title: Nerve-pulp interactions.
abstract: Pulpal haemodynamics are naturally intermeshed with inflammatory responses. Cellular and humoral factors may be the vehicles that aid in physiological regulation, but when these systems are overly activated, they may lead to pathological changes. Sensory nerves may initiate inflammatory reactions when activated, and interestingly, recent findings show that vasoconstrictor nerves in the pulp can inhibit the release of neurally stored vasoactive and inflammatory mediators. Thus, there are options for endogenous control of inflammation. Perhaps a variation in the effectiveness of such control can explain why symptoms of hypersensitivity and pain are so unpredictable and individual. What naturally occurring agents are involved in early tissue changes and how do they act? Some agents exert their effects both on vessels and nerves. Thus, there is an intriguing mutual interplay between nerves and tissue reactions. A prolonged, painful stimulation may generate increased blood flow and inflammation, and vice versa, inflammation may lead to pain. This complexity of mechanisms generates many questions that need answers.
authors.affiliation: Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.
authors.forename: L
authors.initials: L
authors.lastname: Olgart
authors.forename: N P
authors.initials: NP
authors.lastname: Kerezoudis
mesh_terms: D000818:Animals; D002199:Capillary Permeability / Q000502:physiology; D003782:Dental Pulp / Q000098:blood supply* / Q000294:innervation*; D003807:Dentin Sensitivity / Q000209:etiology / Q000503:physiopathology*; D006801:Humans; D018836:Inflammation Mediators; D009475:Neurons, Afferent / Q000502:physiology; D018377:Neurotransmitter Agents / Q000502:physiology; D011671:Pulpitis / Q000150:complications / Q000503:physiopathology*; D014664:Vasodilation / Q000502:physiology*; D014666:Vasomotor System / Q000502:physiology
chemical_list: D018836:Inflammation Mediators; D018377:Neurotransmitter Agents