Orofacial Pain and
Dentistry Management
Attributed to dento-
alveolar and anatomically
related structure disorders
• Hyperalgesia: An increased response to a stimulus that
is usually painful
• Hyperesthesia: An increased sensitivity to a stimulus
that is not painful
• Hyposthesia: A decreased sensitivity to a stimulus that is not painful
• Hypoalgesia: A special case in which pain response to normally
painful stimulus is diminished
• Neuralgia : pain in distribution of a
nerve
• Neuropathy: pathologic change in a
nerve
• Nociorecptors: peripheral receptors
sensitive to noxious (harmful ) stimuli
• vReferred pain: irritation of a certain part
produces pain which is not felt in that part but in
another somatic part that may be a considerable
distance away.
Eg pain that arise from angina pectoris may be not
felt in chest but it is felt in left shoulder
• Radiation pain: Pain is felt both in irritation area
and tends also to spread from the local to the
distance site
Orofacial pain represents one of the most common health problems that negatively affects the
activities of daily living.
However, the mechanisms underlying these conditions are still unclear, and their
comprehensive management is often lacking. Moreover, even if pain is a common symptom in
dentistry, differential diagnostic procedures are needed to exclude other pain origins.
Misinterpretation of the pain origin, can lead to misdiagnosis and to subsequent the pain could
be associated with the hard and soft tissues of the head, face, oral cavity, or to a dysfunction of
the nervous system.
Considering that the origins of orofacial pain can be many and varied, a thorough assessment of
the situation is necessary to enable the most appropriate diagnostic pathway to be followed to
achieve optimal clinical and therapeutic management.
• The most common causes of dental pain are represented by dental caries
or tooth decay.
• Moreover, when untreated, even a simple dental caries can become a
more generalized oral issue, leading to the second group of conditions
most associated with dental and orofacial pain
“An unpleasant sensory and emotional experience associated with
actual or poten- tial tissue damage, or described in term of such
condition”
The obvious relation between a stimulus that causes nerve stimulation
with subsequent sensation of pain led to be classified as a sensation
described in terms of receptors and pathways.
On the other hand, no one can deny the relation of pain and emotional
state.
P(
The neuromatrix is a network of
neurons that is genetically
determined and modified by sensory
experiences.
According to this, pain is considered
an output of the neuromatrix of the
brain to the virtual map of the body
represented on the body surface
known as the homunculus.
The brain will fire this signal
whenever it receives a danger
The neuromatrix concept explains many
different phenomena regarding pain,
such as the absence of correlation
between the degree of tissue damage
and the degree of pain sensation. It also
explains the mechanism of phantom pain
and the mechanism by which stress and
anxiety play a role in chronic
The neuromatrix is a network of neurons, which is
genetically determined and modified by sensory
experiences.
According to this, pain is considered as an output of the
neuromatrix of the brain to the virtual map of the body
represented on the body surface known as homunculus .
The brain will fire this signal whenever it receives a danger
message in case of tissue damage or even by emotional
stress as in the case of chronic pain
Acute vs. chronic pain
In acute pain, the tissue damage and cause
are obvious. Stimulation of nociceptive
receptors occurs due to release of
inflammatory cytokines, and the action of
anti-inflammatory drugs is to interfere with
production of this cytokines .
Dentists and maxillofacial surgeons will train
for diagnosing and managing acute pain.
Chronic pain is a totally different story, and it
is refractory for treatment if it is managed the
same way as acute one. In chronic pain, there
is no presence of acute inflammatory
cytokines, which explains why the use of such
drugs has no/or minimal effect.
The etiology, which triggers the cascade of
central sensitization and activation of the
neuromatrix, is not easy to find in chronic
pain. It is all a suggestion proposed by the
doctor or by the patient himself.
Chronic pain and depression have always
been linked together with a reciprocal
effect that chronic pain induces depression
and depression causes chronic pain
So chronic pain is a result of interacting factors that include the
following:
Genetics, which affect the neurons’ wiring of the neuromatrix of the
brain
Experience, which will modulate the neurons’ connections in the
neuromatrix
Emotional state and sleep quality, a reciprocal relation with chronic
pain
The organic problem as an initiating factor for chronic pain
1.Reffered pain explained by neuromatrix concept
Referral pain is considered one of the causes of misdiagnosis of pain.
Understanding its mechanism using the neuromatrix concept could explain the
confusion of site vs. source of pain.
When we consider pain as an alarming output from the brain, why does the brain send
this alarm to different areas rather than to the area where the danger signal is sent?
At this point, we must differentiate between acute and chronic pain.
