Dental pain evoked by hydrostatic pressures applied to exposed dentin in man: A test of the hydrodynamic theory of dentin sensitivity

1994 ◽  
Vol 20 (3) ◽  
pp. 130-134 ◽  
Author(s):  
Michael Ahlquist ◽  
Ove Franzén ◽  
James Coffey ◽  
David Pashley
2008 ◽  
Vol 87 (9) ◽  
pp. 834-838 ◽  
Author(s):  
T.O. Hermanstyne ◽  
K. Markowitz ◽  
L. Fan ◽  
M.S. Gold

The hydrodynamic theory suggests that pain associated with stimulation of a sensitive tooth ultimately involves mechanotransduction as a consequence of fluid movement within exposed dentinal tubules. To determine whether putative mechanotransducers could underlie mechanotransduction in pulpal afferents, we used a single-cell PCR approach to screen retrogradely labeled pulpal afferents. The presence of mRNA encoding BNC-1, ASIC3, TRPV4, TRPA1, the α, β, and γ subunits of ENaC, and the two pore K+ channels (TREK1, TREK2) and TRAAK were screened in pulpal neurons from rats with and without pulpal inflammation. ASIC3, TRPA1, TREK1, and TREK2 were present in ~67%, 64%, 14%, and 10% of pulpal neurons, respectively. There was no detectable influence of inflammation on the proportion of neurons expressing these mechanotransducers. Given that the majority of pulpal afferents express ASIC3 and TRPA1, our results raise the possibility that these channels may be novel targets for the treatment of dentin sensitivity.


1997 ◽  
Vol 11 (4) ◽  
pp. 487-501 ◽  
Author(s):  
D.G. Gillam ◽  
N.J. Mordan ◽  
H.N. Newman

Dentin sensitivity (DS) is a painful clinical condition which may affect 8-35% of the population. Various treatment modalities have claimed success in relieving DS, although at present there does not appear to be a universally accepted desensitizing agent. Current opinion based on Brannstrom's Hydrodynamic Theory would suggest that following exposure of the dentin surface (through attrition, abrasion, or erosion), the presence of open dentinal tubules, patent to the pulp, may be a prerequisite for DS. The concept of tubule occlusion as a method of dentin desensitization, therefore, is a logical conclusion from the hydrodynamic theory. The fact that many of the agents used clinically to desensitize dentin are also effective in reducing dentin permeability tends to support the hydrodynamic theory. This paper reviews the in vitro evaluation of desensitizing agents, the techniques used to characterize their effects on the prepared dentin surface, and the ability of these agents to reduce permeability through tubule occlusion, and presents recent findings from ongoing research based on the Pashley Dentin Disc model. It can be concluded that the use of this model to determine surface characteristics, and reductions in dentin permeability through tubule narrowing or occlusion, provides a useful screening method for evaluating potential desensitizing agents. Interpreting changes observed in vitro is difficult, and extrapolation to the clinical situation must be tempered with caution.


2013 ◽  
Vol 6 (1) ◽  
pp. 31-36 ◽  
Author(s):  
Gehoon Chung ◽  
Seog Bae Oh

Despite the high incidence of dental pain, the mechanism underlying its generation is mostly unknown. Functional expression of temperature-sensitive transient receptor potential (thermo-TRP) channels, such as TRPV1, TRPV2, TRPM8, and TRPA1 in dental primary afferent neurons and TRPV1, TRPV2, TRPV3, TRPV4, and TRPM3 in odontoblasts, has been demonstrated and suggested as responsible for dental pain elicited by hot and cold food. However, dental pain induced by light touch or sweet substance cannot be explained by the role of thermo-TRP channels. Most of current therapeutics of dentin hypersensitivity is based on hydrodynamic theory, which argues that light stimuli such as air puff and temperature changes cause fluid movement within dentinal tubule, which is then transduced as pain. To test this theory, various TRP channels as candidates of cellular mechanotransducers were studied for expression in dental primary afferents and odontoblasts. The expression of TRPV1, TRPV2, TRPA1, TRPV4, and TRPM3 in trigeminal neurons and TRPV1, TRPV2, TRPV3, TRPV4 and TRPM3 in odontoblasts has been revealed. However, their roles as cellular mechanotransducers are controversial and contribution to generation of dental pain is still elusive. This review discusses recent advances in understanding of molecular mechanism underlying development of dental pain.


