Oral surgery-5th stage

Orofacial pain Dr. sabah alheeti

Orofacial pain
Pain is a complex human psychophysiologic experience associated with actual or
potential tissue damage. It is a multifaceted experience influenced by multiple factors
such as past pain
experiences, physical, cultural, cognitive, emotional and medical aspects.
The physiologic aspects of pain experience involve several processes: transduction,
transmission, and modulation. The sum of these processes, when integrated with higher
centers, yields the human experience of pain.

Classification of orofacial pain

Multiple classification systems for orofacial pain have been proposed.
At the most basic level, it is appropriate to classify orofacial pains as: somatic, .I
neuropathic, and psychological.
Somatic pain arises from musculoskeletal or visceral structures interpreted through
an intact pain transmission and modulation systems.
Neuropathic pain is defined as pain caused by a lesion or disease of the
somatosensory nervous system. The etiology includes trauma, ischemia, infection, or
metabolic disturbances. It arises from damage or alteration to the pain pathways; it can
be classified into paroxysmal (episodic) and continuous neuropathic pain.
2nd classification: according to origin of pain .II

Category Type of pain

Local Dental (include pulpitis, dentin hypersensitivity,
periapical periodontitis, cracked tooth syndrome)
Gingival ( e.g. primary herpetic gingivostomatitis,
ulcerative gingivitis)
Mucosal (e.g. ulceration)
Salivary gland (e.g. sialadenitis)
Temporomandibular joint ( dysfunction and
others)
Maxillary sinuses (sinusitis, malignancy)
Ear disease (otitis media, neoplasm)
Neurological Trigeminal neuralgia
Glossopharyngeal neuralgia
Postherpetic neuralgia
Ramsay- hunt syndrome
Vascular Giant cell arteritis
Migraine and variants
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Cluster headache, Tension headache

Psychogenic Atypical facial pain
Atypical odontalgia
Burning mouth syndrome
Referred pain Cardiac pain

Diagnostic evaluation
The formal diagnostic evaluation contains the following components: chief complaint,
history of present complaint, medical history, physical examination, diagnostic imaging,
and other investigations.
Chief complaint It is the patient’s description of the pain. It may provide ●
valuable information to reach diagnosis; pulpal pains are usually provoked by
thermal stimulation, neuralgias are frequently described as sharp and
lancinating, vascular headaches are throbbing, and muscle pain is described as a
deep, dull ache. Many of these descriptions may overlap.
History of present complaint: It should include the following points: ●
The intensity of the pain needs to be measured against the patient’s own experience
of pain, need for medication, and effect on lifestyle.
The patient should be asked to indicate the site of the pain or the site of maximum
pain intensity and its anatomic distribution should be traced accurately in terms of local
anatomy.
The patient should be encouraged to remember the events surrounding the onset of
the pain.
The time relations of the pain should be clarified in terms of duration and frequency.
Aggravating and relieving factors should be determined.
The presence or absence of associated factors (redness or swelling of the face,
flushing, tearing, nasal congestion, eyelid ptosis, facial numbness, or facial weakness)
needs to be ascertained.

Medical history: A careful medical history should be taken. A thorough review ●

of organ system disease should be performed, including surgical history,
hospitalizations with special emphasis to history of trauma to the face, mouth or
head, allergies, current medical treatments, and current medications, habit
history, and psychosocial history.

