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 DEFINITION

The most recent definition of pain,

produced by task force on Toxonomy of the
international association for the study of
pain (IASP) is'
An unpleasant sensory and emotional
experience associated with actual or
potential tissue damage or described in term
of such damageð
 Incidence of Pain :-

According to Cohen ± it was found

that 21.8% of adult in the United States
experience orofacial pain symptoms
within 6 months of study. The most
common pain was toothache, which was
estimated to have occurred in 12.3% of the
population
Äactors influencing behavior responses
elicited by the painful stimuli are:
Physical
Psychological
Social factors.
 PAIN PATHWAYS
Detection of Pain




    
    


 
      
   
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 Pain Receptors :-

Bare nerve ending serve as pain

receptors whereas other cutaneous
receptors when stimulated
excessively may cause pain. Ärom
tooth, pain sensation is carried by
A delta fibres and C fibres.
 A-Delta Äibres :-
These are myelinated, relatively large fibres,
with fast conduction velocities. They enter the
root canal and divide into smaller branches,
coursing coronally through the pulp. Once
beneath the odontoblastic layer, the A- delta
fibers loose their myelin sheath and
anastomose in to a network of nerves referred
as the plexus of Raschkow
 This circumpulpal layer of nerves sends free nerve
endings on to and through the odontoblastic cell
layers, extending up to 200um into the dentinal
tubules, while also conducting the odontoblastic cell
process. Disturbances of pulp dentinal complex in a
vital tooth initially affect the low thresholds A- Delta
fibers.
Nociceptive signals, transmitted through fast
conducting fibers are perceived as a quick,
sharp, momentary pain.
The clinical symptoms of A delta fiber
pain signify that the pulp dentinal
complex is intact and capable of
responding to an external disturbance
 A-Beta Nerve Äiber :-
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 C-Nerve Äibers
Äibers:: -
Small, unmyelinated nerves that innervate the pulp.
They are high threshold fibers, course centrally in the
pulp stroma. The pain associated with C-fiber is dull
and poorly localized. C fiber have a high threshold and
can be activated by intense heating or cooling of the
tooth crown or mechanical stimulation of the pulp.
Once activated, the pain initiated by C fibers can
radiate to anywhere in the ipsilateral face and jaw.
 Processing :-
Pain is perceived and recognized in the cortex,
because of incoming nociceptive input. The primary
afferents neurons enters the brainstem at the level
of the pons. The cell bodies of the trigeminal nerve
are located in the gasserian ganglion. Trigeminal
brain stem sensory nuclear complex can be
separated in to trigeminal main sensory nucleus
and trigeminal spinal tract nucleus, also Known.
as nucleus of desending tract
The spinal tract nucleus is composed of
three separate nuclei processing from
rostral to caudal direction, subnucleus
oralis, interpolaris and caudalis.
Caudalis is located in the medulla, at
times extending to the level of C2 or C3
and is the principal brain recognizing
site of nociceptive information arising
from the orofacial region.
 Both incoming nociceptive signals to
subnucleus caudalis and projecting
signals on their way to thalamus can be
modified by descending nerve fibers from
higher levels of CNS or by drugs.
 Convergence of Neurons within
Trigeminal Spinal Tract

Nerve fibers from different areas in

the mouth may all synapse on another
neurons in the spinal cord, thus sending
a signal to the brain. Due to convergence
factors, the brain may experience more
difficulty in localizing the pain.
Trigeminal Second Order Neurons 

