DOI•
Inflammation and pain in skin and deep tissues
01 Jan 2015-
TL;DR: Evaluate the change in sensitivity after inflammation inside and outside the irradiated skin and investigate the existence of a mechanism of cumulative effects between cutaneous and deep-tissue hyperalgesia and allodynia induced by UVB irradiation after application of heat stimuli and sensitization of deep tissues.
Abstract: Ultraviolet-B irradiation model has been used for many years as a translational model since it is well known to induce cutaneous inflammatory pain in both animals and humans. The aim of this study project was to evaluate time course and sensory changes induced by UVB and in particular: 1) evaluate the change in sensitivity after inflammation inside and outside the irradiated skin, 2) investigate the existence of a mechanism of cumulative effects between cutaneous and deep-tissue hyperalgesia, 3) investigate the effect on mechanical hyperalgesia and allodynia induced by UVB irradiation after application of heat stimuli and sensitization of deep tissues.
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Book Chapter•
01 Jan 2006
TL;DR: The Wall and Melzack's Textbook of Pain is revised under new editorial leadership, and with a host of new, multidisciplinary international contributors.
Abstract: WALL AND MELZACK'S TEXTBOOK OF PAIN, revised under new editorial leadership, and with a host of new, multidisciplinary international contributors ...
527 citations
TL;DR: Findings point towards a regulatory function for nerve growth factor in vivo in the stimulation of sensory neuropeptide synthesis during prolonged inflammatory processes.
223 citations
TL;DR: In this article, the authors explored the contribution of capsaicin-sensitive nociceptors in the development of mechanical and heat hyperalgesia in humans following ultraviolet-B (UVB) irradiation.
Abstract: Subpopulations of primary nociceptors (C- and Aδ-fibers), express the TRPV1 receptor for heat and capsaicin. During cutaneous inflammation, these afferents may become sensitized, leading to primary hyperalgesia. It is known that TRPV1+ nociceptors are involved in heat hyperalgesia; however, their involvement in mechanical hyperalgesia is unclear. This study explored the contribution of capsaicin-sensitive nociceptors in the development of mechanical and heat hyperalgesia in humans following ultraviolet-B (UVB) irradiation. Skin areas in 18 healthy volunteers were randomized to treatment with 8% capsaicin/vehicle patches for 24 h. After patches removal, one capsaicin-treated area and one vehicle area were irradiated with 2xMED (minimal erythema dose) of UVB. 1, 3 and 7 days post-UVB exposure, tests were performed to evaluate the development of UVB-induced cutaneous hyperalgesia: thermal detection and pain thresholds, pain sensitivity to supra-threshold heat stimuli, mechanical pain threshold and sensitivity, touch pleasantness, trans-epidermal water loss (TEWL), inflammatory response, pigmentation and micro-vascular reactivity. Capsaicin pre-treatment, in the UVB-irradiated area (Capsaicin + UVB area), increased heat pain thresholds (P 0.2). No effects of capsaicin were reported on touch pleasantness (P = 1), TEWL (P = 0.31), inflammatory response and pigmentation (P > 0.3) or micro-vascular reactivity (P > 0.8) in response to the UVB irradiation. 8% capsaicin ablation predominantly defunctionalizes TRPV1+-expressing cutaneous nociceptors responsible for heat pain transduction, suggesting that sensitization of these fibers is required for development of heat hyperalgesia following cutaneous UVB-induced inflammation but they are likely only partially necessary for the establishment of robust primary mechanical hyperalgesia.
1 citations
References
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TL;DR: Mechanisms of exercise-induced delayed onset muscular soreness and the sensation of pain and stiffness in the muscles that occurs from 1 to 5 d following unaccusto
Abstract: Delayed-onset muscular soreness (DOMS), the sensation of pain and stiffness in the muscles that occurs from 1 to 5 d following unaccustomed exercise, can adversely affect muscular performance, both from voluntary reduction of effort and from inherent loss of capacity of the muscles to produce force. This reduction in performance is temporary; permanent impairment does not occur. A number of clinical correlates are associated with DOMS, including elevations in plasma enzymes, myoglobinemia, and abnormal muscle histology and ultrastructure; exertional rhabdomyolysis appears to be the extreme form of DOMS. Presently, the best treatment for DOMS appears to be muscular activity, although the sensation again returns following the exercise. Training for the specific contractile activity that causes DOMS reduces the soreness response. The etiology and cellular mechanisms of DOMS are not known, but a number of hypotheses exist to explain the phenomenon. The following model may be proposed: 1) high tensions (particularly those associated with eccentric exercise) in the contractile/elastic system of the muscle result in structural damage; 2) cell membrane damage leads to disruption of Ca++ homeostasis in the injured fibers, resulting in necrosis that peaks about 2 d post-exercise; and 3) products of macrophage activity and intracellular contents accumulate in the interstitium, which in turn stimulate free nerve endings of group-IV sensory neurons in the muscles leading to the sensation of DOMS.