Physical examination: Patients with orofacial pain should undergo a complete ●

oral cavity, face, head, and neck examination which should include inspection,
palpation, percussion, and auscultation. Muscles of mastication and muscles of
neck and shoulder should be assessed and palpated for tender and trigger points.
Intraoral examination includes dental occlusion and dentition for caries, gingival
and periodontal health in addition to inspection and palpation for any swellings,
masses, lesions, or areas of discoloration.
An important part of the examination is the neurological examination of all the cranial
nerves especially trigeminal and facial nerves in addition to the upper cervical nerve
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roots (C2–C5), since afferents from the upper cervical spinal segments are relayed
through the trigeminal brainstem complex forming trigeminocervical network which
includes the 3 branches of the trigeminal nerve (the ophthalmic branch [V1], the
maxillary branch [V2], and the mandibular branch [V3]) as well as the sensory nerves
for the posterior head and neck (C2, C3, C4, C5).
Activation of this network may result in referred pain perceived on one or both sides of
the head, the eyes or sinuses, and the posterior head and neck. Neurological
examination may include; sensory testing with directional sense, sharp (pain) touch,
light touch, hot, cold and pressure.
Imaging ●
Plain radiographs like panoramic (OPG) and periapical radiographs provide detailed
evaluation for the jaws and teeth. More detailed imaging for the maxillofacial skeleton
can be provided by computed tomography scan (CT scans), Magnetic resonance imaging
(MRI) is best for soft tissue evaluation. Ultrasonography can be used to evaluate the
major salivary glands, carotid arteries, and masses in the neck.
Scintigraphy or bone scan with technetium-99m will highlight areas of increased
metabolic activity within the bone and can help to identify infection, tumor, or
degenerative changes in the TMJ.
Other investigations ●
These may include blood investigations, microbiological studies, diagnostic injections
like local anesthetic, and biopsy of any suspicious mass or lesion.

Odontogenic pain
Dental pain is usually well localized, and the quality of the pain can range from a dull
ache to severe, depending on the specific cause and extent of disease. NSAIDs and non-
opiate analgesics can be used to alleviate most odontogenic pain but definitive
treatment is dental.

Pulpal
Pain may be sharp, throbbing, or dull, it can be spontaneous or provoked or exacerbated
by percussion, thermal or electrical stimuli. It is associated with compromised dental
pulp due to deep caries, crown fracture or recent dental work. Treatment is by removal
of carious lesion, tooth restoration, endodontic treatment, or tooth extraction.

Periodontal
Pain is localized, deep continuous associated with compromised periodontium (gingiva
or periodontal ligament) exacerbated by biting, chewing or percussion. Usually there are
signs of periodontal inflammation or abscess with or without tooth mobility, periapical
radiographs may aid in diagnosis. Treatment options include: drainage and
débridement of periodontal pocket, scaling and root planning, periodontal surgery,
endodontic treatment, or tooth extraction.

Cracked tooth
It is associated with fractured tooth with history of trauma or restorative dental work,
pain is usually sharp, spontaneous or brief provoked by biting, chewing or percussion.
Treatment depends on the level of the tooth fracture; restoration or extraction of the
tooth.
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Dentinal pain
Brief, sharp pain provoked by different kinds of stimuli to the dentin (e.g., hot or cold
drinks), it is caused by stimulation exposed dentin or cementum that may result from
recession of periodontium or possible erosion of dentinal structure. Treatment options
may include; mouthwash (fluoride), desensitizing toothpaste, tooth restoration,
endodontic treatment.

Oral mucous membrane disorders

Diseases of the oral mucosa are numerous and have a variety of local and systemic
causes. Pain may be a symptom of the disease process, secondary to an associated
process (infection), or related to damaged oral mucosa (chewing food, thermal, chemical
stimuli). Typically, pain is associated with oral mucosal lesions including; ulcers,
vesicles, bullae, erosions, erythema, or red and white patches. Treatment depends on
the proper diagnosis; options may include topical or systemic analgesics and
corticosteroids.

Temporomandibular disorders (TMD)

