The role of toothpaste in the aetiology and treatment of dentine hypersensitivity.

Dentine hypersensitivity (DH) is a common, painful dental condition with a multi-factorial aetiology. The hydrodynamic mechanism theory to explain dentine sensitivity also appears to fit DH: lesions exhibiting large numbers of open dentinal tubules at the surface and patent to the pulp. By definition, DH can only occur when dentine becomes exposed (lesion localisation) and tubules opened (lesion initiation), thus permitting increased fluid flow in tubules on stimulation. Erosion, particularly from dietary acids appears to play a dominant role in both processes. Toothbrushing with most toothpaste products alone cause clinically insignificant wear of enamel but are additive, even synergistic, to erosive enamel loss. Additionally, toothbrushing with toothpaste is implicated in 'healthy' gingival recession. Toothbrushing with most toothpastes removes the smear layer to expose tubules and again can exacerbate erosive loss of dentine. These findings thereby implicate toothbrushing with toothpaste in the aetiology of DH. Management of the condition should have secondary prevention at the core of treatment and therefore, must consider first and foremost the aetiology. Fluoride toothpaste at present appears to provide little primary or secondary preventive benefits to DH; additional ingredients can provide therapeutic benefits. Potassium-based products to block pulpal nerve response have caused much debate and are considered by many as unproven, which should not translate to ineffective. Several toothpaste technologies formulated to block tubules are from studies in vitro, in situ and controlled clinical trials considered proven for the treatment of DH.

The systemic theory of dental caries.

There is growing awareness of oral/systemic links, especially with regard to periodontal disease, diabetes, and cardiovascular disease, among others. The process of dental caries has similar links. Bacterial and other acids in the oral environment can erode enamel and potentially initiate an inflammatory response in the dentin. The body's own matrix metalloproteinases, mostly from within the dentin, become activated, resulting in the caries process. A simplified explanation of the oxidative stress causing inflammation is developed from three equations, namely Health, Disease, and Disease. The healthy tooth is nourished by a centrifugal dentinal fluid flow. This flow is controlled by signals from the hypothalamus that are relayed to the endocrine portion of the parotid gland. The first step in the caries process is the reversal of the dentinal fluid flow, rather than the acid attack from the oral environment. A systemic understanding of the actual cause and progression of dental caries creates opportunities for more effective approaches to preventive care.

Mechanisms and treatment approaches of dentine hypersensitivity: a literature review.

PURPOSE: To review major mechanisms of dentine hypersensitivity and the treatment approaches offered. MATERIALS AND METHODS: Medline was used to find relevant literature published up to December 2006. Based on abstracts and full articles, studies (in human and in animals) were identified describing mechanisms and management of dentine hypersensitivity. Additional information was also obtained by using manual library search for relevant topics in standard texts and journals of dentistry. RESULTS: Discussion about the sensitivity of dentine started over a century ago, but it was not until sixty years later that a possible theory was posited. The so-called hydrodynamic theory became popular and was applied to understand the mechanism responsible for hypersensitive dentine. Nevertheless, because of the discrepancies in the pattern by which the dentine responds to various stimuli, several theories of dentine hypersensitivity were proposed which include the hydrodynamic theory, odontoblast transducer mechanism and direct innervation theory. None of these mechanisms was said to fully explain dentine hypersensitivity, thus indicating that as-yet unexplained mechanisms were possibly responsible. A multitude of products were tried and reported to be effective. The efficacy of many was not clearly established and their mechanisms of action were inadequately elucidated. The potential of gene therapy to reduce the burden of dentine hypersensitivity in the future is being examined. CONCLUSIONS: Considerable effort has been made to precisely explain dentine hypersensitivity, but doubt still exists whether any one theory can be applied to understanding this condition. This has led to a constant increase in therapeutic approaches worldwide, but with no conclusive evidence of reliable, successful treatment regimens.

Recent advances in dentin hypersensitivity: clinically proven treatments for instant and lasting sensitivity relief.

PURPOSE: To provide a brief overview of the diagnosis, epidemiology, etiology and clinical management of dentin hypersensitivity, to discuss technical approaches to relieve sensitivity, with special emphasis on dentin tubule occlusion and the clinical evidence for efficacy of desensitizing toothpastes based upon this approach, and to summarize the science behind a new dentifrice technology, based upon arginine and calcium carbonate, and the clinical evidence which proves that it delivers both instant and lasting relief of dentin hypersensitivity. RESULTS: Clinical studies have shown that a new toothpaste, containing arginine and calcium carbonate (known as Pro-Argin technology) with 1450 ppm fluoride, offers clinically proven instant and lasting relief of dentin hypersensitivity. Three 8-week clinical studies have shown that this new toothpaste provides statistically significantly superior efficacy in reducing sensitivity to market leading desensitizing toothpastes containing 2% potassium ion. Importantly, three further clinical studies have shown that a single direct topical application of toothpaste to sensitive teeth, using a fingertip or cotton swab followed by 1 minute of massage, resulted in instant relief of dentin hypersensitivity and that the relief was maintained with subsequent twice-daily brushing. Mechanism of action studies have shown that this technology physically seals dentin tubules with a plug that contains arginine, calcium carbonate and phosphate. This plug, which is resistant to normal pulpal pressures and to acid challenge, effectively reduces dentin fluid flow and thereby relieves sensitivity. A new whitening variant of this desensitizing toothpaste, containing the Pro-Argin technology, fluoride and a high cleaning calcium carbonate system, has now been clinically and scientifically validated. This toothpaste works by the same mechanism of action as its non-whitening counterpart and is clinically proven to provide both instant and lasting relief of sensitivity, while providing proven efficacy in removal of extrinsic stains. No difference in desensitizing efficacy was observed between the whitening and non-whitening versions.

