5. 1. Musculoskeletal
I. Temporomandibular disorders
a. Masticatory muscle disorders
• Myofascial pain
• Myositis
• Myospasm
• Local myalgia
b. Articular disc derangements
• Disc displacement with reduction
• Disc displacement without reduction
c. Temporomandibular joint disorders
• Synovitis/capsulitis
• Osteoarthritis
II. Tension-type headache
Classification of Orofacial Pain
6. 2. Neuropathic
I. Episodic
a. Trigeminal neuralgia
b. Glossopharyngeal neuralgia
II. Continuous
a. Herpetic neuralgia
b. Postherpetic neuralgia
c. Traumatic neuralgia
d. Eagle’s syndrome
7. 3.Vascular
a. Giant cell arteritis
b. Carotid artery dissection
4. Neurovascular
a. Migraine
b. Cluster headache
c. Chronic paroxysmal hemicrania
8. 5. Idiopathic
a. Atypical facial pain
b. Atypical odontalgia
c. Burning mouth syndrome
7.Other diseases that can cause facial pain
a. Local pathology
b. Distant pathology (referred pain)
c. Systemic diseases
6. Psychogenic
a. Somatoform disorders
b. Factitious disorders
c. Malingering
9. A. History
1. Chief complaint.
2. History of present illness.
Pain Characteristics
• Intensity
• Quality
• Location
• Onset
• Associated events at onset
• Duration and timing of pain
• Course of symptoms since onset
• Activities that increase pain
• Activities that decrease pain
• Associated symptoms (eg, altered sensation, swelling)
• Previous treatments and their effects
• Referral
Evaluation and assessment
10. 3. Past medical history
-Connective tissue disease.
-Demylination disorder.
-Metastatic disease.
-Ischemic heart disease.
4. Social history:
-History of traumatic event prior to onset of pain.
-Change in work, or problem regarding marital state.
11. B. Physical examination:
1. Inspection of the head and neck skin,
2. Palpation of masticatory muscles,
3. Assessment and measurement of the range of mandibular movement.
4. Palpation of soft tissue .
5. Palpation of the temporomandibular joint
6. Palpation of cervical muscles and assessment of cervical range of
motion.
7. Cranial nerve examination.
8. General inspection of the ears, nose, and oropharyngeal areas.
9. Examination and palpation of intraoral soft tissue.
10. Examination of the teeth and periodontium (including occlusion.
12. Measurement of Pain
Methods of pain measurement:
1-visual analog scale (VAS)
0 -----------------------------------10
no pain worst possible pain
2-Descriptive rating scales (eg, no pain, mild, moderate, severe
pain).
3-Faces rating scale.
4-The McGill Pain Questionnaire (MPQ) .
13.
14. C. Diagnostic Imaging:
Used to confirm the diagnosis or rule out serious disease.
Extent of an identified disorder.
Most OFP not produce abnormality.
15. 1. Temporomandibular disorders
a. Masticatory muscle disorders
• Myofascial pain
• Myositis
• Myospasm
• Local myalgia
b. Articular disc derangements
• Disc displacement with reduction
• Disc displacement without reduction
c. Temporomandibular joint disorders
• Synovitis/capsulitis
• Osteoarthritis
2. Tension-type headache
Musculoskeletal
16. Myofascial Pain
Myofascial pain is characterized by the presence of focal, exquisitely tender
muscle areas, called trigger points. Trigger points are typically found in taut
muscle bands and produce a characteristic pain referral pattern on palpation.The
patient complains of constant, dull muscle pain that is typically exacerbated by
muscle use. Frequently, the referred pain is the only symptom and the patient is
unaware of the trigger points. Trigger points in the masseter and temporalis
muscles can refer pain to posterior teeth, while trigger points in the
sternocleidomastoid and trapezius muscles often refer pain to the jaw or temple .
Accordingly, the condition may present as toothache or headache and careful
palpation of the head and neck muscles is required to reveal the trigger points.
Palpation of the trigger points will elicit severe local pain, as well as aggravation
of the referred pain. Replication of the patient’s symptoms upon trigger point
palpation will confirm the diagnosis.
17. Contributing factors
• Teeth clenching
• Trauma
• Somatization
• psychological distress
• Sleep disturbances
• central nervous system dysfunction
• nutritional deficiencies or
• fatigue
18. Treatment
• elimination of precipitating factors and inactivation of trigger points by
vapocoolant spray or injection of a local anesthetic, followed by stretching.
• relaxation therapy
• daily stretching of the affected muscles
• physical therapy modalities, and
• medications, such as analgesics, muscle relaxants, and tricyclic
antidepressants in low doses .
19. Myositis
• refers to true muscle inflammation result from a spreading infection or
acute trauma to the muscle tissue
Diagnosis
• cardinal signs of inflammation
• constant pain
• swelling, erythema, and
• elevated temperature over the affected muscle
20. Treatment
• Controlling of underlying infection by antibiotics
• In the case of muscle injury, rest should be advised in the early posttraumatic phase
to limit hematoma formation.
• Supporting therapy may consist of ice and nonsteroidal anti-inflammatory drugs
(NSAIDs).
21. Myospasm:
• an acute condition, characterized by severe muscle pain, marked
limitation of mouth opening and, often, acute malocclusion.
• increase in electromyographic activity, secondary to sustained,
involuntary muscle contraction.
Treatment
• stretching the muscle to full length - achieved only after reducing the pain by
ice, vapocoolant spray, or injection of local anesthetic.
• Injections of botulinum toxin are recommended for severe and recurrent
myospasms.
• In such cases, predisposing factors, including psychological distress and
parafunctional activities, also should be addressed.
