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Peripheral nerve injuries 185
Figure19.1 (a) Radial nerve injury:
wrist drop, together with anaesthesia
of a small area of the dorsal aspect
of the hand at the base of the thumb
and index nger. (b) Median nerve
injury: thenar eminence paralysis with
anaesthesia of the palmar aspect of
the radial three and a half digits and
corresponding palm.
Median nerve
compression at thewrist
(carpal tunnel syndrome)
The median nerve can be compressed as it passes
through the carpal tunnel (formed by the flexor retinaculum stretching from the hook of the hamate and
pisiform medially to the trapezium and scaphoid laterally). This results in a chronic compression neuropathy of the median nerve. Symptoms include tingling,
diminished sensibility and weakness in the hand as
well as pain in the hand and forearm. In the early and
mild stage of carpal tunnel syndrome, the symptoms
are episodic and worse at night (patients are often
woken from sleep).
In the later and more severe stage, the symptoms
are continuous. The thenar muscle area of the hand
can become wasted. Women are affected four times
more commonly than men, and there is an association with systemic conditions including obesity and
diabetes, and also with pregnancy. In most patients,
the diagnosis can be made from review of the history, and the severity confirmed by examination.
Patients with mild carpal tunnel syndrome may benefit from weight loss, use of a splint across the wrist
at night, and injection of steroids into the carpal tunnel. Severe carpal tunnel syndrome is effectively
treated by surgery to divide the flexor retinaculum
atthe wrist.
Ulnar nerve injuries
(Figure19.2)
The ulnar nerve is acutely injured by fractures around
the elbow joint, penetrating injuries to the upper
inner arm and by lacerations of the forearm and the
wrist. Chronic compression of the nerve occurs at the
Figure19.2 Ulnar nerve injury: main en griffe with
anaesthesia of the ulnar one and a half digits and ulnar
border of the hand on both palmar and dorsal aspects.
186 Peripheral nerve injuries
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elbow (in the cubital tunnel) and less commonly at
the wrist (Guyon’s canal
The ulnar nerve supplies all the intrinsic muscles
of the hand apart from the three muscles of the thenar eminence (abductor pollicis brevis, opponens
pollicis and flexor pollicis brevis) and the two radial
lumbricals, all of which are supplied by the median
nerve. The affected intrinsic muscles are the adductor pollicis, the muscles of the hypothenar eminence, the ulnar two lumbricals and the interossei,
which are the abductors and adductors of the fingers
and which also extend the interphalangeal joints. In
the forearm, the ulnar nerve supplies flexor carpi
ulnaris and the medial half of flexor digitorum
profundus.
The function of the ulnar nerve can be reliably
assessed by testing the patient’s capacity to adduct
the thumb (using adductor pollicis) towards the index
finger (Froment’s test
Damage to the ulnar nerve produces the ‘claw
hand deformity’ or main en griffe. This posture
results from the unopposed action of the long flexors and extensors of the fingers. The paralysed
intrinsic muscles of the hand are normally responsible for flexion of the metacarpophalangeal joints
of the fingers. These joints are, therefore, extended
in an ulnar nerve palsy. The flexor profundus and
sublimis, flex the distal and middle phalanges at
the interphalangeal joints, and these joints are held
in a flexed posture. The patient is unable to make a
normal grip around an object and instead flexes the
interphalangeal joints pushing an object down
thepalm.
If the nerve is injured at the elbow, flexor digitorum
profundus to the fourth and fifth finger is paralysed so
that, rather anomalously, the clawing of these fingers
is less intense than in injuries at the wrist. Paralysis of
flexor carpi ulnaris produces a tendency to radial
deviation at the wrist. In late cases, wasting of the
intrinsic muscles is readily evident on inspecting
thedorsum of the hand and the web space between
4
Jean Casimir Félix Guyon (1831–1920), Professor of
Surgical Pathology and Genitourinary Surgery, University
of Paris. He described the canal at the start of his surgical
training in 1861.
5
Jules Fromont (1878–1946) described the sign while
working with Babinski and examining wounded soldiers in
World War 1 at Hôpital Pitié Salpêtrière in Paris.
