Dentine sensitivity Flashcards
Pain producing stimuli - intact tooth
Thermal (enamel conducts)
- heating 45 C
- cooling 27 C
Thermal stimuli reaction times
Nerves stimulated before any T change in pulp
-receptor: detection
Reaction times < by pre-warming and > by pre-cooling tooth for cold stimulus
Pain producing stimuli: enamel removed
Mechanical stimuli Drying -air -responds to dry absorbent paper Hydrostatic pressure Thermal stimuli Chemical stimuli -dentine sensitive throughout thickness -not all stimuli may result in pain in man
Chemical stimuli producing pain in dentine
Algesic substances: bradykinin, histamine, no pain
Conc. sugar solns, related to osmotic p, pain
Topical application of local anaesthetic, no effect on dentine sensitivity
Nerves in pulp: neuroanatomy
Pulp richly innervated
->900 fibres enter apex of human premolars
-extensive branching of fibres into smaller axons, terminate as free nerve endings (no specific receptors such as found in skin)
Structure similar in man, monkeys, dogs and cats
Which nerves are present in pulp?
Myelinated and unmyelinated axons present
A delta, A beta and C fibres
Conduction velocity of nerves in pulp
Within pulp itself: (A delta and C): 1-34m/s
Outside pulp chamber (A beta, A delta and C fibres): 1-58m/s
Where are A beta fibres found?
Outside pulp chamber, can extend into pulp but conduction velocity decreases with < in diameter
Changes in diameter of nerves in pulp
Smaller in diameter near terminals
Dentinal tubule contents
Inner dentine (innervated)
-odontoblast cell process
-smaller process (nerve?)
-100-200µm
-one pulpal axon may innervate 100 dentine tubules; v high density of free nerve endings
Outer dentine: odontoblast cell process?, but not small process
-not innervated but v sensitive
Denervation studies
2 days after nerve section small processes disappear
12 weeks after nerve section small processes return
Correlation of return of responses of intradental nerves to dentine stimulation
Axonal transport studies
Tritiated proline, injected into trigeminal ganglion, transported along nerves into pulps of teeth and inner dentine
Distribution of lavelled material similar to distribution of secondary processes
Role of odontoblast layer in intradental nerve responses
TEM shows tight junctions between odontoblasts and some terminal axons
Attempts to measure resting membrane potential of odontoblasts show values too low to act as receptor
Pain still felt after odontoblasts have been damaged
Responses of intradental nerves to stimulation
Recordings from single pulpal axons demonstrated:
- stimuli that produce pain in man excite intradental nerve
- 2 classes of neurones identified
- smear layer affects response
Classes of intradental afferent neurones
- Cold sensitive neurones
2. Heat sensitive neurones
Cold sensitive neurones
Short latency response to cooling, also respond to drying, mechanical stimulation of exposed dentine, high conc. solns and pressure changes, also respond to heat
Conduction velocity upper part of range for intradental nerves, including A beta fibres
Heat sensitive neurones
Longer latency response to heating, rarely respond to other forms of stimuli
Conduction velocity lower part of range for intradental nerves
Effect of smear layer
Enhanced response after acid etching, affected by dentine permeability
Hydrodynamic theory: Braennstroem 1963
Fluid movement in tubules leads to mechanical distortion of tissue
Most likely mechanism for dentine sensitivity
Some chemical stimuli are isotonic
All stimuli that cause pain
Except electrical
Can produce fluid movement through tubules
A-unit activation
Cold sensitive
Probably hydrodynamic effects
i.e. displacement of tubule contents leads to activation of cold sensitive neurones
C-fibres
Heat sensitive
Do not respond to stimuli producing fluid movement
Are sensitive to direct heating (longer latency)
Summary: sensitivity mechanism
Displacement of tubule contents leads to activation of cold sensitive neurones
Heat sensitive neurones sensitive to direct heating
‘Receptors’ for both classes situated in inner dentine or outer pulp
Role of odontoblast in receptor mechanism
Dentine hypersensitivity
Exaggerated, trnasient response
Affects up to 57% population
No pathology or dental defect
Dentine hypersensitivity: aetiology
Enamel erosion
Whitening
Recession
Viability of cementum
Dentine hypersensitivity affected by
surface permeability
rapid response
Treatment of dentine hypersensitivity mechanisms
- Reducing dentine permeability (<1µm + no.)
2. Altering ionic environment in tubules
Treaments of dentine sensitivity
Management Desensitising toothpastes Adhesive resins Tannic acid Lasers Ozone treatment
Desensitising toothpastes
Arginine
Stannous fluoride
Bioglass
Adhesive resins
Dentine bonding resins - seal dentine surface
- not fluoride
- limited evidence
Tannic acid
Blocks tubuels
Lasers
Fuse tubules by coagulatin proteins
-limited evidence
Ozone treatment
Removes pellicle and allows remineralisation
Injury to the pulp
Mechanical damage: dislocation of odontoblasts
-dentine does not lose sensitivity
-innervation of dentine not prerequisite for sensitivity
Chemical attack:
-osmotic stimulants produce dislocation: mediated by tubule fluid movement
-direct toxicity: acids and neurotoxins
Correlation between pulp pathology and pain sensations
None
Vasodilation, immune cells, odontoblast distortion
Neuropeptides and toxins released locally
Substance P, CGRP, VIP (neuropeptides)
Neurokinins, cytokines (bradykinin, histamine)
Link with microvascular blood flow
Biochemical markers
More subtle indicators or pain
Coronal injury
Aspiration of odontoblasts
Nerves survive operative procedures and placement of materials
Cervical injury
Calcitonin gene-related peptide (CGRP) fibres proliferate after cervical injury
Relates to developing sensitivity after injury
Severe pulpal injury: local pulpitis
Large areas of SP and CGRP containing fibres sprout near injury site
Tertiary dentine forms
Severe pulpal injury: irreversible pulpitis (Necrosis)
CGRP and sprouting at interface between vital and non-vital tissue
Severe pulpal injury
Nerve fibres proliferate:
-odontoblasts distorted, nerve strectched and stimulated (No correlation with pain and nerve density)
-odontoblasts release NGF on stimulation (6 hours after cavity prep)
Nerves have other functions than pain in tooth pulp: role in pulpal healing, chemotactant, protective
Caries and pain
Nerve trunk increase in SP and CGRP expression
Spontaneous pulpitic pain
High levels of SP and VIP
Use of peptide antagonists
To control pulpal inflammation and pain
Calcium oxalate
closes tubules by remineralisation
-limited/ insufficient evidence
Management of dentine hypersenstivity
Reduction of erosive dietary intake
Gentle brushing
