Neuropeptides and Neurogenic Mechanisms in Oral and Periodontal Inflammation

Abstract

ABSTRACT:It is generally accepted that the nervous system contributes to the pathophysiology of peripheral inflammation, and a neurogenic component has been implicated in many inflammatory diseases, including periodontitis. Neurogenic inflammation should be regarded as a protective mechanism, which forms the first line of defense and protects tissue integrity. However, severe or prolonged noxious stimulation may result in the inflammatory response mediating injury rather than facilitating repair. This review focuses on the accumulating evidence suggesting that neuropeptides have a pivotal role in the complex cascade of chemical activity associated with periodontal inflammation. An overview of neuropeptide synthesis and release introduces the role of neuropeptides and their interactions with other inflammatory factors, which ultimately lead to neurogenic inflammation. The biological effects of the neuropeptides substance P (SP), calcitonin gene-related peptide (CGRP), vasoactive intestinal polypeptide (VIP), and neuropeptide Y (NPY) are summarized, and evidence for their involvement in the localized inflammatory lesions which characterize periodontitis is presented. In this context, the role of CGRP in bone metabolism is described in more detail. Recent research highlighting the role of the nervous system in suppressing pain and inflammation is also discussed.

Chemical sympathectomy increases susceptibility to ocular herpes simplex virus type 1 infection

“…Treatment of sympathectomized mice with the NK1R antagonist was found to delay mortality by 3 days although eventually the survival rate was similar to vehicle-treated, sympathectomized mice. The incomplete protection based on survival in the NK1R antagonisttreated animals may be due to the incomplete action of the NK1R antagonist as the levels of substance P rise in the infected, sympathectomized mice outcompetes for NK1R activation or the dual role of substance P associated with pain perception (Lundy and Linden, 2004) as well as an immunomodulator. For example, substance P elicits the production of cytokines including TNF-α (Lotz et al, 1988), and IFN-γ (Lighvani et al, 2005) which are linked to the control of HSV-1 infection.…”

The selective PAC1 receptor agonist maxadilan inhibits neurogenic vasodilation and edema formation in the mouse skin

“…Alterations in the level of the 28 amino acid neuropeptide VIP were shown in several immunological diseases, like sepsis, rheumatoid arthritis, lupus, autoimmune thyroiditis, while its involvement in neurogenic inflammatory disorders has also emerged (Delgado and Ganea, 2013;Lundy and Linden, 2004;Teresiak-Mikołajczak et al, 2013;Wu et al, 2011). We learned from studies with VIP-deficient mice that endogenous VIP exerts anti-inflammatory properties in LPSinduced septic shock, asthma and pulmonary hypertension (Delgado and Ganea, 2013;Hamidi et al, 2006).…”

Gingival immunologic defense index: a new indicator for evaluating dental plaque infection risk in allergic children

“…by van der Kleij. 15 According to Lundy and Linden, 16 this mechanism also occurred in the periodontal tissues, including gingiva. discussion Allergic hyperreactivity is defined as an exaggerated immuneresponse typically immunoglobulin E (IgE) but also non-IgE mediated toward harmless antigenic stimuli.…”