The Orofacial Pain lab at the Center for Oral Biology is focusing on nerve injury related pains, pain modulation and its clinical application. The nervous system has the ability to either facilitate or inhibit pain. Pain, arising from external painful signals or injury, may undergo modulation in the Central Nervous System (CNS) prior to reaching the primary somatosensory cortex, thus modifying the pain experience. Faulty pain modulation mechanisms have been linked to chronic pain conditions such as fibromyalgia, tension-type headache, musculoskeletal pain, chronic low back pain, trigeminal posttraumatic neuropathies, and irritable bowel syndrome. Exercise is a known trigger of pain modulation that has been used to evaluate pain modulation efficacy by means of an effect commonly termed Exercise-Induced Hypoalgesia (EIH).
Recently we developed a rat model of EIH and applied it in the context of peripheral nerve damage to predict the severity of consequent neuropathic pain. This study showed that rats classified as rats with low EIH not only developed significantly more severe neuropathic pain, indicated by heat-allodynia, mechanical allodynia, and hyperalgesia following sciatic nerve injury compared to High EIH rats, but also developed heat allodynia at the contralateral side (indicative of mirror-image neuropathic pain).
In a related clinical study we have demonstrated that patients with less efficient pain modulation are at risk to develop painful post traumatic trigeminal neuropathy following routine dental procedures. Currently we are studying the mechanisms associated with EIH and focusing on the opioid and cannabinoid system and the role of systemic and localizes inflammation on the phenomenon. We also study the use of EIH in support of targeted and prophylactic treatment for patients at risk to develop post surgical neuropathic pain.