Endodontic pain in the context of oro-facial pain. Endodontic pain is typically derived from noxious insults to the pulp and peri-radicular tissues and the inflammation which follows. Nociceptors of the pulp and peri-radicular tissues have their cell bodies located in the trigeminal ganglia. When these primary afferent nociceptors experience membrane depolarization due to a noxious stimulus, they send an action potential to the second-order neurons whose cell bodies reside in the medulla. The second-order neuron then sends a signal to neurons in the higher centres of the brain where processing of the signal results in perception of pain. This is a simplistic explanation of how the mechanism of dental pain perception occurs. There are many …show more content…
Some of the primary-secondary nerve synapses are ineffective and action potentials from the primary neuron will not activate the secondary neuron. Bruxism and other conditions that may cause chronic and/or intense noxious stimulation can result in central sensitization. Central sensitization is the process of these ineffective synapses becoming effective. An example of this is when there is an action potential created from the afferent nerve innervating a muscle of mastication that is experiencing a noxious stimuli (such as bruxism), which activates the secondary afferent nerve through the newly effective synapse. If the secondary afferent nerve, which usually receives nociceptive input from the teeth, further activates the neuron in the brain responsible for pain perception, there will be a perception that the pain is occurring in the teeth rather than the original site of origin, the muscle of mastication. This results in referred pain from the muscle of mastication to the …show more content…
Hyperalgesia from peripheral inflammation may occur due to alterations to inhibitory mechanisms. Chronic pain conditions (such as temporomandibular disorders) can result in a decrease in central inhibitory control mechanisms, which results in an increased central excitatory state causing hyperalgesia.
It is also possible that multiple primary afferent nerves that innervate different structures, such as the teeth and muscles of mastication, may synapse with the same secondary afferent nerve, which then transmits the signal to the neuron that causes perception of pain. This is called convergence and may also result in referred pain perception from a site experiencing a noxious stimuli to a site that is not. The prudent dentist must be aware of the mechanisms and clinical symptoms of referred pain, peripheral sensitization, central sensitization, and convergence. This knowledge will aide the clinician to be able to properly diagnose non-odontogenic oro-facial pain in order to treat the patient properly and to avoid doing irreversible harm to the patient, such as extractions or endodontic treatment on healthy
p.483 The cell bodies of primary-order neurons or pain-transmitting neurons reside in the dorsal root ganglia just lateral to the spine along the sensory pathways that penetrate the posterior part of the cord. The second order neurons are found in the dorsal horn (p.484) Most nociceptive information tranvels by means of ascending columns in the lateral spinothalamic tract (also called the anterolateral funiculus). The principal target for nociceptive afferents is the thalamus (the major relay station of sensory information in general) Third order neurons project to portions of the CNS involved in the processing and interpretation of pain, the chief areas being the reticular and limbic systems and cerebral cortex. (p 484)
The compound action potential adds up all the action potentials that each individual neuron experiences in the sciatic nerve. Different stimulus amplitudes cause different neurons to fire an action potential; this is due to the fact that each neuron has a different threshold potential, or the minimum voltage the neuron needs to fire an action potential. The individual neuron action potential is an ‘all-or-nothing’ event, but the CAP, as a summation of different individual neurons, is not. The CAP amplitude will increase with larger stimulus potentials because more neurons with higher individual thresholds will be recruited. For this frog sciatic nerve, there are three fiber types, A, B, and C. A fibers are further divided, in the order of decreasing diameter, into α, β, γ, and δ fibers. There is an inverse relationship between the diameter of the nerve fiber and the threshold potential: the larger the diameter, the lower the threshold. Thus, as the largest fibers, the Aα neurons will be the first to be stimulated at a low stimulus potential, and the Aδ neuron fibers will be the last to be recruited. Because the sciatic nerve is mostly composed of A fibers, the recruitment of A-subtype nerve fibers are more readily distinguishable from the data. The minimum potential required to stimulate the Aα fibers was between 75 mV and 80 mV. Once the stimulus potential reached 90 mV, Aβ neurons were recruited and contributed to the increase in amplitude of the CAP. At a stimulus
Central sensitization (CS) is a condition of the nervous system that is related to the development and maintenance of chronic pain. When CS happens, the nervous system goes through a process called “wind-up” and gets regulated in a persistent state of high reactivity. This persistent, or regulated, state of reactivity later on maintains pain even after the initial injury might have healed.
Our patient presented with a history much typically suggestive of trigeminal neuralgia. Dental extractions are sometimes considered as the trigger factor for the same. Patient also did not have any neurological deficits including sensory loss over trigeminal nerve distribution making trigeminal neuralgia a strong clinical possibility.
