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Arch3 oral Binl. Vol. 39, Suppl., pp, 113%119s. 1994 Copyright 0 1994 Eisevier Science Ltd

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CONSENSUS REPORT

DENTINE HYPERSENSITIVITY- INTO THE 21ST CENTURY

R. ORCHARDSON,’ L. P. GANGAROSA Sr,2 G. R. HOLLAND,3 D. H. PASHLEY.’ H. 0. TROWBRIDGE: F. P. ASHLEY,’ 1. KLEINBERG and U. ZAPPA’

‘Institute of Physiology, University of Glasgow, Glasgow, Gl2 SQQ, Scotland, *Department of Oral Biology, School of Dentistry, Medical College of Georgia, Augusta, GA 30912, U.S.A., ‘Department of Restorative Dentistry, Faculty of Dentistry, University of Alberta, Edmonton, Alberta, Canada T6G 2N8, 4University of Pennsylvania, Department of Pathology, School of Dental Medicine, Philadelphia, PA 19104, U.S.A., ‘Department of Periodontology and Preventive Dentistry, UMDS, Guy’s Hospital, Tower Bridge, London SEI 9RT, England, 6Department of Oral Biology and Pathology, School of Dental Medicine, SUNY at Stony Brook, Stony Brook, NY 11794, U.S.A. and 7Universitat Ziirich, Zah-

narztliches Institut, Plattenstrasse 11, CH-8028 Zurich, Switzerland

INTRODUCTION

Hypersensitive dentine is a long-standing yet relatively neglected problem in dentistry; current modes of treatment tend to be unpredictable and at best temporary in their effects. Moreover, the prevalence of this condition is likely to increase in the future as individuais retain their dentitions for longer and as a result of altered dietary trends and increased oral hygiene activity. The rational approach to treating hypersensitive dentine is through a better understanding of dentine and pulp biology and greater appreciation of the underIying aetiological factors. Recent advances in the biology of dentine and pulp offer exciting possibilities for the develop- ment of new and more effective treatments for the late 1990s and into the 21st century.

This symposium on ~.y~e~sensiti~e Dentine: B~olo~~col Basis qf T~era~~~ was held to allow active researchers to present and discuss current knowledge in their own areas of expertise and to provide a forum for debate and for updating knowledge and understanding of dentine sensitivity. The aim of the symposium was to influence the direction of future research in this area by identifying key problems concerning hypersensitive dentine and also to offer suggestions about the most fruitful avenues for future research. To facilitate this process the symposium adopted a multidisciplinary approach, including con- tributions from clinicians and scientists representing the various domains of oral biology. The symposium consisted of a series of major reviews from invited speakers, which were supplemented by poster presentations of the results of recent investigations.

This consensus report was prepared by the organiz- ing committee and session chairmen with the aim of providing a summary of the most significant points that emerged during the symposium, and to identify future research priorities in the field. The report is divided into sections according to the six main conference themes. Each section describes current

knowledge and summarizes the main points raised in discussion. Where appropriate, reference is also made to significant information presented at the poster demonstrations. Throughout the conference, discus- sions highlighted several key issues, and in particular the lack of standardization of methods used in the clinical evaluation of treatments for hypersensitive dentine. A separate report setting out an agenda for future discussions in this latter area is included as an Appendix to the proceedings.

BIOLOGY OF DENTINE AND PULP

Structure of dentine and odontoblasts

The dentinal tubule is the portal through which stimuli gain access to the pulp. These channels may be occluded at different points by surface debris, intratubular inclusions, and by deposition of tertiary (or response) dentine. All of these could alter the sensitivity of dentine by affecting the fluid flow from the pulp and diffusion of substances along the tubules. Because of its accessibility, the outer dentine surface has been investigated in some detail, and it has been shown that tubules in hypersensitive dentine surfaces are wider and more numerous than in non- sensitive dentine. However, open tubules have also been demonstrated on non-sensitive surfaces. and so even if tubules are open on the surface they may be occluded deeper in dentine. Factors such as increased formation of peritubular dentine and deposition of tertiary dentine will tend to reduce the overall per- meability of the dentine and may account for the lower incidence of hypersensitive dentine in older people.

