluid in the sensitive tubules would therefore be 16 times greater than that of non-sensitive teeth (Absi et al. 1987). Combining the increase in diameter of open tubules with the greater number of dentine tubules in sensitive teeth, the flow of fluid in sensitive teeth would therefore be expected to be approximately 100 times greater than in non-sensitive teeth (Canadian Advisory Board on Dentine Hypersensitive Teeth, 2003). Illustration of hydrodynamic theory mechanism - movement of fluid in the dentine tubules Photo courtesy of Inside Dental Assisting. Most pain-producing stimuli, especially the most problematic cold and evaporative stimuli, cause an outflow of dentinal fluid. This results in a pressure change across the dentine which activates intradental A-beta and A-delta nerve fibres, via a mechanoreceptor response, to cause pain. In addition, the fluid movement in the tubules can cause an electrical discharge, known as ”streaming potential”, which may contribute by electrically stimulating a nerve response. By contrast, heat causes a relatively slow retreat of dentinal fluid, and the resultant pressure changes activate the nerve fibres in a less dramatic fashion. This is consistent with the fact that heat is generally a less painful stimulus than cold. 7 PROFESSIONALKNOWLEDGE In a study among Australian dentists (Amarasena 2011), cold and air stimuli were reported as the most frequent triggers for dentine hypersensitivity. Triggers Stimuli % n Cold 80,1 % 920 Air 23,2 % 266 Touch 20,7 % 238 Hot 13,0 % 149 Dietary acid 6,9 % 79 Endogenerous acid 0,7 % 8 Other 6,1 % 70 Patient A Patient B Clinical apperance is not necesarily corelated with the reported degree of sensitivity The weight of evidence suggests that this occurs not only because of the subjective nature of pain, but also because of the natural process of tubule occlusion which occurs over extended time periods, as a result of precipitation of calcium phosphate complexes triggered by proteins in saliva (Cummins 2010). For many years it has been known that calcium and phosphate ions in saliva can remineralize tooth defects, such as early carious lesions. Research into the mechanism of natural desensitisation suggests that calcium and phosphate ions, associated with salivary glycoproteins, can also facilitate tubule plugging. Although in periodontal healthy patients dentine hypersensitivity is generally associated with good oral hygiene, it has been shown that general dental hygiene may be hampered by the discomfort arising from dentine hypersensitivity with the consequence that persistent accumulation of dental plaque can increase the risk of caries and periodontal problems (Carranza 1996). This therefore provides a strong clinical reason for dental professionals to assess and treat dentine hypersensitivity, as well as for the patient’s comfort and quality of life. 8 PROFESSIONALKNOWLEDGE Photo courtesy of: Bo Danielsen, Head of SKT, Copenhagen University Photo courtesy of: Chief Dentist, Ulla Pallesen, Copenhagen University Like any other condition that involves subjective experiences such as pain, there is a difference in reported hypersensitivity by patients displaying the same exposure to aetiological factors. Dental practitioners often face the question of ”why some patients with exposed roots experience dentine hypersensitivity whilst others do not?” The clinical observations are not necessarily correlated with the degree of subjective sensitivity reported by the patient. For example, patient A (below) experiences no pain, despite advanced tooth wear lesions, while patient B, with minimal gingival recession in the first premolar reports severe pain. Treatment Principles 1. Desensitising the nerves. 2. Occlusion of open tubules to block the hydrodynamic mechanism. Desensitising the nerves Nerve desensitisation is based on potassium, which can depolarise the excited nerve, thus ‘numbing’ the pain associated with dentine hypersensitivity (Orchardson & Gillam 2000). Potassium nitrate (5%), potassium chloride (3.75%) and potassium citrate (5.5%) have all been used in toothpastes for dentine hypersensitivity relief with each salt providing 2% potassium ions. Nerve desensitisation mechanism Clinical studies have shown that equimolar concentrations of potassium (2%) delivered from any one of these three potassium salts are effective in reducing dentine hypersensitivity in comparison with regular fluoride toothpastes. However using this method to achieve a reduction in dentine hypersensitivity takes at least two weeks of twice-daily use to yield measurable reductions in sensitivity, and longer time periods - generally four to eight weeks - to demonstrate significant levels of pain relief (Chesters et al. 1992, Ayad et al. 1994, Schiff et al. 1994, Hu et al. 2004, Wara-Aswapati et al. 2005). The addition of fluoride for cavity protection, an antibacterial ingredient for plaque and gingivitis control, crystal inhibitors and high cleaning abrasives for tartar control and whitening respectively, to potassium-based toothpaste, do not seem to have a negative impact on sensitivity relief. Based upon the available data, it can be concluded that potassium-based toothpastes do not provide instant relief from dentine hypersensitivity, which seems an important benefit to those in need to address this condition. 9 PROFESSIONALKNOWLEDGE TREATMENT PRINCIPLES Different therapeutic approaches have been used for treating dentine hypersensitivity. Today two basic treatment principles are used: While there is a substantial evidence base for recommending the use of a potassium-based desensitising toothpaste, some authors have suggested that support for the efficacy of such toothpastes is equivocal, as some studies also showed no statistically significant difference, when compared with a regular fluoride toothpaste (Manochehr-Pour et al. 1984, Gillam et al. 1996, West et al. 1997, Poulsen et al. 2006). The variations in the clinical results have been attributed to differences among clinical study parameters, especially population and scoring methods, and to the well-known Hawthorne effect. The fact that placebo control products can reduce sensitivity by as much as 40% from baseline has significantly impacted the ability to differentiate the efficacy of a test product in some studies. In vitro studies of the mechanism of action of potassium salts have shown that they can dramatically reduce the excitability of intra-dental nerves. Specifically, raising the concentration of potassium ion significantly above the physiological level in the extra-cellular fluid induces depolarization of the nerve cells, a brief excitatory burst, following which the nerves become unresponsive to excitatory stimuli. Nevertheless, for the clinical effect to occur, the potassium ion has to diffuse from the oral cavity into the dentin tubules, then through the dentin tubules against the flow of dentin fluid to the site of action at the interface of the inner dentin surface and the pulp chamber, i.e.,the nerve endings. This explains the slow time to action, as to achieve significant pain relief, the concentration of potassium must build up in the fluid surrounding the nerve ending, which typically takes a period of 4 to 8 weeks, and be maintained at that level on an ongoing basis. If and when treatment with potassium-based products is ceased, elevated levels of potassium at the site of action are diffused, and sensitivity relief is lost (Cummins 2010). Occluding dentine tubules The second treatment principle in dentine hypersensitivity aproach is based on agents that block exposed, open tubules, thereby preventing the external stimuli from causing fluid movement and triggering pain (Orchardson, Gillam 2006). There are multiple and complex ways in which different technologies and products could potentially act to occlude tubules, such as: a. b. c. Deposition of a thin film coating: materials such as restorative resins and dentin bonding agents can create an “artificial smear layer” on the exposed dentin and cover the open tubules. Deposition of a layer of fine particles: materials delivered directly from a dentifrice, e.g. fine abrasive particles, or formed as precipate in situ, e.g. strontium, stannous fluoride, and calcium phosphate particles, have been suggested to form a physical barrier on the exposed dentin and in the openings of the tubules. Induction of natural mineral formation in situ: technologies such as the NovaMin® bioactive glass and the new Pro-ArginTM Technology, have been proposed to physically adhere to the exposed dentin surface and the openings of the tubules, to mediate the formation of calcium-and phosphate-rich mineral. 