For undergraduate dental students from this presentation you can get the primary understanding of what the pain related to the oro facial region

1. OROFACIAL
PAIN
Thilanka Umesh Sugathadasa

2. 1
Physiological basis for the pain
Definition for the pain by IASP
Pain is an unpleasant sensory or emotional experience associated with actual or potential
tissue damage, or describe in terms of such damage.
Nature of pain
 Subjective Modified by the Cultural/ Behavioural/ Personality/ Developmental factors
 Protective
 It is a symptom
 Associated with crying/ sweating/ BP/ HR increase
 Having dual nature
Fast pain Slow pain
 Acute
 Pricking type
 Short duration
 Well localized
 Thin myelinated A delta nerve fibers are
involved.
 Chronic
 Throbbing type pain
 Poorly localized.
 Long duration
 Unmyelinated c nerve fibers are involved
Classification on the basis of pain
 Nociceptive pain- Stimulation of the nociceptors due to
Chemical
Thermal
Mechanical events that has the potential to damage the body tissues.
Pain
Duration(Acute/ Subacute &
chronic)
Anatomy(Headache/
chest pain)
Mechanism
somatogenic (axis i)
Nociceptive
Superficial
Somatic
Deep
Somatic Visceral
Neuropathic
Episodic Continuous
psychogenic (Axis ii)
Quality(Sharp/
burning/ tight)

3. 2
 Neuropathic pain- damage to the nerves system itself cause the neuropathic pain
Two types
- Peripheral neuropathic pain (Damge to the peripheral nerves)
- central neuropathic pain(Damage to the brain/ brain stem/ spinal cord)
 Above two are mainly somatogenic pain, psychogenic pain is that caused, increased or
prolonged by Mental / Emotional/ Behavioural factors
Superficial somatic pain
1. Cutaneous pain
2. Mucogingival pain
 Caused by mainly injury to skin or superficial tissues.
 Cutaneous nociceptors terminates just below the skin & They are present in higher
concentrations so produse fast pain. Due to those reasons most of the time cutaneously minor
wounds & minor burns(1st
degree.) present,
 No CNS excitatory effects.
 LA at the site can abolish pain.
Deep somatic pain
1. Musculoskeletal pain
- Periodontal pain
- Osseous pain
- Muscular pain
- TMJ pain
- CT pain
 Most of the time dull pain
 Originates from ligaments, Tendons, Muscles, Bones, Blood
vessels & fascia.
 Detected with somatic nociceptors, but due to the scarcity
of the pai receptors it causes dull, poorly localized pain on
longer duration than the cutaneous pain.
Eg- Broken bones/ Myofascial pain.
 Pain response not always corresponds to the site &
intensity of the stimulus
 CNs excitatory effects are common
 Local anaesthetic block can eliminate the pain.
TMJ pain
 Capsular pain(capsulitis)
 Synovial pain (Synovitis)
 Retrodiscal pain (Retrodiscitis)
 Ligamentous pain
 Arthritic pain
Muscular pain
 Protective core contraction
 Local muscle soreness
 Myofascial pain
 Myospasm
 Centrally mediated myalgia

4. 3
Deep visceral pain
1. Pulpal pain
2. Vascular pain
3. Neuro vascular pain
4. Glandular pain
5. ENT pain
6. Occular pain
7. Visceral mucosal pain
 Originate from body’s viscera, or organs. Visceral nociceptors are located within the body organs
& internal cavities.
 The even greater scarcity of nociceptors in these areas produces pain that is usually more aching
or cramping & of a longer duration than somatic pain.
 Visceral pain may be well localized, but often it is extremely difficult to localize, & several
injuries to visceral tissues exhibit “reffered” pain, where the sensation is localized to an area
completely unrelated to the site of injury.
 Pain has no relationship for the biomechanical activity.
 Pain does not arise until threshold of stimulus is attained.
process involved in nociception
1. Transduction – process of converting noxious stimuli to action potentials.
2. Perception – Central processing of nociceptive pain in order to interpret pain.
Stimuli – Chemicals/ electrical / Thermal/ physical
Neuropathic Pain
 Spontaneous or triggered by non-noxious stimulus.
 Does not corresponds to the intensity of the stimulus.
 No evidence of tissue damage.
Episodic(Intermittent or paroxysmal
pain)
Continuous pain
 Paroxysmal neuralgias
-Trigeminal neuralgias
-Glossopharyngeal neuralgias
- Geniculate neuralgia
- Superior laryngeal neuralgias
- Nervous intermedius neuralgia
 Neurovascular pain(Overlaps to
some extent with deep visceral)
 Centrally mediated
- Atypical odontalgia(Phantom pain)
- Post- herpetic neuralgia
- Burning mouth syndrome
- Chronic regional pain syndromes
 Peripherally mediated
- Neuritic pain(Herpes zoster/ Peripheral Neuritis)
- Differentiation pain(Traumatic neuroma)
- Entrapment neuropathy
 Sympathetically maintained pain
- Causalgia (pain arising on an operating site eg-

