Neurophysiological

mechanisms of TMD
S.C.Ahn

Introduction
1.The charcteristics of peripheral
nociceptors.
->the reason why inflamed tissues
become sensitive to palpation and
movement.
2.Central nociceptive neurons.
->the nature of the pain.
3.Functional changes in central reflex.
->the effect of pain on movement.

Properties of pain receptors in

muscles and joints

Nociceptors ->unencapsulated nerve endings from

small myelinated(A-delta fiber)
unmyelinated(C-fiber)

some of these receptors begin to fire when

noxious stimuli or algesic chemical
another group of these receptors become
sensitized to mechanical stimuli,and respond to
previously innocuous pressure

Properties of pain receptors in

muscles and joints

Properties of pain receptors in

muscles and joints

Peripheral changes
Sensitization of nociceptive ending :
defence
mechanism that protects injured tissues from
repeated injury by providing a sharp reminder to
cease movement or contact

Central changes
Deep pain(poor localization & referral)
Hyperalgesia
-->
these have more to do
with central changes

Properties of pain receptors in

muscles and joints
Noxious
stimuli

Tissue

mast cells
basophils
Endogenous
substances

macrophages
platelets
endothelial cells

Properties of pain receptors in

muscles and joints
some of these endogenous substances
produce pain when they are applied locally
(histamine, bradykinin, serotonin,
potassium)
other substances facilitate the pain evoked
by stimuli, but themselves are relatively
ineffective in evoking pain (prostaglandins)

Roles of sensory & sympathetic

neurons in inflammation
Antidromic stimulation of sensory nerves
causes vasodilation & inflammation in the
areas that they innervate
---->Neurogenic inflammation
The branches of primary afferents that
ramify in tissues outside the site of injury
--->a essential role in the spread of
inflammation

Roles of sensory & sympathetic

neurons in inflammation

Roles of sensory & sympathetic

neurons in inflammation
This process is associated with peripheral
spread of the zone of hyperalgesia or
tenderness of injury
Hyperalgesia
1)primary hyperalgesia : in the primary zone of
injury
2)secondary hyperalgesia : in the secondary
zone that surrounds the primary site

Roles of sensory & sympathetic

neurons in inflammation

The release of neuropeptides from the

terminals of thin afferent fibers is the
critical event in neurogenic inflammation
(sustance P, neurokinin A, somatostatin,
Calcitonin Gene-Related Peptide,
Vasoactive Intestinal Peptide)

Roles of sensory & sympathetic

neurons in inflammation
It is an important transmitter in the
nociceptive pathways because it excites spinal
cord and trigeminal nociceptive neurons.
Sunstance P has many actions : vasodilation,
increases vascular permeability, activate
lymphocyte, initiate pavementation of
lymphocyte, release of histamin and 5hydroxytryptamine(5-HT) from mast cell

Roles of sensory & sympathetic

neurons in inflammation
These promote both vasodilation and
vascular permeability and increase the rate
of release of substance P.
Neural mechanism for suppressing
neurogenic inflammation :
second population of primary afferents
containing somatostatin which inhibits the
liberation

Roles of sensory & sympathetic

neurons in inflammation

Neurogenic effect in inflammation

inflammation is greatest in the joints that have
the highest levels of substance P
When rats were treated systemically with
capsaicin, which destroys unmyelinated
afferent fibers and depletes substance P, they
were protected against the experimental
arthritis.

Roles of sensory & sympathetic

neurons in inflammation

Neurogenic effect in inflammation

in humans gold has been used for many years to treat
rheumatoid arthritis,is now known to be a selective
neurotoxin that attcks unmyelinated nerve fibers

Local microvasculature and the sympathetic

efferent fiber are important in inflammation.
Substance P released from afferent terminals at
the site of injury and in the secondary zone acts
on the blood vessels

Roles of sensory & sympathetic

neurons in inflammation

The substance P causes sympathetic

neurohumoral agents to bo secreted by
sympathetec terminals inderectly via
histamine :
norepinephrine->vasoconstriction
prostanoid PGE2->vascular permeability

Roles of sensory & sympathetic

neurons in inflammation

Nociceptive afferents increase the release of

substances from sympathetic terminals
substance P-containg terminals of sensory neurons
innervate sympathetic ganglia
there are reflex connectons between primary
afferents and sympathetic preganglionic neurons that
aldo lead to increased sympathetic tone.

