Читать книгу Biological Mechanisms of Tooth Movement - Группа авторов - Страница 67

SP and neurokinin A (NKA) are members of the tachykinin (tachy‐swift) neuropeptide family, and as such evoke rapid responses upon release. They exert a wide variety of biological actions and are intimately linked with neurogenic inflammation. The intensity of neurogenic inflammation has been shown to have a dose‐dependent relationship with the levels of SP and/or NKA. SP causes vasodilatation by acting directly on smooth‐muscle cells and indirectly by stimulating histamine release from mast cells in a concentration‐dependent manner. Increased microvascular permeability, edema formation, and subsequent plasma protein extravasation are prominent peripheral effects of the tachykinins, underlying their powerful proinflammatory properties. The SP‐induced contraction of endothelial cells and subsequent plasma extravasation allow substances such as bradykinin and histamine to gain access to the site of injury and to afferent nerve terminals. SP also interacts with other neurotransmitters: indeed, the characteristic edema formation mediated by SP has been shown to be modulated by nitrous oxide (Hughes et al., 1990). Lee et al. (2007), who outlined the mechanism of action of SP on OTM, demonstrated increased expression of the chemokine C–C ligand (CCL) 20 mRNA, CCL20 protein, and heme oxygenase (HO)‐1 in a dose‐ and time‐dependent manner. SP is also responsible for initiating phosphorylation of IkappaB, degradation of IkappaB, and activation of nuclear factor (NF)‐kappaB. This reaction confirms the role of SP, along with other immunoregulators, in inducing HO‐1, and the inflammatory mediator macrophage inflammatory protein (MIP)‐3 alpha/CCL20 in PDL cells in the development of inflammation associated with OTM.