Peripheral Sympathetic Component of the Temporomandibular Joint Inflammatory Pain in Rats

Rodrigues, Luciane Lacerda Franco Rocha; Oliveira, Maria Cláudia G.; Pelegrini-da-Silva, Adriana; Veiga, Maria Cecı́lia Ferraz de Arruda; Parada, Carlos Amílcar; Tambeli, Cláudia Herrera

doi:10.1016/j.jpain.2006.05.006

Cited by 57 publications

(56 citation statements)

References 43 publications

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“…Because deep inputs may be more effective in inducing central neuronal excitation than cutaneous inputs, greater sensory disturbances may occur in pain conditions involving deep tissues than in those involving cutaneous tissues (Imbe et al, 2001). Otherwise, it has been demonstrated that the TMJ tissues are more sensitive to sympathomimetic amines and PGE 2 than cutaneous tissues (Rodrigues et al, 2006). Thus, we hypothesized that TMJ is more sensible to prostaglandins in comparison to paw tissue, which could explain our results.…”

Section: Discussionmentioning

confidence: 69%

15d-Prostaglandin J₂ Inhibits Inflammatory Hypernociception: Involvement of Peripheral Opioid Receptor

Napimoga

Souza²,

Cunha³

et al. 2007

J Pharmacol Exp Ther

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The 15-deoxy-⌬ 12,14 -prostaglandin J 2 (15d-PGJ 2 ) is an endogenous ligand of peroxisome proliferator-activated receptors ␥ (PPAR-␥) and is now recognized as a potent anti-inflammatory mediator. However, information regarding the influence of 15d-PGJ 2 on inflammatory pain is still unknown. In this study, we evaluated the effect of 15d-PGJ 2 upon inflammatory hypernociception and the mechanisms involved in this effect. We observed that intraplantar administration of 15d-PGJ 2 (30 -300 ng/paw) inhibits the mechanical hypernociception induced by both carrageenan (100 g/paw) and the directly acting hypernociceptive mediator, prostaglandin E 2 (PGE 2 ). Moreover, 15d-PGJ 2 [100 ng/temporomandibular joint (TMJ)] inhibits formalininduced TMJ hypernociception. On the other hand, the direct administration of 15d-PGJ 2 into the dorsal root ganglion was ineffective in blocking PGE 2 -induced hypernociception. In addition, the 15d-PGJ 2 antinociceptive effect was enhanced by the increase of macrophage population in paw tissue due to local injection of thioglycollate, suggesting the involvement of these cells on the 15d-PGJ 2 -antinociceptive effect. Moreover, the antinociceptive effect of 15d-PGJ 2 was also blocked by naloxone and by the PPAR-␥ antagonist 2-chloro-5-nitro-Nphenylbenzamide (GW9662), suggesting the involvement of peripheral opioids and PPAR-␥ receptor in the process. Similar to opioids, the 15d-PGJ 2 antinociceptive action depends on the nitric oxide/cGMP/protein kinase G (PKG)/K ATP ϩ channel pathway because it was prevented by the pretreatment with the inhibitors of nitric-oxide synthase (N G -monomethyl-L-arginine acetate), guanylate cyclase ]1H-(1,2,4)-oxadiazolo(4,2-␣)quinoxalin-1-one [, PKG [indolo[2,pyrrolo [3,4-c]carbazole aglycone (KT5823)], or with the ATP-sensitive potassium channel blocker glibenclamide. Taken together, these results demonstrate for the first time that 15d-PGJ 2 inhibits inflammatory hypernociception via PPAR-␥ activation. This effect seems to be dependent on endogenous opioids and local macrophages.

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Section: Discussionmentioning

confidence: 69%

15d-Prostaglandin J₂ Inhibits Inflammatory Hypernociception: Involvement of Peripheral Opioid Receptor

Napimoga

Souza²,

Cunha³

et al. 2007

J Pharmacol Exp Ther

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“…TMJ inflammatory conditions result in the release of several proinflammatory cytokines, especially tumor necrosis factor-α (TNF-α) and interleukins (Kopp, 2001), both of which contribute to joint remodeling and cartilage degradation (Vernal et al, 2008). These cytokines induce the release of a number of pro-nociceptive compounds, such as potassium chloride, leukotriene B4, prostaglandin E 2 (PGE 2 ), bradykinin, serotonin, histamine, glutamate and adenosine triphosphate (ATP), all of which have been shown to excite and induce spontaneous discharge in the TMJ (Flake and Gold, 2005;Kopp, 2001;Oliveira et al, 2005;Rodrigues et al, 2006). Interestingly, in the present study, low doses of 15d-PGJ 2 -NC, but not unloaded 15d-PGJ 2 , were found to inhibit the release of the proinflammatory cytokine IL-1β.…”

