vasoactive-intestinal-peptide and Mouth-Diseases

The nervous system contributes to the pathophysiology of peripheral inflammation and a neurogenic component has been implicated in many inflammatory disease, including oral diseases. Neurogenic inflammation should be regarded as a protective mechanism wich forms the first line of defense and protects tissue integrity. However, prolonged noxius stimulation may result in the inflammatory response. This review focuses on the evidence suggesting that neuropeptides have a pivotal role in the complex cascade of chemical activity associated with oral diseases. The pathophysiology is complex and neuropeptides are not solely responsible for the initiation and progression of the disease. However, since neuropeptides and inflammatory modulators are released together during the inflammatory response, it will be impossible to assign a specific role to each until work with selective antagonists is completed.

Topics: Animals; Disease Models, Animal; Disease Progression; Humans; Microcirculation; Mouth Diseases; Mouth Mucosa; Neurogenic Inflammation; Neuropeptides; Nociceptors; Pain; Rats; Substance P; Swine; Tongue; Vasoactive Intestinal Peptide

The peripheral nervous system was analysed in the oral mucosa of eight patients with oral lichen planus (OLP), five with a lichenoid reaction (LR) and three with mild chronic inflammation (MCI), by morphometric analysis of nerve fibres containing immunoreactive PGP 9.5, substance P (SP), calcitonin gene-related peptide (CGRP), vasoactive intestinal polypeptide (VIP), or C-flanking peptide of neuropeptide Y (CPON). Overall nerve fibre density was higher in OLP (P=0.039) and LR (P=0.026) compared with healthy oral mucosa and was compatible with sprouting and collateral formation. In contrast to the innervation visualized with structural nerve fibre-marker PGP 9.5, the densities of neuropeptide-immunoreactive nerves were low in inflamed tissue. This is consistent with depletion via local release. Retraction and local loss of innervation were found in areas coinciding with the most severe inflammation and basal membrane (BM) damage. Interestingly, LR showed a twenty-eight-fold loss of post-ganglionic CPON-ir sympathetic nerve fibres (P=0.044). In LR, CPON-ir innervation was markedly lower than in OLP. Finally, the pattern of innervation in relation to inflammatory cell infiltrates and tissue structures differed between OLP and LR. In conclusion, the peripheral nervous system is implicated in the immunopathogenesis of lichen planus and lichenoid reactions, with a disorder-specific difference in this involvement.

Topics: Adult; Aged; Analysis of Variance; Basement Membrane; Calcitonin Gene-Related Peptide; Chronic Disease; Humans; Lichen Planus, Oral; Lichenoid Eruptions; Middle Aged; Mouth Diseases; Mouth Mucosa; Nerve Fibers; Nerve Tissue Proteins; Neuropeptide Y; Statistics, Nonparametric; Stomatitis; Substance P; Sympathetic Nervous System; Thiolester Hydrolases; Ubiquitin Thiolesterase; Vasoactive Intestinal Peptide