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Data sources The authors searched Medline via PubMed, Scopus, Web of Science, the Cochrane Library and ClinicalTrials.gov for published and unpublished clinical trials. Only randomised clinical trials, with either a parallel or crossover design, reporting the tooth sensitivity of participants undergoing in-office dental bleaching and comparing pain frequency and severity with oral premedication of a non-steroidal or other anti-inflammatory drug compared with a placebo were used in the review. Studies that evaluated the topical administration of drugs or desensitising agents were not reviewed.Study selection In total,5,050 randomised clinical studies were screened and 11 studies were included in the various meta-analyses. Nine studies examined the effect of pre-emptive analgesics on the risk of sensitivity and ten studies evaluated the effect of drugs on the severity of sensitivity; seven of these studies were assessed as having a low risk of bias.Data extraction and synthesis This systematic review and meta-analysis was conducted a priori and registered at the International Prospective Register of Systematic Reviews. There were two reviewers who extracted data from the study tables and independently performed quality assessments of the selected trials using the Office of Health Assessment and Translation risk of bias rating tool for human and animal studies. Risk ratios were calculated for the dichotomous sensitivity risk data and mean difference for measures of sensitivity intensity.Results The authors found no effect of the drugs on the risk of sensitivity. Using a visual analogue scale, the authors identified a small but clinically insignificant reduction in the level of sensitivity in the drug-treated group evaluated up to one hour after bleaching. This was not observed when a numerical rating scale was used to measure pain intensity. For the 24-hour pain data, the authors did not find any significant intensity difference between groups. Mean pain intensity scores were generally low in both experimental groups in all randomised controlled trials reviewed. Based on a visual inspection of the funnel plots of all outcomes, the authors concluded that there was no publication bias.Conclusions The data did not support the pre-emptive use of anti-inflammatory drugs in preventing or reducing the intensity of pain caused by in-office tooth bleaching.

Objective: Tooth sensitivity is a common, painful dental condition. Consumer dental products, mostly dentifrices, play an important role in sensitivity treatment. The objective of this review is to describe a new mouthwash-based desensitizing technology., Data: Background literature concerning desensitizing products is reviewed. Potassium salts are the most commonly used active ingredients in desensitizing dentifrices. Clinical studies show that while potassium salt dentifrices are generally effective; most formulations require several weeks to exert their desensitizing effect. Recently, a new desensitizing dentifrice containing the amino acid arginine was introduced. This dentifrice acts to occlude the dentinal tubules, and has been shown to be highly effective in multiple clinical studies. This arginine-containing dentifrice has also been shown to provide instant relief of sensitivity pain when applied directly to the sensitive tooth surface. In contrast to dentifrices, there are few desensitizing mouthwashes available. Building on the success of the arginine-based dentifrice, an arginine-based mouthwash formula was developed and tested., Sources: Published studies in peer-reviewed publications., Study Selection: Controlled and blinded clinical studies to provide evidence of efficacy. In vitro studies are included to indicate the mechanism of action. This review includes studies testing the new arginine-based desensitizing mouthwash., Conclusion: Clinical findings indicate that this new desensitizing mouthwash, based on the Pro-Argin™ mouthwash technology effectively reduces sensitivity symptoms and can be used alone or as a adjunct to the use of the arginine-containing dentifrice in the home treatment of tooth sensitivity., (Copyright © 2012 Elsevier Ltd. All rights reserved.)

Vital bleaching procedures are a popular means of improving the appearance of discolored teeth. There is a wide array of whitening products for home and dental office use; all involves placing peroxide containing gels or solutions in contact with the teeth. In order to whiten teeth peroxide has to be able to penetrate tooth structure and oxidize colored compounds in the dentin. Unfortunately beauty comes with a price; many patients undergoing peroxide based whitening procedures complain of bleaching sensitivity (BS) arising in the treated teeth. In BS, pain can occur in healthy intact teeth without any provoking stimulus. Currently the mechanism of nociceptors activation in BS is unknown. A more common form of dental pain-dentin sensitivity (DS) occurs when stimuli such as cold or tactile stimulation contact areas of exposed dentin in otherwise healthy teeth. In DS, stimulation of the dentin results in fluid shifts in the dentinal tubules, these fluid shifts activate mechanosensitive nerve endings in the deep dentin and pulp. Since many aspects of BS and DS symptoms differ, it is hypothesized that that the mechanism of pain generation differs for these two conditions. Recently the functional properties of a chemosensitive ion channel-TRPA1 have been described. This channel is activated by a variety of oxidizer compounds including hydrogen peroxide. Pulpal sensory afferents express TRPA1. It is hypothesized that direct activation of intradental nerve activity via TRPA1 is the mechanism of BS pain. If this theory were correct, tooth sensitivity treatments that reduce the excitability of the intradental nerves such as potassium salts, would be the treatment of choice for BS.

