Hydrodynamic theory (dentistry)
[2] The fluid flow mechanism behind hydrodynamic theory was first introduced by Alfred Gysi in 1900, and subsequently developed by Martin Brännström in the 1960s through a series of experimental studies.
[3] Further supporting evidence has since been collected from epidemiological surveys and experimental data comparing dentinal tubule numbers in hypersensitive and non-hypersensitive teeth.
[19] In his clinical practice, Gysi observed that the removal of fluid from the cavity floor of his patients' teeth produced the sharp, short pain of dentine hypersensitivity.
Physical and thermal forms of stimuli would cause an increase change in the direction of fluid flow, which activated the pulpal nerve endings.
[22] In the 1960s, Brännström provided evidence to support Gysi's hydrodynamic theory through a series of experimental studies in vitro to show that various stimuli caused shifts in fluid movement across dentine, producing pain.
It was shown that various types of cold thermal, evaporative cooling, osmotic stimuli and hypertonic chemical substances could cause an increase in outward fluid flow along the dentinal tubules.
[26] Brännström's multiple publications of both experimental and observational data provided significance evidence to support the theory of hydrodynamic mechanism causing dentine hypersensitivity.
It was proposed that if the hydrodynamic fluid flow was responsible for hypersensitivity, then there must be higher numbers of dentinal tubules exposed at the surface of the root and patent to the dental pulp.
It is uncertain how the physical changes in direction and rate of fluid flow within dentinal tubules actually causes the stimulation of pain receptors in pulp nerves.
[38] Evidence against the theory was presented in an experiment in which dentinal tubules that had been purposely obstructed to prevent fluid flow still exhibited hypersensitivity upon the application of thermal stimuli.
[39] Additionally, it has been noted in clinical cases that hypersensitivity worsened even after dental cavities had significantly destroyed dentinal tubules and made fluid flow impossible.
[49] As acetylcholinesterase is responsible for terminating neurotransmission and synapse signalling, they hypothesised that it helped conduct sensory information to the pulpal nerves from the odontoblast processes.
[50] Further criticism arose from clinical observations indicating that hypersensitivity continued even after the odontoblast layer was destructed by dental cavities and nerve injuries.
As mechanical stimuli have proven to be a major cause of hypersensitivity, preventative strategies include proper hygiene and brushing technique instruction.
To avoid increasing the patency of tubules, patients have been encouraged to schedule regular appointments to check for dental erosion, tooth decay and periodontal disease.
Desensitising treatments are separated into two groups: at-home procedures in the form of mouthwash and toothpaste, or in-office products such as resin sealers, glass ionomers and dentine solutions.