10 PROFESSIONALKNOWLEDGE Occluding dentine tubules mechanism In the following different technolgies are reviewed: Glutaraldehyde and HEMA Glutaraldehyde is an occluding agent which creates a coagulation plug inside the dentine tubules, via precipitation of serum albumin (Dijkman e al. 1994, Bergenholtz et al. 1993, Schüpbach et al. 1997, Qin et al. 2006). In the presence of hydroxyethyl methacrylate (HEMA), glutaraldehyde together with serum albumin induces the polymerisation of HEMA (Qin et al. 2006). Glutaraldehyde +/- HEMA has been used only in-office products. Some clinical trials have shown a reduction in dentine hypersensitivity (Felton et al. 1991; Dondi dall’Orologio G and Malferrari S, 1993; Kakaboura et al. 2005; Ishihata et al. 2009; Ozen et al. 2010; Yu et al. 2010), but others have not shown any benefit (Sobral et al. 2005; de Assis et al. 2006). Strontium salts Strontium salts are said to work by precipitating strontium and depositing fine particles of insoluble strontium compounds on dentine surfaces and within the dentine tubules (Cummins 2010, Earl et al. 2010). Strontium chloride (10%) was the first strontium salt used in toothpastes, but it was not compatible with fluoride, and was largely replaced by potassium-containing toothpastes, as the potassium ion was considered to be a more effective desensitising agent. Later on, strontium was again introduced in desensitising toothpaste in the form of strontium acetate, which is compatible with fluoride. Despite the long history of strontium toothpastes, a review published in 2010 identified that the clinical data regarding long-lasting relief during routine, twice-daily brushing is equivocal (Cummins 2010). More recently, a study suggested that a 8% strontium acetate toothpaste provided significant relief from dentine hypersensitivity, and that there was no significant difference between the strontium toothpaste and an argininecalcium carbonate based toothpaste, which has been previously proven to provide significant reduction in dentine hypersensitivity (Hughes et al. 2010). 11 PROFESSIONALKNOWLEDGE In addition, another study suggested that the 8% strontium acetate toothpaste may be effective in relieving hypersensitivity immediately after direct topical application, compared with a regular fluoride toothpaste (Mason et al. 2010). However, it is noteworthy that the first of these studies did not include a negative control and the second did not include a positive control, precluding meaningful interpretation of their results. For this reason, the results of three new clinical studies published in 2011 (Docimo et al. 2011, Li et al. 2011, Schiff et al. 2011) are important because they clearly showed that 1) the 8% strontium acetate toothpaste provides inferior efficacy in dentine hypersensitivity relief compared with an arginine-based toothpaste, and 2) the 8% strontium acetate toothpaste is no more effective in providing immediate relief of dentine hypersensitivity than a regular fluoride toothpaste (Cummins 2011). Stannous salts Stannous fluoride has also been used as an occluding agent, and is thought to work by precipitating insoluble stannous metal compounds on the dentine surface, thereby occluding the tubules. Stannous fluoride-based products (either as an anhydrous gel or in toothpaste formulations), have been shown significantly to reduce dentine hypersensitivity over four to eight weeks of twice-daily use (Thrash et al. 1994, Schiff et al. 2005, Schiff et al. 2006, Walters 2005). The review by Cummins (2010) confirmed the effectiveness of properly formulated dentifrices containing stannous fluoride, when used over a four to eight week period. It however identified that stannous fluoride does not provide instant relief. In addition, stannous-based products can result in tooth staining and poor taste (Cummins 2010). A more recent clinical trial, however, suggested that a stannous fluoride toothpaste provided improvement in the negative effects of both tactile and air-blast stimuli when compared with a fluoride-containing negative control, after both three days and two weeks of product use (He et al. 2011). Recent clinical studies on a new variant of the technology, containing stannous chloride with sodium fluoride (NaF), demonstrated that four to eight weeks of product use are required for significant improvement in hypersensitivity compared with fluoride-containing negative control toothpastes (Ni et al. Abstract 2825 2011, Du et al. Abstract 2826 2011). In another clinical trial, a stannous chloride, NaF-containing toothpaste provided reductions in dentine hypersensitivity after four to eight weeks of use, comparable with a toothpaste with 2% potassium ion (Ni et al. 2010). Interestingly however, a recent clinical study appears to be the first to compare these two variants of the technology. This study showed that the stannous fluoride toothpaste delivered better sensitivity relief than both the stannous chloride, NaF-containing paste and a sodium fluoride negative control after four and eight weeks of use (CP data on file), while the stannous chloride, NaF-containing paste was not significantly different from the negative control at four and eight weeks. These studies demonstrate the importance of properly stabilising stannous salts in formulation, for optimal hypersensitivity relief. 12 PROFESSIONALKNOWLEDGE Fluorides High-concentration fluorides can reduce dentine hypersensitivity probably through precipitation of calcium fluoride globules within the dentine tubules (Orchardson and Gillam 2006; Porto et al. 2009). Professionally-applied high-fluoride products, such as fluoride varnish (22,600 ppm fluoride) have been shown significantly to reduce dentine hypersensitivity following a single application (Gaffar 1998). Calcium sodium phosphosilicate Calcium sodium phosphosilicate (CSPS) – also referred to as Bioglass® and sold commercially as NovaMin® - is an occluding agent used in toothpastes and in-office products. This technology is thought to work by forming a calcium phosphate layer that occludes open dentinal tubules (Greenspan 2010). In more detail - calcium and phosphate ions are first released into the local environment and then precipitate, resulting in the formation of a calcium phosphate layer, which in turn crystallises into a hydroxyapatite-like material (Greenspan 2010). The CSPS particles remain on the dentin surfaces through interactions with collagen, and serve as a long-term reservoir of calcium and phosphate ions. The effectiveness of CSPS in toothpaste formulations containing 5% and 7.5% NovaMin®, is supported by data showing significant improvement of dentine hypersensitivity compared with baseline, and superiority in comparison with control toothpastes (Du et al. 2008, Burwell 2009, Litkowsky and Greenspan 2010, Sharma 2010, Salian et al. 2010, Pradeep et al. 2010, Gendreau et al. 2011). Moreover, a 5% NovaMin® dentifrice showed a statistically significant greater reduction in dentine hypersensitivity at two and four weeks compared with both a potassium dentifrice and a regular fluoride dentifrice (Salian et al. 2010). Similarly, a 7.5% NovaMin® dentifrice provided significant reductions in dentine hypersensitivity at two and four weeks compared with a potassium-based and a stannous fluoride toothpaste (Sharma et al. 2010). It should be pointed out that a 5% NovaMin® toothapste is significantly more effective that a 10% strontium chloride toothpaste at two and six weeks (Du et al. 2008). However, so far there is no published data showing an instant reduction of sensitivity. The characteristics of an ideal desensitising agent? It is generally recognised that instant relief is a highly motivating factor for patients, and complete and robust dentine occlusion is the most promising strategy to achieve this. Unfortunately, most desensitising agents are unable to provide instant relief. Since 1935 - when Grossman introduced them - the ideal characteristics of a desensitising agent have been accepted as being non-irritant to the pulp, relatively painless on application, easily applied, rapid in action, effective for a long period, without staining effects and consistently effective. 13 PROFESSIONALKNOWLEDGE Ideal Desensitising Agent Non-irritant to the pulp Painless on application Easy to apply Rapid in action Effective for a long period No staining effects Consistently effective Target both underlying causes and symptoms Characteristics of an ideal desensitising agent according to Grossman, Markowitz and Pashley Apart from these traditionally stated requirements, a recent review (Markowitz and Pashley 2007), suggested that new desensitising technologies should target both the underlying causes and the symptoms of dentine hypersensitivity. This could be achieved, firstly, by increasing the mineral density of the dentine surface itself (improving resistance to wear by both acid erosion and abrasion) and secondly, by plugging and sealing open tubules with a calciumand phosphate-containing dentine-like substance (to block diffusion through the tubules into the dentinal sub-surface and increasing acid resistance). The review also suggested that the ideal dentine hypersensitivity treatment would mimic the natural desensitising process that leads to spontaneous occlusion of open dentinal tubules over time. A successful treatment would render dentine non-sensitive and sclerotic - such a state being more desirable than open, patent, sensitive dentine. The authors concluded that any treatment that completely seals dentinal tubules will restore that surface to a healthy state. Arginine and Calcium Carbonate The newly introduced desensitising technology - Pro-ArginTM Technology, based on 8% arginine and calcium carbonate, pushes scientific research (Kleinberg 2002) into examining the role saliva plays in the mouth’s natural tubule occlusion process, to deliver both instant and lasting hypersensitivity relief in a series of published clinical trials (Ayad et al. 2009, Nathoo et al. 2009, Docimo et al. 2009, Schiff et al. 2009, Docimo et al. 2009, Schiff et al. 2009, Hamlin et al. 2009, Fu et al. 2010, Que et al. 2010, Docimo et al. 2011). Scanning Electron Microscope (SEM) photograph of untreated dentine surface with exposed tubules. SEM photograph of dentin surface showing occlusion of dentinal tubules after application of Pro-ArginTM Technology. 