4. Pain and Nociception
Learning Outcomes
Explain the importance of pain to the dentist
Define pain and differentiate it from nociception
Part A: Nociception
Definition of Nociception: Unconscious detection of harmful stimuli through sensory receptors.
Importance of Understanding Pain: Critical for diagnosis in medical fields, particularly dentistry.
Definition of Pain: "An unpleasant sensory and emotional experience primarily associated with tissue damage" (International Association for the Study of Pain).
Structure of the Nociceptor
Type: Simple free nerve endings.
Distribution: Widespread in skin, arterial walls, joint surfaces; sparsely in deeper tissues; significant in oral tissues (tongue, gums, dental pulp).
Types of Nociceptor Fibres
Aδ Fibres: Myelinated, fast conduction (6-30 m/s), highly localised responsible for sharp, immediate pain (fast pain) evoked by mechanical/thermal stimuli.
C Fibres: Unmyelinated, slow conduction (0.5-2 m/s), hard to localize, causing dull, lingering pain (slow pain) evoked by mechanical, thermal, or chemical stimuli.
Example: Fast pain from a needle prick followed by dull pain.
but a and C fires are found in the dental pulp
Nociceptive Pathways - ASCENDING
When a nociceptor in the torso or limbs is activated, pain signals are carried by C fibres or Aδ fibres to the dorsal horn of the spinal cord (1, 2). These fibres, also called 1st order neurons, synapse with 2nd order dorsal horn neurons (DHNs).
Neurotransmitters: - ascending
Glutamate mediates synaptic transmission for Aδ fibres.
Both glutamate and substance P (pause) mediate C fibre transmission.
Pathways: 4 ASCENDING
1. Spinothalamic tract → Main pain pathway
Carries most pain signals from the body to the thalamus.
From the thalamus, 3rd-order neurons relay the signals to the somatosensory cortex, where pain is consciously perceived.
Spinoreticular tract → Emotional and autonomic response to pain
Also carries pain signals but through the reticular formation (in the brainstem).
Some branches go to the hypothalamus (involved in stress response) and the limbic system (involved in emotions), explaining why pain can trigger emotional and physical reactions (e.g., sweating, nausea).
Visceral pain (organs) → Gracile fasciculus pathway
Pain from internal organs (e.g., stomach ache) travels via the gracile fasciculus in the spinal cord.
Signals go to the gracile nucleus in the medulla, then to the thalamus and somatosensory cortex, where it is perceived as visceral pain.
Head and face pain → Cranial nerve pathways
Pain from the head and face is mainly carried by the trigeminal nerve (V).
The signal passes through the trigininal neuclus in pons and medulla, then reaches the thalamus via 2nd-order neurons. → 3rd order neuron to somatosensory cortex
Other cranial nerves involved in facial pain:
Facial nerve (VII) → Carries pain from parts of the face.
Glossopharyngeal nerve (IX) → Transmits pain from the throat and tongue.
Vagus nerve (X) → Carries pain from deeper areas (e.g., throat, chest).
Spinothalamic tract → Main pain pathway (body →dorsal horn neuron → thalamus → cortex).
Spinoreticular tract → Emotional and autonomic pain response.
Gracile fasciculus → Visceral (organ) pain.
Cranial nerves → Head and face pain.
Peripheral pain signal → Dorsal horn neurons:
Pain signals from the C and Aδ fibers enter the spinal cord and synapse with dorsal horn neurons.
This is the first relay point where pain signals are processed.
Dorsal horn → Brainstem (pons and medulla):
From the DHNs, second-order neurons carry the pain signals upward.
The signals travel through the spinothalamic tract or spinoreticular tract, passing through the medulla and pons on their way to the thalamus.
Thalamus → Cortex:
In the thalamus, third-order neurons relay the signals to the somatosensory cortex, where pain is consciously perceived.
dorsal horn neurons (DHNs) are located in the spinal cord, before the pons and medulla in the pain pathway.