TMD encompasses a number of clinical problems that involve the masticatory
musculature, the TMJ, and associated structures. TMD symptoms are more commonly
seen in women than in men, and many symptoms seem to arise in adolescence or the
early twenties and may continue intermittently, well into middle age.
TMJ disorders
Disorders of the TMJ include mainly;
The internal derangements, such as disc displacements with and without reduction.
myofascial pain syndrome
TMJ subluxation and dislocation.
Inflammatory disorders (e.g., capsulitis or synovitis).
Osteoarthritis.
Rheumatoid arthritis.
In TMJ disorders pain is localized to the preauricular area during jaw function with
presence of painful click or crepitus during mouth opening, in addition to limited mouth
opening (<35 mm) and deviated or painful jaw movements. There is pain on palpation
of the TMJ with possible swelling in the acute phase. CT and MRI may be needed to
reach the diagnosis.
Treatment is by:
Patient education and self-care instructions.
Medication: NSAIDs, non-opiate analgesics.
Physical therapy through exercise program.
Occlusal splints.
Surgery; is only indicated when non-surgical therapy has been ineffective, and it is
not indicated in patients who are asymptomatic or mildly symptomatic or as a
preventive measure. Surgical interventions include; arthrocentesis, arthroscopic
surgery, and open surgery.
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Neuropathic pain
It has been estimated that the incidence of orofacial neuropathic pain is 5-10 per
100,000 people. It is divided into episodic (paroxysmal) pain disorders, including
trigeminal neuralgia and glossopharyngeal neuralgia, and continuous pain disorders
that frequently result from deafferentation after injury in the peripheral and central
nervous system, which is the case in neuromas and idiopathic trigeminal neuropathic
pains such as atypical odontalgia.

Trigeminal neuralgia (Tic douloureux)

It is a chronic paroxysmal neuropathic pain condition that is described as a severe,
lancinating, and electric-like unilateral pain. It is localized most often to trigger zones in
both the V2 and V3 distribution (the most common distribution), after which they occur
alone (and in decreasing order of incidence) in the V3, V2, and VI distributions.

There is usually a trigger zone in the trigeminal distribution which, when stimulated,
can result in an excruciatingly painful attack. Pain will occur following mild stimulation
of this trigger area (e.g., washing the face, shaving, eating, brushing one’s teeth, or
being exposed to a breeze).
The pain attacks last seconds to minutes (about 2 minutes) followed by a refractory
period in which stimulation of the trigger zone will not elicit another attack. Numerous
pain episodes can be present daily. This pattern of pain must be met in order for the
diagnosis of trigeminal neuralgia to be made otherwise alternative terms such as
atypical trigeminal neuralgia can be applied.
It may go through periods of remission where the pain can remit for months or even
longer. This disorder is characterized by a protracted clinical course with increasing
frequency and severity of pain. It has one of the highest suicide rates of any disease and
is regarded as one of the most painful conditions known.
It typically affects individuals older than 50 years of age, although it can develop at any
age, including young children. Women are affected more often than men by a ratio of
1.5: 1. The right side of face is more commonly affected. The majority of cases occur
sporadically; however, several reports of familial trigeminal neuralgia have been
described.
Etiology
Primary or idiopathic (classical) trigeminal neuralgia has no definite cause but
localized demyelination may be implicated, the superior cerebellar artery compression
on the trigeminal root has been shown to be responsible for attacks of trigeminal
neuralgia pain.
Secondary or symptomatic trigeminal neuralgia results from nonvascular
compression by a cerebellopontine angle neoplasm, such as acoustic neuromas,
meningiomas, cholesteatomas, and neurofibromas, has also been shown to result in
trigeminal neuralgia. Therefore, MRI and CT scan of the brain should be requested in
order to rule out any intracranial pathology.
Myelin loss due to multiple sclerosis has been shown to be a causative disorder related
to the trigeminal neuralgia.
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Treatment
Treatment of trigeminal neuralgia consists of medical and surgical therapies.

Medical treatment
Anticonvulsants (e.g., carbamazepine which is the drug of first choice, gabapentin).

Antidepressants (e.g., amitriptyline, nortriptyline).

Non-opiate analgesics.
Botulinum toxin injection.
Combination of baclofen (muscle relaxant) and anticonvulsants when
anticonvulsants alone are not effective, or if the therapeutic range cannot be achieved
due to side effects.

Surgical treatment
If medical therapy is unsuccessful or not tolerated, surgical treatment should be
considered which consists of numerous peripheral and intracranial procedures.

Peripheral procedures all have the goal of inducing nerve damage:

Trigeminal nerve block which provide only temporary relief, high concentration
lidocaine (10%) have been used.
Alcohol injection may be effective for about 1 year but are painful, and fibrosis makes
repeat injections technically difficult. The use of alcohol is associated with many
complications include tissue toxicity, inflammation, and fibrosis.
Peripheral neurectomy involves the avulsion or severing of the terminal branches of
the trigeminal nerve with or without obturation of the foramen. Pain may recur after 2
years
Cryotherapy of peripheral branches may provide pain relief for 6 months and may be
repeated with good results.

