Journal of Oral Pathology and Medicine · 2000 · 29 citations · 28 references
Life SciencesNeurobiologyNeuroscienceImmunophysiologyNeuroendocrinologyNeuroimmunologyNervous System PathologyPeripheral Nerve AnatomyPeripheral Nervous SystemPeripheral Nervous System PhysiologyChronic Mucosal InflammationLichenoid DermatitisLichenoid Tissue ReactionOral Lichenoid LesionsOral Lichenoid ReactionsOral Mucosa AnatomyOral Mucosa HistologyOral Mucosal Innervation
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.
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Jens Ove Andreasen · Oral Surgery Oral Medicine Oral Pathology · 1968 · 523 citations
Medicine, Dermatology, Immunology +14
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Medicine, Neurology, Neuroscience +12
Hypothesis: the nervous system may contribute to the pathophysiology of rheumatoid arthritis.
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