14 PROFESSIONALKNOWLEDGE The technology has been formulated into easy-to-apply delivery vehicles, like everyday toothpaste or professional prophylaxis paste, without affecting clinically documented dentine hypersensitivity relief and without detrimental tooth staining or unpleasant flavor. The technology is also compatible with fluoride, to provide additional strengthening of dental hard tissues, delivering virtually all of the attributes of an ideal desensitising agent. When applied immediately before treatment, the in-office desensitising paste has been clinically documented to provide better relief of the dentine hypersensitivity associated with dental prophylaxis than a pumice-based control paste (Hamlin et al.2009). In a second, double-blind clinical trial, a single professional application of the 8% arginine and calcium carbonate desensitising paste after dental scaling provided significant reduction in dentine hypersensitivity immediately after application that was sustained for 28 days (Schiff et al. 2009). Clinical studies have documented that a dentifrice with 8% arginine, calcium carbonate and 1450 ppm fluoride is more effective at reducing dentine hypersensitivity than a fluoride toothpaste (Docimo et al. 2009, Docimo et al. 2009). A series of clinical trials has also documented that direct application of the 8% arginine, calcium carbonate, and 1450 ppm fluoride toothpaste to the sensitive tooth surface delivers immediate improvement in hypersensitivity. Application directly with patient fingertip or with a cotton applicator swab provided an immediate improvement that was maintained during seven days of twice-daily brushing with the arginine-containing dentifrice (Schiff et al. 2009). Two additional double-blind, placebo-controlled clinical studies demonstrated that, after a single fingertip application, the 8% arginine-containing toothpaste provided significant immediate improvement in sensitivity, compared with both a 2% potassium ion with 1450 ppm fluoride positive control and a 1450 ppm fluoride negative control. This significant benefit continued after three days of twice-daily brushing with the arginine-containing toothpaste (Ayad et al. 2009, Nathoo et al, 2009). The 2% potassium-ion dentifrice only showed improvement when compared with the fluoride-only control in one study, and that benefit was only in response to air blast stimulus after three days of product use (Ayad et al. 2009). A modification of this 8% arginine, calcium carbonate and 1450 ppm fluoride dentifrice formulation - including a high-cleaning calcium carbonate system for enhanced extrinsic stain removal (Yin et al. 2010) - has been clinically documented to deliver dentine hypersensitivity relief comparable with the clinically-proven dentifrice containing only the traditional calcium carbonate system (Ayad et al. v2009, Docimo et al. 2009, Docimo et al. 2009) and superior sensitivity relief when compared with a 1450 ppm fluoride-only control dentifrice (Que et al. 2010). An additional clinical study documented that both the instant and three-day improvements in hypersensitivity were comparable for the 8% arginine, calcium carbonate and 1450 ppm fluoride dentifrices, independent of the addition of the high-cleaning calcium carbonate system (Fu et al.2010). 15 PROFESSIONALKNOWLEDGE These studies demonstrate the flexibility of this desensitising technology in incorporating additional patient benefits, such as whitening (Yin et al. 2010). This clinically documented hypersensitivity relief has been shown to be primarily a result of tubule occlusion, by physical plugging of the tubule and formation of a protective surface layer. The amino acid, arginine - which is found naturally in saliva and carries a positive charge at physiological pH -attracts calcium carbonate to the negatively-charged dentinal surfaces. Calcium and phosphate ions are also recruited into dentinal tubules and induce plugging and the formation of a protective surface layer. Occluded dentine tubules with Pro-ArginTM Technology Calcium indicated by green via Energy Dispersive X-Ray (EDX) chemical mapping Dentine treated with Pro-ArginTM Technology The use of the 8% arginine and calcium carbonate technology effectively accelerates this natural mechanism of occlusion. It is documented through the use of advanced imaging techniques, to visualise tubule occlusion and protective layer formulation on the dentinal surface. This, paired with state-of-the-art surface analysis techniques, demonstrates the arginine tubule plug as well as calcium, phosphorous, and carbonate in the dentinal surface layer (Petrou et al. 2009, Lavender, 2010). In addition to demonstrating dentine hypersensitivity relief, two recent clinical studies have documented benefits for an arginine, calcium carbonate and 1450 ppm fluoride toothpaste compared with a silica-based, 1450 ppm fluoride control, in preventing and repairing enamel damage by acid softening. Leveraging an intra-oral erosion model and crossover clinical study design, the arginine-containing toothpaste provided significantly better protection for enamel samples against erosive acid challenges over five days compared with the fluoride-only control toothpaste (CP data on file). A separate intra-oral, clinical study demonstrated better repair of acid-softened enamel after three days use of the arginine-containing toothpaste compared with the fluoride control (CP data on file). The proposed mechanism of action for these clinically-documented enamel benefits is the physical deposition of a calcium-rich layer on the enamel surface. 16 PROFESSIONALKNOWLEDGE Dentine tubule plug Calcium indicated by green via EDX chemical mapping Fractured Sample of Dentine treated with Pro-ArginTM Technology Surface analysis methods demonstrate that both arginine and calcium carbonate form a surface coating on acid-damaged enamel that acts as a ”reparative” layer – both by filling the microscopic gaps in enamel created by acid and in helping in the physical protection of enamel during subsequent acid challenges (CP data on file). Arginine with PVM/MA copolymer and pyrophosphates A mouthwash can provide an alternative delivery system for sensitivity relief, especially in reaching sensitive areas that may be difficult to brush. A mouthwash composed of 0.8% Arginine with a PVM/MA copolymer system, pyrophosphate and 0.05% sodium fluoride in an ethanol-free base has been clinically documented to provide better dentine hypersensitivity relief than a 0.05% sodium fluoride control rinse after two, four and eight weeks (CP data on file). In a second clinical trial, the same 0.8% arginine-containing mouthwash formula provided more effective dentine hypersensitivity relief than both a mouthwash containing 2.4% potassium nitrate and 0.022% sodium fluoride, and the same 0.05% sodium fluoride negative control after two, four and six weeks. The 2.4% potassium nitrate mouthwash required six weeks to deliver effective sensitivity relief to tactile stimulus, but demonstrated improvement on the air blast stimulus at two, four, and six weeks compared with the 0.05% sodium fluoride negative control (CP data on file). For both clinical trials, mouthwash was added to a standard, twice-daily brushing protocol, with a regular, non-hypersensitivity toothpaste and a soft toothbrush. 17 PROFESSIONALKNOWLEDGE Before Treatment After treatment In-vitro Confocal Laser Scanning Microscopy (CLSM) image showing untreated dentine surface with exposed tubules, and coating of dentine tubules with Arginine with PVM/MA Copolymer and Pyrophosphates The proposed mechanism for the clinically documented dentine hyper sensitivity relief from the arginine-containing mouthwash, is reduction in fluid flow of exposed tubules, through occlusion by coating. To support this, in vitro hydraulic conductance studies have shown a 42% reduction in flow rate for the 0.8% arginine/copolymer/pyrophosphate mouthwash formula compared with a 0.05% sodium fluoride negative control (CP data on file). Analytical methods identified the chemical nature of the occlusive coating to be an arginine-rich layer together with phosphate and copolymer (CP data on file). Regimen In addition to proving the individual benefits of the arginine-based toothpaste and mouthwash, a clinical study determined the combined effect of pairing the 8.0% arginine, calcium carbonate and 1450 ppm fluoride dentifrice (for twice daily brushing with a soft-bristled toothbrush) with the 0.8% arginine, PVM/MA copolymer system, pyrophosphate and 0.05% sodium fluoride mouthwash (used twice daily after brushing). This occlusive-technology regimen demonstrated significantly better dentine hypersensitivity relief than both a potassium-based regimen (comprised of a 2% potassium ion toothpaste with 1450 ppm fluoride, soft bristled brush, and mouthwash with 0.27% potassium ion and 230 ppm fluoride) and a placebo regimen after two, four, and eight weeks. The potassium-based regimen demonstrated better dentine hypersensitivity relief than the placebo regimen at two, four, and eight week measures for air blast stimulus and, at two and eight weeks, for tactile stimulus (CP data on file). 