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CHAP TER11 The upper jaw and midface
cTrigeminal neuralgia (‘tic douloureux’)
Trigeminal neuralgia is most commonly a disorder seen in middle- aged
and elderly patients. It is more common in women with a peak incidence
between 50 and 60years of age. In young patients it may be an early feature
of MS, HIV disease, or as a consequence of a lesion irritating the trigeminal
nerve. Patients complain of a sharp, intense, lancing/ ‘electric- type’ pain
induced by a specic trigger point that r adiates across the distribution
of a branch of the trigeminal ner ve. The pain is almost always unilater al,
with over 30 – 40% of patient s showing a distribution aecting both the
maxillary and mandibular divisions. In approximately 20% of patients, the
pain is conned to the mandibular division, and the ophthalmic division
in 3%. Episodes may last up to several hour s. The aetiology of trigeminal
neur algia is presumed to be multifactorial, with local nerve microcom-
pression within the skull base and possible demyelination.
Management
• Always consider skull base pathology and intracranial disease/
demyelination. Imaging may be required.
• The mainstay of treatment remains medical, typically with
anticonvulsant agents. Usually, trigeminal neuralgia responds well
to carbama zepine and/ or amitriptyline, and a muscle relaxant
such as baclofen. Car bama zepine remains the drug of choice
with an initial regime of 10 0 mg three times daily being gradually
increased to a maximum of 1200 mg daily titrated against eect.
About 20% of patients may develop side eects such as tremor,
dizziness, double vision, and vomiting, which will obviously limit
its use. They should have regular monitoring of FBC, electrolytes,
and LFTs. Approximately 20% can develop folic acid deciency with
megaloblastic anaemia, and hyponatraemia in the elderly. Withdraw
therapy slowly.
• Alternative agents include phenytoin, sodium valproate, lamotrigine,
and baclofen.
• Local sur gical procedures may be considered in trigeminal neur algia
not responsive to medical management. This can include cryotherapy
to the nerve, alcohol/ glycerol injections.
• Neurosurgical decompression in severe cases following imaging
conrming there is nerve compression.
• Gamma Knife® (stereotactic radiosurgery). High- resolution imaging
provides excellent denition and allows a focus beam of ionizing
radiation to irradiate the proximal trigeminal ner ve at its entry into the
pons. Results are very promising (see http:// www.gammaknife.org.uk).
cAtypical facialpain
Atypical facial pain has many distinguishing features that make it a clinical
entity in it s own right and not just a ‘catch all’ diagnosis for seemingly
unexplained facial pains. It is, however, essentially a diagnosis of exclusion
that should only be made after all other possible organic causes have been
excluded. These patients therefore often undergo extensive investigation.
FACIAL NUMBNESS
Clinical features
Patie nts ofte n have a ‘at aec t’ and the mo re they are q uestione d about the
pain the more vague their answers become. The pain is typically described
as being a deep, dull ache, sometimes uctuating, sometimes continuous,
with intermittent severe episodes that the patient can nd no causative factor for. Often the pain has been present for several years and analgesics
rarely aect its nature. It is most commonly bilateral, but ill dened, and its
distribution cannot be explained on an anatomical basis. The patient may
say they are kept from sleeping by the pain but usually look well rested.
When they do admit to sleeping, the pain does not wake them. Aproportion of these patients may show symptoms of depressive illness or anxiet y
states, and patients of ten complain of other symptoms such as back and
neck pain and irritable bowel syndrome. Th e patient’s mood ofte n does not
correlate to the description of their symptoms and they may show exaggerated responses to examination and report stressful life events.
Management
Often the ill- dened nature of the patient’s pain result s in unnecessary
dental work being carried out. In light of the association of atypical facial
pain with the neuroses (particularly depression), and the belief that it
essentially has a psychogenic basis, emphasis has been placed on the use
of antidepressant agents as the main treatment option.
