Dental pain originates from peripheral receptors that exist in the pulp tissue or periodontal ligament that will carry an electrical impulse to the cortex where it will be identified as a painful sensation and in the descending pathway a response to this painful sensation. Untreated dental caries begins with the affectation of the enamel, which leads to inflammation of the dental pulp which is caused by the invasion of commensal oral microorganisms in the pulp due to caries, likewise, irritation of the dental pulp by Mechanical, chemical, thermal or electrical stimuli can also cause pulpal inflammation, as pulpitis can be associated with trauma, cracks and periodontal infections. The dental pulp has a rich microvasculature and a dense innervation to maintain the homeostasis of the pulpal microenvironment, preserving its integrity, therefore, when hostile oral environments are evident, the body, specifically the coronal pulp, has a series of neurovascular and cellular mechanisms. that attack the bacterial bodies for the protection of the teeth when the inflammatory symptoms appear. The nerve fibers present in the pulp are in charge of perceiving the stimuli coming from the dentin, either due to sensitivity or some type of aggression produced to it. which allows them to interact with the microvasculature to maintain the pulp in adequate conditions. dental pulp has the activation of the opioid system, contributing not only to mediate pain but also inflammation of neurogenic origin, which in some cases can be so effective with the possibility of causing painless pulpal necrosis through endogenous opioids, these act by coupling to receptors associated with G protein, such as mu, delta, kappa and epsilon receptors, there are four main families of endogenous peptides, being: β-endorphin, enkephalins, dynorphins and nociceptin/orphanin FQ, for which it is essential have clear knowledge regarding its functional organization, the regulation of its neuronal function and neurotransmission.