The precise functions of the odontoblasts remain uncertain; the extent of the odontoblast process appears to vary in different regions of the tooth but the signifi~nce of this finding is not known. A primary function is likely to be in the formation of peritubular and secondary or tertiary dentine, but the odontoblast may also play a part in sensory transduc-

113s

114s R. OKCHAKVSON e! ul.

tion although at present there is no direct evidence for this and it is clear that more detailed investigation is required of the biophysicai properties of odonto- blasts and their relations to intradental nerve termi- nals. The permeability of the odontoblast layer is likely to be a key factor in regulating fluid movement and diffusion of substances between the dentinal tubules and the pulp. This in turn will be governed by the interodontobiastic junctions. The nature of the odontoblast response to injury appears to vary and merits further investigation.

The composition of dentinal fluid is uncertain. nor is it known how this may alter under different conditions, for example in pulp inflammation. The ionic content could influence the excitabihty of intratubular nerve terminals, and any protein content could have a profound effect on the hydrodynamics of fluid flow.

The pulp contains both somatic and autonomic nerves. The patterns of innervation vary in different parts of the tooth, and it has been shown that individual nerves branch extensively to innervate many tubules. lntradental nerves contain a range of peptides and neuromodulators. including substance P and calcitonin gene-related peptide. Neuromodu- lators released from nerve terminals could influence the local mictovasculature and also the responses of the nerves themselves. It is possible that changes in the local state of the nerves and pulp could account for the variations in tooth sensitivity that may occur with time.

The responses of the nerves and odontoblasts to injury have generated much interest. The nerves display plastic changes in response to injuries. such as those caused by dental operative procedures. The severity of the changes increases with the degree of trauma and in relation to how the dentine surface is subsequently treated. In some types of localized injury, where the primary odontoblasts are replaced by secondary odontoblasts. the innervation of the repaired area is greatly reduced. Another feature associated with dentinal injury is the presence of nerve terminal sprouting. Nerve sprouting seems to correlate with inRammation, but this does not establish a causal relation. The sprouting does not begin until l&24 h after injury, some time after the painful symptoms have appeared. It could be due to increased levels of growth factors in the pulp. but bacterial toxins and/or fluid movement could also be involved. It is not known how sprouting would affect sensitivity. There is some limited evidence of in- creased terminal sprouting in pulps of hypersensitive teeth, but this needs confirmation,

In addition to the peripheral changes in the pulp and dentine. it is possible that the heightened sensitivity of hypersensitive dentine may involve changes in the central nervous system. immuno- chemical studies suggest that changes occur within the central nervous system following peripheral in- juries. One example is the rapid expression of the proto-oncogene c@s in central nervous neurones following peripheral noxious stimulation. The presence of c:#iu suggests that neurones in the nociceptivc pathways may display considerable

plasticity of their connections and responses. Thus, far from being exclusively a peripheral problem, hypersensitive dentine may involve increased excitation of second- and higher-order projection neurones, and may turn out to have some similarities to other hyperalgesic states.

The two types of myeiinated afferent pulp nerves (AD and A6 fibres) appear to be excited by a variety of stimuli acting through a hydrodynamic mechanism and the similarities in their properties suggest that they belong to the same functional group. Some pulpal afferents have receptive fields in both coronal and radicular dentine. Also, there are differences in the responsiveness of nerves innervating different areas of dentine, which may correlate with the reported differences in the sensations elicited from dentine in different regions of the tooth. The effective- ness of many dentinal stimuli is increased following acid etching, which will increase the size and numbers of patent tubules. Oxalate treatment reduces the nerve response, presumably by occluding tubules. In man, there is a correlation between the numbers of exposed tubules and subjective pain ratings. In contrast, unmyelinated C fibres generally do not respond to dentinal stimulation, and seem to react to conditions that cause pulp damage or after damage has occurred. Now, attention is turning to the precise role of fluid movement in stimulating intradental nerve terminals and on the nature of the transducer mechanism responsible for converting fluid move- ments into receptor potentials.

Topics for .fiture consideratiorz

(1) What is the nature of the junctional contacts between odontoblasts, and how is the per- meability of the odontoblast layer affected by pulpal conditions’?

(2) What is the relation between odontoblasts and nerve terminals? Do odontoblasts have any role in sensory transduction in teeth?

(3) What is the composition of dentinal fluid? How does this vary in hypersensitive teeth, and in the presence of pulp in~amnlation?