Pain signals travel upward from the DHNs through the brainstem (pons/medulla) before reaching the thalamus and cortex.
Somatosensory cortex organization:
The cortex processes pain signals according to the body region they originated from (e.g., hand signals go to the hand-specific area).
Stimuli Evoking Nociceptive Responses (chemical, mechan. thermal)
Chemical Mediators: K+ from damaged cell, histamine, bradykinin(mast cell), prostaglandins, excess H+, serotonin. → stimulate nociceptor
Temperature- cold-pain receptors respond to pain <15°C
heat-pain receptors respond to pain >45°C
heat or cold stimuli in teeth can be due to dental instruments of high forces/intense heating or cooling (e.g high speed hand-piece)
Mechanical - examples of mechanical stimuli in teeth → mechanical probing, drying
Pain Elicitation in Dental Tissues: Exposed dentine is sensitive to temperature, mechanical force, and hypertonic solutions. pulp also stimulated by chemical stimulators
Autonomic Responses to Pain
Symptoms may include pupillary dilation, sweating, bradycardia, pallor, and nausea.
Importance: Diagnosis may be complicated by these responses, especially in severe pain situations.
Acute vs. Chronic Pain
Acute Pain: physiologic, Sudden onset, linked to specific events, short duration, decreases with healing (e.g., bone fracture).
Chronic Pain: pathologic Persistent >3 months, often unresponsive to analgesics; may arise from nerve injury and has psychological consequences.
Referred Pain
Phenomenon where pain from visceral organs is perceived in a superficial area; e.g., tooth pain referred to nearby regions.
Explanation: Shared synapses of visceral pain and skin pain fibers, leading the brain to misinterpret the pain's origin.
Importance of Pain
Pain acts as a protective mechanism; awareness of harmful stimuli prompts avoidance behavior.
Conditions like congenital insensitivity to pain -result from abnormal low expression of nociceptor illustrate the protective role of pain in physical well-being.
Part B: Neuropathic Pain
Neuropathic pain results from lesions or diseases in the peripheral or central nervous system (e.g., diabetic neuropathy, multiple sclerosis, spinal cord injury).
It may involve allodynia (pain from normally non-painful stimuli) or hyperalgesia (exaggerated pain response).
Orofacial neuropathic pain is often linked to dental treatment and can present with burning, tingling, or unusual sensations.
Peripheral sensitization
Increased expression of Na⁺ channels in C and Aδ fibres lowers the activation threshold, making them more sensitive.
After nerve damage, these fibres may show spontaneous activity or respond to weaker stimuli.
Peripheral sensitization can cause Central sensitization (wind-up):
nervous system becomes hypersensitive to pain, amplifying pain signals even from minor or non-painful stimuli.
Frequent glutamate release from 1st order pain fibres bombards DHNs, increasing the expression of NMDA (glutamate)receptors (ionotropic, permeable to Na⁺ and Ca²⁺)
This lowers the threshold potential of DHNs, making them more likely to fire, even with weaker stimuli.
sprouting of Aβ (mechanoreceptor) fibres occurs when the fibres are damaged allowing them to make connections to 2o order pain fibres in the spinal cord
This means that stimuli normally perceived as innocuous mechanical activity is now perceived as pain.
Phantom limb pain:
Experienced by high % amputees截肢, it results from central sensitization and cortical rearrangement.
The cortical region representing the missing limb receives signals from the stump (residue limb), creating the sensation that pain originates from the absent limb.
Phantom tooth pain can occur at extraction sites, often following repeated dental procedures.
Part C: Psychological Aspects of Pain
Mind-Body Connection: Pain perception influenced by psychological factor; for instance, a child's response to injury is often affected by the parent's reactions.
Chronic Pain and Psychological Disorders: High correlation; vice-versa, chronic pain patients are at risk for anxiety/depression, therefore antidepressants can alleviate some pain. patient with axiety/ depression more likely to experience chronic pain