22. Local Myalgia
• Term adopted by the American Academy of Orofacial Pain to denote
muscle pain conditions that cannot be attributed to a specific cause, such
as trigger points, inflammation, or muscle spasm.
• Characterized by spontaneous muscle pain, muscle tenderness upon
palpation, as well as limited mouth opening due to the pain.
• Symptoms are aggravated by activities requiring jaw movement, such as chewing,
talking, laughing, or yawning.
23. • patient education on painless use of the mandible
• moist heat applications
• jaw exercises, and
• short-term use of NSAIDs or muscle relaxants.
• An intraoral stabilization appliance may be of benefit if jaw
parafunctional activities are suspected
• relaxation therapy can be recommended for patients that report high
stress levels.
Treatment
24. Articular Disc Derangements
• characterized by displacement of the articular disc anteriorly and medially.
Disc Displacement With Reduction:
• An opening joint clicking occurs as the condyle positions itself under the
posterior band of the disc upon mouth opening, and a closing joint clicking
can be heard as the condyle slips off the disc, just before the teeth come
together.
• Pain may or may not be present
• Asymptomatic clicking is a very common sign among the general
population and does not require treatment
25. Disc Displacement Without Reduction
• The displaced disc blocks the condylar movement, resulting in limited
(25 to 30 mm) mouth opening and restricted lateral excursion to the
contralateral side.
• The mandible deflects to the affected side on opening and clicking
noises are absent.
• Pain is typically present in the acute condition, while chronic disc
dislocation may be nonpainful.
26. • Magnetic resonance imaging can be used to substantiate the
clinical diagnosis and rule out other pathological conditions of
the TMJ that would result in blockage of condylar movement.
27. Treatment
• In acute disc dislocation, there should be an effort to reduce the disc
dislocation by manual manipulation, followed by insertion of an anterior
repositioning appliance.
• Management of chronic disc dislocation may include a stabilization
appliance, physical therapy, and NSAIDs if pain is present.
• Surgical arthrocentesis or arthroscopy may be beneficial for patients who
are refractory to conservative treatment.
28. Temporomandibular Joint Disorders
• characterized by inflammation of the synovial lining of the TMJ
and the capsular ligament respectively.
• Grouped together, since they cannot be distinguished on the
basis of historical or clinical findings.
Synovitis and Capsulitis:
29. Clinical features
• characterized by constant deep pain in the TMJ
• tenderness to TMJ palpation
• restricted mouth opening secondary to pain acute malocclusion of
the posterior teeth on the affected side may also be present
30. • Synovitis and capsulitis can be induced by trauma to the jaw or repetitive
chronic microtrauma.
• In the case of acute trauma, ice should be applied to the affected joint 4
to 6 times daily for the first 24 to 36 hours, followed by moist heat
applications for 10 to 15 minutes, 3 to 4 times per day.
• Restriction of jaw movement to a pain free range of motion and
administration of NSAIDs on a regular basis for 10 to 14 days are
recommended.
Treatment
31. Osteoarthritis
• a non-inflammatory arthritic condition characterized by deterioration
of the articular surfaces.
• presents with pain that is exacerbated by mandibular movement,
tenderness upon palpation of the joint, crepitus, and limited
range of mandibular motion.
• The clinical diagnosis is substantiated by radiographic and magnetic
resonance imaging evidence of structural bony changes, such as surface
irregularities, flattening or erosion of the condyle, and osteophytes.
Diagnosis
32. • Conservative approaches including NSAIDs
• moist heat applications
• painless use of mandible
• jaw exercises and stabilization appliance.
For refractory cases
• one or two single injections of corticosteroids in the joint
• arthrocentesis, or
• arthroscopic surgery may be recommended
Treatment
33. Tension-type Headache
• A common primary headache affecting the occipital, parietal, temporal, or
frontal areas.
• The pain is typically bilateral, has a tightening or pressing quality, mild to
moderate intensity, and may last from a few hours to 7 days.
• In contrast to migraine, there is no nausea, vomiting, or aggravation of the
pain by routine physical activity.
• The pain may be precipitated by stress and is usually associated with
fatigue and poor sleep.
34. • Consists of stress management, relaxation training, and
pharmacotherapy.
• Simple analgesics and NSAIDs are typically effective in aborting
the Pain.
Treatment
35. Neuropathic
1. Episodic
a. Trigeminal neuralgia
b. Glossopharyngeal neuralgia
2. Continuous
a. Herpetic neuralgia
b. Postherpetic neuralgia
c. Traumatic neuralgia
d. Eagle’s syndrome
37. Etiology and pathophysiology
TN divided to primary and secondary(symptomatic)
The primary TN
are result of vascular compression of trigeminal nerve near its entry into the
pons (superior cerebellar artery).
Secondary TN
causes include :multiple sclerosis, tumors ,basilar artery eneurysim or actasia.
38. Clinical features
• It presents as episodic ,recurrent unilateral facial pain, described as
sudden high intensity stabbing or electric like shock.
• lasts for a few seconds to minutes ,
• Pain is frequently triggered by trivial stimulation: such as touching of
face, washing ,shaving , chewing and talking.
• It occurs mostly after 5th decade.
• Clinical examination of face is nearly always normal.
• If sensory loss is present a mass lesion is more likely
• In young patients with TN, multiple sclerosis should be considered.
39. TN Diagnosis:
• Diagnosis depend on history and clinical
examination.
• A careful search for ipsilateral dental pathology
should be undertake
• MRI and MRA and performed if there is suspicion of
underlying pathology.