In acute tissue damage, pain must be directed to the area where damage happened, and
this is mostly the case, unless there is a missing information about the location of
damaged area; example of this is acute pulpitis where nociceptive receptors send signal
for tissue damage but the lack of proprioception localization receptors result in pain
signal to the teeth sharing the pathway from where danger is coming.
In case of chronic pain, the sustained alarming pain is generated mainly centrally
where the brain chose the areas suspected to be the cause of danger according to
wired neural network determined by genetics and old experience, which is why
there is specific pattern of chronic pain as we noticed in case of pressure on trigger
points area or the fluctuating pattern of pain from one area to another.
The reflex muscular spasm seenint different muscles can be a vicious cycle where
chronic pain causes impaire,d unbalanced movement of the ja,w and the impaired
movement of the jaw causes more strain on the muscle with sustained pain, adding
to this the emotional effect, making the diagnosis difficult
The biopsychosocial mode
Types of orofacial pain
Psychogenic
It is a physical pain pain
caused, increased, or prolonged by
mental, emotional, or behavioral factors.
It is characterized by:
Psychic causes,
No noxious stimulus,
No abnormality in neural structure.
Examples:
1- Burning mouth syndrome.
2- Atypical orofacial pain & atypical odontalgia.
3-Myofascial pain dysfunction syndrome.
Atypical Facial PAIN
CLINICAL FEATURES
"Persistent facial pain that does not have the characteristics of the
cranial neuralgias and is not associated with physical signs or
demonstrable organic causes”
It affects females more than males (19:1)
Common sites : maxilla & tongue.
Pain characters: Chronic, intermittent dull aching , deep, diffuse &
poorly localized so that the patient is unable to define location of
pain.
It gets worse with fatigue and stress, but doesn't interfere with
eating or sleeping.
Responds poorly to analgesics.
The patient usually has depression.
Diagnosis: by exclusion (teeth & oral mucosa are free).
Treatment:
Reassure the patient that no dangerous disease e.g.; cancer.
Patient referral to psychiatric physician is important.
Antidepressant drug and tranquillizers.
Avoid unnecessary extractions.
Re-evaluate the case every 6 months.
Atypical odontalgia
Other names: Idiopathic, Phantom tooth pain
Tooth ache with no detectable cause .
Pain is unaffected by endodontic therapy or
even extraction of the tooth.
Persistent pain in a single tooth or a group of
teeth that exhibits no abnormality on
percussion or pulp testing .
It is a variant of atypical facial pain.
Diagnosis: usually by exclusion
Clinical features:
• More in female 40-50 years.
• It may be associated with migraine headache.
• Constant dull localized pain usually even after
dental treatment.
• Emotional & mental problems.
• Patient visit more than dentist for pain.
TREATMENT:
Antidepressants.
Patient reassurance.
Burning Mouth Syndrome
(Glossodynia)
Clinical features:
The patient suffering from
burning sensation of mucosa
without definitive causes
Pain dose not follow anatomical
pathway
No lab. Findings
No neurological findings
• Women experience symptoms of BMS seven times
more frequently than men.
• Pt. complain at tongue (main site), lips &cheek.
• Burning intermittent or constant pain.
• Diffuse pain, patient can not identify the site of the
pain.
• Pain is relieved by eating drinking or chewing.
• Normal oral mucosa or mild atrophic.
• Depression symptoms, lack of appetite, insomnia
Etiology:
Systemic causes:
Local causes:
1. Deficiency states (e.g.; Anemias)
1- Muscle
2. Hormonal tension (especially
disturbance with ↓ vertical
(postmenopausal)
dimention)
3. DM
2- Allergic
4. Systemic reaction
disease (e.g; Blood Ds. &
3- Dry mouth
malignancies)
5. CNS &irritation
4- Local psychological problems
& Chronic (e.g.;
rubbing of mucosa
Depression
5- Oral & cancer
candidosis phobia)
(especially atrophic forms)
6. Chronic alcoholism.
Diagnosis:
1-Exclusion of possibility of any oral lesion
2-Careful clinical examination & lab investigation to detect undiagnosed
anemia
3-If it is unilateral, examine the cranial nerves.
Q- what are the most common causes of mouth burning
sensation?
1- Geographic tongue
2-Fissured tongue
3-Atrophy of tongue coating
4-Viral infection
5-Fungal infection
6-Anemia
7-Avitaminosis
8-Erosive lichen planus
The term TMDs is an umbrella
term involving a group of
Temporomandibular dysfunction/disorders
conditions affecting the
masticatory muscles, TMJ/TMJs
and associated structures
a. Disorders of the joints , including disc
disorders
b.Disorders of muscles
c. Headaches associated with TMD
The main complaints of TMD patients are pain,
limitation of the mouth opening, and clicking.
