When pain, thermal, and/or chemical stimulation is present, SP production and release increases. Current studies focus on whether controlling Substance P expression may control tooth pain.In addition, dental caries is more likely to develop pulpitis due to less time for the dental pulp to react and protect itself by occluding the dentinal tubules. Based on the tooth injury, sensory nerve fibers react to pulpitis by growing terminal branches into the adjacent surviving pulp, which also changes the cytochemical phenotype. This neural growth typically lasts few a few days and function and form is retained. Thus, pain is poorly localized, and the level of pain stemming from pulpitis varies based on severity, quality, duration, onset, trigger. As caries invades dentin, the number of permeable dentinal tubules correlates with the degree of pain. Intrapulp pressure have an effect on the sensory nerves of varying diameters: blocking larger diameter Aδ-fibres and activating smaller C-fibers. Under hypoxic environments and pulp degeneration (symptom of pulpitis), C-fibers may still function. Once reparative dentin forms, odontoblasts associated with the dentin change, and the pulpal fibroblasts lose p75 expression, which is a neurotrophin receptor. Diagnosis
Pulp sensibility tests are routinely used in the diagnosis of pulpitis. Pulp testing is combined with information taken from history, examination and other special investigations such as radiographs in order to reach a diagnosis. Pulp sensibility tests assess the pulp’s sensory response to a stimulus.
Enzymatic production of adenosine can be anti-inflammatory or immunosuppressive. Adenosine receptors
All adenosine receptor subtypes (A1, A2A, A2B, and A3) are G-protein-coupled receptors. The four receptor subtypes are further classified based on their ability to either stimulate or inhibit adenylate cyclase activity. The A1 receptors couple to Gi/o and decreases cAMP levels, while the A2 adenosine receptors couple to Gs, which stimulates adenylate cyclase activity. In addition, A1 receptors couple to Go, which has been reported to mediate adenosine inhibition of Ca2+ conductance, whereas A2B and A3 receptors also couple to Gq and stimulate phospholipase activity. Researchers at Cornell University have recently shown adenosine receptors to be key in opening the blood-brain barrier (BBB). Mice dosed with adenosine have shown increased transport across the BBB of amyloid plaque antibodies and prodrugs associated with Parkinsons disease, Alzheimers, multiple sclerosis, and cancers of the central nervous system. Ghrelin/growth hormone secretagogue receptor
Adenosine is an endogenous agonist of the ghrelin/growth hormone secretagogue receptor. However, while it is able to increase appetite, unlike other agonists of this receptor, adenosine is unable to induce the secretion of growth hormone and increase its plasma levels. Mechanism of action
When it is administered intravenously, adenosine causes transient heart block in the atrioventricular (AV) node. This is mediated via the A1 receptor, inhibiting adenylyl cyclase, reducing cAMP and so causing cell hyperpolarization by increasing K+ efflux via inward rectifier K+ channels, subsequently inhibiting Ca2+ current. It also causes endothelial-dependent relaxation of smooth muscle as is found inside the artery walls.