Photobiomodulation-induced analgesia in experimental temporomandibular disorder involves central inhibition of fractalkine

Ferrara-Jr, João Ignácio; Souza, Everton Tiago de; Franciosi, Adriano Cardozo; Toniolo, Elaine F.; Dale, Camila S.

doi:10.1007/s10103-019-02785-6

Cited by 6 publications

(6 citation statements)

References 45 publications

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“…Behavioral testing was conducted on a blind basis, in which the investigators were blinded to the rat treatment. The head withdrawal threshold, which is negatively associated with the mechanical sensitivity of the orofacial region [ 25 ], was conducted as reported previously [ 22 , 24 , 26 , 27 ], and the results were calculated as mean ± standard deviation (SD) based on 5 measurements per joint and 4 rats per group. Briefly, the rats were habituated to rear on their hind paws and recline against the experimenter's working glove.…”

Section: Methodsmentioning

confidence: 99%

Progesterone Attenuates Allodynia of Inflamed Temporomandibular Joint through Modulating Voltage-Gated Sodium Channel 1.7 in Trigeminal Ganglion

Zhang

et al. 2020

Pain Research and Management

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Background. Women with temporomandibular disorders (TMDs) experience some amelioration of pain during pregnancy. Progesterone increases dramatically and steadily during pregnancy. Sodium channel 1.7 (Nav1.7) plays a prominent role in pain perceptions, as evidenced by deletion of Nav1.7 alone leading to a complete loss of pain. In a previous study, we showed that Nav1.7 in trigeminal ganglion (TG) is involved in allodynia of inflamed temporomandibular joint (TMJ). Whether progesterone modulates allodynia of inflamed TMJ through Nav1.7 in TG remains to be investigated. Methods. The effects of progesterone on sodium currents of freshly isolated TG neurons were examined using whole-cell recording. Female rats were ovariectomized and treated with increasing doses of progesterone for 10 days. Complete Freund’s adjuvant was administered intra-articularly to induce TMJ inflammation. TMJ nociceptive responses were evaluated by head withdrawal thresholds. Real-time PCR and Western blotting were used to examine Nav1.7 mRNA and protein expression in TG. Immunohistofluorescence was used to examine the colocalization of progesterone receptors (PRα/β) and Nav1.7 in TG. Results. Whole-cell recording showed that progesterone could attenuate sodium currents. Moreover, progesterone dose-dependently downregulated Nav1.7 mRNA expression and reduced the sensitivity of TMJ nociception in ovariectomized rats. Furthermore, treatment with progesterone attenuated allodynia of inflamed TMJ in a dose-dependent manner and repressed inflammation-induced Nav1.7 mRNA and protein expression in ovariectomized rats. The progesterone receptor antagonist, RU-486, partially reversed the effect of progesterone on allodynia of inflamed TMJ and TMJ inflammation-induced Nav1.7 mRNA and protein expression. Conclusion. Progesterone, by modulating trigeminal ganglionic Nav1.7, may represent a promising agent to prevent allodynia of inflamed TMJ.

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Section: Methodsmentioning

confidence: 99%

Progesterone Attenuates Allodynia of Inflamed Temporomandibular Joint through Modulating Voltage-Gated Sodium Channel 1.7 in Trigeminal Ganglion

Zhang

et al. 2020

Pain Research and Management

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“…Furthermore, astrocyte inhibition by intracisternal administration of fluorocitrate showed an attenuation of CFA-induced hyperalgesia ( 37 ), and direct blocking of CX3CR1 by intracisternal administration of a neutralizing antibody was able to reverse ectopic facial skin allodynia in CFA-treated animals ( 25 ). In a separate study ( 67 ), the analgesic effect of photobiomodulation treatment was tested in CFA-treated male rats on day 7. The reduction of mechanical hyperalgesia by photobiomodulation was associated with a significant reduction in FKN immunoreactivity in the TG when compared with that in CFA-treated rats with no photobiomodulation treatment ( 67 ), indicating that FKN is elevated in the TG of animals suffering pain and further supporting its direct role in pain modulation.…”

Section: Direct Evidence Of Chemokines In Trigeminal Painmentioning

confidence: 99%

“…In a separate study ( 67 ), the analgesic effect of photobiomodulation treatment was tested in CFA-treated male rats on day 7. The reduction of mechanical hyperalgesia by photobiomodulation was associated with a significant reduction in FKN immunoreactivity in the TG when compared with that in CFA-treated rats with no photobiomodulation treatment ( 67 ), indicating that FKN is elevated in the TG of animals suffering pain and further supporting its direct role in pain modulation.…”

