Relationship between levels of neuropeptide <scp>S</scp>ubstance <scp>P</scp> in periodontal disease and chronic pain: a literature review

Ávila, Érica Dorigatti de; Molon, Rafael Scaf de; Gonçalves, Daniela Aparecida de Godoi; Camparis, Cinara Maria

doi:10.1111/jicd.12087

Cited by 28 publications

(16 citation statements)

References 69 publications

(154 reference statements)

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“…While substance P is mostly known for its role in pain and neurogenic inflammation and is found in the central nervous system ( Mantyh, 2002 ), it also mediates effects via receptors in non-neuronal tissues. Substance P modulates cell proliferation and cytokine production, mediates interaction between immune cells and neurons ( de Avila et al, 2014 ; Mashaghi, 2016 ) and is involved in immunoregulation ( Payan and Goetzl, 1985 ; Stead et al, 1987 , 1989 ; Haines et al, 1993 ; Ho et al, 1997 ; Schratzberger et al, 1997 ). The main receptor for substance P is neurokinin 1 receptor (NK1R), which belongs to the tachykinin receptor family of G protein-coupled receptors.…”

Section: Investigation Of C-fiber-derived Neuropeptides As Novel Pulmmentioning

confidence: 99%

The Regulation of Pulmonary Vascular Tone by Neuropeptides and the Implications for Pulmonary Hypertension

Moosavi

Bubb

2018

Front. Physiol.

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Pulmonary hypertension (PH) is an incurable, chronic disease of small pulmonary vessels. Progressive remodeling of the pulmonary vasculature results in increased pulmonary vascular resistance (PVR). This causes secondary right heart failure. PVR is tightly regulated by a range of pulmonary vasodilators and constrictors. Endothelium-derived substances form the basis of most current PH treatments. This is particularly the case for pulmonary arterial hypertension. The major limitation of current treatments is their inability to reverse morphological changes. Thus, there is an unmet need for novel therapies to reduce the morbidity and mortality in PH. Microvessels in the lungs are highly innervated by sensory C fibers. Substance P and calcitonin gene-related peptide (CGRP) are released from C-fiber nerve endings. These neuropeptides can directly regulate vascular tone. Substance P tends to act as a vasoconstrictor in the pulmonary circulation and it increases in the lungs during experimental PH. The receptor for substance P, neurokinin 1 (NK1R), mediates increased pulmonary pressure. Deactivation of NK1R with antagonists, or depletion of substance P prevents PH development. CGRP is a potent pulmonary vasodilator. CGRP receptor antagonists cause elevated pulmonary pressure. Thus, the balance of these peptides is crucial within the pulmonary circulation (Graphical Abstract). Limited progress has been made in understanding their impact on pulmonary pathophysiology. This is an intriguing area of investigation to pursue. It may lead to promising new candidate therapies to combat this fatal disease. This review provides a summary of the current knowledge in this area. It also explores possible future directions for neuropeptides in PH.

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Section: Investigation Of C-fiber-derived Neuropeptides As Novel Pulmmentioning

confidence: 99%

The Regulation of Pulmonary Vascular Tone by Neuropeptides and the Implications for Pulmonary Hypertension

Moosavi

Bubb

2018

Front. Physiol.

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“…Substance P is closely related to neurogenic inflammation and plays a key role in the immune system by regulating the proliferation, migration and activation of immune cells [3]. A number of studies have shown that substance P, which is involved in inflammatory responses [4], exerts certain regulatory functions, such as increasing vascular permeability, affecting vasodilation [5,6], and inducing angiogenesis [7]. One study found that substance P may have a role in the pathogenesis of periodontal disease [8].…”

Section: Introductionmentioning

confidence: 99%

Substance P participates in periodontitis by upregulating HIF-1α and RANKL/OPG ratio