4
).
5
).
the thumb and index finger. Sensory loss occurs over
the dorsal and palmar aspects of the ulnar one and a
half digits and the ulnar border of the hand on both
palmar and dorsal aspects.
If the ulnar nerve is divided at the level of the
wrist, the sensory loss is confined to the palmar
surface, as the dorsal branch of the ulnar nerve,
supplying the dorsal aspects of the ulnar one and a
half fingers, is given off 5cm proximal to the wrist
and thus escapes injury.
Division of the ulnar nerve leaves a surprisingly
efficient hand. The long flexors enable a good grip to
be achieved; the thumb, apart from the loss of adductor pollicis, is intact, and the important sensation
over the palm of the hand is largely maintained.
Indeed, it may be difficult to be certain clinically that
the nerve is injured. A reliable test is loss of the ability
to abduct and adduct the fingers with the hand laid
flat, palm downwards, on a table. This eliminates the
trick movements of adduction and abduction of the
fingers occurring as part of their flexion and extension, respectively.
Ulnar nerve compression
at theelbow (cubital
tunnel syndrome)
The ulnar nerve may be compressed as it passes
through the cubital tunnel between the two heads of
flexor carpi ulnaris and behind the medial epicondyle
and medial collateral ligament of the elbow. In many
patients, this is an idiopathic condition, but it can be
caused by persistent elbow flexion, localized swelling,
and fractures or arthritis of the elbow. Compression
results in weakness in the hand and paraesthesia
(numbness and tingling) in the ring and little fingers
(and the ulnar border of the patient’s hand). In
patients with compression of the ulnar nerve at the
wrist in Guyon’s canal, the pattern of numbness is
confined to the patient’s fingers. Symptoms are worse
at night.
Nerve conduction studies can confirm the diagnosis and its severity. Conservative treatment with
elbow splints, and avoiding flexing or resting on the
elbows may help. Surgery, when appropriate,
involves division of the roof of the cubital tunnel at
the elbow.
Differential diagnosis
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offlexion deformities
ofthe fingers
Peripheral nerve injuries 187
Mallet nger
This follows trauma (common in cricketers) with flexion deformity of the distal interphalangeal joint due
to avulsion of the extensor tendon insertion to the
base of the distal phalanx.
Ulnar nerve lesion
This has been described above; there is hyperextension of the metacarpophalangeal joints and clawing
of the hand, with sensory loss along the ulnar border
of the hand and ulnar one and a half fingers.
Dupuytren’s contracture
This is a common condition in the elderly, usually
male, subject in whom there is fibrosis of the palmar
aponeurosis. This produces a flexion deformity of the
fingers at the metacarpophalangeal and proximal
interphalangeal joints, usually starting at the ring finger and spreading to the little finger and sometimes
the middle finger. As the aponeurosis extends distally
only to the base of the middle phalanx, the distal
interphalangeal joint escapes. The contracture is
often bilateral and may occasionally affect the plantar
fascia of the foot.
6
Volkmann’s contracture7 due to
ischaemic brosis of exors of
the ngers
The fingers will be curled up in the hand with
metacarpophalangeal and interphalangeal joint flexion. This deformity can to some extent be relieved by
flexion of the wrist when the shortened tendons are
no longer so taut and the fingers can be partially
extended.
Congenital contracture
This usually affects the little finger and produces very
little, if any, disability. The proximal interphalangeal
joint is typically affected, the condition is usually
bilateral and, by definition, it dates from birth.
6
Baron Guillaume Dupuytren (1777–1835), Surgeon, Hôtel
Dieu, Paris, France.
7
Richard von Volkmann (1830–1889), Professor of Surgery,
Halle, Germany.
Trauma
Scar formation following burns, injury or surgery to
the fingers or the palm may produce gross flexion
deformities wherever a scar crosses a joint line.