Stress, which increases sympathetic activity,

exacerbates the symptoms of TMDs

Central mechanisms
The spinal cord dorsal horn and trigeminal
subnucleus caudalis are key structrues for pain
perception. They contain neurons with several
different types of somatosensory receptive fields.
Low-Threshold mechanoreceptive(LTM) neurons.
:
Nociceptive specific(NS) neurons :
Wide dynamic range(WDR) neurons :

Central mechanisms
WDR & NS neurons code the intensity and
spatial localization of noxious stimuli. Many
neurons of all three types project to higher
centers and contribute to sensory perception.
A characteristic of many spinal & trigeminal
WDR and NS somatosensory neurons
transmitting deep nociceptive information is that
they receive additional inputs from afferents
supplying other tissues

Central mechanisms

Extensive convergence and large

mechanoreceptive fields are typical of
myofascial or TMJ-activated WDR and NS
neurons in subnucleus caudalis. These
features contribute to the poor localization,
spread and referral of pain that are
characteristic of pain conditions involving
the TMJ and associated musculature.

Central mechanisms
Poor localization

Extensive
convergence

Referral of pain

Spread of pain

Central mechanisms
Central sensitization of spinal dorsal horn
nociceptive neurons can occur
Injection of algesic chemical into muscle or
localized inflammation can result in change in
neurons of the spinal dorsal horn and primary
somatosensory cortex.
Their responsiveness to afferent inputs is
enhanced, not only from the site of inflammation,
but also from other tissues.

Central mechanisms

Hyperalgesia
Peripherial sensitizaton
Hyperalgesia
Central sensitization

Central mechanisms

Responsiveness

Central sensitization

is enhanced
Spinal dorsal
horn

Localized
inflammation

Thalamus
Primary
somatosensory
cortex
Hyperalgesia

Central mechanisms
These process may influence the cutaneous as
well as the deep receptive field properties of
central spmatosensory neurons
Not only more responsive to gentle movement
of the inflamed site, but some also show
prolonged changes in receptive field size.
C-fibers appear to be especially important for
inducing these effects.

Central mechanisms

The remarkable properties of trigeminal

nociceptive neurons, and in particular the
enhanced excitability that follows the
stimulation of small-diameter afferent fibers
from muscle, joints and other deep tissues,
appear to contribute to the tenderness and
hyperalgesia, as well as to the spread and
referral of pain , that characterize conditions
such as TMD.

Central mechanisms
The cause of the pain that is the primary sign of
the TMD is still not known.
It is likely that many of the neural mechanisms
are important in TMJ arthritis and that they will
later be linked to myofascial pain.
1)neurogenic inflammation
2)peripheral sensitization
3)central sensitization

Central mechanisms

The relationship between pain

and muscle dysfunction

Sustained muscle hyperactivity in the

development and persistence of TMD pain is not
a factor in the large majority of cases.

TMD is separated into distinct

1)Myogenous
2)Internal derangement
3)Arthritis

The relationship between pain

and muscle dysfunction

The ability of patients with these conditions to

move the jaws is abnormal. This can be caused
by mechanical impediments to movement and be
related to the presence of pain
At past, it is thought that the soreness and
tenderness lead to overwork and fatigue, and
muscle hyperactivity causes pain, and that pain in
its turn promotes hyperactivity -->a chronic
vicious cycle

The relationship between pain

and muscle dysfunction
Muscle
hyperactivity

Functioning
abnormally

Pain

Chronic vicious cycle

The relationship between pain

and muscle dysfunction

It is certainly true that heavy exercise can

lead to microtrauma in muscles and
connective tissue. This is followed by pain
that peaks in about 24hours.
--->Post-Exercise Muscle Soreness(PEMS)

However, pain interacts with the neurons that

program movements.

