Botox, or onabotulinum toxin type A (BoNT/A), is widely known for its cosmetic uses, but its therapeutic potential extends far beyond wrinkle reduction. In the context of orofacial pain and headaches, Botox has emerged as a powerful tool for alleviating discomfort. But how does it work?
The truth is, we still do not fully understand the exact mechanisms. However, it is believed that Botox targets nerve endings and inhibits the release of neurotransmitters that signal pain. Research involving animal models has shown that Botox inhibits the release of presynaptic calcitonin gene-related peptide (CGRP) in afferent neurons. CGRP is a neuropeptide involved in transmitting pain signals. By inhibiting its release, Botox can potentially reduce pain.
This antinociceptive, or pain-relieving, mechanism was first identified when Botox was administered both peripherally and intrathecally (directly into the spinal canal) in formalin-induced inflammatory pain models. The results suggested that Botox has a modulatory effect on the processes that lead to pain sensitization, a condition where the nervous system becomes more sensitive to painful stimuli.
In another study using a capsaicin-induced inflammatory pain model, pre-treatment with Botox prevented the onset of mechanical and thermal hyperalgesia—a condition where the body becomes excessively sensitive to painful stimuli. This effect was also observed in neuropathic pain models, where Botox administration reduced sensitivity to both mechanical and thermal pain.
These findings suggest that Botox is capable of reducing central sensitization, a key factor in chronic pain. This central effect could explain why Botox has proven effective in treating various types of chronic pain, including those associated with orofacial disorders and headaches.
In summary, Botox’s ability to modulate pain at the molecular level makes it a valuable option for patients suffering from chronic orofacial pain and headaches. By reducing the release of pain-signaling molecules like CGRP, Botox helps to alleviate pain and improve the quality of life for those affected by these conditions.
References
Bach-Rojecky, L., & Lacković, Z. (2005). Antinociceptive effect of botulinum toxin type a in rat model of carrageenan and capsaicin induced pain. Croatian medical journal, 46(2), 201–208.
Cui, M., Khanijou, S., Rubino, J., & Aoki, K. R. (2004). Subcutaneous administration of botulinum toxin A reduces formalin-induced pain. Pain, 107(1-2), 125–133. https://doi.org/10.1016/j.pain.2003.10.008
Dolly, J. O., & O'Connell, M. A. (2012). Neurotherapeutics to inhibit exocytosis from sensory neurons for the control of chronic pain. Current opinion in pharmacology, 12(1), 100–108. https://doi.org/10.1016/j.coph.2011.11.001
Luvisetto, S., Marinelli, S., Lucchetti, F., Marchi, F., Cobianchi, S., Rossetto, O., Montecucco, C., & Pavone, F. (2006). Botulinum neurotoxins and formalin-induced pain: central vs. peripheral effects in mice. Brain research, 1082(1), 124–131. https://doi.org/10.1016/j.brainres.2006.01.117
Moreno-Hay, I., Mishra, P., & Okeson, J. P. (2019). Intraoral Administration of Botulinum Toxin for Continuous Dentoalveolar Neuropathic Pain: A Case Series. Journal of oral & facial pain and headache, 33(2), 160–164. https://doi.org/10.11607/ofph.2031
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