Dentin bonding-variables related to the clinical situation and the substrate treatment.

The wetness of dentin surfaces, the presence of pulpal pressure, and the thickness of dentin are extremely important variables during bonding procedures, especially when testing bond strength of adhesive materials in vitro with the intention of simulating in vivo conditions. The ultimate goal of a bonded restoration is to attain an intimate adaptation of the restorative material with the dental substrate. This task is difficult to achieve as the bonding process is different for enamel and for dentin-dentin is more humid and more organic than enamel. While enamel is predominantly mineral, dentin contains a significant amount of water and organic material, mainly type I collagen. This humid and organic nature of dentin makes this hard tissue very challenging to bond to. Several other substrate-related variables may affect the clinical outcome of bonded restorations. Bonding to caries-affected dentin is hampered by its lower hardness and presence of mineral deposits in the tubules. Non-carious cervical areas contain hypermineralized dentin and denatured collagen, which is not the ideal combination for a bonding substrate. Physiological transparent root dentin forms without trauma or caries lesion as a natural part of aging. Similar to the transparent dentin observed underneath caries lesions, the tubule lumina become filled with mineral from passive chemical precipitation, making resin hybridization difficult. An increase in number of tubules with depth and, consequently, increase in dentin wetness, make bonding to deeper dentin more difficult than to superficial dentin. While the application of acidic agents open the pathway for the diffusion of monomers into the collagen network, it also facilitates the outward seepage of tubular fluid from the pulp to the dentin surface, deteriorating the bonding for some of the current adhesives. Some dentin desensitizers have shown some promise as they can block dentinal tubules to treat and prevent sensitivity and simultaneously blocking the tubular fluid from flowing to the surface. A new approach to stop the degradation of dentin-resin interfaces is the use of MMP inhibitors. Although still in an early phase of in vitro and clinical research, this method is promising.

In-office treatment of dentinal hypersensitivity.

Dentinal hypersensitivity is a common dental complaint, especially in periodontal patients. It is believed to be mediated by a hydrodynamic mechanism in which various stimuli result in increased fluid flow in dentinal tubules, thereby generating action potentials in associated nerve fibers. Although it is often perceived as mild discomfort by the patient, it can be severe. A variety of interventions has been used, although few have been subjected to rigorous study. This article surveys those in-office treatments that are available, and suggests directions for research so that clinicians may treat patients based on best evidence. Until such evidence is available, it seems prudent to employ therapies that are least likely to cause harm and are reversible.

Managing dentin hypersensitivity.

BACKGROUND: The objective of this review is to inform practitioners about dentin hypersensitivity (DH) and its management. This clinical information is described in the context of the underlying biology. TYPES OF STUDIES REVIEWED: The authors used MEDLINE to find relevant English-language literature published in the period 1999 to 2005. They used combinations of the search terms "dentin*," "tooth," "teeth," "hypersensit*," "desensiti*" and "desensitiz*." They read abstracts and then full articles to identify studies describing etiology, prevalence, clinical features, controlled clinical trials of treatments and relevant laboratory research on mechanisms of action. RESULTS: The prevalence of DH varies widely, depending on the mode of investigation. Potassium-containing toothpastes are the most widely used at-home treatments. Most in-office treatments employ some form of "barrier," either a topical solution or gel or an adhesive restorative material. The reported efficacy of these treatments varies, with some having no better efficacy than the control treatments. Possible reasons for this variability are discussed. A flowchart summarizes the various treatment strategies. CLINICAL IMPLICATIONS: DH is diagnosed after elimination of other possible causes of the pain. Desensitizing treatment should be delivered systematically, beginning with prevention and at-home treatments. The latter may be supplemented with in-office modalities.

[Electroanalgesia: operating principles]. / Electroanalgesie: principes de fonctionnement.

We are faced every day with the problem of dental pain arising from the concomitant action of the nerve fibres, the odontoblasts and the dentinal fluid. Its propagation is due to the triggering of the action potential from the resting potential. It can be reduced thanks to a reversible process of anelectrotonus in electro-analgesia.