Tooth brushing, tooth wear and dentine hypersensitivity - are they associated?

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.

An overview of tooth wear, i.e. of non-carious destructive processes affecting the teeth including abrasion, demastication, attrition, abfraction, resorption and erosion is presented. The nomenclature and classification of dental erosion commonly used in the dental literature are summarized. They are based on etiology (extrinsic, intrinsic, idiopathic), on clinical severity (Classes I to III), on pathogenetic activity (manifest, latent) or on localization (perimolysis). Interactions between erosion and abrasion, demastication, attrition, and abfraction as well as caries and low salivary flow rate are highlighted.

In this study the viability and the distribution of bacteria within the radicular dentin and pulp of periodontally diseased caries-free teeth were studied. Healthy teeth served as controls. Samples were obtained from the pulp tissue and from the radicular dentin. Dentin samples were taken from the interdental surfaces in the subgingival area. Starting from the pulpal side, three to five successive dentin layers of approximately 1 mm thickness were sampled. The samples were processed and cultured using an anaerobic technique. Bacterial growth was detected in 87% of the periodontally diseased teeth. In 83% of the teeth, bacteria were present in at least one of the dentin layers. Fifty-nine percent of the diseased teeth, from which the pulp tissue was cultured, contained bacteria in the pulp samples. The mean bacterial concentrations in the pulp and dentin layers ranged from 1,399 to 16,537 colony-forming units (CFU) per mg of tissue. These concentrations were 259 to 7,190 times greater than concentrations found in healthy teeth. It is suggested that the roots of periodontally diseased teeth could act as bacterial reservoirs from which recolonization of mechanically treated root surfaces can occur, as well as infection of the dental pulp. These findings might change current concepts concerning root surface debridement in periodontal therapy.