Tooth sensitivity is a common dental pain condition where sufferers experience brief episodes of sharp well-localized pain when their teeth are subjected innocuous stimuli such as cold, air-currents and probing with a metallic instrument. In this review, we will make no attempt to describe all the treatments that have been developed to treat tooth sensitivity. We will review the basic anatomic and physiological mechanisms responsible for sensitivity. The insights into the dental lesions responsible for tooth sensitivity, as well as the physiological processes linking stimuli and pain generation have suggested several treatments and preventive strategies. Unfortunately, many tooth sensitivity treatments fail to perform better than placebos in clinical trials that seek to assess the effect of agents on pain symptoms. In the case of the most commonly used self-applied desensitizing agent, potassium salts, the mechanism of action established by laboratory and animal models may not apply to clinical use. Thus results obtained with laboratory and animal models must be applied with care to clinical use. Clinical literature suggests that tooth sensitivity is the symptomatic manifestation of significant dental problems, such as wear and other forms of non-carious tooth structure loss. These conditions are increasing in frequency as people age, retaining their natural teeth longer. They are frequently the consequences of aggressive oral hygiene practices and diets rich in acids. Treatments directed at the underlying causes rather than the symptoms of tooth sensitivity would hinder the development of these lesions and provide researchers with objective targets for assessing therapeutic efficacy.

Tooth sensitivity is a common complaint encountered in clinical practice. Exposed superficial dentin is free of nerve endings, yet sensitive. Experimental evidence indicates that stimuli, such as probing the dentin surface and air blasts, induce fluid movements in the dentinal tubules and these fluid movements, in turn, activate the intradental nerves. The condition of the dentin surface is critically important in allowing this process. In addition, the internal environment of the pulp may influence nerve excitability. Therapies for tooth sensitivity include both agents that obstruct the dentinal tubules and agents that can decrease the excitability of the intradental nerves. The exact treatment used depends on the etiology of the individual's problem and the extent of dentinal tissue damage.

Dentinal sensitivity is a common complaint of patients. Removal of cementum or enamel leaves the dentin exposed allowing various stimuli to produce fluid movement through the dentinal tubules. These fluid movements are believed to activate pulpal sensory nerves leading to pain. Various therapeutic approaches have been investigated to treat this problem. Resins, fluoride compounds and oxalate solutions have been used to block the dentinal tubules. KNO3 and SrCl2 are active ingredients in desensitizing tooth pastes but neither compound reduces the permeability of dentine. The ability of various solutions to decrease hypertonic (3M NaCl) evoked nerve activity was tested in the canine teeth of anesthetized cats. Excitatory and desensitizing solutions were placed into a deep dentinal cavity prepared over the incisal pulp horn. An electrode used to record nerve activity was also placed into this deep cavity. KNO3 and other K+ ion containing solutions elicit a biphasic effect on nerve activity. Immediately following application of these solutions into the deep dentinal cavity there is a brief burst of high frequency spike activity. Following this brief period of excitation, the intradental nerves are silent and respond weakly to hypertonic NaCl. CaCl2 and other divalent cation solutions also inhibit hypertonic NaCl induced nerve activity, but have a weaker effect than that exerted by K+. These observations can be explained based on the effects of various ions on nerve excitability. Increasing the K+ ion concentration in the vicinity of the dentinal nerve terminal depolarize and activates the nerve fibers. Following a prolonged period of depolarization the action potential mechanism is inactivated. Divalent cation solutions stabilize the nerve membrane without changing the membrane potential. Desensitizing solutions do not decrease nerve activity by an effect on pulpal blood flow. This experimental model does not entirely explain the clinical action of these desensitizing agents. The role of inflammation in hypersensitivity and dental pain is currently being investigated.

The effect of dentinal desensitizing agents on nerve activity was tested. Effective agents such as KNO3 reduce dentinal sensory nerve activity. This effect is due to the depolarizing action of the K+ ion.