5. 4
after extraction )
- Reflex sympathetic dystrophy
 Metabolic polyneuropathies
 Rapid, Piercing, electric type of
pain
 Incapacitating, very severe pain
 Short duration
 No pain between episodes
 Pain occur in the distribution of
the concerned nerve
 No evidence of tissue damage.
 Dull, burning pain
 Ongoing pain without remission
 Intensity can vary
 Additional neurological signs may be presents(Loss
of sensation, Paresthesia)
 No evidence of tissue damage
Causes (Origin) of orofacial pain
1. Dental pain – Pain from dentine, pulp, periapical periodontal tissues, gingivae, lateral
periodontal tissues, tooth socket.
2. Pain arising from the mucosa(Labio buccal, lingual, floor of mouth & palate)
3. Pain arising from the jaw bone
4. Pain arising from temporomandibular joints & masticatory muscles.
5. Pain arising from the salivary glands & ducts
6. Pain arising from the maxillary & other sinuses.
7. Neuralgic pain- Neuropathic pain
8. Vascular pain – From cranio facial & blood vessels
9. Referred pain – Cervical spine, eyes, heart
10. Psychogenic pain- tension headache & other headaches, Atypical facial pain, Burning mouth
syndrome, Atypical odontalgia.
Dental pain
 Exposure of Dentine
-Dentinal caries
-Fracture of tooth
-Cracked tooth syndrome
-Attrition of tooth
-Abrasion/ Erosion
 Pulpitis
 Apical periodontitis & Apical abscess
 Periodontal abscess
 ANUG
 Desquamative gingivitis
 Pericoronitis
 Alveolar osteitis(Dry socket)

6. 5
Mucosal pain
 Traumatic ulcers
 Apthous ulcers
 Erythema migrans(Tongue)
 Foliate papilitis (Tongue)
 Oral LP
 Oral submucous fibrosis
 DLE
 Erythema multiforme
 Malignancy
 Radiation induced mucositis
Neuralgic pain
1. Trigeminal neuralgia
2. Glossopharyngeal neuralgia
3. Post-herpatic neuralgia
Pain arising from maxillary & other sinuses
1. Acute maxillary sinusitis
2. Frontal sinusitis
3. Ethmoidal sinusitis
4. Chronic maxillary sinusitis
Pain from jaw bones
1. Fracture of the jaw(Mandible/ zygoma/
Maxilla)
2. Osteomyelitis of mandible
3. Osteoradionecrosis
4. Bisphosphonate induced osteonecrosis
Pain arising from the salivary glands
1. Not all pathologies if salivary glands
cause pain.
2. Acute parotitis including recurrent
juvenile parotitis.
3. Mumps
4. Submandibular sialadenitis
5. Sialolithiasis
6. Sialodochitis(Infection of the duct)
Vascular pain
1. Migraine
2. Migranous neuralgia
3. Temporal(cranial arteritis)
Headaches
1. Tension headache
2. Other headache
Management of Orofacial pain
Mx of Dental pain
Mucosal pain is on other notes
Differential diagnosis from non-odontogenic
pain
1. TN
2. TMJ pain & pain of muscle origin
3. Maxillary sinusitis pain
4. Salivary gland pain
5. Migraine & migranous neuralgia
6. Glossopharyngeal neuralgia
7. Post herpetic neuralgia
8. Atypical odontalgia
9. Temporal arteritis
10. Oral dysaesthesia or burning pain in the
mouth.
11. Burning mouth syndrome
12. Atypical facial pain
TN
1. A characteristic neuropathic pain in the
distribution of one or more branches of
the fifth cranial nerve.
2. It occurs in paroxysms, with each
episode lasting from a few seconds to 2
minutes.
3. Frequency of paroxysms varies from
hundreds of attacks a day to long
period.

