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Updated: May 22, 2026
Temporomandibular Joint Pain Measurement by Bite Force and Von Frey Filament Assays in Mice
Published on: September 13, 2024
Participation of microglial p38 MAPK in formalin-induced temporomandibular joint nociception in rats
Kyoung A Won1, Young M Kang, Min K Lee
1Department of Oral Physiology, School of Dentistry, Kyungpook National University, Daegu, Korea.
Aims:
To investigate nociceptive behavior and the immunoreactivity of microglia and phosphorylated-p38 (p-p38) mitogen-activated protein kinase (MAPK) following intracisternal administration of SB203580, a p38 MAPK inhibitor, or minocycline, a microglia inhibitor, in rats with temporomandibular joint (TMJ) inflammation.
Methods:
The number of nociceptive behavioral responses was recorded for nine successive 5-minute intervals following formalin injections into the left TMJ. SB203580 or minocycline was administered intracisternally 2 hours prior to the formalin injection. Statistical analysis used one-way analysis of variance followed by least significant difference post-hoc analysis.
Results:
The intra-articular injection of formalin increased the expression of p-p38 MAPK in the ipsilateral medullary dorsal horn. Most of the p-p38 MAPK co-localized with OX42, a microglial marker, but not with GFAP, an astrocyte marker. Intracisternal injections of SB203580 (0.5, 1, or 5 Μg) attenuated the number of nociceptive behavioral responses and the expression of p-p38 MAPK in the medullary dorsal horn. Intracisternal injections of minocycline (25 or 50 Μg) also attenuated the responses and the expression of OX42 and p-p38 MAPK in the medullary dorsal horn.
Conclusion:
These findings suggest that p38 MAPK in microglia plays an important role in the central processing of inflammatory TMJ nociception in rats. The data further indicate that a targeted blockade of the microglial p38 MAPK pathway is a potentially important new treatment strategy for inflammatory TMJ nociception.
Insights
In rats with temporomandibular joint inflammation, inhibiting p38 mitogen-activated protein kinase (MAPK) or microglia reduced pain behaviors. Targeting the microglial p38 MAPK pathway may offer a new treatment for TMJ pain.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Temporomandibular joint (TMJ) inflammation causes nociception.
- Microglia and p38 mitogen-activated protein kinase (MAPK) are implicated in pain signaling.
Purpose of the Study:
- To investigate the role of microglia and p38 MAPK in TMJ inflammation-induced nociception.
- To evaluate the effects of p38 MAPK and microglia inhibition on nociceptive behavior and central pain processing.
Main Methods:
- Rats with TMJ inflammation received formalin injections.
- Intracisternal administration of SB203580 (p38 MAPK inhibitor) or minocycline (microglia inhibitor).
- Nociceptive responses and medullary dorsal horn p-p38 MAPK and OX42 expression were assessed.
Main Results:
- Formalin induced TMJ inflammation, increasing p-p38 MAPK in the medullary dorsal horn, co-localizing with microglia.
- SB203580 and minocycline significantly attenuated nociceptive behavior.
- Both inhibitors reduced p-p38 MAPK and microglial activation in the medullary dorsal horn.
Conclusions:
- p38 MAPK within microglia is crucial for processing inflammatory TMJ pain.
- Blocking the microglial p38 MAPK pathway presents a potential therapeutic strategy for TMJ nociception.