(4) How are the structure and properties of intraden- tal nerves altered in hypersensitive teeth?

(5) To what extent are central nervous neurones affected in cases of hypersensitive dentine?

?IETIOLOGY AND CLINICAL FEATURES

Hypersensitive dentine is characterized by transient pain in response to evaporative, tactile, thermal, or chemo-osmotic stimulation of exposed dentine in teeth where there is no evidence of other defects or pathology. The terminology for this condition is extremely varied: in addition to ‘hypersensitive dentine’ other names such as sensitive dentine, cervical dentinal sensitivity and root sensitivity have been applied. There is a need for a uniform nomencla- ture and a precise definition of the condition, as well as agreement about what should be included within its classification.

Consensus Report 115s

Hypersensitive dentine affects between IO-20% of the population. The prevalence appears to be fairly similar in different parts of the world, although there are some regional differences, which are at present difficult to explain. Hypersensitive dentine may affect any tooth, but most studies agree that it is most common in canines and first premolars, and is almost exclusively found on the vestibular surfaces. Hypersensitive dentine may also be present on other surfaces, including cuspal and incisal edges, and on lingual or palatal surfaces; in the latter case, it is usually indicative of acid regurgitation. However, not all exposed dentinai surfaces are sensitive, and not all regions of hypersensitive dentine are the same: they vary in extent, and also in sensitivity to different stimuli. For example, it is often found that hypersen- sitive teeth are sensitive to one form of stimulus e.g. cold, but not to another, e.g. probing. The reasons for these differences require further investigation.

Aetiology und predisposing factors

By virtue of its relation with the pulp, dentine is naturally sensitive, but for this sensitivity to manifest clinically the dentine must be exposed to the mouth. The way in which dentine is exposed can influence its sensitivity. Dentine freshly exposed by cutting or root planing may not be particularly sensitive because of the presence of a smear layer. In hypersensitive dentine, the smear layer is generally absent and the tubules are patent. There is still some debate about the origins of hypersensitive dentine. One school of thought is that dental plaque or plaque products promote dentine hypersensitivity, and that plaque control is important in preventing its development. It is suggested that discomfort on brushing promotes plaque accumulation, with further increases in sensitivity. In contrast, others report that the highest incidence of hypersensitive dentine is found in areas that are almost plaque-free. That this may be associated with over-zealous tooth brushing is supported by observations of good correlations between low plaque scores and incidence of hypersen- sitive dentine. However, not all exposed dentine is sensitive. Abrasive factors, such as tooth brushing or attrition, tend to produce a smear layer, but a tooth may become hypersensitive if the smear layer is removed by localized acid erosion, due to dietary acids such as fruit drinks or reduced salivary buffer- ing. It is also noteworthy that hypersensitive dentine is seldom found on lingual surfaces even in the presence of plaque. These two disparate positions can be reconciled by recognizing that small amounts of acidogenic plaque could demineralize exposed dentine as effectively as dietary acids. Brushing of these softened surfaces will accelerate loss of dentine and may lead to sensitivity. It is agreed that plaque alone is insufficient to cause hypersensitive dentine in the absence of brushing.

Another unresolved question is whether the traditional hypersensitive dentine is different from that occurring after periodontal surgery. Periodontal surgery-related dentine sensitivity has a relatively low level of sensitivity at first, followed by a rapid increase as the smear layer created by root planing is lost by dissolution. Sensitivity then falls over a period of 3-4 weeks as a result of tubular occlusion. How-

ever, in around lo-15% of these patients the sensi- tivity persists. The reasons for failure of the normal protective mechanisms in a few patients is unknown, but may be related to local factors such as salivary composition or flow. Attempts to draw a sharp distinction between spontaneously hypersensitive dentine and hypersensitive dentine following periodontal therapy seem arbitrary. If patients who have had periodontal surgery remain sensitive after 3 months, they should be regarded as having chronic sensitivity.