et al. 2020

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Background: Both substance P and hypoxia-inducible factor 1 alpha (HIF-1α) are involved in inflammation and angiogenesis. However, the relationship between substance P and HIF-1α in rat periodontitis is still unknown. Methods: Ligation-induced rat periodontitis was established to observe the distribution and expression of substance P and HIF-1α by immunohistochemistry. Rat gingival fibroblasts were cultured and stimulated with Porphyromonas gingivalis lipopolysaccharide (LPS). Recombinant substance P was applied to elaborate the relationship between substance P and HIF-1α in gingival fibroblasts in vitro. Primary mouse bone marrow-derived macrophages (BMMs) were isolated and cultured to observe the effect of substance P on receptor activator of NF-κB ligand (RANKL)-induced osteoclastogenesis by TRAP staining. Western blotting was used to investigate the expression of HIF-1α, osteoprotegerin (OPG) and RANKL. Results: Rat experimental periodontitis was successfully established 6 weeks after ligation. Gingival inflammatory infiltration and alveolar bone loss were observed. Positive expression of substance P was found in the infiltrating cells. Higher HIF-1α levels were observed in periodontitis compared to that of normal tissues. Substance P upregulated the level of HIF-1α in gingival fibroblasts with or without 1 μg/ml LPS in vitro (*P < 0.05). Substance P upregulated the expression of HIF-1α in RANKL-stimulated BMMs in vitro. Substance P also increased the RANKL/ OPG ratio in gingival fibroblasts (*P < 0.05). Both 10 nM and 50 nM substance P promoted RANKL-induced osteoclast differentiation (*P < 0.05). Conclusion: Substance P participates in periodontitis by upregulating HIF-1α and the RANKL/OPG ratio.

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“…SP is a member of tachykinin family and is known to be extensively involved in the neurogenic inflammatory process [ 11 ]. Upregulated SP levels in synovium and synovial fluid (SF) have been observed in patients with RA [ 12 ]. In addition, SP has been demonstrated to facilitate vasodilatation and plasma extravasation into the synovial cavity, which probably contributes to arthritis progression [ 13 ].…”

Section: Introductionmentioning

confidence: 99%

Increasing expression of substance P and calcitonin gene-related peptide in synovial tissue and fluid contribute to the progress of arthritis in developmental dysplasia of the hip

Wang

Zhang

et al. 2015

Arthritis Res Ther

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IntroductionDevelopmental dysplasia of the hip (DDH) is a common musculoskeletal disorder that has pain and loss of joint function as major pathological features. In the present study, we explored the mechanisms of possible involvement and regulation of substance P (SP) and calcitonin gene-related peptide (CGRP) in the pathological and inflammatory processes of arthritis in DDH.MethodsBlood, synovial tissue and fluid samples were collected from patients diagnosed with different severities of DDH and from patients with femoral neck fracture. Levels of SP, CGRP and inflammatory cytokines in synovium and synovial fluid (SF) in the different groups were evaluated by immunohistochemistry, real-time PCR and enzyme-linked immunosorbent assay (ELISA). Correlations between neuropeptides and inflammatory cytokines in SF were evaluated by partial correlation analysis. The proinflammatory effects of SP and CGRP on synoviocytes obtained from patients with moderate DDH were investigated in vitro by real-time PCR and ELISA. The mechanisms of those effects were evaluated by Western blot analysis and nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) DNA binding assay.ResultsSignificantly increased levels of neuropeptides and inflammatory cytokines were observed in synovium and SF from patients in the severe DDH group compared with the moderate DDH and control groups. In moderate DDH samples, SP in SF correlated with tumor necrosis factor (TNF)-α, and CGRP in SF correlated with TNF-α and interleukin (IL)-10. In the severe DDH group, SP in SF correlated with interleukin (IL)-1β, TNF-α and IL-10. CGRP in SF correlated with TNF-α. Additionally, SP might have had obvious proinflammatory effects on synoviocytes through the activation of NF-κB.ConclusionsThe upregulation of SP and CGRP in synovium and SF might participate in the inflammatory process of arthritis in DDH. The activation of the NF-κB pathway seems indispensable in the proinflammatory effect of SP on synoviocytes. This original discovery may indicate a potential clinical drug target and the development of innovative therapies for DDH.

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Relationship between levels of neuropeptide Substance P in periodontal disease and chronic pain: a literature review

Cited by 28 publications

References 69 publications

The Regulation of Pulmonary Vascular Tone by Neuropeptides and the Implications for Pulmonary Hypertension

The Regulation of Pulmonary Vascular Tone by Neuropeptides and the Implications for Pulmonary Hypertension

Substance P participates in periodontitis by upregulating HIF-1α and RANKL/OPG ratio

Increasing expression of substance P and calcitonin gene-related peptide in synovial tissue and fluid contribute to the progress of arthritis in developmental dysplasia of the hip

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