Sciatic nerve injuries
This nerve may be injured in penetrating injuries or
torn in posterior dislocation of the hip associated with
fracture of the posterior lip of the acetabulum, to
which the nerve is closely related. Injury is followed
by paralysis of the hamstrings and all the muscles of
the leg and foot; there is loss of all movement below
the knee joint with foot drop deformity. Sensory loss
is complete below the knee, except for an area extending along the medial side of the leg over the medial
malleolus to the base of the hallux, which is innervated by the saphenous branch of the femoral nerve,
the longest cutaneous nerve in the body.
Common peroneal nerve
injuries
The common peroneal nerve is in a particularly vulnerable subcutaneous position as it winds around the
neck of the fibula. It may be injured at this site by
direct trauma or compression, such as the pressure of
a tight plaster cast, or in severe adduction injuries to
the knee. It is the most common peripheral nerve
injury in the lower limb and the majority of cases
result from iatrogenic causes. Damage is followed by
foot drop (due to paralysis of the ankle and foot extensors) and inversion of the foot (due to paralysis of the
peroneal muscles with unopposed action of the foot
flexors and inverters). There is anaesthesia over the
anterior surface of the leg and foot. The medial side of
the foot, innervated by the saphenous branch of the
femoral nerve, and the lateral side of the foot, supplied
by the sural branch of the tibial nerve, both escape.
188 Peripheral nerve injuries
t
s
r
u
s
e
ps
s
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Ptosis: drooping upper
eyelid
Enophthalmos: apparent,
no
not real
M
Meiosis: small pupil
Dry skin and
D
flushing on side of
fl
lesion (sudomotor
le
and vasoconstrictor
denervation)
d
Ipsilateral hand often
I
also involved
al
Lateral cutaneous nerve
ofthe thigh compression:
meralgia paraesthetica
The lateral cutaneous nerve of the thigh (L2, 3) may be
trapped as it emerges beneath the inguinal ligament,
a finger’s breadth medial to the anterior superior iliac
spine. It commonly occurs in overweight middlemen and in athletes undergoing physical training.
Symptoms comprise painful paraesthesiae over the
anterolateral aspect of the thigh, worse on standing
and relieved on sitting (hip flexion). Sensation in the
distribution of the nerve is diminished.
aged
Figure19.3 Horner’s syndrome.
• Meiosis: paralysis of the dilator pupillae, resulting
in constriction of the pupil.
Ptosis: paralysis of the sympathetic muscle fibres
•
transmitted via the oculomotor nerve to the levator palpebrae superioris results in drooping of the
upper eyelid.
• Anhidrosis: loss of sweating on the affected side of
the face and neck.
•
Enophthalmos: the eye appears sunken within the
orbit, an illusion due to the ptosis.
Horner’s syndrome may follow operations on, or injuries to, the neck in which the cervical sympathetic
trunk is damaged, malignant invasion from lymph
nodes or adjacent tumour or spinal cord lesions at the
T1 segment (e.g. syringomyelia).
Cervical sympathetic
nerve injuries: Horner’s
syndrome
If the T1 contribution to the cervical sympathetic
chain is damaged, the result is known as Horner’s
syndrome (Figure 19.3), in which there are the
following characteristics.
8
Johann Horner (1831–1886), Professor of Ophthalmology,
Zurich, Switzerland.
8
Additional resources
Case 38: A lacerated wrist
Case 39: A hand deformity
Case 40: A deformed nger
Case 41: A boy with a droopy eyelid
The oral cavity
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Kanwalraj Moar
Learning objectives
✓ To understand the embryology and anatomy of the oral cavity and lips.
✓ To know the common features of acquired and congenital diseases of
the oral cavity and lips.
20
It is a useful exercise (and a favourite examination
topic) to consider what can be learned by examining a
specific anatomical site, such as the fingers, nails or
eyes, in making a clinical diagnosis. The mouth and
tongue can be conveniently used to illustrate how
best to deal with this subject, which can be considered under three headings.
Information about local disease. Tumours of the
1
mouth and tongue and congenital anomalies are
diagnosed by local examination.
Local manifestations of disease elsewhere.
2
•
Crohn’s disease: oral ulceration, cobble stoning,
gingival hyperplasia, fissuring of lips, perioral
erythema and angular cheilitis. Symptoms may
precede gastrointestinal disease.