7. 6
Primary TN
TN Epidemiology Aetiology
 Between successive episodes of
pain, the patient is pain free.
 A severe pain that is intense,
sharp, superficial, stabbing,
shooting, incapacitating & often
like an electric shock.
 In a single pts different attacks of
the pain have the same
character.
 Pain provokes brief muscle spasm
of the facial muscles, thus
producing tic- patient grimaces
with contortion of the face.
 Light touch in a specific area or
talking, washing the face or
brushing the teeth may trigger an
attack.
 No neurological deficit can
detectable.
 Incidence in the UK 27
cases per 100,000
persons in the
population.
 Previous studies USA
6/100,000 women’s &
3.5/100,000 men’s in a
F:M ratio of 1.75:1
 In men aged>80
incidence is
45.2/100,000
 More common after the
age of 40
 Right side of the face is
more commonly
affected than the left.
 Idoipathic – 90%
 Compression
Blood vessels may press on
the trigeminal nerve as it
leaves the brainstem at its
nerve root in the cerebello-
pontine angle. Compression
of the nerve leads to
demyelination resulting in
spontaneous generation of
the electric impulses.
 Degeneration
Some have postulated it to be
part of the aging process, as
with increasing age the brain
atrophies, leading to
redundant arterial loops
which can cause
compression.
 Myelin sheath infiltration
In tumor or Amyloidosis
Secondary
(Symptomatic) TN
Atypical TN Pre TN
 Cerebello- pontine
angle tumor may
cause compression
in some pts
(Younger patients)
 Multiple sclerosis:
2-3% of patient
with TN may have
MS
 Hypertension is a
risk factor (More in
females)
 Without treatment, typical
TN (TN1) may transform
over time to become
atypical TN (TN2).
 A change in the character of
the pain occurs to more
constant & background pain
& the development of
sensory impairment.
 Therefore, some authorities
recommend early
intervention to give the
opportunity of pain relief
without sensory deficits.
 There are some reports of the existence of a
pain condition termed pre TN.
 Patients who subsequently develop typical TN
may experience a prodromal pain termed
“Pre TN”.
 The prodromal pain is experience as a
toothache or sinusitis like pain lasting up to
several hours sometimes triggered by jaw
movements or by drinking hot or cold liquid.
 Typical TN develops a few days to several
years later, and in all cases affected the same
division of the trigeminal nerve.
 This becomes pain free when using
carbamazepine or baclofen.
 Recognition avoids unnecessary irreversible
dental procedures.

8. 7
Diagnostic criteria for classical TN
A. Paroxysmal attacks of pain lasting from a fraction of a second to 2 minutes, affecting one or
more divisions if the trigeminal nerve & fulfilling criteria B-C.
B. Pain has at least 1 of the following characteristics:
Intense/ Sharp/ Superficial/ Stabbing/ precipitated from trigger areas or by trigger factors.
C. Attacks are stereotyped in the individual pts.
D. There is no clinically evident neurological deficit.
E. Not attributed to another disorder.
Diagnosis of TN
1. History
2. Clinical examination to rule out other pathology including dental causes.
3. Cranial nerve function test
4. Diagnosis is conclusive if one or more attacks occur during history taking or clinical examination
when clinician can witness the “tic”
5. MRI to rule out the tumors in the cerebello- pontine angle mostly in young patients and
medically uncontrollable cases.
Treatment of trigeminal neuralgia.
Pharmacological Surgical intervention
1. Single drug therapy
2. Multiple drug therapy in “breakthrough pain”
- Carbamazepine/ oxcarbazepine is the mainstay of
treatment.
- Other drugs (usually in combination) in
breakthrough pain or when carbamazepine is
contraindicated.(Valproate/ phenytoin/
clonazepam/ gabapentin/ lamotrigine/pregabalin/
baclofen etc)
- Carbamazepine is started at a low dose: 100mg bd
or 8 hourly & increased gradually to obtain
optimum response with or without amitriptyline.
- Side effects (Dizziness) may affect compliance.
- Serious adverse effects have to be watch
Older methods
1. Peripheral (Inferior alveolar, mental, & infra
orbital branch resection) - considered less
effective.
2. Gasserian ganglion procedures- Alcohol/
phenol injections now largely abandoned.
3. Nerve root procedures- Wide sectioning of
roots – rhizotomy
Newer methods
1. Percutaneous procedures
2. Stereotactic radiosurgery or radiotherapy.
3. Posterior fossa exploration & micro vascular
decompression (MVD) of the trigeminal
root(more surgical morbidity, however)
Prognosis of TN
- 1/3 of patients will have mild symptoms.
- Some pts only ever have one episode
- Many peoples have period of remission with no pain for months or years.

