TMJ Flashcards

1
Q

Define noxious stimuli, allodynia and hyperalgesia

A
  • Noxious stimuli: A stimulus that is painful
  • Allodynia: Pain due to a non- noxious (non painful) stimuli, for example, pain due to touch
  • Hyperalgesia: A state of increased pain to a noxious (painful) stimuli
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2
Q

Explain the process of pain perception (nociception) in terms of nerve fibres and the general pathway of pain transmission

A

There are two types of afferent nociceptive nerve fibres:
• Aδ fibres: myelinated thus sharp, pricking pain that’s well localised

• C fibres: unmyelinated, thus dull pain that is poorly localised. It is a secondary or slow pain

General pathway involved in the transmission of pain:
• First, the fibres detect pain and transmit this information to second order neurons into dorsal horn of the spinal cord, then this is transmitted to the thalamus of the brain

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3
Q

Explain the process of orofacial pathway of pain transmission

A
  • Trigeminal nociceptive nerve fibres in the TMJ, PDL or orofacial muscles will travel to the trigeminal ganglion as “first order neurones”.
  • From here, they travel to the trigeminal sensory complex in the brainstem.
  • These first order will synapse with second order neurones in the “subnucleus caudalis”
  • Second order neurones ascend to the nucleus of the thalamus.
  • Here, second order neurons synapse with third order neurons in higher order centres in the brain , which will discriminate where the pain is coming
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4
Q

Explain peripheral sensitisation in the scenario of tissue damage (e.g. tooth abscess)

A

This is known as an increased sensitivity to a stimuli that is received by afferent nerves (nerves that travels from the skin to the brain)
• Injury/ cell damage recruits mast cells, macrophages and neutrophils
• These immune cells releases chemicals such as H+, bradykinin, interleukin and pro-inflammatory cytokines
• These chemicals bind to nociceptors, which has two effects
• Firstly, it causes an action potential strong enough that it will travel to the brain = pain sensation
• Secondly, it sensitises nociceptors by bringing their membrane potential closer to the depolarization threshold. This up-regulates ion channels, causing an influx of ions -> fast and/or prolonged depolarisation -> action potential -> pain

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5
Q

Provide 3 oral examples of peripheral sensitisation

A
  • Abscessed tooth painful to bite upon, painful to percussion
  • Ulcer/sore spot under over-extended denture flange
  • Tender jaw muscles; tender TMJ
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6
Q

Explain central sensitisation, and how this can also contribute to allodynia

A
  • An increased responsiveness of nociceptors in the central nervous system
  • The brain has adapted to over react to the normal signals of movement/pressure/temperature etc and the brain misinterprets this information and sends a protective signal: pain - results in hyperalgesia and allodynia
  • 2nd order neurones are much more likely to be involved in this. A very strong response from first order neurones could cause a barrage of chemicals that result in constant depolarisation of second order neurones, thus continually firing off action potentials that go to the brain
  • Low inputs may end up easily activating second neurones
  • Tactile input can also illicit pain because 2nd order neurones not only conduct nociception, but also are responsible for tactile input/ pressure/ temperature
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7
Q

Explain why an abscessed tooth is tender to touch

A
  • The patient is experiencing allodynia
  • The nociceptive pathway to higher centres of the brain is being activated

Mechanisms involved in allodynia:
• Peripheral sensitization of nociceptive endings (inflammatory changes etc.)
• Central sensitization of neurons conveying information along the nociceptive pathway to higher centres - their subnucleus caudalis is sensitised
• Combination of both

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8
Q

State why central sensitisation is considered a disease entity

A
  • Possibility where periphery heals but central brain changes perpetuate the pain
  • This is why peripheral nociceptive input is blocked during GA surgery; it reduces the chances of central sensitisation
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9
Q

Explain the mechanism of referred pain in the orofacial region

A
  • Referred pain is pain felt at a site distant from the site of injury
  • Nociceptive afferents from different orofacial regions may converge onto the same 2nd order neurone. These are known as “silent connections”
  • This is the case for the temporalis muscle, where its nociceptors converge with forehead and upper molars nociceptors
  • Prolonged and/or intense noxious stimulus in the temporalis muscle (star) could sensitise/ activate these “silent connections” with other neurones. The brain is therefore confused as to which nociceptive afferent is the source of the problem
  • Thus, pain source may not be the pain site
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10
Q

List the the management of referred pain (4)

A

Reduce pain

Restore comfortable jaw function

Improve quality of life by addressing stressors

Long term management

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11
Q

Explain the possible mechanism behind persistent pain in a patient where the suspected source of pain is removed