41. Treatment of trigeminal neuralgia
1- Medical treatment:
Carbamazepine 200 mg _ 1600mg bid .(effective in 75% as
first line of treatment)
Oxcarbazepine 600mg _3000mg It used in patients who are
sensitive to Carbamazepine.
Baclofen 15mg _80mg tid.
Gabapentine 900mg _3600mg tid.
Lamotrigine 25mg _300mg.
Clonazepam 1.5 mg _ 6mg
Phenytoin 300 mg
Valproate sodium 500mg _1500mg
42. 2- Surgical treatment(invasive):
indicated If medical treatment (carbamazepine) has been ineffective after 4 weeks at
maximum tolerated dose .
• Surgical treatment divided into 3 groups:
a) peripheral procedures :include alcohol injection, cryosurgery ,nerve avulsion
b) Percutaneous ganglion procedure: include radiofrequent thermocoaglation ,glycerol injection ,
balloon compression,Gamma knife.
c) Open operations : microvascular decompression ,trigeminal root section,
43. Glossopharyngeal Neuralgia
• Characterized by severe, sudden, unilateral, stabbing pain in the
ear, base of the tongue, tonsillar fossa, or beneath the angle of the
mandible.
• Pain typically lasts a few seconds to 2 minutes and can be triggered
by swallowing, chewing, talking, coughing, or yawning.
44. • Pain similar to character of TN.
• Affect tonsil ,tongue base, ear,and intra articular area.
• Patient often point just to behind mandible angle.
• Triggered by yawing and swallowing.
• may be associated with a vasovagal reflex,
• The application of a topical anesthetic to the
pharyngeal mucosa eliminates glossopharyngeal
nerve pain.
Clinical features
45. Management
• Anti convulsion drugs,carbamezipine.
• Vascular decompression.
• Percutaneous R.F. at the jugular foramen.
• Intracranial or extra cranial neuroectomy.
Etiology:
The most common causes of glossopharyngeal neuralgia areintracranial or extracranial
tumors and vascular abnormalities that compress CN IX.
46. Herpetic And Postherpetic Neuralgia
• Following a chickenpox infection, the varicella zoster virus
becomes latent in the cranial nerve and dorsal root ganglia.
• Reactivation of the virus later in life can result in herpes zoster,
which is characterized by vescicular eruption and associated
severe pain in the distribution of the affected branch.
• The trigeminal ganglion is involved in approximately 10% of
cases, with the ophthalmic division being most commonly
affected. Antiviral drugs and systemic corticosteroids are the
mainstreams of treatment;
• Pain that persists longer than 3 to 4 months following the
outbreak of herpes zoster eruption is referred to as
posteherpetic neuralgia.
47. • continuous severe, burning pain with sharp exacerbations.
• Tactile allodynia (pain in response to an innocuous stimulus) and
hyperalgesia (exaggerated pain in response to a noxious stimulus) are
often present, compromising significantly the patient’s quality of life.
• Since no apparent peripheral pathology is evident upon clinical examination,
careful questioning is needed to rule out a history of vesicular/ulcerative lesions,
which would lead to a definite diagnosis.
Clinical Features
48. Treatment
• Medications that have been proven effective in controlled clinical trials
include:
• lidocaine patch 5%
• Gabapentin
• tricyclic antidepressants, and
• opioids
49. Traumatic Neuralgia:
• Traumatic neuralgia occurs following direct neural injury and
deafferentation. The pain is typically described as constant and
burning, while superimposed lancinating exacerbations may also
occur.
50. • Pharmacological consists of
• tricyclic antidepressants;
• administration of anticonvulsant medications, such as carbamazepine or
gabapentin.
• Topical applications of capsaicin may desensitize the affected area and alleviate the
symptoms, while sparing the patient of the adverse effects of systemic drugs.
Management
51. Eagle’s Syndrome
• An uncommon condition resulting from compression of the
glossopharyngeal nerve by an elongated styloid process or an
ossified stylohyoid ligament.
52. • The chief signs and symptoms include dull and persistent neck and throat
pain, dysphagia, otalgia, and a foreign body sensation.
• Radiation of the pain to the TMJ or the upper limb has also been
reported.
• The pain may have a neuralgic component, mimicking glossopharyngeal
neuralgia, and it is usually exacerbated by rotation of the head to the
contralateral side, swallowing, extending the tongue, and yawning
Clinical Features
53. • Plain radiographs and computed tomography examination will reveal elongation of
the styloid process or ossification of the stylohyoid ligament. In addition, patients
with bilateral elongation frequently complain of unilateral neck pain. Therefore,
establishment of the diagnosis is greatly facilitated by replication of the patient’s
symptoms on palpation of the tonsillar fossa, aswell as alleviation of the pain by
injection of local anesthetic
Diagnosis
54. • Surgical resection of the styloid process or the calcified
stylohyoid ligament, through an intraoral or extraoral approach,
results in resolution of the symptoms in most patients.
• Concurrent treatment with NSAIDs is advocated, in order to
prevent re-ossification following the surgical procedure.
Treatment
56. Giant Cell Arteritis
• Giant cell arteritis (GCA) is a multifocal vasculitis, characterized
by granulomatous infiltrates in the wall of medium-sized and
large cranial arteries, especially the extracranial branches of the
carotid arteries also referred to as temporal arteritis, because
the superficial temporal artery is most commonly affected.
Other commonly involved arteries include the maxillary, the
ophthalmic, and the posterior ciliary arteries.
57. • The etiology of GCA is unknown; however, autoimmunity to the
vessel wall has been implicated. Involvement is characterized by
chronic inflammation of the intima and tunica media, as well as
edema and proliferation of the intima, resulting in narrowing of
the lumen and ischemic complications.