• Dothiepin, a tr icyclic antidepressant, has been shown to be eective
in reducing the painful symptoms (as it has in TMJ dysfunction).
• Selective serotonin re- uptake inhibitors (SSRIs).
cFacial numbness
Facial numbness is a problem that presents from time to time. In most
cases either the cause is benign or cannot be found. Many cases spontaneously resolve without a rm diagnosis ever being made— idiopathic
facial numbness. Nevertheless, numbness, especially if it corresponds to the
distribution of a nerve, should be taken seriously. It can occasionally be the
rst symptom of a serious problem.
Causes
• Idiopathic
• Migraine
• Following dental treatment (nerve injury)
• Post- trigeminal neuralgia
• Viral trigeminal neuropathy. Temporary dysfunction of the nerve
following a viral infection
• Demyelinating diseases (notablyMS)
• Tumours (sinus, intr acranial, skull base, nerve sheath)
• Sinus pathology (including large odontogenic cysts) aecting the
infraorbitalnerve
• AVM
• Hypothyroidism
• Peripheral neuropathy (common causes are vitamin deciency,
diabetes, excessive alcohol int ake, and lead poisoning, but there are
many other causes).
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CHAP TER11 The upper jaw and midface
Investigations
These are tailored towards the suspected cause, but include the
following:
• FBC and ESR/ CRP
• Electrolytes (notably calcium, potassium, and sodium)
• LF Ts
• Thyroid functiontests
• Measurement of vit aminlevels
• Heavy metal or toxicology screening
• Imaging may include MRI or CT. MRI is useful for demyelinating and
other intracranial disease, CT in the assessment of the sinuses, but it
is often best to discuss these with a radiologist.
Management
This is directed to the underlying cause (if one is found). Sometimes reas-
surance and review is all that is required.
cFacialpalsy
Assessment of a patient with facial palsy requires careful examination of the
ear— see E Chapter 6 for details.
The cranial nerve VII (facial nerve) supplies:
• Motor bres to the muscles of facial expression, post belly of
digastric, and a branch to the stapedius muscle in the middleear.
• Taste sensation from the anterior two- thirds of the tongue via the
chorda tympani.
• Secretomotor bres to the submandibular, sublingual salivary glands,
and to the lacrimal glands.
Extracranial course ofthe facialner ve
The facial nerve exits the st ylomastoid foramen, just in front of the mas-
toid process and passes almost immediately into the parotid gland. Here
it lies in a brous plane separating the deep and supercial lobes of the
gland. The nerve then divides into t wo major divisions:an upper ‘tempo-
rofacial’ and lower ‘cervicofacial’ branch. These then divide further into
its ve terminal branches:
• Temp o r a l
• Zygomatic
• Buccal
• Marginal mandibular
• Cervical branch.
Sometimes the marginal mandibular branch divides immediately into
two, making six main branches of note. Frequent interconnections exits
between these branches— the ‘pes anserinus’.
Causes offacialpalsy
• Cerebrovascular accidents
• Cerebral tumours
• Bell’spalsy
• Acute/ chronic otitis media/ other middle ear diseases
• Ramsay Hunt syndrome (her pes zoster infection of the geniculate
ganglion)
• Trau m a
• Surgical (iatrogenic— possibly intentional)
• Temporal bone fracture (see E Chapter 6)
• Bir thinjury
• Neoplastic — malignant disease of the middle ear and acoustic
neuroma
• Parotid tumours and inltrative disease(TB)
• Sarcoidosis— Heerfordt’s syndrome is sarcoidosis resulting in parotid
enlargement, fever, anterior uveitis, and facial nervepalsy
• MS
• Guillain– Barré syndrome (acute idiopathic polyneuritis). Facial palsy
does not occur in isolation. An ascending peripheral neuropathy
is usually associated. It is believed to occur following a recent viral
infection. Potentially a serious condition.