Post Obturation pain can be defined as pain of the facial soft tissues and the oral mucosa after the initiation of root canal treatment of the endodontically treated tooth that
Parafunctional habits can result in injury to the PDL, alveolar bone loss, sensitivity to hot and cold, cervical erosion, mobility, and may even cause tooth fracture. Pain referred from the PDL can be confused with pulpitis. If endodontic treatment is initiated there will be no pain relief. Therefore, good history taking and intra-oral and extra-oral examinations are essential. Pain from oral mucosal lesions can produce localized or diffuse pain that is usually described as soreness or burning sensation and is usually associated mucosal breakdown. However, toothache is usually distinguishable from pain of the oral
Pain medications and nonsteroidal anti-inflammatory drugs (NASAIDs) can provide some relief, and some dentists recommend oral appliances called splints to be worn for a short period of time. Additionally, there’s a lot your employees can do to ease their painful symptoms, like eating soft foods, applying ice packs and avoiding extreme jaw movements, such as yawning widely, singing loudly or chewing gum. Many dentists refer their patients with jaw problems to a physical therapist, who may suggest exercises that can provide relief. Learning stress-reducing techniques is also beneficial when dealing with facial pain.
Chronic pain and inflammation increases serotonin receptor density in the DRG and spinal cord (Bardin, 2011). Spinal 5-HT3 receptors in particular are implicated in central sensitization (Kayser et al., 2007; Zeitz et al., 2002). 5-HT3 antagonists relieve pain intensity in patients with FMS (Vergne-Salle et al., 2011; Wolf, 2000). While they do appear to play a role in decreasing acute pain in tail-flick and thermal plate tests in rats (Glaum, Proudfit, & Anderson, 1988) they also increase wind-up and sensitization, two phenomena that characterize FMS pain, and are most often associated with pronociceptive signaling (D'Mello & Dickenson, 2008; Suzuki et al., 2004). 5-HT3 receptors are believed to have an important role in supraspinal facilitation and hyperalgesia (Dogrul et al., 2009). These receptors enhance the release of nociception promoting substances such as substance P, calcitonin gene-related peptide, and neurokinin A (Bannister et al., 2009). Symptoms that
Neuropathic pain is a common condition resulted ref from pathology of the nervous system. It is a common syndrome comprising hyperalgesia, allodynia and spontaneous pain. The chronic constriction injury (CCI) of the sciatic nerve is a widely used model of neuropathic pain which evokes a series of molecular, biochemical and cytoarchitectural changes in primary sensory neurons and produces neuropathic
An important fundamental paper by Brannstrom and Astrom1 explored a possible mechanism to explain dentinal pain and sensitivity. In an experiment where air was blown on exposed dentin, they noticed a significant outflow of fluid from the dentinal tubules. They postulated that dentinal sensitivity may be caused by the rapid flow of fluid in either an inward or outward direction at the pulpo-dentinal border.
Endodontic refers to that field of dentistry that deals with diagnosing and treating pulpal and periapical diseases as to preserve the surrounding tissue. (1) Until recently, root canal treatment therapy was traditionally performed using tactile sensation of the clinician and the root canal system could only be seen on a two-dimensional radiograph. To perform an endodontic treatment regularly means to work in a dark and narrowed place, and little bit of millimeters may decide the outcome of therapy, as it relays on the dentist knowledge and expertise many results were achieved by chance. (2)
While pain is a subjective feeling, and an unpleasant sensation there is not one definition that explains what exactly pain is. We do however know that a pain pathway helps understand what pain is. Pain begins from a painful stimulus which activates nociceptor or pain receptors. This receptor sends pain signals to the spinal cord synapse. At this point a reflex response to the pain, which helps move the body away from the source of pain. Neurons then communicate to the ascending tracts to the brain. Two tracts; one for acute sharp pain called neospinothalamic tract and the paleospinothalamic tract for slower impulses. The tracts connect to the reticular formation in the brainstem, hypothalamus, thalamus and other structures. (Karin C. VanMeter,
Cavities can be a serious pain, especially if they get down into the nerve of your tooth. If you are experiencing pain with a cavity then it has likely done this, or you may have an infection
According to the European Federation of Neurological Societies (EFNS) guidelines on neuropathic pain assessment and the American Acade-my of Neurology (AAN)-EFNS guidelines on TN management (Cruccu G et al., 2006) the neurophysiological recording of trigeminal reflexes represents the most useful and reliable test for the neurophysiological diagnosis of trigeminal pains. (Figure 1.1). In patients presented with pain in the trigeminal territory, trigeminal reflexes offer the clinician with useful information. Abnormalities are often discovered in divi-sions that appear clinically unaffected. An objective demonstration of dysfunction is provided in all patients with pain secondary to a docu-mented disease, such as symptomatic trigeminal neuralgia,
Take to 2-3 tender guava leaves and chew them. Keep the chewed leaves on the affected tooth and soon you will find the difference in the pain.