Central procedures:
Percutaneous trigeminal rhizotomy. These procedures are directed at the trigeminal
ganglion aims to use controlled injury to interfere with the nerve's ability to transmit
signals. They include radiofrequency thermal rhizotomy, glycerol injection, or
balloon compression. The three modalities provide approximately equal initial pain
relief (around 90%) but are each associated with different rates of recurrence and
complications. Overall, radiofrequency rhizolysis consistently provides the highest rates
of sustained pain relief but is associated with high frequencies of facial and corneal
numbness.
Posterior fossa exploration and microvascular decompression of the trigeminal root.
It is based on the premise that trigeminal neuralgia caused by vascular compression of
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the nerve root, and surgically separating them may offer a permanent cure. Initial
success rates for microvascular decompression are very high (approximately 90%), but
long-term follow-up shows that after 10 years 30% to 40% of patients will experience a
relapse
Gamma Knife stereotactic radiosurgery; it is a minimally invasive technique that
precisely delivers radiosurgical doses of 70 to 90 Gy to the trigeminal nerve root at the
point of vascular compression as mapped using MRI, it provides good to excellent
(60%–90%) initial pain relief.

Glossopharyngeal neuralgia
Glossopharyngeal neuralgia is a rare condition (0.2-1.3% of facial pain syndromes)
associated with pain in the area supplied by the glossopharyngeal nerve (9th cranial
nerve). Painful sites may include the nasopharynx, posterior part of the tongue, throat,
tonsil, larynx, and ear.
This disorder presents shooting paroxysms of pain that can occur multiple times a day
with stimulation of the oropharyngeal region. Common triggers may include mechanical
stimulation of the trigger zone as well as activities including chewing, swallowing,
coughing, talking, and head movement.
It occurs in middle-aged or older individuals with no sex predilection. Due to the
proximity of the vagal sensory nerves, glossopharyngeal neuralgia may coincide with a
cardiac dysrhythmia such as bradycardia, asystole, and syncope in about 10% of the
cases (vagoglossopharyngeal neuralgia). Like trigeminal neuralgia, it can be
classified as classical or secondary but it is uncommon for glossopharyngeal neuralgia to
be associated with multiple sclerosis.
Treatment
The management of GN typically parallels that of TN.

Postherpetic neuralgia
It is a potential sequela of shingles, also known as herpes zoster which is the clinical
manifestation of the reactivation of a lifelong latent infection with varicella zoster virus,
usually contracted after an episode of chickenpox in early life where the virus lay
dormant in the ganglia of peripheral nerves but in 10-15% of the cases the trigeminal
nerve is involved in which the dermatome of the ophthalmic branch (V1) is affected in
about 80% of the cases.
Postherpetic neuralgia occurs immediately after the skin rash or after about 1, 3 or 6
months. Pain is spontaneous burning and tingling, but may present as dull and aching
and occasional lancinating evoked pain. Clinically there may be small cutaneous vesicles
or scarring, usually affecting the forehead, loss of normal skin color, corneal ulceration
can occur. Sensory changes in affected area (e.g., hyperesthesia, dysesthesia).
Treatment is by acyclovir in the acute phase, anticonvulsants, antidepressants, non-
opiate analgesics. Rhyzotomy and Gamma knife may be indicated in nonresponsive
cases.
A related condition, Ramsay Hunt Syndrome, is a herpes zoster infection of the
sensory and motor branches of the facial nerve (VII) and in some cases the auditory
nerve (VIII). Symptoms include facial paralysis, vertigo, deafness, and herpetic eruption
in the external auditory meatus
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Vascular pain
Giant cell arteritis (Temporal arteritis)
It is an immune-mediated vasculitis that affects medium-sized and larger arteries,
leading to vascular occlusion and ischemia, although it is considered as a systemic
condition and can affect any vessel but the superficial temporal artery is the most
commonly affected site. Patients are usually above 50 years of age with female
predilection, presenting with symptoms of severe headache and scalp tenderness.
A highly characteristic feature is jaw claudication, which is described as cramping pain
of the masseter and temporalis muscles that increases with usage (chewing or talking)
but is relieved by rest. The superficial temporal artery is sensitive to palpation and
eventually appears erythematous, swollen, tortuous, or sometimes ulcerated.
Rare examples of unilateral or bilateral tongue necrosis secondary to lingual artery
involvement also have been described. The most significant complication in the head
and neck region is vision loss, which usually is due to vasculitis of the posterior ciliary
artery and ischemic optic neuropathy. If pain and stiffness affecting the shoulders,
upper arms and pelvis are present in addition to the characteristic unilateral headache, a
diagnosis of polymyalgia rheumatica should be considered.
Investigations include elevated ESR, biopsy of the temporal artery is required which
shows skip lesions of inflammatory tunica intima and media with giant cells, and usually
there is narrowing of the lumen.
Treatment
Treatment is by high-dose systemic corticosteroid therapy, the dose can be reduced as
the ESR starts to fall. Methotrexate or azathioprine sometimes will be added for their
steroid-sparing effects.