Topics ,fOr future consideration

(1)

(2)

(3)

(4)

(5)

A universally accepted definition and terminol- ogy is required, together with agreement about what clinical states come within the definition of hypersensitive dentine. More extensive longitudinal studies are required to quantify (a) prevalence and incidence. (b) natural variations in symptoms, and (c) aetiolog- ical factors in hypersensitive dentine. What is the role if any of plaque in the development of hypersensitive dentine? How do demineralization and remineralization affect dentine sensitivity? Do agents that prevent remineralization sustain hypersensitive dentine? What is the influence of salivary composition, flow rate and buffering capacity, on the develop- ment of hypersensitive dentine? Why does sensitivity persist in a proportion of patients after periodontal surgery? What mechan- isms fail to operate in these patients?

DENTINEPULP REACTIONS

Pulp haemodynamics

An adequate blood supply is important for the health of any tissue, and techniques such as laser Doppler flowmetry have provided valuable information about the control of pulp blood flow. It appears that pulp blood vessels are subject to essentially the same neural and humoral controlling influences as those in other tissues. Stimulation of the sympathetic fibres to the pulp causes vasoconstriction and reduced pulp blood flow. Vasoconstrictors such as noradrenaline applied directly to the exposed pulp decrease pulp blood flow, whilst drugs such as acetyl- choline, bradykinin and substance P increase pulp blood flow. Although the pulp contains both a- and /3-adrenoreceptors, the effects of the /I-receptors seem to be limited and they are probably of lesser physio- logical importance in regulating pulp blood flow.

A relatively recent concept is the role of oxygen-de- rived free radicals, such as the superoxide ion (‘0; ) and its derivative the hydroxyl radical (‘OH), in vascular control. Oxygen-derived free radicals produce complex vascular effects, and depending on circumstances, can cause either vasoconstriction or vasodilation. Free radicals may act directly on the blood vessels, or they may modify the effects of other endogenous mediators such as noradrenaline and the endothelium-derived relaxing factor (nitric oxide). Although some effects of oxygen-derived free radicals and nitric oxide have been demonstrated in the pulp, it is not known to what extent these actions occur

116s

naturally. This is likely to be an area of vigorous research in the future.

It is now clear that the tooth pulp can no Ionger be regarded as a passive recipient of stimuli, but rather reacts to them in a way that can modify its own responsiveness. St~mulatjon of dentine causes the release of a host of transmitters and modulators that can affect both blood vessels and afferent and efferent nerves: these effects constitute neurogenic inflam- mation. In addition to exciting afferent nerves through hydrodynamic mechanisms, physiological stimulation sf dentine generally causes an increase in pulp blood flow and increased permeability of microvessels. Even relatively mild tactile stimuli can increase pulp blood flow. Subsequent changes in tissue-fluid pressures may further affect puIp bfood Bow. Blood-flow changes do not appear to be due to a direct action on vasomator nerves, but are mediated by axon reflexes initiated by activation of the myeti- nated afferent nerves. These reactions can be further influenced by vasomotor nerves, which now appear to act not only on the blood vessels, but may also modify the responsiveness of afferent nerve terminals.

It is possible that sustained, low-grade stimulation of the pulp could produce neurogcnic inflammation, and this may be responsible for the characteristic features of hypersensitive dentine, including the spontaneous changes in the degree of clinical ‘sensitivity’ that occur with time. But as yet, very little is known about the nature of any neuropharm~~- cological differences between the pulps of normal and hypersensitive teeth. Because neurogenic infIam- mation might be present in hypersensitive teeth, it has been suggested that anti-inflammatory drugs such as aspirin could reduce dentinal hypersensitivity, but this does not appear to have been fully investigated.

Is there an inflammatory component in hyperscn- sitive teeth? Could aspirin or other non~steroidal anti-inflammatory agents reduce dentinal hyper- sensitivity? Is there any evidence of neuropharm~coIogicaI changes in the pulps of hypersensitive teeth? What is the role of oxygen-derived free radicals and nitric oxide in pulp haemodynamics? What are the long-term effects of altered pulp blood flow? Under what conditions can sustained vasoconstriction lead to pulp necrosis? Do any pulpal changes in hypersensitive teeth resolve, or wi17 they progress to pulpitis?

