Displacement of the contents of dentinal tubules and sensory transduction in intradental nerves of the cat. (1/14)

Experiments were performed on anaesthetized cats to test the hypothesis that fluid flow through dentinal tubules is part of the mechanism involved in the transduction of pain-producing stimuli in teeth. In 11 animals, fluid flow through dentine and single- and multi-unit activity in intradental nerves were recorded simultaneously during the application of changes in hydrostatic pressure (-500 to +500 mm Hg) to exposed dentine. Seventeen A-fibres (conduction velocity (CV), 10.6-55.1 m s(-1)) were isolated that were pressure sensitive. The thresholds of these units in terms of dentinal fluid flow were in the range 0.3-2.1 nl s(-1) mm(-2) during outward flow from the pulp and 2.0-3.5 nl s(-1) mm(-2) during inward flow. All the units were more sensitive to outward than inward flow. Twenty-eight units (CV, 0.6-48.8 m s-1) were not pressure sensitive, and 12 of these had conduction velocities in the C-fibre range (< 2.5 m s(-1)). The velocities of the tubular contents were calculated by estimating the number and diameters of dentinal tubules exposed. At the threshold of single-fibre responses these velocities were in the range 31.7-222.9 microm s(-1) during outward flow 211.4-369.6 microm s-1 during inward flow. Repetitive pressure stimulation of dentine resulted in a progressive reduction in the evoked discharge, which was probably due to pulp damage. In seven animals, 10 single intradental nerve fibres were selected that responded to hydrostatic pressure stimuli and their responses to the application of hot, cold, osmotic, mechanical and drying stimuli to exposed dentine were investigated. With these stimuli dentinal fluid flow could not be recorded in vivo for technical reasons and was therefore recorded in vitro after completion of the electrophysiological recordings. With each form of stimulus, the discharge evoked in vivo was closely related to the flow predicted from the in vitro measurements. The results were therefore consistent with the hypothesis that the stimuli act through a common transduction mechanism that involves fluid flow through dentine.  (+info)

Invasion of dentinal tubules by oral bacteria. (2/14)

Bacterial invasion of dentinal tubules commonly occurs when dentin is exposed following a breach in the integrity of the overlying enamel or cementum. Bacterial products diffuse through the dentinal tubule toward the pulp and evoke inflammatory changes in the pulpo-dentin complex. These may eliminate the bacterial insult and block the route of infection. Unchecked, invasion results in pulpitis and pulp necrosis, infection of the root canal system, and periapical disease. While several hundred bacterial species are known to inhabit the oral cavity, a relatively small and select group of bacteria is involved in the invasion of dentinal tubules and subsequent infection of the root canal space. Gram-positive organisms dominate the tubule microflora in both carious and non-carious dentin. The relatively high numbers of obligate anaerobes present-such as Eubacterium spp., Propionibacterium spp., Bifidobacterium spp., Peptostreptococcus micros, and Veillonella spp.-suggest that the environment favors growth of these bacteria. Gram-negative obligate anaerobic rods, e.g., Porphyromonas spp., are less frequently recovered. Streptococci are among the most commonly identified bacteria that invade dentin. Recent evidence suggests that streptococci may recognize components present within dentinal tubules, such as collagen type I, which stimulate bacterial adhesion and intra-tubular growth. Specific interactions of other oral bacteria with invading streptococci may then facilitate the invasion of dentin by select bacterial groupings. An understanding the mechanisms involved in dentinal tubule invasion by bacteria should allow for the development of new control strategies, such as inhibitory compounds incorporated into oral health care products or dental materials, which would assist in the practice of endodontics.  (+info)

Consensus-based recommendations for the diagnosis and management of dentin hypersensitivity. (3/14)

These consensus recommendations for the diagnosis and management of dentin hypersensitivity were developed by a broadly constituted board of dentists and dental hygienists drawn from general dental practice, specialist practice, academia and research from across Canada, joined by 2 international dentists with subject matter expertise. The need for consensus recommendations was made evident by the lack of clear and robust evidence in the dental literature, as well as confusion about diagnosis and management demonstrated by an educational needs assessment survey. High prevalence of the condition, underdiagnosis and widespread availability of noninvasive, efficacious and inexpensive preventive treatment further underscored the need for direction. This paper outlines the key elements of the scientific basis for the causes, diagnosis and management of dentin hypersensitivity; where such evidence is deficient, the document relies on the compound experience of the board. A simple algorithm was developed to guide clinicians through the diagnostic process and assist them in determining appropriate case management. Finally, the board makes a series of recommendations to raise awareness, to improve dental education, to develop symbols for charting, to develop an index for case assessment and for further research.  (+info)

Influence of intrapulpal pressure simulation on the bond strength of adhesive systems to dentin. (4/14)

 (+info)

Dental pulp neurophysiology: part 1. Clinical and diagnostic implications. (5/14)

Diagnosis in endodontics requires an understanding of pulpal histology, neurology and physiology, and their relationship to the various diagnostic tests commonly used in dental practice. Thermal changes in the oral environment cause rapid displacement of dentinal tubular contents, resulting in pain. This effect, known as the hydrodynamic effect, is the regulator of pain sensation in thermal-pulp testing. Hundreds of axons enter the tooth from the apical foramen to provide it with its sensory supply. The nerve supply of the dentin-pulp complex is mainly made up of A fibres (both delta and beta) and C fibres. They are classified according to their diameter and their conduction velocity. The A fibres are mainly stimulated by an application of cold, producing sharp pain, whereas stimulation of the C fibres produces a dull aching pain. Because of their location and arrangement, the C fibres are responsible for referred pain. This first part of a 2-part review examines the relation between clinical sensations during the diagnostic visit and the neurophysiology of the dental pulp to explore the connection between the art (clinical diagnosis) and the science (neurophysiology) of endodontics.  (+info)

Dentin permeability: the basis for understanding pulp reactions and adhesive technology. (6/14)

 (+info)

Prevention of water contamination of ethanol-saturated dentin and hydrophobic hybrid layers. (7/14)

PURPOSE: This in vitro study evaluated the amount and distribution of outward fluid flow that occurred when an experimental etch-and-rinse hydrophobic adhesive was applied to ethanol-saturated dentin before and after oxalate pretreatment. MATERIALS AND METHODS: Measurements of dentin permeability were performed under a constant pulpal pressure of 20 cm H2O in deep and middle dentin. A lucifer yellow solution was placed in the pulp chamber to determine the distribution of the water contamination of the hybrid layers. RESULTS: The distribution of fluorescence in dentin specimens that were not pretreated with oxalate revealed that the dye permeated around the resin tags and filled the hybrid layer. Dentin specimens pretreated with oxalate prior to resin bonding, showed 80% to 83% less (p < 0.05) water contamination compared to controls. The dentin permeability results obtained before and after oxalate pretreatment showed that oxalate decreased dentin permeability by 98% (p < 0.05) compared to acid-etched controls. This prevented outward fluid movement during bonding, resulting in better resin sealing of dentin due to the formation of a double seal of resin tags over calcium oxalate crystals in the tubules. CONCLUSION: Outward dentinal fluid flow may contaminate hybrid layers during adhesive bonding procedures. Pretreatment of acid-etched dentin with 3% oxalic acid prior to bonding procedures can prevent outward fluid flow during bonding and water contamination of the hydrophobic hybrid layers.  (+info)

Fluid mechanics in dentinal microtubules provides mechanistic insights into the difference between hot and cold dental pain. (8/14)

 (+info)