Section: Direct Evidence Of Chemokines In Trigeminal Painmentioning

confidence: 99%

Chemokines and Pain in the Trigeminal System

2021

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Chemotactic cytokines or chemokines are a large family of secreted proteins able to induce chemotaxis. Chemokines are categorized according to their primary amino acid sequence, and in particular their cysteine residues that form disulphide bonds to maintain the structure: CC, CXC, CX3C, and XC, in which X represents variable amino acids. Among their many roles, chemokines are known to be key players in pain modulation in the peripheral and central nervous systems. Thus, they are promising candidates for novel therapeutics that could replace current, often ineffective treatments. The spinal and trigeminal systems are intrinsically different beyond their anatomical location, and it has been suggested that there are also differences in their sensory mechanisms. Hence, understanding the different mechanisms involved in pain modulation for each system could aid in developing appropriate pharmacological alternatives. Here, we aim to describe the current landscape of chemokines that have been studied specifically with regard to trigeminal pain. Searching PubMed and Google Scholar, we identified 30 reports describing chemokines in animal models of trigeminal pain, and 15 reports describing chemokines involved in human pain associated with the trigeminal system. This review highlights the chemokines studied to date at different levels of the trigeminal system, their cellular localization and, where available, their role in a variety of animal pain models.

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“…MM inflammation was induced by unilateral injection of complete Freund's adjuvant (CFA, Sigma F5881, Sigma-Aldrich, Saint Louis, MO, USA; 0.5 mg/mL, heat-killed Mycobacterium tuberculosis suspended in 1:1 oil: saline emulsion), as reported in previous studies. [24][25][26] The protocol details are described in our previous study. 24 Briefly, rats were anesthetized with 4% isoflurane (Forane, Abbott Laboratories Ltd, Queenborough, UK) in a gas mixture O 2 :N 2 =1:2 to abolish righting and corneal reflexes.…”

Section: Establishment Of Bilateral Hypersensitivity Following Unilatmentioning

confidence: 99%

“…The previously described rat head withdrawal threshold (HWT) method was used to evaluate nocifensive behavioral changes. [25][26][27][28] The method details are reported in our previous study. 24 Briefly, a von Frey anesthesiometer (VFA; type 2391, IITC Inc., Woodland Hills, CA, USA) was used bilaterally at different time points to establish the nocifensive response.…”

Section: Mechanical Nocifensive Behavior Measurementsmentioning

confidence: 99%

P2Y2 Receptors Mediate Masseter Muscle Mechanical Hypersensitivity in Rats

Knežević

Vukman

Uhač

et al. 2020

JPR

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Purpose: P 2 Y 2 receptors (P 2 Y 2 Rs) are among the various receptors that play an important role in nociception. The goal of this research was to investigate possible P 2 Y 2 R expression changes in the trigeminal ganglion (TRG) in bilateral masseter muscle (MM) hypersensitivity following unilateral MM inflammation. The impact of unilateral intramasseteric administration of P 2 Y 2 R antagonist on bilateral MM hypersensitivity was also explored. Materials and Methods: Bilateral MM hypersensitivity was provoked by unilateral intramasseteric injection of complete Freund's adjuvant (CFA). The head withdrawal threshold (HWT) was assessed bilaterally 4 days later. Bilateral TRG and MM isolation were followed, and quantitative real-time polymerase chain reaction (qRT-PCR) and histopathological analysis were carried out on these tissues, respectively. The involvement of P 2 Y 2 Rs in nocifensive behavior was evaluated by administering two doses of P 2 Y 2 R antagonist AR-C118925 (0.2 or 1 mg/100 μL) in inflamed MM 4 days post-CFA administration. Bilateral HWT was assessed at different time points following antagonist injection. Results: qRT-PCR analysis demonstrated P 2 Y 2 R up-regulation in TRG ipsilateral to the site of CFA administration. Compared to the controls, both doses of AR-C118925 injected ipsilateral to the TRG increased the bilateral HWT at 30, 60, 90, and 120 minutes after antagonist administration. Conclusion: The findings suggest that P 2 Y 2 Rs may affect MM inflammatory hypersensitivity owing to its up-regulation in the TRG in MM inflammatory pain states.

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Photobiomodulation-induced analgesia in experimental temporomandibular disorder involves central inhibition of fractalkine

Cited by 6 publications

References 45 publications

Progesterone Attenuates Allodynia of Inflamed Temporomandibular Joint through Modulating Voltage-Gated Sodium Channel 1.7 in Trigeminal Ganglion

Progesterone Attenuates Allodynia of Inflamed Temporomandibular Joint through Modulating Voltage-Gated Sodium Channel 1.7 in Trigeminal Ganglion

Chemokines and Pain in the Trigeminal System

<p>P<sub>2</sub>Y<sub>2</sub> Receptors Mediate Masseter Muscle Mechanical Hypersensitivity in Rats</p>

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