Clinical features
Varying degrees of weakness of the muscles of the face may beseen:
• Upper motor neuron lesions will cause a unilateral facial palsy with
sparing of the muscles of the upper face. The upper face receives
innervation bilaterally from both motor cortices. All muscles may
move normally during emotional responses.
• Lower motor neuron lesions will show a unilateral paralysis of all the
muscles, both voluntarily and to emotional stimulus.
This can result in the following:
• Facial asymmetry is exagger ated when attempting to show the teeth,
whistle, or close the eyes tightly (the eyes roll upwards— Bell’s
phenomenon).
• Food collects in the vestibule because of buccinator paralysis.
• Loss of the nasolabial fold as the commissure of the mouth droops.
• Epiphora— tears overow to thecheek.
• Reduced lacrimation (lesions above the geniculate ganglion).
• Hyperacusis:loss of stapedius reex (lesions above ner ve to
stapedius).
• There may also be loss of taste and reduced salivation.
cHerpes zoster infection (Ramsey Hunt syndrome)
This is a viral infection, usually chickenpox, aecting the geniculate gan glion. In addition to facial weakness, vesicles are visible on the ear canal,
phar ynx, and face. Management requires the use of systemic antiviral
agents (aciclovir). Some specialists also advise steroids.
cBell’spalsy
Idiopathic facial palsy (Bell’s palsy) should be a ‘diagnosis of exclusion’. All
other causes must be eliminated clinically or following investigations (notably
parotid tumours and acoustic neuroma). There is unilateral facial paraly-
sis, sometimes associated with loss of taste and hearing, or occasionally
hyper acusis. It is often preceded by mastoid discomfor t. High- dose IV
steroids may be of use, although this is controversial, and if the diagnosis
is wrong (e.g. it is herpes zoster instead) this may lead to rapid spread
FACIALPALSY
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CHAP TER11 The upper jaw and midface
and deterioration in the patient. Bell’s palsy can be easily confused with
Ramsey Hunt syndrome (in which the use of steroids is controver sial). To
dierentiate bet ween the two, consider the history and carefully exam-
ine for vesicles in the external meatus. The prognosis for Bell’s palsy is
generallygood.
Management offacialpalsy
This is dependent on thecause.
Non- infective lumps and swellings
cParotid obstruction
Obstruction of any part of the duct system of the gland may result in
a build- up of salivary secretions and swelling. The classic histor y is of
unilateral swelling on the side of the face, associated with meal times.
Patient may also report that the swelling set tles a few hours after the end
of eating. Parotid calculi are not as common as submandibular and are
usually not visible on plain lms. Sialography is of ten required to locate
them. Stones may be removed endoscopically. With recur rent bouts of
obstruction, infection may eventually super sede due to st agnation of
secretions.
cParotid tumours
70– 80% of all salivary gland tumours arise in the parotid. Of these,
approximately 80% are pleomorphic adenomas and 10– 15% are malig-
nant. Classication of salivary gland tumours is complex. This includes
(not an exhaustivelist):
• Benign epithelial tumours (pleomorphic and monomorphic adenoma,
myoepithelioma, and Warthin’s tumour)
• Malignant epithelial tumour s (acinic cell, mucoepidermoid, and
adenoidcystic carcinoma, salivary duct carcinoma)
• Soft tissue tumours (lymphangioma, haemangioma, and lymphomas)
• Metastatic tumours (skin cancers metastasizing to parotid nodes).
A lump associated with facial nerve weakness suggests inltrative patholog y
(i.e. tumour). Patients may present with the following clinical features:
• Swelling
• Pain
• Facial weakness
• Skin changes
• Poor hearing or earache.
Most parotid tumours present as a painless, localized swelling, which
have been present for several years. Pain in the gland suggests infection or
malignancy. Other features suggestive of malignancy include facial ner ve
weakness, tethering of the lump, and rapid growth. Investigations include
CT or MRI scan. FNAC is often under taken but its value is debatable.