Pain is more than a mere sensation. It does not always occur in direct proportion to the intensity of a noxious stimulus or the extent of tissue damage. The nociceptive system is not a passive relay mechanism, but actively modulates the sensations and perceptions resufting from tissue damage or injury. The amount of pain felt is influenced by many things, such as the individual’s sex and age. the

circumstances and present context, previous experi- ences and current expectations. Personality charac- teristics also influence how the individual reacts to noxious stimuli. The emotive reactions differ in acute and chronic pains; the former often cause anxiety, whilst the latter tend to cause depression. All of these factors that can affect pain experience and perception may also affect the response to treatment. The effects of these variables are recognized in systemic pain management, but they are not always considered when dealing with conditions such as dentinal hypersensitivity. Hypersensitive dentine tends to be regarded as a purely peripheral phenomenon, but the role of central factors can no longer be ignored. It is pertinent to consider to what extent expectations and emotional factors contribute to dental pain.

Pain may be measured in terms of the stimuli that cause it or by subjective ratings of the intensity of the experience. Pain thresholds are relatively simple to measure, but they arc limited in what they convey, and do not provide the comprehensive information about the overall nocieeptive system that can be revealed by more global rating methods. Pain severity can be assessed by psychophysical rating methods such as visual analogue scales, whilst the multiple and interacting components may be revealed by verbal indices such as the McGill pain questionnaire.

Most methods for studying dentinal sensitivity use thermal, mechanical. osmotic, evaporative or electrical stimuli, all of which can elicit dental pain. However. not all of these are equally suitable or sufficiently quantifiable for use in clinical assess- ments. Ideally, the stimuli chosen for evaluation ought to be measurable and reproducibIe, but should also be clinically relevant and take account of the pain experience of the individual, In practice, dentine sensitivity can be measured either as pain thresholds to graded stimuli or by using one of the various forms of subjective rating scales. However. there are few standard methods and stimulators are often custom made, although this is not necessarily a problem as long as the specifications are clearly defined. In order to obtain a more comprehensive picture, clinical studies often employ more than one form of stimulus. Some, but not all, studies report good correlations between the degree of sensitivity measured by differ- ent methods.

Electrical stimuli differ from most other dentinal stimuli in that they bypass the normal receptor mechanisms and excite nerves directly in the pulp. The relative merits of constant-current and constant- voltage stimulators generated intense debate. Nerve thresholds are defined in terms of current, but most electrical stimulators vary the applied voltage, so that any changes in voltage threshold coufd arise from alterations to the resistance or impedance of the combined tooth-electrode system. Impedance changes could also reflect changes in the dentine structure, such as deposition of peritubular dentine or tertiary dentine, that might underlie a change in tooth sensitivity. The use of electrical stimulation methods can be defended by observations that teeth classed as hypersensitive on the basis of air or tactile stimuli are consistently found to have lower thresholds to

Consensus Report 117s

electrica stimuli than non-sensitive teeth. Although the stimulating electrodes are placed on enamel rather than on the exposed root surface, hypersensitive teeth show lower thresholds to electrical stimuli than non- sensitive contralateral controls. These findings might suggest lowered pulp thresholds, but this has not been confirmed. As yet, there is no direct evidence that nerves in inflamed pulps have lowered thresholds or that pufp thresholds correlate with the pathological state of the pulp. Hence one might need to consider the possibility that changes in the response to electri- cal stimulation may be due to altered processing in the central nervous system, rather than in the periph- ery. However, one can argue that this may not be important, provided the method used is capable of detecting any change in the responsiveness of the nociceptive system as a whole.

Topics for future consideration

(1)

(2)

(3)

(4)

Is hypersensitive dentine significantly more sensi- tive than normal dentine, or does it represent one extreme of a normal continuum of sensibility? To what extent do personality and other individ- ual psychological characteristics influence the pain experienced from hypersensitive dentine? Are there differences in the way in which people with hypersensitive dentine process nociceptive information: do they, for example, have lowered pain thresholds or pain tolerance levels? What are the best ways to quantify the global aspects of dental pain?

MECHANISMS OF SENSITIVITY AND DESENSITIZATION

flentine per~eabi~it?