2011 ◽  
Vol 11 (01) ◽  
pp. 205-219 ◽  
Author(s):  
M. LIN ◽  
Z. Y. LUO ◽  
B. F. BAI ◽  
F. XU ◽  
T. J. LU

Noxious thermal and/or mechanical stimuli applied to dentine can cause fluid flow in dentinal microtubules (DMTs). The fluid flow induces shear stress (SS) on intradental nerve endings and may excite pulpal mechanoreceptors to generate dental pain sensation. There exist numerous studies on dental thermal pain, but few are mathematical. For this, we developed a computational fluid dynamics (CFD) model of dentinal fluid flow (DFF) in innervated DMTs. Based on this model, we systematically investigated the effects of various parameters (e.g., biological structure, DFF velocity, and fluid properties) on the SS experienced by intradental nerve endings and thus provide a quantitative interpretation to the hydrodynamic theory. The dimensions of biological structures, odontoblastic process (OP) movement, dentinal fluid velocity, and viscosity were found to have significant influences on the SS while dentinal fluid density showed negligible influence under conditions studied. The results indicate that: (i) dental pain study of animal models may not be directly applied to human being and the results may even vary from one person to another and (ii) OP movement caused by DFF changes the dimension of the space for the fluid flow, affecting thus the SS on nerve endings. The present work enables better understanding of the mechanisms underlying dental pain sensation and quantification of dental pain intensity resulted from clinical procedures such as dentine sensitivity testing and dental restorative processes.


2021 ◽  
Vol 10 (37) ◽  
pp. 3289-3293
Author(s):  
Mrinalini Mrinalini ◽  
Urvashi B. Sodvadiya ◽  
Mithra N. Hegde ◽  
Gowrish S. Bhat

BACKGROUND Dentinal hypersensitivity is a common clinical disease that occurs as a result of dentin exposure. Though the term dentin hypersensitivity and dentin sensitivity is used interchangeably, dentin hypersensitivity is an exaggerated form of dentinal sensitivity which arises due to localized pulpal inflammation, pulpal nerve sprouting, and development of inflammatory sodium channels. It is characterised by short sharp pain emerging from exposed dentinal tubules in reaction to various stimuli. Such dentin exposure could be due to either enamel loss or cemental loss. This is followed by removal of smear layer by mechanical or chemical means. At present, the hydrodynamic theory, which describes fluid movement in response to stimuli within exposed dentinal tubules, is a commonly recognized explanation for dentin hypersensitivity. It is more common in premolars and canines, and it affects the facial surfaces of the teeth towards the cervical aspect. Studies suggested microscopic changes in the structure of sensitive dentin compared with normal dentin. The diagnosis of dentinal hypersensitivity requires careful clinical examination and eliciting the response using various stimuli. Dentinal hypersensitivity is usually managed by the use of physical or chemical agents. They work either by disturbing the neural response to pain stimulus or block fluid flow by occluding the tubule. The desirable features of a desensitising agent include the ability to give instant and longlasting pain relief, being simple to use, well accepted, not harmful to the pulp. It is recommended that the desensitizing agent is used for at least two weeks. Some of the newer agents used for management includes CPP-ACP, proarginine, nanomaterials, herbal products, propolis etc. In cases where there is tooth structure loss, appropriate restorative material is used to cover the exposed dentin. Root canal therapy is considered the last resort for pain relief after all other options have failed to provide relief. The present article outlines the etiopathogenesis, risk factors, diagnosis, prevention and treatment of dentinal hypersensitivity. KEY WORDS Dentinal Hypersensitivity; Dentin Sensitivity; Desensitizing Agents; Iontophoresis


Analgesia ◽  
1994 ◽  
Vol 1 (1) ◽  
pp. 65-71 ◽  
Author(s):  
Stephen A. Cooper ◽  
Elliot V. Hersh ◽  
Norman J. Betts ◽  
David Wedell ◽  
Peter Quinn ◽  
...  

Energies ◽  
2021 ◽  
Vol 14 (12) ◽  
pp. 3425
Author(s):  
Huanping Li ◽  
Jian Wang ◽  
Guopeng Bai ◽  
Xiaowei Hu

In order to explore the changes that autonomous vehicles would bring to the current traffic system, we analyze the car-following behavior of different traffic scenarios based on an anti-collision theory and establish a traffic flow model with an arbitrary proportion (p) of autonomous vehicles. Using calculus and difference methods, a speed transformation model is established which could make the autonomous/human-driven vehicles maintain synchronized speed changes. Based on multi-hydrodynamic theory, a mixed traffic flow model capable of numerical calculation is established to predict the changes in traffic flow under different proportions of autonomous vehicles, then obtain the redistribution characteristics of traffic flow. Results show that the reaction time of autonomous vehicles has a decisive influence on traffic capacity; the q-k curve for mixed human/autonomous traffic remains in the region between the q-k curves for 100% human and 100% autonomous traffic; the participation of autonomous vehicles won’t bring essential changes to road traffic parameters; the speed-following transformation model minimizes the safety distance and provides a reference for the bottom program design of autonomous vehicles. In general, the research could not only optimize the stability of transportation system operation but also save road resources.


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