Clinical trials on dentine hypersensitivity have been numerous and protocols varied. To date there is little consensus as to the conduct of studies on this poorly-understood yet common and painful dental condition. A committee of interested persons from academia and industry was convened to discuss the subject of clinical trials on dentine hypersensitivity and a consensus report is presented. A double-blind randomized parallel groups design is recommended, although cross-over designs may be used for the preliminary screening of agents. Subjects may have multiple sites scored. Sample size will be determined by estimating the variability in the study population, the effect to be detected and the power of the statistical test to be used. Subject selection is based on a clinical diagnosis of dentine hypersensitivity, excluding those with conflicting characteristics such as currently-active medical or dental therapy. The vestibular surfaces of incisors, cuspids and bicuspids are preferred as sites to be tested. A range of sensitivity levels should be included. Tactile, cold and evaporative air stimuli should be applied. Negative and benchmark controls should be incorporated. Most trials should last 8 weeks. Sensitivity may be assessed either in terms of the stimulus intensity required to evoke pain or the subjective evaluation of pain produced by a stimulus using a visual analog or other appropriate scale. The subject's overall assessment may be determined by questionnaire. Outcomes should be expressed in terms of clinically significant changes in symptoms. Follow-up evaluation is required to determine the persistence of changes. At least 2 independent trials should be conducted before a product receives approval.

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There are limited studies specifically on the prevalence of root dentine hypersensitivity or root sensitivity per se; most of the published information relates to the prevalence of dentine hypersensitivity (DH). Several investigators have suggested that there may be some justification on the basis of differing pathologies of distinguishing between those individuals complaining of DH who have relatively healthy mouths with those who complain of DH as a result of periodontal disease and/or its treatment. It is generally recognized that those individuals diagnosed with periodontal disease and having periodontal therapy including scaling procedures may have a higher prevalence than those who present with healthy mouths and evidence of gingival recession. The availability of a vast array of treatments, however, would indicate either that there is no one effective desensitizing agent for completely resolving the discomfort or that the condition, due to its highly subjective nature, is difficult to treat irrespective of the available treatment options. The importance of implementing preventative strategies in identifying and eliminating predisposing factors in particularly erosive factors (e.g. dietary acids) cannot be ignored if the practitioner is going to treat this troublesome clinical condition successfully. This paper will review the published literature and provide information as to the prevalence of the condition, its etiology and causal factors, as well as recommendations for the clinical management of the problem.

Potassium ions in dentifrices for treating 'hypersensitive' dentin are believed to act directly on intradental nerves by raising extracellular potassium ion concentration ([K+]o) sufficiently to prevent action potential generation by axonal accommodation. However, the [K+]o necessary to block nerve conduction is not precisely known, nor is it certain that K+ can diffuse from a dentifrice in sufficient amounts to inactivate intradental nerves. To establish more accurately the [K+]o required to block nerve conduction under controlled conditions, we studied the effects of increased [K+]o on the sizes of compound action potentials (CAP) recorded from rat spinal nerves in vitro. [K+]o was increased by the addition of either KCl or KNO3 to Krebs' solutions applied to the central portion of the nerves. CAP attenuation increased in a dose-dependent manner as [K+]o was raised in the 8 to 64 mmol/L range, and complete block was generally produced with solutions containing at least 32 mmol/L K+. CAP attenuation was reversible, and recovery times increased with increasing [K+]o. The effects of KCl and KNO3 solutions were the same for all [K+]o tested. Half-maximal (50%) reduction in the A beta-fiber component of the CAP occurred with 17.4 mmol/L K+, and with 17.8 mmol/L and 19.3 mmol/L K+, respectively, for the A delta- and C-fiber components. Control experiments with glucose and choline chloride confirmed that the conduction block observed with increased [K+]o was not due to increased solution osmolarity or ionic strength.(ABSTRACT TRUNCATED AT 250 WORDS)

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