As fluid movements across dentine are thought to provide the stimulus-response coupling mechanism involved in dentine sensitivity, the factors that regulate fluid distribution across the pul~entine complex require careful study. Measurement of hy- draulic conductance in vitro has provided important basic information about the physical factors governing tubular fluid movement and dentine per- meability, as well as showing how these are affected by clinical procedures and the chemicals present in desensitizing preparations. These methods can be applied in viva to study pulpal pressures and outward fluid flows. Several new concepts were introduced that require more study. Evaporative water loss in response to air blasts can now be accurately measured in vitro. The outward movement of dentinal fluid has been shown to slow the inward diffusion of substances both in vitro and in vivo. Fluid and solute exchange between the pulp and tubular fluids will also be influenced by the nature and permeability of the barrier formed by the odontoblasts. There is limited information about the permeability of the odontoblast barrier, or how its permeability might be altered in the presence of pulpal inflammation or after repair following disruption of the odontoblast layer.

Neroe excitability

Treatment of hypersensitive dentine has been directed at methods that either occlude dentinal

tubules or reduce the excitability of intradental nerves. Nerve excitability is affected by the ionic composition of the local extracellular environment. This environment can be affected by the state of the pulp and also by substances diffusing inwards from the mouth. The therapeutic potential of potassium and divalent cations in reducing intradental nerve activity was discussed in some detail. Laboratory studies of the effects of these ions and other agents on nerve conduction have identified the local concen- trations that are required to modify nerve activity. However, it is not certain if substances applied to the outer dentine in uivo can diffuse along the tubules in sufficient amounts to affect the excitability of intradental nerves.

Measurement of diffusion in dentine can pose technical difficulties, and mathematical modelling may provide an aitemative method for studying diffusion. Computer models can be used to predict the time course of ion accumulation at different points along the tubules under a variety of con- ditions, including concentration gradients, assumed diffusion coefficients, dentine thickness, tubular dimensions, hydraulic conductance, pulpal pressure, presence or absence of odontoblasts and the permeability of the cell junctions. Such models necessarily require certain assumptions to be made, but the predictions can be tested experimentally to assess the validity of the model.

interactions between ~~id~o~ and nerve activity

Novel techniques for measuring fluid flow across cat dentine in uivo have established that the resting outward fluid flow is around 13 pi/s. The mean flow per tubule is 0.6fl/s, which corresponds to a mean tubular fluid velocity of 1.4pm/s near the outer dentine surface. The rate of outward fluid Aow is increased by pulpal vasodilation produced by stimulation of the inferior alveolar nerve, whilst constriction of pulp blood vesseis by stimulating the sympathetic supply reduces dentinal fluid flow, or causes it to reverse and go towards the pulp.

Recently devised techniques allow simultaneous recordings to be made of dentinal IIuid IIow and activity in intradental and pulp afferent nerves. The experiments show that the direction and magnitude of dentinal fluid flow produced by positive or negative hydrostatic-pressure stimuli is correIated with intradental and single-unit nerve activity. Spontaneous outward fluid flow is well below the threshold for nerve activation. The lowest thresholds for initiating action potentials in intradental nerves are approx. 50 times greater than resting flow rates. Thresholds for nerve activation are lower for negative pressures (causing outward fluid movements) than for positive pressures (causing inward fluid movements). For units that respond to both inward and outward flows, the neural responses are greater with outward than inward flows of the same rate. It is now necessary to investigate the transducer mechanism in greater detail to establish why outward fluid movement is a more effective stimulus than inward.

Stimulation of dentine sufficient to activate A6 fibres also causes an increase in pulpal blood flow and outward fluid flow via axon reflex activity. It is suggested that one function of intradental nerves is to

118s R. OKCHAKVWN et nl.

detect open dentinal tubules. Increased activity in intradental nerves may bring about pulp changes that result in increased outward fluid flow, which may provide a defence against the ingress of possible toxic agents along tubules.

Topics .for future consideration

(I) How do junctional complexes between odonto- blasts modify the permeability of the pulp dentine complex? Are these junctions intact or absent in hypersensitive teeth?

(2) How are the intrad~ntal receptors activated by hydrodynamic stimuli? What is the critical stimu- lus (e.g. fluid velocity, shear forces, pressure changes) and does the stimulus threshold change in inflammation?

(3) Why are intradental nerves more responsive to outward rather than inward fluid movements?

(4) What is the magnitude of dentinal tubular fluid flow in hypersensitive teeth?

(5) Does neurogenic inflammation have a protective role, or does it cause persistance of dentine sensitivity’?

(6) Can topically applied therapeutic agents reach the pulp in effective concentrations? What con- ditions are necessary to optimize the delivery of topically applied agents to the pulpdentine com- plex?