Postural activity in TMD

It was accepted for a long time that people
suffering from TMD had an abnormally high
level of postural activity in their jaw closing
muscles, and that this was the cause of fatigue,
ischemia and pain.
In EMG activity of the masseter and temporalis
muscles of TMD patients and people without
pain, the average activity in the patients was a
few millivolts higher than normal.

Postural activity in TMD

It seems a little extravagant to label such
small increases hyperactivity, because they
represented only 1~2% of the maximum
output of the muscle.
These small differences between the patients
and the other proups were due to other factors
that were not controlled in the experiments,
such as sex, age and prevalence of bruxism

Postural activity in TMD

Chronic bruxers have higher resting activity

than non-bruxers, presumably because their
jaw muscles are relatively hypertrophied,
there is no difference between the resting
activity of bruxers who report pain and those
who do not. The evidence does not support
the idea that there is a systematic increase in
the postural activity of muscles in TMD.

Biting force
Chronic pain patients cannot exert maximal force.
The maximal biting force of TMD patients is
significantly less than controls.
Biting force increased over time as pain fell.
The pain does not even have to be associated with
muscles or joints to cause a fall in bite force. For
example, the bite force after extraction was lower
and that there was a weak inverse correlation with
pain intensity

Voluntary jaw movements and

mastication
Pain often changes movement.
TMD patients cannot open their mouths
widely without pain
The restriction on movement must rarely be
structural, because the TMD subjects could
open an average of more than 7mm more if
they were encouraged or assisted.

Voluntary jaw movements and

mastication
Hyperalgesia and tenderness cause most TMD
patients to reduce the amplitude of voluntary
movements so as to avoid pain, it also seems
that unconscious reflexes, heightened by the
peripheral and central sensitization, participate.
Jaw-closing muscles were more active in TMD
patients than in controls during the jaw-opening
phase of mastication.

Voluntary jaw movements and

mastication

The mean activity of the masseter and

temporalis muscles of individual TMD
patients is significantly greater during the
jaw-opening phase of painfl masticatory
cycles than during pain-free cycles.

Voluntary jaw movements and

mastication
Pain in the masseter muscle :
1)A decrease in the velocity and amplitude of
jaw movement
2)The activity of masseter muscles are less
active
3)EMG of the masseter become more active
during jaw-opening

The pain-adaptation model

Pain has a similar effect on muscle activity
throughout the body.
Vicious cycle theory has been rejected
Pain-adaptation model proposed to explain the
effects of pain on motor activity.
It incorporates how sensory-motor interactions
take place, and it can account for the changes
in motor patterns that accompany chronic pain.

The pain-adaptation model

Pain in a body part causes agonist muscles to

become less active and antagonist muscles to
become more active than normal

A decrease in the amplitude and speed of

movements, which probably reduces the chance of
aggravating the injury and therefore aids healing.

The pain-adaptation model

At least, part of the effect of pain is
involuntary.
Pain can change movements by acting at the
level of the brainstem or spinal cord.

Summary

Inflammatory processes, the peripheral

sensitization of muscle and joint
nociceptors, and the central sensitization of
the nociceptive neurons in the spinal cord
and brainstem is important for pain on TMJ.

Summary

The properties of the peripheral and central

neural elements can explain many of the
signs and symptoms of TMD, including the
tenderness the poor localization, spread and
referral of pain, as well as the limitation of
jaw-opening and slowing of movement

Reference
George A.Zarb. Gunnar E.Carlsson.
Temporomandibular joint and masticatory
muscle disorders. 158-207
Epker J.et al. A model for predicting
chronic TMD : practical application in
clinical settings. J Am Dent Assc. 1999 Oct:
130(10):1470-5

Wight EF. Referred craniofacial pain patterns

in patients with temporomandibular disorder.
J Am Dent Assoc.2000 Sep:131(9):1307-15
Maixner W.et al. Sensitivity of a patients with
painful temporomandibular disorders to
experimentally evoked pain: evidence for
altered temporal summation of pain.
Pain..1998 May:76(1-2):71-81

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