18 PROFESSIONALKNOWLEDGE Management of dentine hypersensitivity and underlying conditions Before initiating any kind of treatment for dentine hypersensitivity, it is important to understand that many oral conditions exhibit similar symptoms and that dentine hypersensitivity therefore is a differential diagnosis reached by first excluding other diseases and/or defects (Olsson and Lindhe 1991, Dowell and Addy 1983, Hallmon and Harrel 2004, West 2008). History When screening has shown that the patient has a problem with sensitive teeth, it is essential to let the patient use his/her own words to describe the symptoms and the pain triggers. Once pain characteristics are described, closed questions can be used to help to confirm the diagnosis such as: “Does it persist after stimulus?” As always, it is important to obtain and record the patient’s dental, medical and dietary history. It is advisable to check for any history of excessive intake of acid food and drink (citrus juices and fruits, carbonated drinks, wines or ciders) in the diet, and to probe for evidence of gastric reflux and eating disorders. Photos courtesy of Prof. Nicola West Clinical examination The clinical examination shall include controlled assessment of the sensitive teeth, such as mechanical/tactile stimuli (running a sharp explorer over the area of exposed dentine) and/or thermal and evaporative stimuli (a blast of cold air from the 3-in-1 syringe). Cold airblast from triple syringe Sharp explorer over the area of exposed dentine 19 PROFESSIONALKNOWLEDGE EXAMINATION Screening As suggested in the recommendations of the Canadian Advisory Board of Dentine Hypersensitivity (2003), all dental patients shall be actively screened for dentine hypersensitivity by dental professionals at each dental check-up, as sensitivity is often unreported by the patient. By actively asking the patients if they have, or have had, any problems with sensitivity, the vast majority of dentine hypersensitivity suffers will be detected, enabling the dental professional to help these suffers. The application of a controlled stimulus would be expected to result in a short sharp pain that generally lasts just for the duration of the stimulus, but may sometimes continue for a short while post stimulation, if the patient has dentine hypersensitivity. Differential diagnosis The combined history and clinical examination are essential to exclude other factors or conditions like dental caries, pulpitis, cracked tooth syndrome, fractured restorations, gingival inflammation, chipped teeth, lack of care while contouring restorations, fractured restoration and TMJ disorders. Differential Diagnosis Caries P Pulpitis A IN Gingivitis Short, sharp pain Cracked tooth syndrome Fractured restoration Traumatic occlusion TMJ disorders Other pain symptoms - such as dull and throbbing pain, pain that lasts long after the removal of the stimulus, pain that keeps the patient awake at nights, the need for pain killers, pain irradiating from original site, pain occur at the chewing/biting surfaces, pain during air travel or when laying down - may indicate other dental diseases or defects that require further investigation. By excluding all other potential causes of the same or similar symptoms, the diagnosis of dentine hypersensitivity can be confirmed as the most likely cause of pain. It is then a good idea to measure and record the severity of the pain in order to allow this to be monitored over time. 20 PROFESSIONALKNOWLEDGE Measurement and registration of dentine hypersensitivity Usually, dentine hypersensitivity is measured by (a) tactile (pressure) stimulus or (b) thermal/evaporative (cold air blast) stimulus. The air blast measurement is a very simple and often-used technique to measure dentine hypersensitivity. The sensitive tooth is isolated from the adjacent teeth. A short blast of air, from a 3-in-1 dental syringe, is directed at the exposed dentine surface. The response of the subject to the air blast stimulus is usually scored by the clinical examiner, based upon the subject’s response, using an analogue scale, such as the commonly used Schiff scale. Schiff scale Value Response of the patient to the air blast stimuli 3 Responds, requests discontinuation and considered it painful 2 Responds and requests discontinuation 1 Responds 0 Does not respond Visuel analog scale (VAS) Another way to determine and record the pain response to the stimulus is for the subject to rate his/her experience using an open scale, like a visual analog scale (VAS). Directions for use • The patient mark the level of pain on the line. • The distance from ”No Pain” to the paitients mark is meassured (in mm). This meassurement is the patient’s VAS-score. • The VAS-score is registered in the paitient records. VISUAL ANALOG SCALE (VAS) AS) SCALE FOR MEASURING THE LEVEL OF PAIN Unbearable pain No pain Example of a visual analog scale 21 PROFESSIONALKNOWLEDGE Treatment Plan As dentine hypersensitivity is not a disease in itself, but rather a symptom of one or more of a number of underlying causes, all possible conditions, which could have led to dentine hypersensitivity need to be identified. The management of dentine hypersensitivity should first aim to eliminate, or at least minimise, all the underlying and predisposing factors. These include both those leading to lesion localisation (exposure of dentine) and those leading to lesion initiation (opening of tubules). By treating the underlying causes, as well as the dentine hypersensitivity itself, it is possible to reduce the frequency of dentine hypersensitivity attacks, or even to prevent further dentine hypersensitivity episodes. SCREENING Symptoms of DHS ? Patient describes pain & triggers No NO TREATMENT required Yes CLINICAL EXAMINATION Examine to exclude other causes such as: • Caries • Pulpitis • Gingival inflammation • Traumatic occlusion • Chronic pain syndrome • Cracked tooth syndrome • TMJ disorders • Fractured restoration • Marginal leakage • Post-restorative sensitivity • Refered pain • Neuropathic pain CASE HISTORY Anamnesis Review medical history of patient (dental and general) CONFIRM DHS Diagnosis MAINTAIN DHS TREATMENT PLAN AND MONITOR UNDERLYING CONDITION MEASUREMENT OF DHS Measure and record level of DHS IDENTIFY and ADDRESS UNDERLYING CONDITIONS Refer to Treatment Strategy Options further described. FOLLOW UP YES Re-assesment fo DHS and underlying condition Does DHS still persist ? NO NO FURTHER TREATMENT OF DHS REQUIRED Continue to control underlying conditions 22 PROFESSIONALKNOWLEDGE Dentine can become exposed through gingival recession or through enamel loss. Experts have concluded that gingival recession, rather than cervical enamel loss, is the key predisposing factor for dentine hypersensitivity. However, several others conditions also seem to be associated with an elevated incidence of dentine hypersensitivity. In the following section, the most common predisposing factors will be reviewed and intuitive flowcharts will be presented for guidance on how to manage dentine hypersensitivity, and any related underlying conditions. Dentine hypersensitivity and gingival recession due to improper brushing Gingival recession is a multifactorial condition rendered more complex by anatomical factors. Overzealous and improper tooth brushing techniques have been associated with gingival damage and loss of gingival tissue through mechanical forces. Once gingival recession occurs, the cement covering the dentine surface is easily removed exposing the vulnerable underlying dentine and increasing the risk of dentine hypersensitivity. Based on in vitro and in situ studies, it appears that normal tooth brushing does not cause significant enamel loss. However, erosion from acidic foods and drinks, in combination with tooth brushing, can result in significant tooth wear on any part of the tooth surface, especially the cervical area. Dentine hypersensitivity and lesions resulting from tooth wear Photo courtesy of Prof. Roger Elwood Photo courtesy of Chief Dentist Ulla Pallesen, Copenhagen University Tooth wear in general means loss of tooth substance. It covers four types of lesions - abrasion, attrition, erosion and abfraction. Sensitive teeth due to a combination of erosive and abrasive damages Sensitive teeth due to erosion 23 PROFESSIONALKNOWLEDGE TREATMENT PLAN Exposed dentinal tubules are loosely occluded by a coating, known as the smear layer, comprised of protein components and calcium phosphate deposits derived from saliva. On the basis of in vitro studies, it has been suggested that both chemical and physical forces can remove the smear layer to open exposed dentinal tubules. While there seems little doubt that acidic foods and drinks are able to remove the smear layer and soften dentine - rendering the softened dentine tissue susceptible to physical forces such as tooth brushing - clinical data suggests that physical forces alone are not a key factor in removing the smear layer and opening exposed dentinal tubules. In the last few years, basic research has suggested that acid erosion combined with abrasion can have the