739 citations
TL;DR: Systemic administration of anti-NGF neutralizing antibodies prevent the behavioral sensitivity, the up-regulation of neuropeptides and the inflammation-induced expression of the immediate early gene c-fos in dorsal horn neurons, without modifying swelling and erythema.
723 citations
"Inflammation and pain in skin and d..." refers background in this paper
...The role of NGF in the inflammation has been investigated by several groups (Donnerer et al., 1992; Rueff and L.M. 1996; Woolf et al., 1994)....
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...A large number of studies have also investigated the possibility of reversing inflammatory pain by blocking the action of NGF using anti-NGF antibodies or similar agents able to bind free molecules of NGF (Frade and Barde 1998; Rueff and L.M. 1996; Woolf et al., 1994)....
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...It has also been demonstrated that the exposure of nociceptors to NGF increases th release of the neuropeptides such as substance P and calcitonin gene-related peptide (CGRP), both related to the development of pain and hyperalgesia (Greco et al., 2008; Rueff and L.M. 1996; Woolf et al., 1994)....
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TL;DR: This review focuses on the molecular determinants of network plasticity in the central nervous system (CNS) and discusses their relevance to the development of new therapeutic approaches.
Abstract: Chronic pain is a major challenge to clinical practice and basic science. The peripheral and central neural networks that mediate nociception show extensive plasticity in pathological disease states. Disease-induced plasticity can occur at both structural and functional levels and is manifest as changes in individual molecules, synapses, cellular function and network activity. Recent work has yielded a better understanding of communication within the neural matrix of physiological pain and has also brought important advances in concepts of injury-induced hyperalgesia and tactile allodynia and how these might contribute to the complex, multidimensional state of chronic pain. This review focuses on the molecular determinants of network plasticity in the central nervous system (CNS) and discusses their relevance to the development of new therapeutic approaches.
648 citations
"Inflammation and pain in skin and d..." refers background in this paper
...The acute pain, considered as a protective phenomenon, appears quickly after tissues injury and disappears gradually by a he ling process (Kuner 2010)....
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TL;DR: While sensory fibres normally respond to a range of physical and chemical stimuli their activity and metabolism are profoundly altered by a variety of mediators generated by tissue injury and inflammation, which can profoundly affect the properties of nociceptors and their ability to transmit pain signals.
Abstract: While sensory fibres normally respond to a range of physical and chemical stimuli their activity and metabolism are profoundly altered by a variety of mediators generated by tissue injury and inflammation. These include substances produced by damaged tissue, substances of vascular origin as well as substances released by afferent fibres themselves, sympathetic fibres and various immune cells. The effects of inflammatory mediators, to activate or sensitize afferent fibres, are produced by changing membrane ion channels which are coupled directly via receptors or more commonly are regulated through receptor-coupled second messenger cascades. These latter processes also have the potential to alter gene transcription and thereby induce long-term alterations in the biochemistry of sensory neurones. This can have far-reaching consequences as the expression of novel proteins for ion channels (Na channels) and receptors (capsaicin, NPY) as well as the induction of novel enzymes (i-NOS) can profoundly affect the properties of nociceptors and their ability to transmit pain signals. However, such changes may be targeted successfully for the development of new analgesic and anti-inflammatory agents.
576 citations
"Inflammation and pain in skin and d..." refers background in this paper
...A large number of these mediators such as nitric oxide, histamine, bradykinin, prostaglandins, cytokines, 15 and NGF are involved in the sensitization of the peripheral nociceptors located on the sensory neurons innervating the region of the irradiation (Dray 1995; Kidd and Urban 2001)....
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...15 and NGF are involved in the sensitization of the pe ripheral nociceptors located on the sensory neurons innervating the region of the irradiation ( Dray 1995; Kidd and Urban 2001)....
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TL;DR: Findings point towards a regulatory function for nerve growth factor in vivo in the stimulation of sensory neuropeptide synthesis during prolonged inflammatory processes.
575 citations