In these complaints, pain is the main cause for
the patient to seek treatment .
People with clicking without pain are not
bothered by it. .
TMD symptoms
• Painless clicking during opening
• Intermittent locking with limitation of mouth opening
to finger breadth and accompanied by pain
• Limitation of opening with pain with history of the
previous symptoms
• Limitation of the mouth opening without history of
previous symptoms
• Clicking at the end of opening and the beginning of
closure
There are several supposed methods for management of TMD.
This includes different surgical procedures, considered as invasive
irreversible non-conservative methods.
Other methods like occlusal splints, occlusal adjustment,
physiotherapy, psychological treatment, and injections (joints or
muscles) are consideredconservativee.
Tooth grinding and some types of occlusal splint are also considered
non-inva- sive methods, but they are irreversible
The recommended policy is to try conservative method first for about 6 months; if no
improvement, then the last resort is surgical interference.
On what basis the 6 months was chosen?
What if the surgical interference does not also improve the condition?
The lack of rational guidelines for TMD leads to every doctor choosing the method of
treatment according to his own beliefs or specialty
Acute pain cases, whether it is muscular or joint, are
straightforward cases to manage as the cause and effect are clear
In chronic pain cases, there are no obvious etiological factors, and all explanations of
pain are based on assumptions.
Brain activity is considered the main factor for chronic pain in the absence of tissue
damage.
In chronic pain, the wired area of the brain becomes sensitized (central sensitization).
Brain reprogramming should be the main step of treatment in any case of chronic pain,
including TMD patients.
People with chronic pain are trapped in their thoughts, worrying about the
future; they think about how they will go on with this kind of dysfunction,
unable to chew,
unable to speak, and even unable to do simple tasks like yawning.
They use their mouth, expecting pain and more tension in the muscles.
The subsequent result is a decrease in the mouth opening. The problem of
negative thoughts with their reflection on
body function is more than a mental process, but about a wired neural
network in the brain generating these thoughts and pain.
So, the question is how to stop this neural network from firing?
This process can be done in different ways. Mirror therapy has been used
for chronic and phantom pain conditions.
Another method is known as pain reprocessing therapy.
We applied those principles by using the mirror and engaging active
patient brain feedback during mouth opening with gradual stretching of
the contracture muscles, mainly masseter, medial pterygoids, and
temporalis.
After 2 weeks of brain reprogramming exercises, the pain and mouth
opening improved.
This method of brain reprogramming exercise is continued by the
patient at home after being sure that the patient has understood how to
perform it exactly.
1.Protocol for managing TMD patients
After careful history and clinical examination of the patient ensuring no organic pathological
conditions or sleep breathing disorders, the following protocol is applied:
a. Patient education, regarding the difference between acute and chronic pain, the role of the
brain in chronic pain and brain sensitization, and how abnormal mandibular movements,
habits, or body posture play a role in precipitating and aggravating the condition.
b.Training the patient on how to use the mirror for brain reprogramming exercise and follow-up
after 2 weeks. Most of the patients who follow the rules show improvement.
a. Patient referred to physiotherapy in cases needs assistant exercise or involvement of
other body muscles like neck, shoulder, or gross postural adjustment.
b.Patient with advanced degree of depression refers to psychotherapy in addition to brain
deprogramming program.
c. Stabilizing appliance therapy is used only in cases of unstable mandibular resting
position or occlusion.
d.Botox injection is used if there is hypertrophy of masticatory muscles, espe- cially
masseter muscle
e.Surgical interference is only applied in the form of TMJ replacement where severe
osteoarthritic degenerative changes occur. Most of these cases have undergone disc
removal operation in the past.
Temporomandibular Joint (TMJ) Dilemma: How to Resolve?
DOI: http://dx.doi.org/10.5772/intechopen.1009276
Neurogenic pain
Neurogenic pain
Discomfort that results within the nervous system
without any noxious stimulus, due to:
Neuropathy:
It refers to a functional abnormality of
nerves that may be due to: Neuritis
resulting from inflammatory change of
the nerve, that causes burning
sensation. Neuralgia:
It refers to pain along the course of
the nerve caused by vascular spasm
and CNS diseases, (poorly localized, &
of electric shock like pain).
Compare BETWEEN NEURALGIC & NEUROPATHIC PAIN.