Pernicious anaemia: smooth tongue.
•
• Agranulocytosis/leukopaenia: ulcerated
mouth with no inflammatory halo.
• Leukaemia: oral ulceration, petechiae, gingival
haemorrhage and swelling, loose teeth.
• Addison’s disease
gingiva and areas of trauma.
1
omas Addison (1773–1860), Physician, Guy’s Hospital,
London, UK.
Ellis and Calne’s Lecture Notes in General Surgery, Fourteenth Edition.
Edited by Christopher Watson and Justin Davies.
© 2023 John Wiley & Sons Ltd. Published 2023 by John Wiley & Sons Ltd.
Companion website: www.wiley.com/go/Watson/GeneralSurgery14
1
: brown pigmentation of
• Peutz–Jeghers syndrome2 : perioral
pigmentation.
•
Vitamin C deficiency: swollen bleeding gums
and loosened teeth.
Hypoglossal nerve palsy: hemihypertrophy of
•
the tongue.
•
Human immunodeficiency virus (HIV): many
oral manifestations including candidiasis,
hairy leukoplakia, gingivitis, acute necrotizing
ulcerative gingivitis (ANUG), Kaposi’s
Sarcoma, atypical ulceration.
• Sjogren’s Syndrome: xerostomia leading to
caries, candidiasis, dry mucosa and lobulated
tongue. Patient symptoms include disturbed
taste, speech and swallow and enlarged major
salivary glands.
• Hereditary haemorrhagic telangiectasia:
telangiectasia on lips and intraoral mucosa.
3 Information given about the general condition and
habits of the patient. Examples include the dry
tongue of dehydration, the brown dry tongue of
uraemia and the coated tongue with foetor oris of
acute appendicitis.
2
Johannes Peutz (1886–1957), Physician, the Hague, the
Netherlands. Harold Jeghers (1940–1990), Professor of
Medicine, Georgetown University School of Medicine,
Washington, DC, and Tufts University Medical School,
Boston, MA, USA.
190 The oral cavity
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The oral cavity
The oral cavity (see Figure20.1) is an integral part of
the orofacial skeleton and is a unique combination
of hard and soft tissues. It is the cephalic limit of the
oro-
digestive tract and forms the junction between
the external and internal aspects of the body. The
external boundary is the vermillion of the lips anteriorly and buccal mucosa of the cheeks laterally. It
extends posterior and inferior where it adjoins the
oropharynx, at the anterior pillars of the fauces.
Posteriorly, the oropharynx comprises the soft palate, tonsillar fossae, tongue base and posterior and
lateral walls inferiorly to the epiglottis. The distinction between oral cavity and oropharynx is of particular importance when treating cancers of the
head and neck.
The oral cavity is divided into several regions by
the dental alveolus and teeth into the oral vestibule
between teeth and cheeks, and the oral cavity
proper internally. The hard and soft palate form the
superior margin or ceiling. The lower border is limited by oral mucosal membrane overlying the mylohyoid muscle and formed from the floor of mouth
and tongue.
Embryology
The embryology of the face, oral cavity and lips is
complex, but is important in understanding the
pathology in this region. The various structures within
the orofacial region are derived from the four primary
germ layers and summarized as follows:
•
Ectoderm: enamel of teeth, adjacent oral epithe-
lium, tastebuds and major salivary glands.
•
Mesoderm: muscle of tongue, cementum and peri-
odontal ligament of teeth.
Endoderm: minor salivary glands and pharyngeal
•
pouch derivatives.
•
Neural crest: underlying skeleton, cartilages and
musculature, the inner layers of the tooth –
dentine and pulp.
Oral facial development is recognizable from 14days
conception (see Figure20.2) with the formation
postof a prechordal plate in the bilaminar germ disc. This
will contribute to the oropharyngeal membrane; a
junction of ectoderm and endoderm with no intervening mesoderm (mimicked by the cloacal membrane of the hindgut) that will separate the primitive
oral cavity from the forming pharynx.