Nordborg C, Nordborg E, Petursdottir V. Giant cell arteritis. Epidemiology, etiology and
pathogenesis. APMIS. 2000;108:713–724.
58. Symptoms
• Temporal headache is one of the most common symptoms, occurring in
approximately 90% of patients. The headache is typically described as
severe and throbbing, and is aggravated upon recumbence. Pain in the
masticatory muscles upon chewing (jaw claudication), secondary to
inflammation of the maxillary artery, Involvement of the lingual artery
can result in pain and blanching of the tongue and rarely in tongue
necrosis. Occlusion of the optic arteries may result in transient or
persistent visual disturbances, including blindness. Constitutional
symptoms not directly related to the affected arteries may also be
present; these include malaise, fatigue, low-grade fever, anorexia, and
weight loss. Also, giant cell arteritis frequently overlaps with polymyalgia
rheumatica, which presents with bilateral pain and morning stiffness in
the shoulders and/or hips.
59. Clinical Examination
• The superficial temporal artery is usually extremely sensitive to palpation
and appears erythematous, swollen, and tortuous; temporal artery
pulsations may be decreased or absent. Laboratory studies reveal an
erythrocyte sedimentation rate greater than 50 mm/h, and a marked
elevation of nonspecific acute-phase reactants, such as C-reactive
protein. Temporal artery biopsy constitutes the gold standard for the
diagnosis of giant cell arteritis.
60. Treatment
• Corticosteroids constitute the cornerstone in the treatment of GCA. High-
dose corticosteroid therapy should begin immediately upon clinical
suspicion of GCA to prevent cranial ischemic complications, such as acute
visual loss and cerebrovascular accidents. Recent research10 suggests that
parallel administration
• of low-dose aspirin attenuates
• the incidence of these complications. Duration of corticosteroid
• therapy should be based on laboratory
• values and clinical signs and symptoms
61. Carotid Artery Dissection
• Dissection of extracranial carotid arteries,
• namely splitting of the arterial wall by a mural
• hematoma, may occur spontaneously or following
• minor trauma and involves most commonly
• the internal carotid artery.
• The patient usually
• presents with unilateral pain that may start
• in the neck and radiate to the face or manifest
• itself only in the face and/or head. Headache is present in
approximately 70% of
• patients and is reported as the initial symptom
62. • Cranial nerve palsies due to diminished
• blood supply may also result in various signs
• and symptoms, such as difficulty protruding
• the tongue or speaking (hypoglossal nerve),
• decreased facial sensation or difficulty chewing
• (trigeminal nerve), and drooping of the
• face (facial nerve). Magnetic resonance
• imaging and angiography of the head and
• neck constitute valuable diagnostic tools that
• can demonstrate the dissection and substantiate
• the diagnosis.
63. t/t
• Administration of anticoagulant,
• or antiplatelet agents, for 3–6
• months is advocated in an attempt to prevent
• arterial thrombosis and embolism, while
• the hematoma resorbs. Ultrasonography
• is useful in monitoring recanalization of the
• vessel and guiding treatment.16 Endovascular
• stent placement is an alternative treatment
• approach, recommended for patients refractory
• to anticoagulation
64. Neurovascular Pain- Migraine
• a highly prevalent, recurrent
• headache that involves the frontal, temporal,
• and retro-orbital areas. the pain
• is unilateral, of moderate to severe intensity
• and pulsating quality, and it is aggravated by
• routine physical activity. The headache attacks
• last 4 to 72 hours and are accompanied
• by sensitivity to light (photophobia), sensitivity
• to sound (phonophobia), nausea, and/or
• vomitingPain may be precipitated by various
• factors, such as stress, alcohol, tyraminecontaining
• foods, menstruation, and bright
65. two main types
• 1. migraine
• without aura, which is the most common,
• 2. Migraine with
• aura is characterized by an aura, namely
• focal neurological symptoms that precede
• the headache. These symptoms most often include visual
disturbances, such as flickering
• lights, and less often unilateral numbness,
66. Management
• should begin
• with an effort to modify triggering factors.
• Acetaminophen or nonsteroidal antiinflammatory
• drugs (NSAIDs) when taken at
• the onset of a mild attack may abort the
• pain. If the patient fails to respond, triptans
• or ergotamine should be tried.25 Overuse
• of abortive medications (acute anti-migraine
• drugs and/or opioids or combination analgesics
• taken on ≥10 days per month, or simple
• analgesics taken on ≥15 days per month)
67. Cluster Headache
• also called alarm clock
• headache, or suicide headache
• male to female sex ratio was 6:1
• Cluster headache is characterized
• by unilateral pain attacks and ipsilateral
• symptoms of autonomic dysfunction.31 The
• pain is localized in the orbital, supraorbital,
• and/or temporal region and is described as
• excruciating and throbbing. Associated autonomic
• features include conjuctival injection,
• ipsilateral lacrimation, nasal congestion, rhinorrhea,
68. • Cluster headache is
• characterized by regular periodicity; it occurs
• in discrete time periods lasting a few months
• (cluster periods) separated by remission periods
• lasting months or years. Notably, during
• the cluster periods, the pain attacks occur
• usually at the same time each 24 hour period,
• often in the middle of the night, awakening
• the patient. In contrast to migraine where retreat
• to a dark quiet room is desired, the CH
• patient tends to exhibit hyperactivity or restlessness
69. t/t
• Pharmacological therapy is the mainstay
• of treatment, with an emphasis on attack
• prevention during active periods of cluster
• headache. Effective prophylactic treatments
• include verapamil, ergotamine, methysergide,
• and steroids; lithium is also recommended
• for chronic CH.31 Acute therapies,
• aiming at aborting individual attacks, include
• subcutaneously administered sumatriptan,
• inhalation of 100% oxygen (7 L/min for
• 15 min), and intranasal dihydroergotamine.31
• Alcohol should be avoided during the cluster
70. Chronic Paroxysmal Hemicrania
• Chronic paroxysmal hemicrania (CPH) is a
• rare type of headache that, similar to cluster headache, is
characterized by daily, multiple,
• attacks of severe pain and associated autonomic
• symptoms. The pain attacks
• are more frequent but shorter-lasting
• than those of CH; they occur 1 to 40 times per
• day and last 2 to 120 minutes, with a mean
• of approximately 15 minutes. The pain
• presents most commonly in the ocular, temporal,
• maxillary, and frontal regions. It is described
• as excruciating and has a throbbing
71. • The pain episodes
• are typically accompanied by a variety of autonomic
• signs and symptoms, including ipsilateral
• lacrimation, rhinorrhea, conjunctival
• injection, and nasal congestion.39 Attacks occur
• around the clock and interrupt the patient’s
• sleep. Head flexion or rotation can
• precipitate the paroxysms in approximately
72. t/t
• Notably, CPH shows a very robust response
• to indomethacin prophylactic treatment.
