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Questions and Answers
What is a consequence of peripheral sensitization in response to repeated noxious stimuli?
What is a consequence of peripheral sensitization in response to repeated noxious stimuli?
What phenomenon occurs when noxious stimuli produce an even greater perceived intensity of pain?
What phenomenon occurs when noxious stimuli produce an even greater perceived intensity of pain?
⭐️Which of the following best describes allodynia?
⭐️Which of the following best describes allodynia?
Which of the following substances contributes to the sensitization process in peripheral tissues?
Which of the following substances contributes to the sensitization process in peripheral tissues?
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Spontaneous pain can develop as a result of which of the following changes in nociceptor activity?
Spontaneous pain can develop as a result of which of the following changes in nociceptor activity?
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Which mechanism can lead to hyperalgesia through changes in sensory nerve fibers?
Which mechanism can lead to hyperalgesia through changes in sensory nerve fibers?
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What role do inflammatory mediators play in the development of allodynia?
What role do inflammatory mediators play in the development of allodynia?
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What characteristic is NOT associated with hyperalgesia?
What characteristic is NOT associated with hyperalgesia?
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Which mechanism contributes to the development of spontaneous discharges of nociceptors during hyperalgesia?
Which mechanism contributes to the development of spontaneous discharges of nociceptors during hyperalgesia?
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What role does NGF play in hyperalgesia?
What role does NGF play in hyperalgesia?
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⭐️What factor is associated with increased sensitivity of dentin when the pulp is acutely inflamed? Making it hard to 麻醉。
⭐️What factor is associated with increased sensitivity of dentin when the pulp is acutely inflamed? Making it hard to 麻醉。
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Which of the following explains the difficulty in anesthetizing a tooth with inflamed pulp?
Which of the following explains the difficulty in anesthetizing a tooth with inflamed pulp?
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The presence of which channels is primarily responsible for the increased excitability of nerves in inflamed dental pulp?
The presence of which channels is primarily responsible for the increased excitability of nerves in inflamed dental pulp?
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Study Notes
Peripheral Sensitization
- Nociceptors (sensory receptors that detect pain) are sensitized following repeated noxious stimuli.
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Sensitization manifests as three key changes in nociceptor response patterns:
- Decreased firing threshold: Non-noxious stimuli can trigger discharges, leading to allodynia (pain caused by normally non-painful stimuli).
- After-discharges: Noxious stimuli produce increased intensity of pain (hyperalgesia).
- Spontaneous firing: Leads to the development of spontaneous pain.
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Chemical mediators released in inflamed pulp and periradicular tissues contribute to sensitization:
- Damaged tissue products
- Vascular agents
- Peptides from nerve fibers themselves.
- These changes are commonly observed in patients with endodontic pain.
Inflammatory Mediators
- Inflammatory mediators like prostaglandins, bradykinin, and substance P contribute to hyperalgesia and allodynia by sensitizing nociceptors
- These mediators lower the threshold for activation of nociceptors, which are pain-sensing neurons
- They also increase their responsiveness to painful stimuli
Afferent Fiber Changes
- Afferent fibers, which transmit sensory information to the central nervous system, undergo significant changes during hyperalgesia and allodynia
- Activation and sensitization: These fibers can become more sensitive to both mechanical and thermal stimuli, leading to heightened pain perception
- Sprouting: New nerve endings can sprout from existing afferent fibers, increasing the density of pain receptors in the affected area
- Proteins: Changes in the expression of proteins involved in pain signal transduction, such as TRPV1 and Nav1.8, contribute to the sensitization of afferent fibers
Additional Mechanisms
- Tissue pressure: Increased pressure in inflamed tissue can directly activate nociceptors and contribute to hyperalgesia
- Tissue temperature: Changes in temperature can also modulate nociceptor activity. Heat can exacerbate pain, while cold can sometimes provide temporary relief
- Sympathetic primary afferent fiber interactions: Interactions between sympathetic nerves and primary afferent fibers can influence pain perception and contribute to chronic pain states
Aβ Fiber Plasticity
- Aβ fibers, typically responsible for non-painful touch sensations, can become involved in pain transmission during chronic pain conditions
- This can lead to allodynia, where normally innocuous stimuli like light touch elicit pain
### Hyperalgesia
- Hyperalgesia is defined as increased sensitivity to pain:
- Spontaneous pain
- Decreased pain threshold
- Increased response to painful stimuli
- Hyperalgesia can be caused by:
- Sustained inflammation
- Upregulation of tetrodotoxin-resistant (TTX-resistant) sodium channels in inflamed neural tissue
- Nerve Growth Factor (NGF) regulating chronic inflammatory hyperalgesia
- Localized elevations in tissue pressure and inflammatory mediators play a role in inflammation and hyperalgesia.
Allodynia
- Allodynia is a condition where previously non-noxious stimuli cause pain.
- Thermal allodynia: pain from normally innocuous thermal stimuli (e.g., drinking cold beverages).
- Mechanical allodynia: pain from normally innocuous mechanical stimuli (e.g., biting on a tooth).
### Pulpal Inflammation & Sensitization
- Pulpal inflammation can lead to hyperalgesia and allodynia.
- Inflammation upregulates genes and their products, potentially increasing sensitivity of peripheral nerve endings in the pulp and periradicular tissues.
- Normal pulpal tissue contains silent nerve fibers that are not excited by ordinary external stimuli.
- Inflammation sensitizes these silent nerve fibers, making them responsive to hydrodynamic stimuli, potentially contributing to dentin hypersensitivity.
### Dentin Sensitivity and Inflammation
- Dentin sensitivity can increase when the pulp is inflamed.
- This increase in sensitivity can make it harder to anesthetize the tooth.
- The increase in sensitivity is linked to the upregulation of tetrodotoxin-resistant (TTX-resistant) sodium channels.
- These channels are present in inflamed neural tissue.
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