potential significantly to accelerate wear on teeth. Detailed in vitro and in situ studies have shown that the mechanical process of brushing with a toothbrush alone has no measurable effect on enamel, and that tooth brushing with toothpaste contributes little, if anything, to the loss of enamel over a lifetime of use. In contrast, similar studies have shown that the chemical process of erosion caused by acidic foods and drinks, particularly when combined with mechanical cleaning, can result in significant tooth wear and, ultimately, exposure of dentine. Research has suggested that acid erosion combined with abrasion can have the potential to significantly accelerate tooth wear. Patients with abrasion and erosion should, therefore, be considered as predisposed to suffering from sensitive teeth with a need for prevention and treatment. A desensitising mouthwash may be a valid option for dentine hypersensitivity sufferers whose condition has resulted from excessive brushing, used in between the morning and evening brushings. Dentine hypersensitivity management strategy options for patients with gum recession due to improper brushing and toothwear lesions DIAGNOSIS Identified gum recession and/or tooth wear lesions caused by excessive brushing or improper brushing technique, and/or erosion as primary underlying cause of DHS PATIENT EDUCATION FOLLOW-UP • Show patient the site and what likely has caused the problem • Adjust brushing technique (if appropriate to diagnosis) • Instruction in modifying frequent intake of acidic food & drink & avoiding brushing before and after acidic intake (if appropriate to diagnosis) Regular assessment on tooth wear and dietary habits AT HOME ORAL HYGIENE ROUTINE Brushing with Colgate® Sensitive Pro-ReliefTM Toothpaste & Toothbrush x 2 daily Rinsing with Colgate® Sensitive Pro-ReliefTM Mouthwash 2 x daily ( 20 ml for 30 sec) In between brushing use of Colgate® Sensitive Pro-ReliefTM Mouthwash may be considered for reducing the risk of gingival and hard tissue trauma with improper/excessive brushing. TREATMENT In-office DHS treatment to provide instant pain relief Application of Colgate® Sensitive Pro-ReliefTM Desensitising Polishing Paste 24 PROFESSIONALKNOWLEDGE Dentine hypersensitivity and periodontal disease and treatment Photo courtesy Prof. M Wolff Periodontal disease results in periodontal tissue damage and loss of gingival tissue through biological breakdown processes. Exposed dentine due to periodontal disease Once gingival recession occurs, the cementum covering the exposed dentine surface is easily removed by physical and/or chemical forces, thereby exposing the underlying dentinal tubules and increasing the risk of dentine hypersensitivity. Patients suffering from dentine hypersensitivity as a result of periodontal disease, are recommended to receive a two-component treatment and prevention plan addressing periodontal health and sensitivity. The primary task must be to focus on the periodontal problem, by initiating both the systemic phase (general disease and smoking habits control) and the initial phase of the periodontal therapy including scaling and root planing (SRP) and motivation for rigorous oral hygiene practices, to control dental plaque effectively. After these are completed, a re-evaluation will indicate the need to plan for corrective and maintenance therapies based on the projected desired outcome of the periodontal treatment (Lindhe et al. 2008). Several clinical studies have attempted to analyse the contribution of different clinical variables to the development of dentine hypersensitivity, during both initial and corrective periodontal therapy phases (Wallace et al. 1990, Fischer et al. 1991, Tammaro et al. 2000). A meta-analysis showed that periodontal therapy appears to be a significant cause of dentine hypersensitivity (von Troil 2002). After periodontal therapy, reduction of the gingival protective barrier may result from excision of tissue that exposes the root surfaces, while SRP may remove 20 to 50 micrometers of cementum and expose the dentinal tubules to external stimuli. Two studies (Fischer et al. 1991 and Tammaro et al. 2000) reported significant change in dentine hypersensitivity after SRP, with about 55% of patients experiencing characteristic pain one week after treatment. A systematic review showed that dentine hypersensitivity occurred in approximately half of patients after they underwent SRP (von Troil et al. 2002). Tamminen and colleagues (1998) determined that dentine hypersensitivity also occurred after periodontal surgery. Clinicians have observed that the intensity of pain or discomfort differs considerably among patients (Karadottir et al. 2002). 25 PROFESSIONALKNOWLEDGE Dentine hypersensitivity needs to be addressed, whenever it occurs during the periodontal therapy, by using an in-office product that provides instant relief. Such an approach can not only help to relieve pain, but can also help ensureproper plaque control following therapy, through effective home oral hygiene procedures. In patients with a history of discomfort during periodontal procedures, pre-procedural application of a dentine hypersensitivity treatment may also be considered. At home, management of dentine hypersensitivity in periodontal patients may be handled through a range of options, like the use of a desensitising mouthwash, while the daily brushing with an antimicrobial toothpaste is continued. Dentine hypersensitivity management strategy options in the context of the periodontal treatment DIAGNOSIS Identified periodontal disease as primary underlying cause PATIENT EDUCATION • Motivation for oral hygiene and recommendation of at home oral hygiene routine • Instruction on ways of reducing periodental risk factors (local factors, general diseases, smoking, etc) TREATMENT Pro-Relief INITIAL PHASE • SRP • DHS TREATMENT Apply Colgate® Sensitive Pro-ReliefTM Desensitising Polishing Paste to reduce discomfort before/after non-surgical procedures Re-evaluation Follow-up assessment on periodontal status and DHS CORRECTIVE PHASE • Surgical periodontal treatment Other required therapeutic measures (implant surgery, endodontic, restorative, prosthodontic etc.) • DHS TREATMENT Apply Colgate® Sensitive Pro-ReliefTM Desensitising Polishing Paste to reduce discomfort before/after surgical procedures AT HOME ORAL HYGIENE ROUTINE a) Short period, if needed 0.2% CHX mouthwash for plaque control b) Regularly brushing with Colgate® Total Toothpaste + 3600 Toothbrush 2 x daily for plaque control Colgate® Sensitive Pro-ReliefTM Mouthwash x 2 daily (20 ml for 30 sec) for DHS control FOLLOW UP MAINTENANCE PHASE • Supportive periodontal therapy • Continuous monitoring • DHS TREATMENT Apply Colgate® Sensitive Pro-ReliefTM Desensitising Polishing Paste to reduce discomfort before/after supportive perioodontal therapy procedures (eg. professional cleaning) 26 PROFESSIONALKNOWLEDGE Dentine hypersensitivity and restorative treatments Tooth preparations for restorative treatments on vital teeth inevitably open up hundreds of dentinal tubules. Hypersensitivity after crown preparation is very common, especially in young teeth with large pulp and minimum secondary dentine formation. The resultant smear layer is not able to block the freshly-cut dentine so a certain degree of fluid movement within the dentinal tubules is still possible, hence causing dentine hypersensitivity. It has been shown that the application of a 8% arginine and insoluble calcium carbonate containing desensitising paste did not have a significant effect on the shear bond strength of the composites, enabling the safe use of restorative adhesive techniques (Garcia-Godoy 2010), with a proper control of dentine hypersensitivity, for direct or indirect restorations (Seow Liang Lin 2012). Dentine hypersensitivity management strategy options for patients with restorative treatments DIAGNOSIS TREATMENT Decision about restorative treatment on vital teeth RESTORATIVE PREPARATION Perform the required filling and/or crown preparation procedure AT HOME ORAL HYGIENE ROUTINE FOLLOW-UP Inspect restoration Brushing with Colgate® Sensitive Pro-ReliefTM Toothpaste & Toothbrush x 2 daily Rinsing with Colgate® Sensitive Pro-ReliefTM Mouthwash 2 x daily ( 20 ml for 30 sec) DHS TREATMENT Apply Colgate® Sensitive Pro-ReliefTM Desensitising Polishing Paste on all exposed dentine FINAL RESTORATION Filling or crown cementation Dentine hypersensitivity and professional tooth whitening The demand for having white teeth has increased during the last decade and tooth whitening has become more common. Products that are used for professional tooth whitening have been found to be linked with tooth sensitivity (Pohjola 2002, Auschillet al. 2005). Sensitivity often occurs during both in-office and at-home tooth whitening treatments, and has been considered to be the most common complication of at-home tray treatments. The problem will commonly manifest itself as generalised hypersensitivity to cold stimuli, but often also occurs as a spontaneous sharp pain, sometimes limited to one or a few teeth (Haywood 1991). Reported incidence is most commonly in the 60% range and the degree of hypersensitivity in these reports ranges from very mild to intolerable. The latter can be severe enough for patients to interrupt or even stop their treatment. (Haywood 2005, Sterrett 1995, Jorgensen 2002). The cause of the sensitivity experienced during whitening treatments is considered to be multifactorial - involving acidic pH, dentinal fluid outflow caused by osmotic stimuli and penetration of peroxides through enamel and dentine. The latter supposedly results in a reversible pulpal irritation (Hewlett 2007). Pain needs to be prevented and treated to avoid negative effects on treatment compliance. Pre-existing dentine hypersensitivity is considered one of the best predictors of post-whitening hypersensitivity, and the use of classic desensitising agents applied topically, has proven effective in managing the pain (Haywood 2002, Seow Liang Lin 2012). 