• Accordingly, a drug trial is advocated
• when the frequency of headache episodes
• is higher than 4 per day. The recommended
• dose is 75 mg per day for 3 days, followed,
• if necessary, by 150 mg per day for another
• 3 days
74. • Idiopathic facial pain is a diagnosis of exclusion,
• after other conditions have been considered
• and eliminated. A thorough clinical examination
• and extensive diagnostic tests are
• warranted in order to rule out an underlying
• organic cause before the facial pain is labeled
• as “idiopathic.”
75. Atypical Facial Pain
• more common in
• women than in men
• Although any area
• of the face can be involved, the most commonly
• affected area is the maxillary region.
76. symptoms
• characterized by continuous,
• daily pain that is described as dull
• and aching.43 The pain is usually deep and
• diffuse and does not interfere with sleep.28,43
• At onset, the pain may be confined to a limited
• area on one side of the face, while later
• it may spread to involve a larger area. Psychological
• distress, including anxiety and depression,
• is prevalent among patients with
• atypical facial pain
77. • A small subset of patients develops
• typical features of trigeminal neuralgia later
• in the course of the condition; these cases
• are referred to as pretrigeminal neuralgia.43
• Pretrigeminal neuralgia is described as dull,
• constant pain that precedes the development
• of trigeminal neuralgia by days or years.44
78. management
• Management of the patient is
• better achieved through a multidisciplinary
• approach intended to relieve the pain and
• improve the patient’s quality of life. This involves
• reducing the disability caused by the
• pain often with an improvement in mood
• and an increase in activity and social contact.
• Medical management of idiopathic facial
• pain is mainly through the use of tricyclic
• antidepressant and anticonvulsant drugs.45,46
• Education, physical therapy, psychological
79. Atypical Odontalgia
• Atypical odontalgia, or phantom tooth pain,
• affects mainly women in the fourth and fifth
• decades of life.
• This condition is a variation
• of atypical facial pain, where chronic
• pain is centered on apparently normal teeth
• or endodontically treated teeth and occasionally
• in extraction sites.47,49 The pain is typically
• continuous, dull, aching or burning, and
• of moderate intensity. It can occur in any
• tooth or teeth group, but most commonly it
80. m/x
• Atypical odontalgia patients are usually
• subjected to many unsuccessful dental procedures
• before the correct diagnosis is
• reached.49,51 Dental treatment is contraindicated,
• since it can result in further deterioration
• of the patient’s dentition without
• any beneficial effect on the pain. Moreover,
• aggravation or spread of the pain
• following invasive dental interventions is
• not uncommon.48,52 In some occasions, the
• pain even begins following a deafferentation
• procedure, such as dental pulp extirpation
81. Burning Mouth Syndrome
• Burning mouth syndrome (BMS) is characterized
• by constant, chronic burning pain in
• clinically normal oral mucosal sites. Burning
• mouth syndrome has a higher prevalence
• in postmenopausal women.53 The anterior
• two thirds and tip of the tongue are
• most commonly affected;
• may constitute a primary (is
• idiopathic; the clinical examination and the
• results of laboratory testing and diagnostic
• imaging fail to detect any systemic or local
82. • can be unilateral or bilateral
• or can start on one side and spread
• to the opposite side. The pain does not disrupt
• the patient’s sleep, it is usually milder
• upon awakening and progressively increases
• in the course of the day.53 Eating, drinking,
• or chewing gum often attenuate the symptoms.
• Precipitating factors include stress, fatigue,
• cold, hot, or spicy foods. Associated
• symptoms may include dry mouth, taste alterations,
• thirst perception, and “draining
• fluid.”53 Spontaneous partial remission within
83. etiopathogenesis
• psychological distress may play a prominent
• role in individual cases; these should be
• identified and treated appropriately.58 Abnormal
• responses in quantitative sensory tests
• among BMS patients suggest a neuropathic
• Etiology.
