Temporomandibular disorders (TMDs) represent a set of musculoskeletal disorders associated with the masticatory system and a number of symptoms. Pain is the most common symptom usually concentrated in masticatory muscles and/or temporomandibular joints (TMJs), but exacerbated by mandibular movement and stomatognathic functions. TMD seems to be of multifactorial etiology, including parafunctional habits, bruxism, deleterious body posture, occlusal features, growth abnormalities, trauma, overload and stress.
Although there is yet no conclusive evidence that central sensitization (CS )is a common etiological factor of TMD and comorbid CSS, several studies have made a convincing argument in favor of such an etiology. In many cases, CS is the basis …show more content…
In addition, it is promoted and maintained by neural activity among key regions in the brain involved in pain processing. The general assumption is that the central nervous system is altered in ways that amplify pain processing.
Work by Iggo and Perl had identified specific high threshold sensory neurons tuned to respond only to noxious stimuli, hence their name nociceptors , a term first coined by Sherrington based on his studies on noxious stimulus evoked flexion reflexes. Furthermore, first Perl and then others showed that nociceptor peripheral terminals could become ‘‘sensitized” after injury, reducing their threshold, mainly to heat stimuli, and only within the site of injury where the terminal was exposed to inflammatory modulators, the zone of primary hyperalgesia.
While this phenomenon is clearly a very important contributor to inflammatory pain hypersensitivity , it cannot account for dynamic tactile allodynia, the temporal summation of pain, or secondary hyperalgesia. Some other explanation was needed as the neurobiological basis for these symptoms, which turned out to be increased synaptic function triggered within the CNS by nociceptive …show more content…
The investigators then showed that the secondary mechanical hyperalgesia required sensory inflow to the CNS because local anesthesia prior to the capsaicin injection blocked it. In addition because the pain sensitivity crossed a tight band that prevented circulation in the skin, they concluded that it was not due to a local spread of the capsaicin or any peripheral inflammatory mediator.
Central amplification of Ad nociceptor fiber test input following a Cfiber conditioning input was shown to contribute to pinprick/ punctate secondary hyperalgesia, again using the intradermal capsaicin model , underscoring the different identity of the afferent signals that elicit central sensitization as a conditioning stimulus (Cfibers) from those that elicit allodynia or hyperalgesia
, a further clear manifestation of heterosynaptic
Although there is yet no conclusive evidence that central sensitization (CS )is a common etiological factor of TMD and comorbid CSS, several studies have made a convincing argument in favor of such an etiology. In many cases, CS is the basis …show more content…
In addition, it is promoted and maintained by neural activity among key regions in the brain involved in pain processing. The general assumption is that the central nervous system is altered in ways that amplify pain processing.
Work by Iggo and Perl had identified specific high threshold sensory neurons tuned to respond only to noxious stimuli, hence their name nociceptors , a term first coined by Sherrington based on his studies on noxious stimulus evoked flexion reflexes. Furthermore, first Perl and then others showed that nociceptor peripheral terminals could become ‘‘sensitized” after injury, reducing their threshold, mainly to heat stimuli, and only within the site of injury where the terminal was exposed to inflammatory modulators, the zone of primary hyperalgesia.
While this phenomenon is clearly a very important contributor to inflammatory pain hypersensitivity , it cannot account for dynamic tactile allodynia, the temporal summation of pain, or secondary hyperalgesia. Some other explanation was needed as the neurobiological basis for these symptoms, which turned out to be increased synaptic function triggered within the CNS by nociceptive …show more content…
The investigators then showed that the secondary mechanical hyperalgesia required sensory inflow to the CNS because local anesthesia prior to the capsaicin injection blocked it. In addition because the pain sensitivity crossed a tight band that prevented circulation in the skin, they concluded that it was not due to a local spread of the capsaicin or any peripheral inflammatory mediator.
Central amplification of Ad nociceptor fiber test input following a Cfiber conditioning input was shown to contribute to pinprick/ punctate secondary hyperalgesia, again using the intradermal capsaicin model , underscoring the different identity of the afferent signals that elicit central sensitization as a conditioning stimulus (Cfibers) from those that elicit allodynia or hyperalgesia
, a further clear manifestation of heterosynaptic