MANAGEMENT AND CLINICAL TREATMENT OF HYPERSENSITIVE DENTINE

The treatment of any condition is more likely to be successful if it is based on an l~nderstanding of what is causing the problem. Normally, this is achieved through a logical process of history taking and clinical examination. This leads on to making a diagnosis, which is usually linked to the aetiological factors contributing to the condition. Finally, a treatment plan is made, which is based ideally on elimination of known aetiological factors. If aetiolog- ical or predisposing factors cannot be identified or eliminated, their effects must be negated by treatment. Treatment of hypersensitive dentine may be professionally applied or undertaken by the individual at home.

Dentist -upplied treatments

The traditional obtundants introduced before the advent of local anaesthetics are caustic and irritant, and should be avoided. Agents currently used for treating hypersensitive dentine include: corticosteroid preparations, oxalates, potassium salts and fluorides; topical applications of these agents may be augmented by techniques such as iontophoresis. Cavity varnishes, dentine-bonding agents and glass- ionomer cements are also used for covering sensitive dentinal surfaces. The role of newer methods such as laser treatments for hypersensitive dentine remains unclear, as they have not yet been fully evaluated nor are their long-term effects known. In addition, there is a question of whether the state of the underlying pulp is likely to affect the treatment of choice.

There was some ‘discussion of the mechanism of action of iontophoresis, and in particular whether its effects were due to the specific actions of the applied

agents or to the effects of the electric current. The exact mode of action of iontophoresis in dentinal desensitization remains unclear. If the current intensi- ties used clinically were sufficient to excite intradental nerves, they could alter pulp blood flow and the fluid flow in dentinal tubules with subsequent alterations in dentine sensitivity.

Restorative materials applied to dentine appear to reduce dentinal sensitivity as long as they remain on the tooth surface, but sensitivity tends to return after the material is lost. As hypersensitive dentine is most common at the cervical margins of teeth, adequate moisture control can be difficult, although this is less of a problem with some of the newer dentine primers. Opinions are divided about whether it is necessary to remove any smear layer before applying an adhesive agent. Treatment by restorations is not always applicable, for example in the case of multiple sensitive teeth, and there is a need for more durable materials that will provide more permanent and effective surface barriers.

Self-applied treatments

Self-applied treatments are popular because they are economical and easy to use. They are most commonly in the form of dentifrices, but gels and solutions are also available over the counter. Active agents used in home-care preparations include: potassium salts (nitrate, chloride and citrate), stron- tium salts (chloride or acetate), sodium citrate and various fluoride compounds. The type of abrasive included in the formulation also seems to play some part in altering dentine sensitivity. possibly by causing tubular occlusion. The disadvantages of self- applied treatments include compliance, difficulty of delivery to specific sites, slow onset of action, and the requirement for continuous use. A particularly rel- evant question is whether a small but statistically significant reduction in sensitivity is clinically meaningful. Reductions in the degree of dentinal hypersensitivity can be difficult to observe objectively and depend to a large extent on individual interpret- ation. Many of the initial reports on desensitizing agents were essentially anecdotal, but while it is easy to criticize these early clinical studies, they cannot readily be compared with more recent work employ- ing different and more refined methods.

In terms of future developments, should we wait for more information about the biological mechan- isms of dentinal sensitivity, or seek new agents, or simply repeat earlier work using more refined methods? There was no clear answer, but it was agreed that reproducibility of findings between inves- tigations was essential, and that there was an urgent need for standardization of methods used in future studies.

Clinical trial design

The effectiveness of treatments for hypersensitive dentine can be investigated by controlled clinical trials, which should follow established principles and employ well-designed protocols. Discussion highlighted the problems resulting from the lack of standardization of methods used in clinical studies, and delegates were challenged to establish a ‘gold standard’ for the clinical evaluation of desensitizing

Consensus Report 119s

agents. Without clearly defined criteria and operating and making recommendations about future studies. principles, it was felt that no significant progress To this end, a paper setting out a possible agenda for towards developing new desensitizing treatments future discussions on the development of a standard would be made in the foreseeable future. It was code of practice for clinical evaluations of desensitiz- agreed that a statement should emerge from this ing preparations is included in the following symposium identifying the most controversial issues Appendix.