Parotid lumps need urgent referral to a head and neck specialty (e.g.
maxillofacial/ ENT ). Imaging is usually required (CT/ MRI or ultrasound).
Management is usually surgical removal.
NON-INFECTIVE LUMPS AND SWELLINGS
Not all swellings of the parotid gland are due to salivary tumour s.
Tumours can also arise from associated blood vessels, nerves, fat , and
lymphatic tissue. ‘Tumour- like’ conditions presenting as swellings include
sarcoid, toxoplasmosis, and sialosis. The latter is painless swelling, which
may be associated with alcoholic cirrhosis, diabetes, acromegaly, or bulimia. Heerfordt’s syndrome is sarcoidosis resulting in parotid enlargement,
fever, anterior uveitis, and facial nervepalsy.
cOdontogenic cysts and tumours
As a group these form the commonest cause of non- infective swelling in the
upper and lower jaws. The vast majority which present are benign. The term
‘odontogenic’ refers to structures arising from the tissues that make up
the teeth. Classication of odontogenic cysts and tumours is very complex. Some pathologist s specialize in just these and other oral pathology.
Odontogenic cysts and tumours can be considered as follows:
Benign odontogenic tumours
• Ameloblastoma
• Squamous odontogenictumour
• Calcifying epithelial odontogenic tumour (Pindborg tumour)
• Ameloblastic broma
• Calcifying odontogeniccyst
• Odontoma
• Odontogenic broma
• Myxoma (odontogenic myxoma, myxobroma)
• Cementoblastoma.
Malignant odontogenic tumours
• Malignant ameloblastoma
• Primar y intraosseous carcinoma
• Malignant variant s of other odontogenic epithelial tumour s
• Malignant changes in odontogeniccysts
• Odontogenic sarcomas
• Odontogenic carcinosarcomas.
Non- neoplastic bone lesions
• Fibrous dysplasia of thejaws
• Cemento- osseous dysplasia
• Periapical cemental dysplasia (periapical brous dysplasia)
• Cherubism (familial multilocular cystic disease of thejaws)
• Central giant cell gr anuloma
• Aneur ysmal bonecyst
• Solitary bonecyst
• Traumatic bone cystofjaw
• Simple bone cystofjaw
• Haemorrhagic bonecyst.
This is not an exhaustivelist.
bOdontogeniccysts
Many types of cyst can occur in the jaws and the classication of these
is also very complicated. The vast majority of these present a s a welldened, cor ticated, radiolucency in the bone, often incident al. A few
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CHAP TER11 The upper jaw and midface
Figure11.4 Large dentoal veola r cyst in the r ight maxilla. T he over lying bone
was eg gsh ellth in.
have characteristic calcication that enables diagnosis. Many can be diag-
nosed with reasonable certaint y from the X- r ay (see Figure 11.4). Some
require biopsy. All should be referred, but not necessarily on an ur gent
basis (if small and asymptomatic). The more common ones encountered
include:
• Dentigerouscyst
• Odontogenic keratocyst (may be considered as an intraoral basal cell
carcinoma)
• Periapicalcyst
• Residual cyst of thejaw
• Traumatic bone cystofjaw
• Stafnecyst.
Other causes of a ‘cyst’ in the jaws include:
• Ameloblastoma
• Metastases, including lymphoma
• Squamous cell carcinoma invading thebone
• Multiple myeloma
• Periapical abscess
• Giant cell granuloma
• Aneur ysmal bonecyst.
Again, this list is not exhaustive but demonstrates the diculty in triaging
and diagnosis of cysts and growths of thejaws.