• Moreover, the presence of taste
• abnormalities in BMS patients has led to the
• theory that there is a dysfunction of the
• chorda tympani and/or the glossopharyngeal
• nerves resulting in loss of central inhibition
• and hyperactivity of the nociceptive trigeminal
84. m/x
• Treatment of secondary BMS targets the
• underlying disease. In contrast, since the etiology
• of primary BMS is unclear, its treatment
• is empiric and still unsatisfactory. Commonly
• used pharmacological agents include
• tricyclic antidepressants, benzodiazepines,
• anticonvulsants, and topical capsaicin; however,
• there is no conclusive scientific evidence
• supporting their effectiveness.53,62,63
• Recent studies suggest that alpha lipoic acid,
• the trometamol salt of thioctic acid that has
• antioxidant and neuroprotective capacities,
85. Other diseases that can cause facial pain
1. Local pathology
2. Distant pathology (referred pain)
3. Systemic diseases
86. Local Pathology
• Pain in the orofacial region
• may be secondary to local pathology affecting
• any of the following structures: eyes, ears,
• nose, sinuses, pharynx, teeth (most common), periodontium,
• mucogingival tissues, salivary glands, cranial
• bones, and temporomandibular joint.
Dental
pain is among the most common types
of orofacial pain and can be referred to various
head and neck areas. On the other
hand, muscular, neuropathic and neurovascular
pain may be felt in teeth, mimicking a
toothache and confusing the clinician. Dental pain is usually
intensified by local
provocation of the teeth and it tends to get
87. Pain in the orofacial region may also be
due to a variety of oral mucosal and gingival
disorders, such as acute necrotizing ulcerative
gingivitis, recurrent apthous stomatitis,
herpes simplex, candidiasis, lichen planus,
and other vesiculobullous and ulcerative diseases
Acute sinusitis
presents with periorbital pressure and pain
over the affected sinuses. Maxillary sinusitis
can refer pain to maxillary teeth; typically
the pain is described as dull and constant,
and the teeth are sensitive to percussion
and may feel extruded.70,71 The accompanying
malaise, fever, nasal obstruction, and
purulent nasal discharge facilitate the diagnosis,
while radiographic examination is
needed to confirm it.71 Administration of antibiotics,
such as penicillin or amoxicillin,
for 7 to 14 days constitutes the mainstay of
treatment.72
88. Salivary pain, intensified immediately
prior to and during eating, is often due to
blockage of a salivary duct by calculus, which
causes chronic sialadenitis.73 Salivary gland
tumors may also cause pain; tumors occurring
in the deep lobe of the parotid gland may
cause temporomandibular joint symptomatology,
simulating a number of primary temporomandibular
disorders (see Figure 2).74
Orofacial pain that has worsened rapidly in
a short period of time may indicate malignancy,
which may affect almost any soft
or hard tissue component of the oral and
maxillofacial region,
Sjogren’s
syndrome, which is characterized by dry
mouth and eyes and bilateral parotid
swelling, may also be associated with facial
pain. Sjogren’s syndrome affects women 9
times more than men. It is an autoimmune
disorder whose etiology is unknown and its
treatment is primarily symptomatic, consisting
of artificial salivary substitutes, cholinergic
agonists, NSAIDs, and antirheumatic
drugs
89. Distant Pathology (Referred Pain)
• Cranial
• nerves V, VII, IX, X, as well as the upper
• cervical nerves converge in the trigeminal
• spinal tract nucleus, providing an anatomical
• substrate for pain referral in the orofacial
• Region
• Accordingly, pathology in distant
• structures, including the neck, heart muscle,
• brain, and lung can be the source of referred
• orofacial pain.
90. • Distant Pathology (Referred Pain)
• Referral of pain in the orofacial structures is
• not uncommon and can constitute a significant
• challenge in the diagnostic process. Cranial
• nerves V, VII, IX, X, as well as the upper
• cervical nerves converge in the trigeminal
• spinal tract nucleus, providing an anatomical
• substrate for pain referral in the orofacial
• region.78 Accordingly, pathology in distant
• structures, including the neck, heart muscle,
• brain, and lung can be the source of referred
• orofacial pain. Palpation of the neck
91. Systemic Diseases
• Rheumatic diseases, such as
• rheumatoid arthritis, psoriatic arthritis, and
• systemic lupus erythematosus can affect the
• temporomandibular joints and are often associated
• with musculoskeletal facial pain and
• dysfunction.
Notably, fibromyalgia affects
15% to 20% of temporomandibular disorders
(TMD) patients, while its population prevalence
ranges from 0.5% to 5%.85−87 Moreover,
75% of fibromyalgia patients meet the
diagnostic criteria for TMD.86 Fibromyalgia,
according to the criteria established by the
American College of Rheumatology, is characterized
by chronic, widespread pain, as
well as pain on palpation of 11 out of 18 specific
tender points.88 The disorder is also associated
with fatigue, sleep disturbances, cognitive
dysfunction, and psychological distress.89
The prominent overlap between fibromyalgia
and TMD, combined with the fact that
most TMD patients report pain in multiple
body sites,90 suggest that the two disorders
share common underlying pathophysiological
mechanisms, such as dysfunction
of pain processing in the central nervous
system.
92. • The clinical manifestation of Lyme disease
• may also mimic various orofacial pain
• disorders.93,94 Associated signs and symptoms
• include facial and dental pain, headache,
• temporomandibular joint and masticatory
• muscle pain, as well as facial nerve palsy.94,95
• Lyme disease should be included in the differential
• diagnosis when dealing with multisystemic
• presentation and vague, nonspecific
• face and/or head pain.94 History of exposure
• to the spirochete, development of erythema
• migrans, and positive serologic studies
93. • Neurological disorders, such as multiple
• sclerosis, may constitute the underlying cause
• of neuropathic facial pain. Multiple sclerosis
• is a chronic central nervous system disease,
• characterized by discrete areas of demyelination,
• axon damage, and associated
• inflammation.97−99 Multiple sclerosis lesions are disseminated in
time and space and
• can result in a wide variety of symptoms
• and signs, including numbness, paresthesias,
• pain, weakness, spasticity, fatigue, vertigo,
• visual difficulties, gait dysfunction, bladder
94. Psychogenic Pain
• Various mental disorders have been associated
• with chronic orofacial pain, including
• somatoform disorders, factitious disorders,
• and malingering.28 A diagnosis of psychogenic
• pain requires not only exclusion of
• other organic disorders, but also fulfillment of
• specific diagnostic criteria.
