Orofacial Sensations Flashcards
List some functions of sensory info
Protection/safety Control of movement Future reference Maintain consciousness Emotion
How are receptors classified? And what are the different types?
By type:
- Mechano (hearing, touch)
- Chemo (taste, smell)
- Photo (light)
- Thermo (temperature)
- Proprio (position)
- Noci (pain)
By range
- Telo (source of stimulus far from target, e.g. sight, sound)
- Extero (source of stimulus must make contact e.g. touch, smell, taste)
- Intero (detect internal conditions e.g. carotid sinus baroreceptors)
By speed of adaptation:
Phasic: fast e.g. touch
Tonic: slow e.g. pain
What is kinaesthesia? How is it different from proprioception?
Detection of position of body parts, involves use of teloreceptors (sight, sound), internoreceptors (proprioceptors) and exteroreceptors (touch+pressure)
Proprio different in that it only detects muscles/joints–>part of kinaesthesia
What are the main types of extero + interoreceptors in the oral cavity and where are they found?
Extero: -PMR’s: PDL, gingiva, alveolar mucosa, periosteum
Intero: -TMJ receptors: muscle spindles
What is the pre-dominant type of PMR receptor? They are most sensitive to force applied in which direction? Are they more sensitive to high force or low force?
- Ruffini endings
- Force applied in labial direction
- Low force
What do TMJ receptors mainly consist of? What is their function?
- Ruffini endings + GTO’s: Static mechanoreceptors that detect proprioception (slow adapting)
- Nociceptors: Detect pain
- Vater-pacinian corpuscles: Dynamic mechanoreceptors for proprioception (fast adapting)
What factors affect conversion of stimulus to a signal/influence properties of signal?
Modality
Intensity
Duration
Location
What is the distribution of cold receptors relative to warm receptors?
-More of cold + cold located more superfically
How is referred pain produced?
When two primary neurons from different locations converge, resulting in receptor field of secondary neuron encompassing both primary neurons. This results in painful stimulus in one area potentially also causing painful sensations in another location.
What can measuring oral stereognosis give an indication of?
- Effectiveness of therapy
- Extent of oral dysfunction
- Current oral function
What functions does OSA play physiologically?
- Control of mastication
- Speech
- Swallowing
- Denture adaptation
(think of this like proprioception)
What can affect OSA?
Test piece
-Size, shape, order of presentation, texture
Subject:
- Number of teeth present
- All teeth present>dentures>edentulous/no denture
- Age
- Perio breakdown
- Muscle spindle dystrophy
External factors:
-LA reduce OSA
What are the types of receptors involved in OSA?
- Muscle spindles
- PMR’s
- Tongue + palate mucosal receptors
- TMJ + jaw muscle receptors
List 3 different types of abnormal pain response.
Allodynia: Non-painful stimulus produce pain
Phantom pain: No stimulus but pain produced
Neuropathic pain: pain due to damage to somatosensory system
What are some factors that affect pain intensity?
- Race/ethnicity
- Emotions
- Intensity of stimulus/extent of damage
- Concomitant experience
- Placebo
- Memory of experience
What is a polymodal nociceptor?
Detects pain from multiple sources (i.e. chemical, thermal, mechanical) rather than from just one source type
What do nociceptors respond to?
Thermal, chemical, mechanical
Explain the double pain sensation?
A-delta fibres located more superfically and thus stimulated first
Results in initial short, sharp pain sensation that is well localised
C fibres are located deeper and thus are stimulated a short time after, resulting in a dull, throbbing poorly localised sensation (the receptors are polymodal)
What chemicals can produce pain and sensitise nociceptors?
Produce pain:
- Potassium: damaged cells
- Bradykinin: damaged vessels
- Serotonin: damaged endothelial cells + platelets
- Histamine: mast cells
Sensitise:
- Prostaglandin: From damaged cells
- Substance P: from primary afferent neurons
Explain antidromic activation of receptor endings.
Rather than nociceptors detecting pain and transmitting signal to CNS, the opposite occurs.
I.e., CNS sends signal to nociceptors to release substances which cause them to become sensitised (e.g. substance P)
Describe what occurs in hot pulps.
Release of substance P:
- Release of histamine-> increase pain in nociceptors
- Cause increased permeability + extravasation -> edema -> Trigger release of bradykinin
CGRP-> vasoliation->edema->release of bradykinin
-Bradykinin increases pain
Explain central sensitisation?
- Activation of slow conducting C fibres
- Alters second messengers
- Activation of protein kinases
- Results in increased excitibility and synaptic efficiency
What are the effects of P substance?
- Vasodilation
- Increased blood flow
- Increased blood pressure
- Increased permeability
- Synthesis of pro-inflammatory cytokines
- Chemotaxis of inflammatory cells
- Increased pain sensitisation
What are WDR neurons?
-Detect both noxious and non-noxious (touch, pressure, temp,etc.) stimuli (i.e. responsible for both pain and non-painful stimuli)