CHRONIC HEADACHE
When headaches recur regularly, the majority will be diagnosed as one of the primary
(no other cause) headaches: migraine, tension-type headache, or cluster headache.
Although most headaches are centered in the Orbits and temples, many may present in
the lower half of the face, teeth, or jaws.
Migraine
Migraine is a common headache afflicting approximately 18% of woman and 8% of men.
The first migraine headache typically occurs in the teenage years or in young adulthood.
An "aura" may develop several minutes to 1 hour before headache onset in
approximately 40% of patients. The aura is a neurologic disturbance, frequently
expressed as flashing or shimmering lights or a partial loss of vision.
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INH criteria for migraine without aura

The mechanism for migraine headache appears to involve neurogenic inflammation of

intracranial blood vessels secondary to neurotransmitter imbalance in certain brain
stem centers.

Preventive treatment is directed at normalizing neurotransmitter imbalance with

antidepressants, anticonvulsants, beta-blockers, and other drugs. Treatment of acute
attacks is with the "triptans" (e.g., sumatriptan, zolmitriptan), ergots (ergotamine and
dihydroergotamine ), nonsteroidal anti-inflammatory drugs (NSAIDs), opioid
analgesics, antiemetics, and other agents

Cluster Headache
Cluster headache is an overwhelmingly unilateral head pain typically centered around
the eye and temporal regions.
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Treatment, as in migraine, is either preventive or symptomatic. Preventive treatment is

accomplished with verapamil, lithium salts, anticonvulsants, corticosteroids, and certain
ergot compounds. Symptomatic treatment is with "triptans," ergots, and analgesics.
Oxygen inhalation at 7 to 10 L/min may be an effective abortive treatment.

Atypical odontalgia
Atypical odontalgia presents as pain in a tooth or site of dental extraction in the absence of
clinical or radiographical evidence of pathological dental condition. This pain may affect 3-6% of
patients who undergo endodontic therapy. Its most common in the 5th decade with female bias.
Molar and premolar sites are involved more frequently, and maxillary teeth are more likely.

The pain is a persistent sharpness, aching, burning or throbbing of moderate severity. The
patient may have increased sensitivity to pressure, unresponsive to analgesics, surgery or other
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dental procedure, not lessen entirely to local anesthesia. Sleep is not affected although the pain
recommences on awakening. The patient has other symptoms like headache, hyperesthesia,
alloydynia and exacerbation of pain by temperature, palpation or percussion.

The exact pathogenesis of atypical odontalgia remains unknown. The present favored theory is
mild trauma to the orofacial structures (including even inferior alveolar nerve block) alters
neural continuity of the tissue and create deafferentation.

The treatment of atypical odontalgia remains unsatisfactory. The treatment includes:

Topical application of capsaicin (0.025%) and EMLA 5% (mixture of lidocaine and .i
prilocaine)
TAD .ii
Anxiolytics such as clonazepam .iii
Gabapentin .iv