Hard palate
Soft palate
Uvula
Posterior
wall
(Pharyngopalatine
arch)
Palatine tonsil
Figure20.1 The oral cavity and
oropharynx viewed from the front.
Forebrain
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The oral cavity 191
Olfactory pit
Stomodaeum
Facial prominences
The face forms from the three embryological prominences (frontonasal, paired maxillary and paired
mandibular) surrounding a central stomodeum (a
depression with will go on to become the mouth). The
frontonasal prominence will develop the nasal and
optic placodes from ectodermal thickenings that will
form forehead, nose and upper lip.
The upper lip is a fusion of the nasal and maxillary
prominences, separating mouth from nose. The
medial nasal prominence also forms the tip of nose
and ‘primary’ palate or premaxilla. Midline fusion of
the paired mandibular prominences forms the lower
lip and jaw, with the commissures of the oral aperture
formed by lateral fusion of the maxillary and mandibular prominences. Failure of fusion at any of the
sites can give rise to the more common cleft lip or less
frequent facial clefts.
The separation of nasal from oral cavity occurs with
formation of the palate from horizontal extensions of
the frontonasal and maxillary prominences to form
the primary palate and two lateral palatal shelves.
These will fuse horizontally in a Y shape, with the
nasal septum superiorly, to form the hard and soft
palate at 6–8 weeks. Mesenchyme migrates into the
posterior third, which remains unossified, to form the
musculature of the velum.
Development ofthe tongue
The anterior two- thirds of the tongue develops from
the fusion of two lateral lingual swellings of first
branchial arch origin. The posterior part of the tongue
develops from median swellings of second, third and
Medial
Lateral
Eye
Frontonasal
Maxillary
Mandibular
Nasal fold
Process
fourth branchial arch, with the central junction of first
arch and second arch swellings being the foramen caecum. The innervation of the tongue reflects its
branchial arch origin. The body of the tongue receives
sensory supply from the lingual nerve (V), special taste
sensation from chorda tympani (VII) and motor innervation from the hypoglossal (XII). The palatoglossus
muscle and the root of the tongue are innervated by a
plexus of glossopharyngeal (IX) and vagus (X) nerves.
Figure20.2 The ventral aspect
of a foetal head showing
the three prominences–
frontonasal, maxillary and
mandibular– from which the
face, nose and jaw are derived.
Embryology ofteeth
Teeth are unique in their structure and development
and derive from their own dedicated epithelium
known as ‘odontogenic’ epithelium.
Teeth develop initially within the alveolar crypt of
the jaw and uniquely erupt from their bony envelopment into the oral cavity. Buds for permanent teeth
form on the lingual side of the deciduous teeth during
embryological development. They remain dormant
until around the sixth year of life, when they push
through the underside of the deciduous teeth. The
roots of the deciduous teeth undergo osteoclasis and
reabsorption.
Congenital disease ofthe
oral cavity andlips
Cleft lip andpalate
Cleft lip and palate is second only to talipes as the
most common congenital deformity with a UK incidence of approximately 1:800 live births, although
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there is significant worldwide variation being more
common in Chinese and less common in people of
Caribbean descent. Many of these children
Africanwill have additional congenital malformations with
the musculoskeletal, circulatory and digestive systems most commonly affected.
Aetiology
Cleft lip and palate can be caused by a single gene
defect in which case it is associated with a syndrome.
It more commonly arises due to the interaction of several genes (polygenic) with associated environmental
factors (epigenetic), such as smoking, alcohol usage,
folate deficiency, obesity and medications including
steroids and anticonvulsants. This results in sporadic
cases and unpredictable inheritance.
Manifestations
Cleft deformities may involve the lip (44%), the palate (23%), or a combination of the two with either a
single cleft lip (22%) or bilateral cleft lip (11%). It may
be complete, incomplete, microform (lip) or submucous (palate), and may extend beyond the lip as a
facial cleft.
Embryology andanatomy
Cleft pathologies are an example of what happens
when embryological development is disrupted. The
deformities can be understood by understanding the
embryology of the developing face and oral cavity.