95. INTERNAL DERANGMENT OF THE TMJ
• Pain on palpation directly over TMJ.
• Limitation in joint range of motion.
• Deviation on opening.
• Joint noises consistently associated with pain.
• Joint crepitus.
• Mahan sign (+ve in Wilkes II,III and IV).
99. NEURALGIA-INDUCING CAVITATIONAL
OSTEONECROSIS
Rare pain disorder characterized by continuous
lancinating like pain in site of previous tooth
extraction.
Usually in lower 3rd molar region.
Pain not interfere with sleep.
Radiographically appear as moth eaten or soap
bubbles in site of previous extraction.
Treated by resection of bone area with pain ,
102. • -Pain is typically aching,buring,or shock like.
• -Potential sequela of infection with herpes zoster.
• Pain persist longer than one month after
healing vesicle classified as PHN.
Post-herpetic neuralgia
103. Management:
• -Antiviral and corticosteroids after presentation of
rash reduce incidence of postherptic neuralgia.
• -Anticonvulsant drugs
• -Local anesthesia injected to painful site.
104. Occipital Neuralgia
presents as a paroxysmal stabbing pain in the distribution of
the greater or lesser occipital nerves.
It may be caused by trauma,
Palpation below the superior nuchal line may reveal a tender
spot .
Treatment has included occipital nerve block,
neurolysis, C2 dorsal root gangionectomy ,
105. Post -Traumatic Neuropathic Pain
Its caused by Trigeminal nerve injuries may result from facial
trauma or from surgical procedures, such as the removal of
impacted third molars, the placement of dental implant
Clinical Manifestations: The pain may be persistent or occur
only in response to a stimulus, such as a light touch.
Patients with nerve damage may experience anesthesia ,
paresthesia, allodynia , or hyperalgesia .
106. Post -Traumatic Neuropathic Pain
Treatment:
may be surgical ,nonsurgical, or both,
Systemic corticosteroids a when administered within the first
week after a nerve injury.
TCAs
Anticonvulsant drugs, Gabapentin.
Topical capsaicin .
107. Complex Regional Pain Syndrome( CRPs)
chronic pain conditions that develop as a result of injury.
patients suffer from allodynia, hyperalgesia, and spontaneous pain that
extends beyond the affected nerve dermatome.
it accompanied by motor and sweat abnormalities, atrophic changes in
muscles and skin, edema,
108. Complex Regional Pain Syndrome
Types of CRPs :
1- CRPS I was previously termed reflex sympathetic dystrophy
(RSD),
2- CRPS II was previously termed causalgia.
Etiology and Pathogenesis:
believed to result from changes after trauma that couples
sensory nerve fibers with sympathetic fibers.
109. Complex Regional Pain Syndrome
Treatment:
physical therapy.
block of regional sympathetic ganglia or regional intravenous
blockades with guanethidine ,reserpine, or
phenoxybenzamine,
Bisphosphonates such as alendronate or pamidronate.
110. Paroxysmal pain of facial nerve, may result of herpes zoster of
geniculate ganglion.
-Clinical features:
-Pain at the ear, anterior tongue, soft palate.
-Not intense like T.N.
- Ramsay-hunt syndrome may develop(Facial paralysis ,vesicle
,tinnitus & vertigo)
Nervous Intermedius (Geniculate) Neuralgia
111. Management:
• -High dose of steroid for 2-3weeks.
• -Acyclovir is significant in reduce the duration.
• -Anti convulsion ,Carbamezipine.
• -Surgery: section of nerve intermedius.
112. CENTRAL POSTSTROKE PAIN
Condition secondary to damage caused by a
cerebrovascular accident .
its is characterized by constant or paroxysmal pain
accompanied by sensory abnormalities ,
113. CENTRAL POSTSTROKE PAIN
Treatment:
anticonvulsant ( Lamotrigine,Gabapentine)
sodium channel blocker(Mexiletine).
TCAs (Amitriptyline).
Short-term relief may be obtained with intra venous lignocaine
or propofol .
Note: the anticonvulsants are preferred
114. Bell's palsy
In about 50% of patient with Bell's palsy, pain occur
in or near the ear but sometimes spreading down the
jaw, either precedes or develops at the same time as
the facial palsy.
Treatment: prednisolone 60-80 mg per day, acyclovir.
115. Atypical facial pain
Constant dull aching pain , deep ,diffuse variable
intensity in absence of identifiable organic disease.
Its more common in female .
Most patient middle age and elderly .
116. Atypical facial pain
Clinical features:
Often difficult for patients to describe their symptoms .
Most frequently described as deep , constant ache or burning .
Doesn't awake patient.
Doesn't follow anatomical pattern and may be bilateral.
Affect maxilla more than mandible.
Often initiated or exacerbated by dental treatment .
Examination entirely normal .
Often have other complaints such as IBS ,dry mouth and
chronic pain syndrome .
117. Atypical facial pain
Treatment :
Often rewarded with limited response.
Tricyclic antideprssant drugs have some effect in some patients .
30% of patient respond to Gabapentine
Cognitive behavior therapy
118. occurs most frequently in women in the fourth and fifth
decades of life,
constant dull, aching pain without an apparent cause that can
be detected by examination ,
it occur after dental extraction or endodontic treatment ,
Period of pain free after secondary dental management.
