Role of histamine in the development of neurogenic inflammation of rat oral mucosa

Györfi, A; Fazekas, Á; Posch, E.; Irmes, F; Rosivall, László

doi:10.1007/bf01980879

Cited by 10 publications

(3 citation statements)

References 37 publications

(29 reference statements)

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“…Evidence for the development of neurogenic inflammation in the oral cavity was first presented just over a decade ago (Fazekas et al, 1990). Further work showed that SP was a major mediator of the neurogenic inflammatory response in the oral mucosa (Gyorfi et al, 1991(Gyorfi et al, , 1992(Gyorfi et al, , 1993(Gyorfi et al, , 1995. Factors associated with neurogenic inflammation in cutaneous tissues are also present in orofacial tissues.…”

Section: (B) Neuropeptides and Oral Diseasementioning

confidence: 99%

Neuropeptides and Neurogenic Mechanisms in Oral and Periodontal Inflammation

Lundy

Linden

2004

Critical Reviews in Oral Biology & Medicine

148

165

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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.

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Section: (B) Neuropeptides and Oral Diseasementioning

confidence: 99%

Neuropeptides and Neurogenic Mechanisms in Oral and Periodontal Inflammation

Lundy

Linden

2004

Critical Reviews in Oral Biology & Medicine

148

165

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“…Gyorfi et al (1991) reported effects derived from application of histamine and capsaicin, along with stimulation of the inferior alveolar nerve, on the oral mucosa covering the mandibula of rats. These authors observed a marked vasodilation and increased vascular permeability of the tissue following such stimulation, typical features of the (sensory) axon reflex or neurogenic inflammation (Jancsó et al 1968).…”

Section: Introductionmentioning

confidence: 98%

Tissue-selective inflammation in the oral cavity of the rat

et al. 2016

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In the current study, carrageenan (CG; 100-1000 μg/site) was injected intraorally in the cheeks of Holtzman or Wistar rats to evaluate the consequences of administration of a non-immunogenic stimulus in the orofacial region. Subsequent inflammation was measured as oedema (increased thickness of the cheek wall using digital calipers), relative to the other cheek injected with saline. Oedema formation and tissue collection for histopathological studies were assessed at 0.5, 1, 2, 3, 4, 6, 24, 48, 72, 96, 120 and 144 h after injection. In parallel, other groups of rats were injected with CG in the hind paw, to provide a reference response. The inhibitor of prostaglandin biosynthesis, indomethacin, and antagonists of histamine, serotonin and NK1 receptors were injected s.c., 0.5 h before CG. CG induced a dose-related oedema more rapidly from 0 to 2 h which lasted for at least 72 h, showing a biphasic profile (peak at 2 and 24 h), compared with the monophasic oedema induced in rat paws (maximal duration of 24 h). Histopathological analysis of the CG-injected cheek revealed oedema formation with little leukocyte recruitment at 1-3 h, mast cell degranulation at 6 h, and a mixed polymorphonuclear and mononuclear cell infiltrate by 24 h. Histamine and serotonin antagonists and indomethacin, but not the NK1 antagonist, decreased cheek oedema in the first 4 h following carrageenan. Taken together, our data indicated important differences in the pattern of inflammation between the oral cavity and the paw which will determine the therapeutic approach to the treatment of inflammatory conditions in the oral cavity.

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“…Although histamine is not the main compound responsible for HC development, it may be considered to belong to such a group of substances, stored inside both immune cells and newly synthesized pro-inflammatory factors. Moreover, for the past 20 years it has been commonly accepted that histamine plays an essential role in the development of neurogenic inflammation [13,14]. Thus, histaminic mechanisms contributing to HC pathogenesis may also be a potential pharmacological target.…”

Section: Introductionmentioning

confidence: 99%

The influence of pemirolast on autonomic imbalance in rat cystitis model

2013

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AbstractCyclophosphamide (CP) treatment is associated with the risk of haemorrhagic cystitis (HC). Moreover, CP-induced HC is complicated by autonomic nervous system (ANS) dysfunction. Pemirolast is thought to be a mast cell stabiliser that inhibits the release of many inflammatory mediators and sensory neuropeptides, and thus, it may be considered a potential chemoprotective HC agent. The aim of the study was to indirectly estimate the effect of pemirolast in experimental HC by measuring ANS activity with the heart rate variability (HRV) method. In CP-treated rats, we found a decreasing trend of overall autonomic activity, together with an imbalance between the main components, and a dominant very low frequency (VLF) power component. Pemirolast treatment did not improve the total HRV power value or the main non-normalized HRV components. Moreover, CP-HC animals treated with pemirolast displayed a different disproportion of normalized spectral components as compared to both control and CP-HC animals without pemirolast treatment, with the balance between normalized low frequency (nLF) and normalized high frequency (nHF) shifted towards nLF. This finding, together with a relatively high VLF tension, indicates that the pemirolast treatment resulted in high sympathetic activity that may contribute to HC exacerbation; thus, this agent seems to be ineffective in CP-induced HC.

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Role of histamine in the development of neurogenic inflammation of rat oral mucosa

Cited by 10 publications

References 37 publications

Neuropeptides and Neurogenic Mechanisms in Oral and Periodontal Inflammation

Neuropeptides and Neurogenic Mechanisms in Oral and Periodontal Inflammation

Tissue-selective inflammation in the oral cavity of the rat

The influence of pemirolast on autonomic imbalance in rat cystitis model

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