Section: Discussionmentioning

confidence: 99%

15d-PGJ2-loaded in nanocapsules enhance the antinociceptive properties into rat temporomandibular hypernociception

et al. 2012

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Aims: To verify whether the nanoencapsulation of 15d-PGJ 2 in poly(D,L-lactide-co-glycolide) (PLGA) nanocapsules (15d-PGJ 2 -NC) might potentialize its antinociceptive activity into rats' temporomandibular joint (TMJ). Main methods: Transmission electron microscopy (TEM) and atomic force microscopy (AFM) were used to evaluate the morphology and suspension of the PLGA nanocapsules. Rats were pretreated (15 min) with an intra-TMJ injection of unloaded 15d-PGJ 2 or 15d-PGJ 2 -NC at concentrations of 10, 100 or 1000 pg followed by an ipsilateral intra-TMJ injection of 1.5% formalin. The nociceptive behavioral response was observed during 45 min; animals were then sacrificed and the periarticular tissue was removed for IL-1β measurements. Key finding: TEM and AFM analyses showed that 15d-PGJ 2 -NC is spherical without any aggregates or adhesion confirming that this formulation is a good drug carrier system for 15d-PGJ 2 . Pretreatment with 15d-PGJ 2 -NC (100 and 1000 pg/TMJ), but not unloaded 15d-PGJ 2 , was found to significantly decrease the release of IL-1β cytokine and the animals' nociceptive behavioral response induced by intra-TMJ injection of formalin. Significance: The compound 15d-PGJ 2 -NC might be used as a potential antinociceptive and anti-inflammatory agent to treat temporomandibular disorders in clinical practice.

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“…A second TMJ injection was given 1 h later, when the carrageenan-induced TMJ hyperalgesia was in its peak, as previously described (Oliveira et al, 2005;Rodrigues et al, 2006). Although this concentration of carrageenan did not elicit nociception by itself, it induced TMJ hyperalgesia dependent on prostaglandin synthesis (Rodrigues et al, 2006).…”

Section: Experimental Designmentioning

confidence: 95%

Nerve growth factor acts with the β2-adrenoceptor to induce spontaneous nociceptive behavior during temporomandibular joint inflammatory hyperalgesia

et al. 2008

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Peripheral Sympathetic Component of the Temporomandibular Joint Inflammatory Pain in Rats

Cited by 57 publications

References 43 publications

15d-Prostaglandin J₂ Inhibits Inflammatory Hypernociception: Involvement of Peripheral Opioid Receptor

15d-Prostaglandin J₂ Inhibits Inflammatory Hypernociception: Involvement of Peripheral Opioid Receptor

15d-PGJ2-loaded in nanocapsules enhance the antinociceptive properties into rat temporomandibular hypernociception

Nerve growth factor acts with the β2-adrenoceptor to induce spontaneous nociceptive behavior during temporomandibular joint inflammatory hyperalgesia

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Peripheral Sympathetic Component of the Temporomandibular Joint Inflammatory Pain in Rats

Cited by 57 publications

References 43 publications

15d-Prostaglandin J2 Inhibits Inflammatory Hypernociception: Involvement of Peripheral Opioid Receptor

15d-Prostaglandin J2 Inhibits Inflammatory Hypernociception: Involvement of Peripheral Opioid Receptor

15d-PGJ2-loaded in nanocapsules enhance the antinociceptive properties into rat temporomandibular hypernociception

Nerve growth factor acts with the β2-adrenoceptor to induce spontaneous nociceptive behavior during temporomandibular joint inflammatory hyperalgesia

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Product

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15d-Prostaglandin J₂ Inhibits Inflammatory Hypernociception: Involvement of Peripheral Opioid Receptor

15d-Prostaglandin J₂ Inhibits Inflammatory Hypernociception: Involvement of Peripheral Opioid Receptor