Pulpal haemodynamics are naturally intermeshed with inflammatory respo
nses. Cellular and humoral factors may be the vehicles that aid in phy
siological regulation, but when these systems are overly activated, th
ey may lead to pathological changes. Sensory nerves may initiate infla
mmatory reactions when activated, and interestingly, recent findings s
how that vasoconstrictor nerves in the pulp can inhibit the release of
neurally stored vasoactive and inflammatory mediators. Thus, there ar
e options for endogenous control of inflammation. Perhaps a variation
in the effectiveness of such control can explain why symptoms of hyper
sensitivity and pain are so unpredictable and individual. What natural
ly occurring agents are involved in early tissue changes and how do th
ey act? Some agents exert their effects both on vessels and nerves. Th
us, there is an intriguing mutual interplay between nerves and tissue
reactions. A prolonged, painful stimulation may generate increased blo
od flow and inflammation, and vice versa, inflammation may lead to pai
n. This complexity of mechanisms generates many questions that need an
swers.