A
  • Central sensitization helps explain these somewhat bizarre signs and symptoms –changes have occurred in the excitability of 2nd order (and higher) neurones in the Trigeminal Brainstem Sensory Nuclear Complex
  • Tactile input is eliciting pain because 2nd order neurones not only conduct nociception, but also are responsible for tactile input/ pressure/ temperature

• Therefore, even though the periphery has calmed down, the changes in the 2nd order neurones is causing nociception

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12
Q

Describe the management of central sensitisation

A
  • Short term management goals: pain reduction, improvement of psychosocial factors and restoration of function
  • Medications: Amitriptyline (Tricyclic antidepressants) 10 mg at bedtime or capsaicin 0.075% cream (apply to the skin of the cheek where pain is)
  • Commence exercises and muscle relaxation techniques
  • Further psychological assessment and cognitive therapy and strategies for coping with the pain and improving family relationships.
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13
Q

Explain the possible mechanism behind TMJ pain. (refer to TMJ lecture notes)

A

Peripheral sensitisation:
• Excessive stretching of the jaw can be injurious

  • Injury/ cell damage recruits mast cells, macrophages and neutrophils
  • These immune cells releases chemicals such as H+, bradykinin, interleukin and pro-inflammatory cytokines
  • These chemicals bind to nociceptors which has two effects
  • Firstly, it causes an action potential strong enough that it will travel to the brain = pain sensation
  • Secondly, it sensitises nociceptors by bringing their membrane potential closer to the depolarization threshold. This up-regulates ion channels, causing an influx of ions -> fast and/or prolonged depolarisation -> action potential -> pain

Central sensitisation:
• An increased responsiveness of nociceptors in the central nervous system
• The brain has adapted to over react to the normal signals of movement/pressure/temperature etc and the brain misinterprets this information and sends a protective signal: pain - results in hyperalgesia and allodynia
• 2nd order neurones are much more likely to be involved in this. A very strong response from first order neurones could cause a barrage of chemicals that result in constant depolarisation of second order neurones, thus continually firing off action potentials that go to the brain
• Low inputs may end up easily activating second neurones
• Tactile input can also illicit pain because 2nd order neurones not only conduct nociception, but also are responsible for tactile input/ pressure/ temperature
• This is thought to be one of the main mechanisms of chronic pain; Possibility where periphery heals but central brain changes resulting in hyperexcitable 2nd order neurones perpetuate the pain

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14
Q

Describe the concept of “reducing pain”

A
  • Education of problem and the pain
  • Awareness of habits/jaw use patterns; clenching, grinding, jaw posturing
  • Diet modifications
  • Positioning of jaw to avoid tooth contact habit
  • Avoid wide jaw openings
  • Moist heat/ice or
  • Analgesics: moderate pain = NSAID + codeine, severe pain = opioid
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15
Q

Describe the concept of “restoring comfortable jaw position” and “improving quality of life by addressing stressors”

A

Restore comfortable jaw function:
• Jaw exercises/heat packs to increase jaw mobility

Improve quality of life by addressing stressors:
• Chronic pain is often associated with severe physical and/or emotional stresses
• Relaxation strategies; deep breathing, muscle relaxation
• Reduction of work stressors; improve work station ergonomics, discuss with employer work goals

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16
Q

Describe the concept of “long term pain management”

A
  • Review and re-emphasize above short-term strategies
  • Reassurance and encouragement
  • Change medication regime
  • Occlusal appliance to minimise teeth wear from sleep bruxism

Reduce need for future health care through avoiding:
• Excessive mouth opening
• Heavy chewing
• Lengthy dental procedures
• Oral habits that may strain the jaw muscles or overload the TMJs

17
Q

List the three dimensions of pain (refer to TMJ lecture notes)

A
  • Sensory: discriminative
  • Motivation: affective
  • Cognitive: evaluative
18
Q

Describe the three dimensions of pain (refer to TMJ lecture notes)

A

Sensory: discriminative
• Relates to the location, intensity, duration and quality of pain

Motivation: affective
• Conscious or unconscious drive for a person to remove themselves from the source of pain
• Interpreted in relation to the actual situation, e.g. fearful dental patient
• You want to escape from the pain

Cognitive: evaluative
• Pain is evaluated in terms of current and past experience
• Scared of dentist due to past experiences of pain

19
Q

Define and describe acute pain

A

Acute pain:
• Evoked by a noxious stimuli e.g. pin prick

  • Dental examples include tooth abscess, ulcer under dental flange
  • Useful biological function: it is protective and demands immediate attention and action
  • Much dental practice is treatment of acute pain
20
Q

Define and describe chronic pain, providing some examples.

A

Chronic pain:
• Pain lasting >3 months

  • No clear biological role
  • Often associated with severe physical and/or emotional stresses

Chronic orofacial pain examples:
• Temporomandibular disorders
• Burning mouth syndrome
• Trigeminal neuropathic pain