NON-INFECTIVE LUMPS AND SWELLINGS
bExtramedullary haematopoiesis
This should be considered in the dierential diagnosis of any diuse jaw
swelling in patients with chronic anaemia. It is the production of blood in
sites other than the long bones, pelvis, spine, and ster num. This occurs
as a response to increased production of erythropoietin in chronically
anaemic patients (such as those with chronic haemoly tic anaemia). There
is usually hepatomegaly and splenomegaly. Extramedullary haematopoiesis rarely involves the facial bones but has been repor ted to involve the
mandible, maxilla and orbit. It may be misdiagnosed as sinusitis.
cMyeloma
Myelomatous involvement of the maxilla is very rare, but may present
as an expansile jaw lesion. Patients may also present with renal failure,
bone pain, fatigue, recurrent infections, and neurological dysfunction.
Oral manifestations may be the rst sign. Treatment involves mainly irradiation and chemotherapy and the prognosis is generallypoor.
bOsteoradionecrosis(ORN)
ORN of the upper jaw is less common than the lower, due to its relatively
better blood supply. The clinical spectrum of presentation of ORN is
wide. The patient will usually have a non- resolving painful mucosal ulcer
with evidence of exposed bone or sequestrum. There may be trismus
and this usually appears 3– 6months following radiotherapy. At the other
end of the spectrum the patients may present with an orocutaneous stula, increasingly mobile teeth, or a pathological fracture. Typically radiological appearances will include a moth- eaten appear ance to the bone,
which is best seen on CT. Management pr inciples are based on controlling any acute superadded infection, strict oral hygiene, analgesia, and
nutritional suppor t as well as minimal surgical debridement. In severe
cases, resection of the bone involved and reconstr uction with a free tissue transfer may be required.
bBisphosphonate- related osteonecrosis
ofthe jaw (BRONJ)
Bisphosphonates inhibit osteoclastic action and reduce bone loss in
patients with multiple myeloma, bony metastasis in breast cancer,
Paget’s disease of bone, and postmenopausal osteoporosis. However,
osteonecrosis can occur as a serious side eect in both jaws. Patients
present with pain and swelling aecting the mucosa of the jaw, which
may be confused with chronic osteomyelitis, ORN, or even malignancy.
CT usually shows regions of mottled bone and sequestrum formation.
Treatment usually involves meticulous or al hygiene, antibiotics and gen tle debridement. Cessation of the drug, if not contraindicated may help
some recovery.
bPaget’s disease
Paget’s disease is a localized disorder of bone remodelling. Usually the
bone is mechanically weaker, larger, less compact, more vascular, and
more susceptible to fracture than normal adult lamellar bone. Patients
can present with bone pain associated with marked deformity. Clinical
examination may reveal excessive warmth, due to hypervascularit y and
paraesthesia of the infraor bital ner ve due to bony compression. These
symptoms may be confused with chronic infection or a tumour.
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CHAP TER11 The upper jaw and midface
bFibrous dysplasia
This is a disorder of bone grow th where normal bone is replaced with
immature brous bone. It can occur in any part of the skeleton but the
skull and face are commonly involved. Patients present with a smooth
hard swelling and deformity usually in childhood or early adulthood.
During rapid growth this may become painful. Two types of brous dys-
plasia are described.
McCune– Albright syndrome, includes endocrine diseases (precocious
puberty) and skin pigmentation. Fibrous dysplasia may also be associated with neurobromatosis. Management include bisphosphonates and
surgical contouring of a cosmetic deformity.
Chapter12
347
The lower jaw andface
Common presentations 348
Common problems and their causes 348
Useful questions and what to look for 351
Examination of the lower jaw and face 356
Useful investigations 358
Injuries to the lower jaw 359
Temporomandibular joint dislocation 365
Infec tive swellings around the lower jaw and face 366
Non- infective swellings around the lower jaw and face 372
Temporomandibular joint dysfunction syndrome 375
Limitation of mouth opening 377
Tris mus 379
Bleeding from the lower jaw (non- traumatic) 380
Cutaneous sinuses and stulae overlying the lower jaw 382
Pain in the lower jaw 384
Altered sensation of the lower lip 388