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Systemic chemical desensitization of peptidergic sensory neurons with resiniferatoxin inhibits experimental periodontitis.

Breivik T, Gundersen Y, Gjermo P, Fristad I, Opstad PK - Open Dent J (2011)

Bottom Line: Desensitization with RTX significantly reduced bone loss as measured by digital X-rays.LPS provoked a significantly higher increase in serum levels of the pro-inflammatory cytokine tumour necrosis factor (TNF)-α, but lower serum levels of the anti-inflammatory cytokine interleukin (IL)-10 and the stress hormone corticosterone.The results may partly be explained by the attenuated transmission of immuno-inflammatory signals to the brain.

View Article: PubMed Central - PubMed

Affiliation: Department of Periodontology, Faculty of Dentistry, University of Oslo, Norway.

ABSTRACT

Background and objective: The immune system is an important player in the pathophysiology of periodontitis. The brain controls immune responses via neural and hormonal pathways, and brain-neuro-endocrine dysregulation may be a central determinant for pathogenesis. Our current knowledge also emphasizes the central role of sensory nerves. In line with this, we wanted to investigate how desensitization of peptidergic sensory neurons influences the progression of ligature-induced periodontitis, and, furthermore, how selected cytokine and stress hormone responses to Gram-negative bacterial lipopolysaccharide (LPS) stimulation are affected.

Material and methods: Resiniferatoxin (RTX; 50 μg/kg) or vehicle was injected subcutaneously on days 1, 2, and 3 in stress high responding and periodontitis-susceptible Fischer 344 rats. Periodontitis was induced 2 days thereafter. Progression of the disease was assessed after the ligatures had been in place for 20 days. Two h before decapitation all rats received LPS (150 μg/kg i.p.) to induce a robust immune and stress response.

Results: Desensitization with RTX significantly reduced bone loss as measured by digital X-rays. LPS provoked a significantly higher increase in serum levels of the pro-inflammatory cytokine tumour necrosis factor (TNF)-α, but lower serum levels of the anti-inflammatory cytokine interleukin (IL)-10 and the stress hormone corticosterone.

Conclusions: In this model RTX-induced chemical desensitization of sensory peptidergic neurons attenuated ligature-induced periodontitis and promoted a shift towards stronger pro-inflammatory cytokine and weaker stress hormone responses to LPS. The results may partly be explained by the attenuated transmission of immuno-inflammatory signals to the brain. In turn, this may weaken the anti-inflammatory brain-derived pathways.

No MeSH data available.


Related in: MedlinePlus

The mean distance from the cemento-enamel junction to the alveolar bone crest in resiniferatoxin-treated rats, and vehicle-treated control rats as measured on digital radiographs. (* p < 0.01 vs. controls).
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Figure 1: The mean distance from the cemento-enamel junction to the alveolar bone crest in resiniferatoxin-treated rats, and vehicle-treated control rats as measured on digital radiographs. (* p < 0.01 vs. controls).

Mentions: The RTX-treated animals had significantly less alveolar bone loss than the controls (615 ± 22 µm vs. 700 ± 15 µm; p < 0.01; Fig. 1). Since the RTX-treated rats weighed less, the length of their teeth could be shorter. We therefore compared the root-length of the right 2nd molar teeth in the two groups by measuring the distance between the cemento-enamel junction (CEJ) and apex on mesial root surfaces. There wasno difference between the root-length in the RTX- and saline-treated control rats.


Systemic chemical desensitization of peptidergic sensory neurons with resiniferatoxin inhibits experimental periodontitis.

Breivik T, Gundersen Y, Gjermo P, Fristad I, Opstad PK - Open Dent J (2011)

The mean distance from the cemento-enamel junction to the alveolar bone crest in resiniferatoxin-treated rats, and vehicle-treated control rats as measured on digital radiographs. (* p < 0.01 vs. controls).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3040995&req=5

Figure 1: The mean distance from the cemento-enamel junction to the alveolar bone crest in resiniferatoxin-treated rats, and vehicle-treated control rats as measured on digital radiographs. (* p < 0.01 vs. controls).
Mentions: The RTX-treated animals had significantly less alveolar bone loss than the controls (615 ± 22 µm vs. 700 ± 15 µm; p < 0.01; Fig. 1). Since the RTX-treated rats weighed less, the length of their teeth could be shorter. We therefore compared the root-length of the right 2nd molar teeth in the two groups by measuring the distance between the cemento-enamel junction (CEJ) and apex on mesial root surfaces. There wasno difference between the root-length in the RTX- and saline-treated control rats.

Bottom Line: Desensitization with RTX significantly reduced bone loss as measured by digital X-rays.LPS provoked a significantly higher increase in serum levels of the pro-inflammatory cytokine tumour necrosis factor (TNF)-α, but lower serum levels of the anti-inflammatory cytokine interleukin (IL)-10 and the stress hormone corticosterone.The results may partly be explained by the attenuated transmission of immuno-inflammatory signals to the brain.

View Article: PubMed Central - PubMed

Affiliation: Department of Periodontology, Faculty of Dentistry, University of Oslo, Norway.

ABSTRACT

Background and objective: The immune system is an important player in the pathophysiology of periodontitis. The brain controls immune responses via neural and hormonal pathways, and brain-neuro-endocrine dysregulation may be a central determinant for pathogenesis. Our current knowledge also emphasizes the central role of sensory nerves. In line with this, we wanted to investigate how desensitization of peptidergic sensory neurons influences the progression of ligature-induced periodontitis, and, furthermore, how selected cytokine and stress hormone responses to Gram-negative bacterial lipopolysaccharide (LPS) stimulation are affected.

Material and methods: Resiniferatoxin (RTX; 50 μg/kg) or vehicle was injected subcutaneously on days 1, 2, and 3 in stress high responding and periodontitis-susceptible Fischer 344 rats. Periodontitis was induced 2 days thereafter. Progression of the disease was assessed after the ligatures had been in place for 20 days. Two h before decapitation all rats received LPS (150 μg/kg i.p.) to induce a robust immune and stress response.

Results: Desensitization with RTX significantly reduced bone loss as measured by digital X-rays. LPS provoked a significantly higher increase in serum levels of the pro-inflammatory cytokine tumour necrosis factor (TNF)-α, but lower serum levels of the anti-inflammatory cytokine interleukin (IL)-10 and the stress hormone corticosterone.

Conclusions: In this model RTX-induced chemical desensitization of sensory peptidergic neurons attenuated ligature-induced periodontitis and promoted a shift towards stronger pro-inflammatory cytokine and weaker stress hormone responses to LPS. The results may partly be explained by the attenuated transmission of immuno-inflammatory signals to the brain. In turn, this may weaken the anti-inflammatory brain-derived pathways.

No MeSH data available.


Related in: MedlinePlus