Pain Perception and Types of Pain

Pain Perception

• Pain is an unpleasant sensory and emotional experience.
• Nociceptors are receptors stimulated by potentially tissue damaging stimuli.
• Pain is a symptom, subjective, protective, and modified by developmental, behavioral, personality and cultural factors.
• Pain can be acute or chronic.

Types of Pain

• Fast pain: Also called sharp, pricking, acute pain, felt within 0.1 seconds after the stimulus is applied. Well localized. Not felt in deeper tissues.
• Slow pain: Also called slow burning, aching, throbbing, nauseous, chronic pain. Felt after 1 second or more, increasing over time. Poorly localized, often associated with tissue destruction, and can lead to prolonged, almost unbearable suffering.

Nerve Fibers

• Different nerve fibers transmit pain signals, categorized by myelination, diameter, and speed.
• A delta fibers are fast pain fibers and myelinated thin nerves associated with sharp, localized pain.
• C fibers are slow pain fibers, unmyelinated, associated with dull, poorly localized lingering pain.

Pain Receptors and Stimulation

• Pain receptors are free nerve endings.
• Located in superficial skin layers, somatic tissues, and some internal tissues (excluding brain and lung parenchyma).
• Stimulated by mechanical, thermal, and chemical factors.
• Fast pain is elicited by mechanical or thermal stimuli.
• Slow pain is triggered by all three types of stimuli.

Neurotransmitters

• Chemicals (e.g. bradykinin, histamine, serotonin, K+ ions) released cause pain and sensitize nociceptors.
• Prostaglandins and substance P increase sensitivity, without directly stimulating nociceptors.

Pain Receptors and their Stimulation

• Pain receptors are free nerve endings.
• Widespread in superficial skin and somatic tissues.
• Stimuli include mechanical, thermal, and chemical.
• Chemicals like bradykinin, serotonin, K+ ions, histamine, H+, lactic acids, ACh, proteolytic enzymes, leucotrienes, cytokines & capsaicin.

Pain Modulation

• Pain perception is variable due to endogenous & exogenous mechanisms, which can increase or decrease pain threshold.
• Enhancement and inhibition occur at all nervous system levels.
• Modulation at nerve, spinal cord and brain levels influence pain perception.

Pain Suppression (Pain Modulation)

• Includes periaqueductal gray and periventricular areas of the mesencephalon and pons, raphe magnus nucleus, as well as a pain inhibitory complex in the spinal cord's dorsal horns.
• Transmitters like enkephalin (pre- and post-synaptically inhibit pain fibers - Aδ,C) and serotonin (which stimulates enkephalin release).
• Brain opioid system: endorphins (hypothalamus/pituitary), enkephalins and dynorphins (brain stem).

Opioid Actions

• Endogenous opioid peptides, such as endorphin, enkephalin, and dynorphin, and exogenous substances like morphine, codeine, fentanyl, pethidine and heroin.
• Act presynaptically or postsynaptically to block calcium channels, inhibiting neurotransmitter release (e.g. glutamate, substance P) and trigger potassium channel opening, resulting in membrane hyperpolarization and inhibiting pain neurotransmitter activity.
• Activate descending pain modulatory inhibitory pathway and inhibit GABA-mediated inhibition of descending pathways.

Gate Control Theory

• Non-painful input closes gates to painful input.
• This occurs at the substantia gelatinosa in the dorsal horn of the spinal cord, and stimulation in the Aδ or C neurons will activate it.
• Stimulation of Aβ fibers opens the gates.
• The theory helps explain methods of pain relief through massage, applying irritants, transcutaneous electrical stimulation and acupuncture.

Varieties of Pain

• Phantom pain: occurs when there's no stimulus but a feeling of pain in the missing limb/tissue.
• Psychogenic pain: originates from emotional or psychological factors.
• Neuropathic pain: a pain caused by damage or disease to the somatosensory nervous system.

Pain in Dentistry

• Pulpal Origin: Visceral pain; threshold type pain. responds to various stimuli, but not usually mastication.
• PDL Origin: Deep somatic musculoskeletal pain. more localized than pulpal pain, is related to biomechanical function & can be precisely localized.
• A-delta fibers and C-fibers contribute to pain sensations from different parts of the mouth and teeth.

Orofacial Pain Pathway

• Somatic inputs from facial structures travel through the trigeminal nerve (CN V) to various brain nuclei.
• Different nerves transmit sensations in the face and mouth directly to specific central nervous system nuclei.

Orthodontic Pain Pathway

• The trigeminal neurons receive nociceptive signals.
• These first-order neurons synapse with second-order neurons in the trigeminal nucleus caudalis, which then decussate (cross to the opposite side) before synapsing with third-order neurons in the thalamus.
• The thalamus then relays the signals to the somatosensory cortex where the pain perception is integrated.

Dental Pain of Pulpal Origin

• Characterized by visceral pain, threshold, and widespread stimuli response.
• Non-localized and doesn't always persist.
• Can become chronic or spread to the periodontal ligament.

Dental Pain of PDL Origin

• Deeper somatic musculoskeletal pain.
• More localized than pulpal pain.
• Intimately related to biomechanical function (e.g. mastication).
• Highly localized & related to biting pressure or discomfort localized to a specific area.