The simple answer is the research proven discovery and development of sub-sensory waves of electric energy that is delivered via a specialized probe to the area of nerve bundles blocks the electrical nerve signal from ever causing a pain signal in the brain. This is called neuro-modulation.
More advanced description:
Pain sensory fibers in the periodontal complex (including supporting mucosal tissue, attached gingival, periodontal ligament, attachment fibers, dental structure including dentinal tubules with odontoblasts, pulpal tissue, and neural complex leading to ganglia) are blocked using sub-sensory High Frequency Kilohertz Alternating Current (HFKAC) used in the Dental Pain Eraser.
Blocking of pain fiber action firing, which also includes odontoblasts below relating to dental hypersensitivity, will also block the release of neurotransmitters and neuropeptide cascade pain response.
Blocking of neuropeptides such as Substance P can also reduce the vasodilation, mast cell activation (histamine response), and reduce swelling and inflammation in the area.
Another neuropeptide that is blocked or reduced is Calcitonin gene-realted peptide (CGRP). CGRP is a 37-amino acid peptide found primarily in the C and Aδ sensory fibers arising from the dorsal root and trigeminal ganglia, as well as the central nervous system. Calcitonin gene–related peptide was found to play important roles in cardio-vascular, and sensory functions. Although the vasodilatory properties of CGRP are well documented, it has been shown to modulate neuronal sensitization. CGRP plays a key role in the development of peripheral sensitization and the associated enhanced pain. Calcitonin gene–related peptide is implicated in the development of neurogenic inflammation and it is upregulated in conditions of inflammatory and neuropathic pain. It is most likely that CGRP facilitates nociceptive transmission and contributes to the development and maintenance of a sensitized, hyper-responsive state not only of the primary afferent sensory neurons but also of the second-order pain transmission neurons within the central nervous system, thus contributing to central sensitization as well.
Dentine hypersensitivity and pulpitis-associated pain are among the most common types of dental pain. Patients with these conditions feel pain upon exposure of the affected tooth to various external stimuli. Numerous ion channels and receptors localized in the dental primary afferent neurons (DPAs) and odontoblasts have been implicated in the transduction of dental pain, and functional expression of various polymodal transient receptor potential (TRP) channels has been detected in DPAs and odontoblasts. External stimuli-induced dentinal tubular fluid movement can activate TRP channels on DPAs and odontoblasts. Blockage of the ionic potential and firing of the “neuronal” properties of the odontoblasts with the DPE, can in turn block the DPAs by paracrine signaling through ATP and glutamate release.
In pulpitis, inflammatory mediators may sensitize the DPAs. DPE current delivery through dentinal tubules, lateral canal pulpal communication, can also block DPA sensitization. This will in turn block post-translational modifications of TRP channels, decrease increase trafficking of these channels to nerve terminals, and decrease the sensitivity of these channels to stimuli.
In our studies, we found that the pain relief from one single administration of DPE, providing pain relief relating to dental and periodontal pain for up to 48 hours. The main methods that this can occur are divided into peripheral and central mechanisms of pain reduction.
Peripheral system of pain reduction occurs by blocking the cascade effect of the neurotransmitter and neuropeptide response relating to sensory pain. This can occur directly through reduction of the firing of the above discussed odontoblastic method, and by direct block of pain fibers in the pulp directly.
The immediate block of pain when applying it directly to the tooth surface prior to a polishing (ionic air and pressure change in the tubule), tells us that the ionic potential on the odontoblast cell has been disrupted, preventing firing and sensitization of the polishing procedure that is to follow.
The central system of pain reduction occurs by communicating directly to ganglia and brain, causing a communication change in the process of pain response, signaling the central system to “shut down” pain response centers temporarily.