27 PROFESSIONALKNOWLEDGE Patients undergoing tooth-whitening procedures can be offered an in-office dentine hypersensitivity treatment, as well as preventive advice and instruction on the daily use of home dentine hypersensitivity products. An in-office treatment with a desensitising paste containing 8% arginine and calcium carbonate, followed by the use of a desensitising toothpaste containing 8% arginine, calcium carbonate and fluoride, was effective in achieving immediate and lasting sensitivity relief after professional tooth-whitening procedures in subjects with pre-existing dentine hypersensitivity. A majority of the subjects noticed a remarkable improvement in the condition immediately after in-office application of the desensitising paste, and claimed that twice-daily brushing with the respective toothpaste helped them to maintain, and even improve, the desensitising effect achieved in the dental office (Data on file, Colgate-Palmolive 2011). Dentine hypersensitivity management strategy options for patients in professional tooth-whitening treatment DIAGNOSIS Assessment of potential for whitening. Define whitening needs and shade improvement goals. Assessment of baseline tooth sensitivity before tooth whitening treatment FOLLOW-UP Follow-up assessment on DHS and whitening treatment PATIENT EDUCATION DHS TREATMENT Patient counseling in reducing risk factors (acidic drinks & food, abrasive toothbrushing) Apply Colgate® Sensitive Pro-ReliefTM Desensitising Polishing Paste to reduce baseline hypersensitivity DAT HOME ORAL HYGIENE ROUTINE If further control of DHS is needed Brushing with Colgate® Sensitive Pro-ReliefTM Toothpaste & Toothbrush x 2 daily Rinsing with Colgate® Sensitive Pro-ReliefTM Mouthwash 2 x daily (20 ml for 30 sec) WHITENING TREATMENT Perform professional tooth whitening procedure Development lesions (Hypomineralized teeth / MIH) Molar incisor hypomineralisation (MIH) is a type of dental defect which seems to occur frequently in various populations around the world, raising interest in further research and understanding of its aethiology and management in the dental community. Prevalence varies from 6% in Germany to almost 40% in Denmark (Alalussua 2010). According to a recent EAPD (European Academy of Paediatric Dentistry) policy document (Ligidakis et al. 2010) the aetiology of this condition is still not entirely understood. Several existing studies suggest a multifactorial involvement of medical problems during the prenatal, neonatal and postnatal periods. 28 PROFESSIONALKNOWLEDGE Photo courtesy of Dr. J. Kühnisch, München Universitet, Tyskland MIH can have several dental consequences for the individual affected, including detine hypersensitivity. In fact, hypersensitivity is one of the diagnosis criteria for MIH as established by the EAPD (Weerheij et al 2003). Hypersensitivity often results in the child avoiing brushing the affected teeth, thus increasing their risk of developing caries. In this context adequate control of pain is part of the initial management of MIH. Hypomineralised molar An in-office treatment may be recommended to try to achieve immediate relief and increase the ability of the child to maintain proper oral care. Considering also the mineralisation effect Pro-ArginTM Technology has on enamel, the recommendation to continue to use a toothpaste with such a formulation at home seems consistent with proposed approaches for the management of MIH for partially erupted teeth. This holds true for preventive care, regardless of the severity of the defect or development stage of the affected teeth. Mineralisation could also be achieved with a high-fluoride varnish (William et al 2006a, Mathu-Muju and Wright 2006). Dentine hypersensitivity management options for patients with MIH DIAGNOSIS DHS diagnosed in the context of MIH FOLLOW-UP DHS, plaque control and caries prevention PATIENT EDUCATION Provide appropriate dietary and preventive advice. Involve parents if needed. AT HOME ORAL HYGIENE ROUTINE Brushing with Colgate® Sensitive Pro-ReliefTM Toothpaste & Toothbrush x 2 daily for further control of DHS and remineralization. Brushing with fluoridated toothpaste minimum 1000 ppm F (Smiles Toothpaste &Toothbrush) for children under the age of 6. Additionally Colgate® Sensitive Pro-ReliefTM Mouthwash 2 x daily (20 ml for 30 sec) (children 6+) 29 PROFESSIONALKNOWLEDGE TREATMENT DESENSITISATION Apply Colgate® Sensitive Pro-ReliefTM Desensitising Polishing Paste to sensitive MIH teeth. REMINERALISATION Apply Duraphat Varnish RESTORATION Depending on severity of deficiency PROFESSIONALKNOWLEDGE 30 NO Yes, with regular 2/daily use of toothpaste Sr-chloride NO Sr-acetate YES (with NaF and MFP) NO NO Yes, with regular 2/daily use of toothpaste YES (with NaF and MFP) Not applicable Lasting Relief Compatibility with Fluoride Superior efficacy vs K+ as positive control Toothpaste Instant Relief Toothpaste Tubule occlusion through deposition of insoluble strontium compounds on the dentine surface Desensitisation of dental nerve Mode Of Action Product Form Strontium Salts Potassium Salts (K+) Depolarising Agents No data available YES Yes, with 2-3 application in 10 days YES In-office varnish Tubule occlusion through deposition of calcium fluoride globules on the dentine surface Fluorides (high concentration) No data available YES Yes, with regular 2/ daily use of toothpaste or gel NO 1)Toothpaste 2)Gel Tubule occlusion through deposition of insoluble stannous compounds on the dentine surface Stannous Salts YES vs. K+ and Sr2+. Salts YES (with MFP) YES, with regular 2/ daily use of toothpaste or single application of in-office paste NO 1)In-office paste 2)Toothpaste 3)RX toothpaste Tubule occlusion through formation of a hydroxy-apatite-like calcium phosphate layer on dentine surface Calcium Sodium Phosphosilicate (NovaMin®) YES, vs. K+ and Sr2+. Salts YES (with MFP) YES, with regular 2/ daily use of toothpaste or single application of in-office paste YES 1)In-office paste 2)Toothpaste Tubule occlusion through formation of a calcium- and phosphate-rich layer on dentine surface which is triggered by arginine and calcium carbonate Arginine-Calcium Carbonate Pro-ArginTM Technology Overview of different technologies for treatment of dentine hypersensitivity References (listed alphabetically) 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;14:280-4. Addy M. Dentine hypersensitivity: new perspectives on an old problem. Int J Dent . 2002;52:367375. Addy M. Etiology and clinical implications of dentine hypersensitivity. Dent Clin North Am. 1990;34:503-514. Alaluusua S, Lukinmaa PL, Koskimies M, Pirinen S, Hölttä P, Kallio M, Holttinen T, Salmenperä L. Developmental dental defects associated with long breast feeding. Eur J Oral Sci. 1996 ; Oct-Dec 104(5-6):493-7. Alaluusua S. Aetiology of molar-incisor hypomineralisation. A systematic review. Eur Archs Paediatr Dent. 2010; 10:53-58. Albers H. At-home bleaching. Adept Report. 2000 (vol. 6) Santa Rosa: Adept Institute,. Auschill TM, Hellwig E et al. Efficacy, side effects, and patients’ acceptance of different bleaching techniques (OTC, in-office, at-home). Oper Dent. 2005;30:156-63. Ayad F, Ayad N, Delgado E, Zhang YP, DeVizio W, Cummins D, Mateo LR. Comparing the efficacy in providing instant relief of dentine hypersensitivity of a new toothpaste containing 8.0% arginine, calcium carbonate, and 1450 ppm fluoride to a benchmark desensitising toothpaste containing 2% potassium ion and 1450 ppm fluoride, and to a control toothpaste with 1450 ppm fluoride: A three-day clinical study in Mississauga, Canada. J Clin Dent . 2009;20:115–122. Ayad F, Ayad N, Zhang YP, DeVizio W, Cummins D, Mateo LR. Comparing the efficacy in reducing dentine hypersensitivity of a new toothpaste containing 8.0% arginine, calcium carbonate, and 1450 ppm fluoride to a commercial sensitive toothpaste containing 2% potassium ion: An eightweek clinical study on Canadian adults. J Clin Dent. 2009;20 (Spec Iss):10–16. Ayad F, Berta R, DeVizio W, McCool J, Petrone ME, Volpe AR. Comparative efficacy of two dentifrices containing 5% potassium nitrate on dentinal sensitivity: A twelve-week clinical study. J Clin Dent. 1994; 5 (Spec Iss): 97–101. Azarpazhooh A and Limeback H. Clinical efficacy of casein derivatives. A systematic review of the literature. JADA. 2008;Vol. 139. Bekes K, John MT, Schaller HG, Hirsch C. Oral health-related quality of life in patients seeking care for dentin hypersensitivity. J Oral Rehabil. 