Neuropathic pain tends to be:
• Constant pain
• It has a burning quality
• No presence of trigger zones
However, neuralgic pain is characterized by:
• Paroxysmal pain along the course of the nerve
• It has an electrical nature
• Presence of trigger zonese
Neurogenic pain
Paroxysmal Non paroxysmal
1. Trigeminal neuralgia 1. Peripheral neuritis
2. Glossopharyngeal n. 2. Post herpetic neuralgia
3. Occipital neuralgia. 3. Post traumatic pain
4. Atypical odontalgia
5. Bell’s palsy
6. Trotter’s syndrome
7. Frey’s auriculo-temporal
syndrome
FACIAL NEURALGIAS
The classic neuralgias that affect the craniofacial region are
characterized by:
1. Pain-free periods
Brief episodes between attacks; & Trigger zones
of shooting, often 2. Refractory periods on the skin or
electric shock–like immediately after mucosa that
pain along the an attack, during precipitate painful
which a new attacks when
course of the episode cannot be touched.
affected nerve triggered
branch.
Facial (CN VII)
Bell’s Palsy
peripheral paralysis
It is a peripheral facial weakness of unknown etiology affecting any age
group of either sex.
7th cranial nerve is enclosed in a closely fitting bony canal from the
geniculate ganglion to stylomastoid foramen.
The content of the canal is slightly bounded by fibrous connective tissue
sheath which is slightly bounded by a fibrous connective tissue sheath
adheres to the epineurium
Blood Supply: petrosal artery branch of the middle meningeal supplying
the horizontal portion and geniculate ganglion, stylomastoid artery
branch of external carotid supplying the lower part of the vertical
portion
Pathophysiology
• Idiopathic and there is no local or systemic cause can be
identified.
• Immunolgical mediated
• Trauma
• Associated with viral infection like Herpes simplex
Pathogenesis of Bell’s palsy
Middle External carotid
meningeal
Petrosal artery Stylomastoid
artery
Geneculate
ganglion
Facial nerve Fibrous C T
Stylomastoid
foramen
Inflammation of Facial
nerve inside the canal
demyelination & edema
loss blood
• Vasospasm occurs in the canal producing ischemia.
• Prolonged Vasospasm leads to edema, and the
underlying bony canal it causes compression.
• Further reduces the blood supply to the nerve,
which aggravates the ischemia
• If untreated necrosis and fibrosis may result
• The degree and duration of ischemia determine
the course and prognosis
Clinical feature
Rapid onset or preceded by pain along the
angle of the jaw
Patient unable to : raise eye brow, whistle, and
close the eye , retract the angle of the mouth
Change in facial expression
Retract the angle of the mouth unilateral talking
and smiling deviation to the unaffected side
The patient can not hold liquid in mouth saliva
dribbles, weakness of buccinator muscle
Swallowing is not affected but taste may be
diminished
• Remarkable changes in facial expression
• Loss of taste sensation on the ant two third of the tongue with
reduce salivary secretion due to involvement of the chorda tympani
• Eyelid drooping and difficulty closing one (or both) upper eyelids
are classic findings in Belle’s palsy.
• Asymmetric or incomplete smiles, decrease in forehead wrinkling,
nasal stuffiness, and mild difficulty with speaking are also
common signs.
• Frequent early symptoms include abrupt onset of dry eye and
tingling around the mouth, with progression to more complete
facial palsy occurring within one to several days.
Treatment
Analgesic for pain
Eye shield eye baths
For paralysis
ACTH given early and IM
1-5 days 80 units
6th day 60 units
7th day 40 units
8th day 20 unitsa
9-10th day 10 units
Predinison high dose for 5 days the tailing off for 5 days
• Systemic corticosteroids within the first few days after the onset of
paralysis.
• Combining steroids with antiherpetic drugs such as acyclovir may
decrease the severity and length of paralysis.
• It is also helpful to protect the eye with lubricating drops or ointment
and a patch if eye closure is not possible.