These second order nociceptive neurons

in Nucleus caudalis can be classified in to
two main categories

Nociceptive specific (NS) neurons

Wide dynamic range (WDR) neurons
 NS neurons respond exclusively to
noxious stimuli i.e heat and pinch. Their
receptive fields are small and may
include skin and muscle.
WDR neurons are excited by both
noxious stimuli and non-noxious tactile
stimuli over a wide range of intensities.
Their field are large.
 In addition nucleus caudalis also
contain low threshold
mechanoreceptors (LTM) which are
activated by light tactile stimuli.
Axon from the spinal nucleus cross
to the opposite side and ascend to
nuclei of thalamus
 A delta fibers from pulp synapse in
the lamina-I area of SC and C fiber
synapse in the lamina II and III
areas. A-delta fiber pass to the
thalamus directly, by way of the
neospinothalamic tract and is said to
carry fast pain.
The 2nd order C-fiber neuron carries impulse
by paleospinothalamic tract. This passes
through the reticular formation, where the
impulse are influenced by many modulator
interneurons before they reach the thalamus,
this type of pain is called slow pain
 Third Order Neurons :-
The next major synaptic connection in
pain transmission is in the thalamus,
where axon traveling in the
trigeminothalamic tract synapse with
third order neurons.
Thalamus act as primary relay station
between the brainstem and different parts
of somatosensory cerebral cortex.
 Äor all nerve pathway from thalamus to
cerebral cortex, there are reciprocal
connections from the cortex to the thalamus.
In the thalamus, action potential will be
subjected to extensive processing through
interactions among its various nuclei and by
inter connections with the limbic,
hypothalamic and cortical regions of the
brain.
 Pain Modulation :-
Definition
Human nervous system has an inherent
ability to alter the intensity of nociceptive
signals and reduce the pain experience.
The key pathway start in the pre-aqueductal
gray region in the mid brain. Signals from
this area of the brain descend to the spinal
cord dorsal horn where further neuron inter
connection serve to reduce the transmission
of the primary pain signal.
This modulation also takes place within the
spinal trigeminal nucleus.
 Pain Perception :-

The final process of perception of

pain take place in the posterior
parietal cortex of the brain.
ð

Cranial and cervical nerves that provide

somatic and visceral sensation to the
orofacial area
area

1.Trigeminal Nerve
2. Äacial Nerve
3. Gloss pharyngeal Nerve
2. Vagus Nerve
3. Cervical Nerve-2
4. Cervical Nerve-3.
 MEASURMENT OÄ PAIN AND
DISABILITY:--
DISABILITY:
There is no simple method of measuring
pain. In assessing OÄP patients, pain
intensity, emotional distress, and
associated disability are important and
cannot be captured with one scale or
questionnaire. Pain intensity can be
measured by using rating such as a visual
analog scale (VAS).
 A VAS consist of a 10cm line on which
0cm is ³no pain´ and 10cm is pain as bad
as it could be´. The patient marks the
point along the line that best represents
his or her pain and score is measured
from the no pain end of the scale. Visual
analog scale are sensitive to treatment
effects, can be incorporated into pain
diaries and can be used with children.
 MC Gill Pain Questionnaire (MPQ)
It is used to measure the motivational,
affective and the cognitive evaluative
qualities of pain, in addition to the sensory
experience. It provides quantitative
measures of clinical pain that can be
treated statistically.
The questionnaire enables patients to choose from
78 adjectives that describe pain, the form is
designed to assess the sensory (Group-10),
affective (Gp-11-15) and evaluative (Gp 16)
dimensions of pain and to produce a pain rating
index. VAS and numeric scales require no
specific forms and are easily administered. The
MPQ is available from the (IASP) and is used in
pain clinics and by clinicians focusing on pain
management.
 |

 
 

 





 





 









 




 

 
 
 


 








 

  

 PAIN MEDIATORS
Nociceptors can be activated by intense
thermal and mechanical stimuli, noxious
cold and noxious chemicals. They are also
activated by stimulation from endogenous
algesic chemical substances (Inflammatory
mediators) produced by the body in
response to tissue injury.
Pain mediators include:

bradykinin (BK)
potassium (K+)
histamine
serotonin
arachidonic acid and others
 
 
 
 



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General Origin of Pain Quality of Pain

Classification
Extra cranial Craniofacial region Varies
Structure
Referred pain from Distant organs and Aching and
remote pathologic structures pressing
sites
Intracranial Brain and related Varies
pathosis structures
Êeurovascular Blood Vessels Throbbing,
pulsing or
pounding
Êeuropathic Sensory nervous Shooting, sharp,
system burning pain

Causalgic Sympathetic Burning

nervous system
Muscular Muscles Deep aching, tight

Unclassifiable Etiology unknown Any

 


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Typical Pain Disorders Atypical Pain Disorders

Periodontalgia
Êeuralgic (trigeminal neuralgia)
Vascular (migraine, cluster
headache)
Otic (Otitis media)
Sinus (Sinusitis)
Heart (cariogenic jaw pain)
Salivary gland Disorder
Musculo skeletal disorder
Causalgia
Reflex sympathetic dystrophy
Atypical facial pain
Phantom tooth pain
Êeuralgia including
cavitational osteonecrosis
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223
 



 

Etiology:
Precise cause is unknown. Evidence indicates it
may be due to vascular compression of gasserian
ganglion, viral infection of neuron or nerve
sheath may be there.
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