2009 Jan;36(1):45-51. Bergenholtz G, Jontell M, Tuttle A, Knutsson G. Inhibition of serum albumin flux across exposed dentine following conditioning with GLUMA primer, glutaraldehyde or potassium oxalates. J Dent. 1993 Aug;21(4):220-7. Blong MA, Volding B, Thrash WJ, Jones DL. Effects of a gel containing 0.4 percent stannous fluoride on dentinal hypersensitivity. Dent Hyg (Chig). 1985; 59: 489–492. Brännström M, Astrom A, The hydrodynamics of the dentine. its possible relationship to dentinal pain. Int Dent J. 1972;22:219-27. Brännström M, Aström A. The hydrodynamics of the dentine, its possible relationship to dentinal pain. Int Dent J. 1972;22:219-27. Browning WD, Blalock JS, Frazier KB, Downey MC, Myers ML. Duration and timing of sensitivity related to bleaching. J Esthet Restor Dent. 2007;19: 256-64. Burwell AK, Litkowski LJ, Greenspan DC. Calcium sodium phosphosilicate (NovaMinTM): remineralization potential. Adv Dent Res. Jul 31, 2009. 21(1):35-9.. Chesters R, Kaufman HW, Wolff MS, Huntington E, Kleinberg I. Use of multiple sensitivity measurements and logit statistical analysis to assess the effectiveness of a potassium citrate-containing dentifrice in reducing dentinal hypersensitivity. J Clin Periodontol. 1992;19:256–261. Clark RE, Papas AS. Duraphat versus Extra Strength Aim in treating dentinal hypersensitivity. J Dent Res. 1992; 71 (Sp Is): 734 (Abstr 628). Cummins D. Dentin hypersensitivity. From diagnosis to a breakthrough therapy for everyday sensitivity relief. J Clin Dent. 2009; 20 (Spec Iss):1–9. Cummins D. Recent advances in dentine hypersensitivity. Clinically-proven treatments for instant and lasting sensitivity relief. Am J Dent. May 2010; 23 Spec No A:3A-13A. de Assis C, Antoniazzi RP, Zanatta FB, Rösing CK. Efficacy of Gluma Desensitiser on dentine hypersensitivity in periodontally treated patients. Braz Oral Res. 2006; 20(3):252-6. Dijkman GE, Jongebloed WL, de Vries J, Ogaard B, Arends J. Closing of dentinal tubules by glutardialdehyde treatment. A scanning electron microscopy study. Scand J Dent Res. 1994 Jun;102(3):144-50. Docimo R, Montesani L, Maturo P, Costacurta M, Bartolino M, Zhang YP, DeVizio W, Delgado, E, Cummins D, Dibart S, Mateo L. Comparing the efficacy in reducing dentine hypersensitivity of a new toothpaste containing 8.0% arginine, calcium carbonate, and 1450 ppm fluoride to a benchmark commercial desensitising toothpaste containing 2%potassium ion. An eight-week clinical study in Rome, Italy. J Clin Dent. 2009; 20:137–143. REFRENCES 31 PROFESSIONALKNOWLEDGE Docimo R, Perugia C, Bartolino M, Maturo P, Montesani L, Zhang YP, DeVizio W, Mateo LR, Dibart S. Comparative evaluation of the efficacy of three commercially available toothpastes on dentine hypersensitivity reduction. An eight-week clinical study. J Clin Dent. 2011;22(Spec Iss):121-7. Docimo R, Montesani L, Maturo P, Costacurta M, Bartolino M, DeVizio W, Zhang YP, Cummins D, Dibart S, Mateo LR. Comparing the efficacy in reducing dentine hypersensitivity of a new toothpaste containing 8.0% arginine, calcium carbonate, and 1450 ppm fluoride to a commercial sensitive toothpaste containing 2% potassium ion. An eight-week clinical study in Rome, Italy. J Clin Dent. 2009; 20 (Spec Iss):17–22. Dondi dall’Orologio G, Malferrari S. Desensitising effects of Gluma and Gluma 2000 on hypersensitive dentin. Am J Dent. 1993;6(6):283-6. Dowell P, Addy M. Dentine hypersensitivity - a review. Clinical and in vitro evaluation of treatment agents. J Clin Periodontol. 1983 Jul;10(4):341-50. Review. Felton DA, Bergenholtz G, Kanoy BE. Evaluation of the desensitising effect of Gluma dentine bond on teeth prepared for complete-coverage restorations. Int J Prosthodont. 1991; MayJun;4(3):292-8. Fischer C, Wennberg A, Fischer RG, Attström R. Clinical evaluation of pulp and dentine sensitivity after supragingival and subgingival scaling. Endod Dent Traumatol. 1991;7(6):259-65. Flynn J, Galloway R, Orchardson. The incidence of ’hypersensitive’ teeth in the West of Scotland. R. J Dent. 1985 Sep;13(3):230-6. Gaffar A. Treating hypersensitivity with fluoride varnishes. Compend Contin Educ Dent. 1988; 19: 1088-1097. Gillam DG. An overview on conducting clinical studies for evaluation of desensitising products for the treatment of dentine hypersensitivity. Oral Health Dialogue. 2011 Issue 2:6-14. Gillam DG, Bulman JS, Jackson RL, Newman HN. Comparison of two desensitising dentifrices with a commercially-available fluoride dentifrice in alleviating cervical dentine sensitivity. J Periodontol. 1996; 67:737–742. Gillam DG, Coventry JF, et al. Comparison of two desensitising agents for the treatment of cervical dentine hypersensitivity. Endod Dent Traumatol. 1997; 13:36-9. Gillam DG, Mordan AD, et al. The effects of oxalate-containing products on the exposed dentine surface. An SEM investigation. J Oral Rehab. 2001; 28:1037-44. Graf H, Galasse R. Morbidity, prevalence and intra-oral distribution of hypersensitive teeth . J Dent Res. 1977; abstract 479. Grossman LI. A systemic method for the treatment of hypersensitive dentine. J Am Dent Asso. 1935;22:592. Gysi A. An attempt to explain the sensitiveness of dentine. Br J Dent Res. 1900; 43:865-368. Hallmon WW, Harrel SK. Occlusal analysis, diagnosis and management in the practice of periodontics,. Periodontol 2000. 2004;34:151-64. Review. Hamlin D, Williams KP, Delgado E, Zhang YP, De Vizio W, Mateo LR. Clinical evaluation of the efficacy of a desensitising paste containing 8% arginine and calcium carbonate for the in-office relief of dentine hypersensitivity associated with dental prophylaxis. Am J Dent. 2009; 22 (Sp Is A):16A-20A. Haywood VB. Dentine hypersensitivity. Bleaching and restorative considerations for successful management. Int Dent J. 2002;52:376-384.. Haywood VB, Leonard RH, et al. Effectiveness, side effects, and long-term status of nightguard vital bleaching. J Am Dent Assoc. 1994; 125:1219-26. Haywood VB. Treating tooth sensitivity during whitening.Compend Contin Educ Dent 26 (supp 3):11-20, 2005. Haywood VB. Tooth whitening. Indications and Outcomes of Nightguard Vital Bleaching. Quintessence Publishing Co., 2007. Hodosh M. A superior desensitiser—Potassium nitrate. JADA. 1974; 88:831–832. Holland GR, Narhi MN, Addy M, Gangarosa L, Orchardson R. Guidelines for the design and conduct of clinical triials on dentine hypersensitivity. J Clin Periodontol. 1997; 24: 808-813.. Hu D, Zhang YP, Chaknis P, Petrone ME, Volpe AR, De Vizio W. Comparative investigation of the desensitising efficacy of a new dentifrice containing 5.5% potassium-citrate. An eight-week clinical study. J Clin Dent. 2004;15: 6–10. Ishihata H, Kanehira M, Nagai T, Finger WJ, Shimauchi H, Komatsu M. Effect of desensitising agents on dentine permeability. Am J Dent. 2009; Jun;22(3):143-6. Jaeggi T, Lussi A. Prevalence, incidence and distribution of erosion. Monogr Oral Sci. 2006;20:4465. 32 PROFESSIONALKNOWLEDGE Jorgensen MG, Carroll WB, Incidence of tooth sensitivity after home whitening treatment. J Am Dent Assoc. 2002; 133:1076-82. Jälevik B. Prevalence and Diagnosis of molar incisor hypomineralisation (MIH). A systematic review. Eur Archs Paediatr Dent. 2010; 10: 59-64. Kakaboura A, Rahiotis C, Thomaidis S, Doukoudakis S. Clinical effectiveness of two agents on the treatment of tooth cervical hypersensitivity. Am J Dent. 2005 Aug;18(4):291-5. Kanapka JA. Current treatment for dentine hypersensitivity. A new agent. Compend Contin Educ Dent. 1982; (Suppl):S118–S120. Karadottir H, Lenoir L, Barbierato B, et al. Pain experienced by patients during periodontal maintenance treatment. J Periodontol. 2002;73(5):536-42. Kowalczyk A, Botulinski B, Jaworska M, Kierklo A, Pawinska M, Dabrowska E. Evaluation of the product based on Recaldent technology in the treatment of dentine hypersensitivity. Adv Med Sci. 2006;51 (suppl 1):40-42. Li Y, Lee S, Zhang YP, Delgado E, De Vizio W, Mateo LR. Comparison of clinical efficacy of three toothpastes in reducing dentine hypersensitivity. J Clin Dent. 2011;22 (Spec Iss):113-20. Lindhe J, Lang N P, & Karring T. Clinical periodontology and implant dentistry. 2008; 5th edition, Oxford: Blackwell Munksgaard. Litkowski L, Greenspan DC. A clinical study of the effect of calcium sodium phosphosilicate on dentine hypersensitivity--proof of principle. J Clin Dent. 2010;21(3):77-81. Litkowski L, Greenspan DC.: A clinical study of the effect of calcium sodium phosphosilicate on dentin hypersensitivity -proof of principle. J Clin Dent2010; 21(3):77-81. Lygidakis NA. Treatment modalities in children with teeth affected by molar incisor hypomineralisation (MIH). A systematic review. Eur Arch Paediatr Dent. 2010; 11: 65-74. Manochehr-Pour M, Bhat M, Bissada N. Clinical evaluation of two potassium nitrate toothpastes for the treatment of dentinal hypersensitivity. Periodont Case Rep. 1984; 6:25–30. Markowitz K, Kim S. The role of selected cations in the desensitisation of intradental nerves. Proc Finn Dent Soc. 1992; 88 (Suppl):39–54. Markowitz K, Pashley DH. Discovering new treatments for sensitive teeth. The long path from biology to therapy. J Oral Rehabil. 2007; 35:300–315. Mathu-Muju K, Wright JT. Diagnosis and treatment of molar incisor hypomineralisation. Compend Contin Educ Dent. 2006; 27(11): 604-10. Miller S, Truong T, Heu R, Stranick M, Bouchard D, Gaffar A. Recent advances in stannous fluoride technology. Antibacterial efficacy and mechanism of action towards hypersensitivity. Int Dent J. 1994; 44 (Suppl):83–98. Nagata T, Ishida H, Shinohara H, Nishikawa S, Kasahara S, Wakano Y, Daigen S, Troullos ES. Clinical evaluation of a potassium nitrate dentifrice for the treatment of dentinal hypersensitivity. J Clin Periodontol. 