Atypical odontalgia(phantom)
120. Burning sensation of oral mucosa , usually tongue, in
absence of any identifiable clinical abnormality or
cause.
Epidemiology: 5 per 100,000 ,higher in middle age
and elderly, affect female more than male .
Causes: unknown but hormonal factors , anxiety ,and
stress have been implicated.
Burning mouth syndrome
121. Clinical features:
• Complain of dry mouth with altered or bad taste.
• Burning sensation affecting tongue , anterior palate and less
common lips.
• May be aggravated by certain foods.
• Usually bilateral.
• Doesn't awake patient . But may present at awaking
• Examination entirely normal .
122. Burning mouth syndromeInvestigation: FBC ,haematinics ,swab for Candida .
Treatment:
Reassurance .
Avoidance of stimulating factors.
Some patients may respond to TCA, SSRIs
topical clonazepam, sucking and spitting 1 mg three
times daily for 2 weeks.
2-month course of 600 mg daily alfa-lipoic acid.
Cognitive behavior therapy.
123. Eagle’s syndromea series of symptoms caused by an elongated styloid
process (more than 3 c.m) and/or the ossification of part
or the entire stylohyoid Ligament.
124. Types of Eagles syndrome:1-Classic :
the symptoms are persistent pharyngeal pain
aggravated by swallowing and frequently radiate to the
ear , with sensation of foreign body within pharynx ,
This pain arise following tonsillectomy due to
development of scar tissue around the tip of the
styloid process.
125. 2- stylo-carotid artery syndrome(vascular):
Attributed to impingement of the carotid artery by the styloid
process This can cause a compression when turning the head
resulting in a transient ischemic accident or stroke.
3-Traumatic Eagle syndrome:
in which symptoms develop after fracture of a mineralized
stylohyoid ligament.
126.
127. Diagnosis:(1)clinical manifestations,
(2) digital palpation of the process in the tonsillar fossa,
(3) radiological findings .
(4) lidocaine infiltration test.
Treatment:
COSERVATIVE: involves injecting steroids
or long-lasting anesthetics into the lesser cornu of
the hyoid or the inferior aspect of the tonsillar fossa
I,NSAID
Surgical: intra oral or extra oral styloidectomy
128. Before puberty , female more than male .
Aura may developed before headache in
40%.
It may be triggered by foods such as nuts,
chocolate, and red wine ; stress; sleep
deprivation; or hunger.
Migraine
129. Clinical manifestation:
A-classic migraine (start with prodromal aura occurring
over 20-30 minutes )
• Flashing lights
• Scotoma (localized area of vision depression )
• Sensitivity to light
• Sensory and motor deficit
• Aura is followed by severe unilateral throbbing pain.
• Headaches may last for hours or up to 2 or 3 days.
B-common migraine (not preceded by aura)
• Severe unilateral throbbing pain
• Sensitivity to light and noise
• Nausea and vomiting
130. C-facial migraine(carotidynia):
• 30-50 years of age.
• Pain last for minutes to hours and recurs several times
per week.
• Throbbing pain of neck and jaw.
• Patients often seek dental consultation,
• Tenderness of carotid artery
D-Basilar migraine :
• The symptoms are primarily neurologic and include
aphasia,temporary blindness, vertigo, confusion, and
ataxia.
• may be accompanied by an occipital headache.
132. Cluster headache
Clinical Manifestations:
• 80%of patients with CH are men.
• The attacks are sudden, unilateral, and stabbing ,causing
patients to pace, cry out, or even strike objects. Some patients
exhibit violent behavior during attacks.
• pain as a hot metal rod in or around the eye.
• Each attack lasts from 15 minutes to 2 hours and recurs several
times daily.
• A majority of the painful episodes occur at night, often
awaking the patient from sleep.
133. Cluster headache
Clinical Manifestations:
• The pain is associate nasal congestion and tearing Sweating of the face,
ptosis, increased salivation, and edema of the eyelid.
• Cluster headache produce pain in posterior maxilla that mimic dental pain.
• Trigger by alcohol.
134. Cluster headache
Treatment:
An acute attack:
100% oxygen (its effectiveness is diagnostic), Injection of sumatriptan or
sublingual or inhaled ergotamine
Prophylaxis : lithium, ergotamine, prophylactic
prednisone, and calcium channel blockers.
135. Chronic Paroxysmal Hemicrania
is believed to be a form of CH that occurs predominantly in
women between the ages of 30 and 40 years.
The episodes of pain tend be shorter, but attacks of 5 to 20
minutes’ duration can occur up to 30 times daily.
It responds dramatically to therapy with indomethacin , which
stops the attacks within 1to 2 days.
136. Temporal Arteritis
-Its inflammation(vasculitis) of cranial arterial
tree.secondary to giant cell granulomatous.
Clinical features:
most frequently affects adults above the age of 50
years.
Dull aching or throbbing temporal pain.
accompanied by generalized symptoms , including
fever, malaise, and loss of appetite.
Jaw claudication during mastication.
137. Temporal ArteritisDiagnosis:
elevated ESR 50-100 .
elevated CRP.
Biopsy.
-Treatment:
high dose of steroid(prednisolone) 60 -100mg daily.
the steroid is tapered once the signs of the disease are
controlled.
Patients are maintained on systemic steroids for 1 to 2 years
after symptoms resolve.
138. 1-Burket,s oral medicine.
2-Neville , Oral & Maxillofacial PATHOLOGY
3-Fonseca Oral and Maxillofacial surgery.
4- Booth Oral & Maxillofacial surgery.
5-Lecture notes in oral and maxillofacial surgery.
6- Orofacial pain ,from basic to management
References