• In chronic condition, surgical decompression of the nerve in the
stylomastoid canal is effective
Dental implication difficult to maintain oral hygiene and food is usually retained in
the buccal and labial vestibule
The skin at the corner of the mouth becomes wet by saliva and become susceptible
to candidal infection
To restore facial appearance
Edentulous patient build up premolar canine region
Dentulous patient hooks are cemented to full crowns on premolar region to hold
the angle of the mouth
Major Neuralgia
Trigeminal neuralgia
(Tic douloureux)
It’s a rare disease characterized by:
It ‘s one of common cranial neuralgias
• Electric shock like very severe sharp lancinating, shocking paroxysmal
unilateral pain involving mainly maxillary, mandibular division of
trigeminal nerve
Pain is brief lasts seconds to minutes, precipitated by touching trigger
zone within trigeminal territory chewing talking or swallowing
Etiology and Pathogenesis
Unknown may be due to
Idiopathic trigeminal neuralgia:
-vascular compression of the trigeminal ganglion by nearby vessels (cerebral arteries)
-Progressive degeneration and demyelination of the trigeminal nerve leads to decrease in
the ratio of myelinated to unmyelinated nerve fiber and so may alter the central sensory
processing
-stretching of the nerve over the petrous part of temporal bone which is larger on the
right side
Secondary trigeminal neuralgia:
Secondary to CNS lesion tumor, vascular malformation
Multiple sclerosis demyelination of axons within CNS. Its
etiology is not clear and the pain is commonly bilateral
In MRI contact between a blood vessel and the trigeminal
nerve root was much greater on the affected side
Trigger zone (area)
Patient point to the area with forefinger without touching it (half an inch
finger sign to avoid initiation of pain) nasolabial fold& corner of the lip is
the most common sites.
Pain free intervals between attacks is characteristic where the patient is
completely asymptomatic. After each attack there is usually a refractive
period during which stimulation of the trigger zone will not induce the pain
The attack ranges from several per day to few per year
It is common in women at age 50-70 years
If it occurs in younger individuals suspect underlying lesion as; tumor,
aneuresm or multiple sclerosis
Clinical features
-Sharp lancinating unilateral electric shock like pain along the course of the
nerve
-Pain is brief lasts seconds to minutes
- Appears and disappears suddenly
- Episodic attacks ranges from several per day to few per year
- Between the intervals the patient is completely free
- precipitated by touching trigger zone within trigeminal territory chewing
talking or swallowing
- After each episode, there is refractory period where stimulation of trigger
zone will not induce pain
• The maxillary branch is most affected followed by mandibular
then ophthalmic branch.
• Shaving, showering, eating or even exposure to air or cold can
trigger a painful episode, patient tend to protect the trigger
zone
• Intraoral trigger zone cane be misdiagnosed with dental
disorders
• It may mimic pain of cracked tooth, DD was reached if gentle
touch to T.Z will precipitate pain
Unilateral distribution Trigeminal nerve branches
Pain in TN is
precipitated
by light
touch on a
“trigger
zone”
It may be
present on
the skin or
mucosa
within the
distribution
of the
involved
nerve
branch.
Diagnosis
• History of pain& trigger zone
• Cranial nerve examination may be normal in idiopathic pts,
but sensory/ or motor changes observed in tumor or CNS
involvement
• LA block will identify the specific nerve involved
• Neurologic examination to rule out tumors or multiple
sclerosis
• MRI
Management
I-Conservative drug use: II-Surgery:
It is done in cases refractory to
medications in which continuous pain
1. Anticonvulsants (e.g.; phenytoin & rather than separate attacks.
Gabapentin ).
2. Carbamazepine (Pts. Should be 1. Alcohol injection in nerve or
monitored for hepatic, renal fuctions ganglion.
& hematologic disorders). 2. Cryosurgery for peripheral nerve.
3. Baclofen (used alone or combined 3. Sectioning of part of the nerve
with drug no. 2). (permanent numbness may result).
4. Injection of LA in the trigger zone
Notice that; maybe also effective.
Drug therapy should be slowly 5. Percutaneous radiofrequency
withdrawn if a patient remains pain thermo-coagulation of the nerve,
free for 3 months. is recently applied.
percutaneous radiofrequency thermo-coagulation of the
trigeminal nerve.
Clinically, The neuralgic stabbing pain can mimic
the pain of A cracked tooth, especially if the
trigger zone is intra-oral …
HOW CAN WE DIFFERENTIATE?
Pain of A cracked tooth
The stabbing pain
• TN pain will be triggered by • Pressure on the tooth is required
touching the soft tissue. to cause pain from a cracked
tooth (stimulation).
• Just after an attack, there is a
refractory period when touching • Pain is always precipitated by any
the trigger zone will not stimulation of the tooth.
precipitate pain (pain free).
• A local cause (affected tooth)
• There may not be any dental should be present.
problem.
• Neurogenic pain • Somatic pain
Post Herpitic Neuralgia
The most common complication of shingles.
It causes a burning pain in nerves and skin.
The pain lasts long after the rash and blisters of shingles go
away.
The risk of postherpetic neuralgia rises with age.
Prophylactic Gabapentin,
Treatment
Antidepressants