9. 8
- Unconfirmed evidence that in many people it becomes more severe & less responsive to treatment
with time.
Condition Factors
Maxillary
sinusitis
 Can be unilateral or bilateral, felt on the face
 Acute or chronic stage of sinusitis
 Dull ache exacerbated by head movements particularly lowering the head- more
in bilateral than in unilateral.
 Pain may be felt in the maxillary teeth. TTP may present mostly in acute
 Nasal congestion may be present.
 Occipitomental radiograph may reveal radio opacity/cloudiness of the maxillary
sinus(es) A fluid level may be seen in the acute maxillary sinusitis.
Mx
 Mostly medical
 Antibiotics given mainly for the chronic sinusitis.
 Nasal decongestant
 Antihistamines
 Steam inhalation
 Functional endoscopic sinus surgery (FESS) by ENT surgeons
Migraine
 A neurovascular pain sometimes proceeded by visual or sensory aura
 Throbbing or pulsatile pain
 Localized in the fronto-temporal & ocular area, but can be felt anywhere around
the head.
 Photophobia or phonophobia may be found
 Nausea & vomiting may occur
 DD of TN
Migranous
neuralgia(Cluster
headache)
 Nuerovascular pain
 No aura
 Severe pain, strictly unilateral, retro orbital or periorbital radiating to the jaws
sometimes.
 May be confused with TN(but consider as worse than the TN. Because each
attack last longer than in the TN)
 Accompanied by ipsilateral lacrimation, conjunctival injection, nasal discharge or
congestion
 Each cluster is consists of 8 attacks per day or less during sleep or early morning
hours.
 Attacks lasts from 5-100 minutes to few hours.
Glossopharyngeal
neuralgia
 Repeated episodes of severe unilateral pain in the following areas which can
lasts from a few seconds to few minutes with similar characteristics as TN
Back of the nose & throat
Back of the tongue
Ear
Throat
Tonsil area
Voice box(Larynx)
 Management on similar lines as for TN

10. 9
Atypical
Odontalgia
 A form of tooth ache present in apparently normal teeth.
 Intra oral equivalent of atypical facial pain.
 Generally dull pain, often moves from one tooth to another – lasts for period of
4 months to several years.
 Cause is not yet clear
 Diagnosis by exclusion.
 Rx is tricyclic or other types of antidepressants.
Temporal
arteritis
 Commonest form of giant cell arteritis affecting the Head & Neck blood vessels.
 An autoimmune disease.
 Affects mostly superficial temporal artery & ophthalmic branch.
 Affects mostly the elderly.
 Insidious in development over weeks/ months commonly presents as headache
in the temporal region with tenderness along the course of the artery.
 Jaw pain brought on by chewing/ talking due to ischemia of masseters.
 Risk of blindness due to ophthalmic artery involvement.
 Diagnosis may require temporal artery biopsy.
 ESR or C - reactive protein is very highly elevated.
 Treatment is by steroids/ immunosuppressive therapy.
Oral dysaesthesia
or Burning pain
in the mouth.
 Due to clinically identifiable pathology.
Ulcerations
OSMF
 Due to causes that are not visible in the mouth
Dry mouth
Deficiency of hematinic
Drugs eg captopril
DM
Depression
Burning mouth
syndrome
 This term is not applied for burning sensation due to identifiable causes except in
association with psychogenic depression.
 However it is also considered a continuous neuropathic pain
 A diagnosis by exclusion
 Patient should be handle with empathy.
 Rx is by counseling & antidepressant therapy
Atypical facial
pain
 Not attributed by any identifiable causes.
 Diagnosis by exclusion
 Patient should be handle with empathy.
 Rx is counseling & antidepressants.

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