1994; 21:217–221. Nathoo S, Delgado E, Zhang YP, De Vizio W, Cummins D, Mateo LR. Comparing the efficacy in providing instant relief of dentine hypersensitivity of a new toothpaste containing 8.0% arginine, calcium carbonate, and 1450 ppm fluoride relative to a benchmark desensitising toothpaste containing 2% potassium ion and 1450 ppm fluoride, and a control toothpaste with 1450 ppm fluoride. A three-day clinical study in New Jersey, USA. J Clin Dent. 2009; 20:123–130. Newman Michael G, Takei Henry H, Klokkevold Perry R, Carranza Fermin A. Carranza’s clinical periodontology – 10th Edition, Philadelphia : W.B. Saunders Co, 2006. Olsson M, Lindhe J. Periodontal characteristics in individuals with varying forms of the upper central incisors. J Clin Periodontol. 1991 Jan;18(1):78-82. Orchardson R, Collins WJ. Clinical features of hypersensitive teeth. Br Dent J. 1987 Apr 11;162(7):253-6. Orchardson R, Gillam DG. Managing dentine hypersensitivity. JADA. 2006;137:990–998. Orchardson R, Gillam DG. The efficacy of potassium salts as agents for treating dentine hypersensitivity. J Orofac Pain, 2000;14:9–19. Ozen T, Orhan K, Avsever H, Tunca YM, Ulker AE, Akyol M. Dentine hypersensitivity. A randomised clinical comparison of three different agents in a short-term treatment period. Oper Dent. 2009 Jul-Aug;34(4):392-8. Papas AS, Clark RE. Accrued desensitization with repeated Duraphat treatment of hypersensitivity. J Dent Res. 1995; 74:134. Petrou I, Heu R, Stranick M, Lavender S, Zaidel L, Cummins D, Sullivan RJ, Hsueh C, Gimzewski JK. A breakthrough therapy for dentine hypersensitivity. How dental products containing 8% arginine and calcium carbonate work to deliver effective relief of sensitive teeth. J Clin Dent. 2009;20 (Spec Iss):23-31. 33 PROFESSIONALKNOWLEDGE Pohjola RM, Browning WD, et al. Sensitivity and tooth whitening agents. J Esthet Rest Dent .2002;14:85-91. Poulsen S, Errboe M, Lescay Mevil Y, Glenny AM. Potassium-containing toothpastes for dentine hypersensitivity. Cochrane Database Syst Rev 3: CD001476, 2006 Qin C, Xu J, Zhang Y. Spectroscopic investigation of the function of aqueous 2- hydroxyethylmethacrylate/glutaraldehyde solution as a dentine desensitiser. Eur J Oral Sci. 2006 Aug;114(4):354-9. Salian S, Thakur S, Kulkarni S, La Torre G.. A randomised controlled clinical study evaluating the efficacy of two desensitising dentifrices. J Clin Dent. 2010;21(3):82-7. Salvato AR, Clark GE, Gingold J, Curro FA. Clinical effectiveness of a dentifrice containing potassium chloride as a desensitising agent. Am J Dent 5:303–306, 1992. Schiff T, Delgado E, Zhang YP, De Vizio W, Mateo LR. Clinical evaluation of the efficacy of a desensitising paste containing 8% arginine and calcium carbonate in providing instant and lasting in-office relief of dentine hypersensitivity. Am J Dent. 2009; 22 (Sp Is A):8A-15A. Schiff T, Dos Santos M, Laffi S, Yoshioka M, Baines E, Brasil KD, McCool JJ, De Vizio W. Efficacy of a dentifrice containing 5% potassium nitrate and 1500 ppm sodium monofluorophosphate in a precipitated calcium carbonate base on dentinal hypersensitivity. J Clin Dent. 1998; 9:22–25. Schiff T, Dotson M, Cohen S, De Vizio W, McCool J, Volpe A. Efficacy of a dentifrice containing potassium nitrate, soluble pyrophosphate, PVM/MA copolymer, and sodium fluoride on dentinal hypersensitivity. A 12-week clinical study. J Clin Dent. 1994; 5 (Spec Iss):87–92. Schiff T, Mateo LR, Delgado E, Cummins D, Zhang YP, De Vizio W. Clinical efficacy in reducing dentine hypersensitivity of a dentifrice containing 8.0% arginine, calcium carbonate, and 1450 ppm fluoride compared to a dentifrice containing 8% strontium acetate and 1040 ppm fluoride under consumer usage conditions before and after switch-over. J Clin Dent. 2011;22 (Spec Iss):128-38. Schiff T, Saletta L, Baker RA, Winston JL, He T. Desensitising effect of a stabilised stannous fluoride/sodium hexametaphosphate dentifrice. Compend Contin Educ Dent. 2005; 26 (Suppl):35–40. Schüpbach P, Lutz F, Finger WJ. Closing of dentinal tubules by Gluma desensitiser. Eur J Oral Sci. 1997 Oct;105(5 Pt 1):414-21m Seow L L. Novel clinical applications of Colgate® Sensitive Pro-Relief™ in the management of dentine hypersensitivity. J Clin Dent. 2012; 23:7–10. Sharma N, Roy S, Kakar A, Greenspan DC, Scott R. A clinical study comparing oral formulations containing 7.5% calcium sodium phosphosilicate (NovaMinTM), 5% potassium nitrate, and 0.4% stannous fluoride for the management of dentine hypersensitivity. J Clin Dent. 2010;21(3):88-92. Sharma N, Roy S, Kakar A, Greenspan DC, Scott R. A clinical study comparing oral formulations containing 7.5% calcium sodium phosphosilicate (NovaMinTM), 5% potassium nitrate, and 0.4% stannous fluoride for the management of dentine hypersensitivity. J Clin Dent. 2010;21(3):88-92. Silverman G, Berman E, Hanna CB, Salvato A, Fratarcangelo PA, Bartizek RD, Bollmer BW, Campbell SL, Lanzalaco AC, MacKay BJ, McClanahan SF, Perlich MA, Shaffer JB. Assessing the efficacy of three dentifrices in the treatment of dentinal hypersensitivity. JADA. 1996; 127:191–201. Silverman G, Gingold J, Clark GE: The effectiveness of potassium nitrate and sodium monofluorophosphate dentifrices in reducing dentinal hypersensitivity. J Dent Res. 1988; 67:247. Silverman G, Gingold J, Clark GE. The effectiveness of potassium nitrate and sodium monofluorophosphate dentifrices in reducing dentinal hypersensitivity. J Dent Res. 1988; 67:247. Silverman G, Gingold J, Curro FA. Desensitising effect of a potassium chloride dentifrice. Am J Dent. 1994; 7:9–12,. Silverman G..The sensitivity-reducing effect of brushing with a potassium nitrate-sodium monofluorophosphate dentifrice. Compend Contin Educ Dent. 1985; 6:131–136. Snyder RA, Beck FM, Horton JE. The efficacy of a 0.4% stannous fluoride gel on root surface hypersensitivity. J Dent Res. 1985; 62:237. Sobral MA, Garone-Netto N, Luz MA, Santos AP. Prevention of postoperative tooth sensitivity. A preliminary clinical trial. J Oral Rehabil. 2005 Sep;32(9):661-8. Sterrett J, Price RB, Bankey T. Effects of home bleaching on the tissues of the oral cavity. J Can Dent Assoc. 1995;61:412-20. Tammaro S, Wennström JL, Bergenholtz G. Root-dentine sensitivity following non-surgical periodontal treatment. J Clin Periodontol 2000;27(9):690-7. Tamminen V, Kontturi-Narhi V, Narhi M. Development of pulp and dentine sensitivity in flap operated teeth.. J Dent Res 1998;77(special issue):671,(abstract 322). Tarbet WJ, Silverman G, Fratarcangelo PA, Kanapka JA. Home treatment for dentinal hypersensitivity. A comparative study. JADA. 1982; 105:227–230. 34 PROFESSIONALKNOWLEDGE Tarbet WJ, Silverman G, Stolman JM, Fratarcangelo PA. Clinical evaluation of a new treatment for dentinal hypersensitivity. J Periodontol. 1980;51:535–540. Thrash WJ, Dodds MW, Jones DL. The effect of stannous fluoride on dentinal hypersensitivity. Int Dent J. 1994; 44 (Suppl):107–118. von Troil B, Needlemen I, Sanz M. A systematic review of the prevalence of root sensitivity following periodontal therapy. J Clin Periodontol. 2002;29(supplement 3):173-7. Wallace JA, Bissada NF. Pulpal and root sensitivity related to periodontal therapy. Oral Surg Oral Med Oral Pathol. 1990;69(6):743-7. Walters PA. Dentinal hypersensitivity. A review. J Contemp Dent Pract. 2005; 6:107-17. Walters PA. Dentinal hypersensitivity. A review. J Contemp Dent Pract. 2005; 6:107–117. Wara-aswapati N, Kringnawakul D, Jiraviboon D, Adulyanon S, Karimbux N, Pitiphat W. The effect of a new toothpaste containing potassium nitrate and triclosan on gingival health, plaque formation and dentine hypersensitivity. J Clin Periodontol. 2005;32:553–558. Weerheijm KL, Duggal M, Mejare I, et al. Judgement criteria for molar incisor hypomineralisation (MIH) in epidemiologic studies. A summary of the European meeting on MIH held in Athens 2003. Eur Archs Paediatr Dent. 2003;3:110-113. West NX, Addy M, Jackson RJ, Ridge DB. Dentine hypersensitivity and the placebo response. A comparison of the effect of strontium acetate, potassium nitrate and fluoride toothpastes. J Clin Periodontol. 1997; 24:209–215. West NX. Dentine hypersensitivity. Preventive and therapeutic approaches to treatment. Periodontol 2000. 2008;48:31-41. Review. William V, Messer LB, Burrow MF. Molar incisor hypomineralisation. Review and recommendations for clinical management. Pediatr Dent. 2006 May-Jun;28(3):224-32. Willmott NS, Bryan RA, Duggal MS. Molar-incisor-hypomineralisation. A literature review. Eur Arch Paediatr Dent. 2008 Dec;9(4):172-9. Wogelius P, Haubek D, Poulsen S. Prevalence and distribution of demarcated opacities in permanent first molars and incisors in 6-to 8-year old Danish children. Acta Odontologica Scandinavia, 2008; 66:58-64. Yu X, Liang B, Jin X, Fu B, Hannig M. Comparative in vivo study on the desensitising efficacy of dentine desensitiser and one-bottle self-etching adhesives. Oper Dent. 2010 May-Jun;35(3):279-86. Zapera, Survey among dental professionals in Nordic about dentine hypersensitivity. YouGov, 2009. Zapera, Survey among the Nordic adult population. Experience about dentine hypersensitivity. Zapera.com 2007. 35 PROFESSIONALKNOWLEDGE