Cleft lip
The lip is formed from the conjunction of the nasal
and maxillary processes. Fusion begins as the tripoint
junction of the premaxilla (from the nasal process)
and the secondary palatal shelves (from the maxillary
processes), which later becomes the incisive foramen. In the lip, fusion travels from posterior to anterior in a V shape, fusing anterior palate, alveolus and
lip from nasal sill to vermillion. The earlier the failure
of fusion the more significant and complete the cleft.
Cleft lip is the result of failure of fusion resulting in
discontinuity of the skin, muscle (orbicularis oris and
nasalis) and mucosa. This can be continuous, through
the nasal floor, with a discontinuity in the anterior
maxilla and alveolus. Although the nose is intact,
there is a characteristic nasal deformity due to adverse
muscle activity resulting in asymmetry (flat and wide
nostril on cleft side) and internal obstruction of the
ipsilateral nasal passage due to a bowed and deviated
septum.
Diagnosis can be as early as 12 weeks postconception by ultrasound scan or at birth. If there is
no palate involvement, a baby should be able to
suckle and feed normally, but this is dependent on
the severity of the lip deformity and ability to form a
lip seal.
Cleft palate
The palate is formed from the fusion of the secondary
palatal shelves with the premaxilla anterior and the
vomer superior. Fusion progresses from the future
incisive foramen anteriorly in a posterior direction
towards the uvula.
Cleft palate is a result of failure of fusion in the midline between the shelves of the secondary palate and
the vomer. It can be a complete cleft of hard and soft
palate or incomplete. When the hard palate is
involved, there may be bilateral or unilateral failure of
fusion of the palatal shelves with the vomer. On occasion, there will be continuity of the oral/nasal mucosa
but failure of fusion of the underlying bone or musculature resulting in a submucous cleft palate which is
often diagnosed later in life. A submucous cleft is typified by bifid uvula, notching of the posterior border of
hard palate, and a central sagittal lucid zone in the
soft palate.
Diagnosis of cleft palate is usually made at birth
either by direct observation and palpation of the palate or following failure to feed and associated nasal
regurgitation; occasionally, it is identified on antenatal ultrasound scan. The difficulty in feeding is
because of the inability to form a seal between mouth
and nose, so the baby cannot suck. Patients may also
suffer from recurrent otitis media due to tensor palatine dysfunction resulting in reduced hearing with an
associated impact on speech development.
Management ofclefts
Cleft lip and palate is ideally treated in specialist centres by a multidisciplinary team typically comprising
cleft surgeons (maxillofacial, plastic and ENT), cleft
nurse specialist, speech and language therapist, psychologist, paediatric dentist, orthodontist and audiologist. While advice on how to feed the baby is
crucial, the ultimate treatment is surgical, the aim
The oral cavity 193
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being to return the anatomy to as normal form and
function as possible. This is done in three stages.
Cleft lip and anterior palate repair (age 3–6months).
1
Repair by 6months will allow parents to form a bond
with their child and improves lip function including
speech, as babble starts from around this time.
Cleft palate repair (age 9–12 months). At least
2
3months following lip repair. Exact timing depends
on the width of the cleft and any underlying medical conditions. There is a tradeing the palatal apparatus in time to facilitate
normal speech to develop and the potentially negative impact of surgery on the growing maxilla.
3 Alveolar bone graft (age 8–10 years). A cleft of the
lip will often involve a discontinuity of the bone in
the underlying anterior maxilla and through the
alveolus. This will have an impact on the ability of
teeth, particularly the adult canines, to erupt and
so a bone graft may be considered.
off between repair-
Other craniofacial clefts
Intrauterine failure of fusion in other areas of the face
can result in other craniofacial clefts. These are rare
and complex clefts involving underlying bone and
organs with the severity dictated by the anatomical
position and extent. They may be associated with
ocular defects and communications between the cranial and oral cavity.
Acquired disease ofthe
oral cavity andlips
Dental disease
Anatomy
The human body has two sets of teeth:
Deciduous (milk) teeth
These 20 teeth erupt after birth, and are exfoliated by
age 13 to be replaced by the permanent dentition.
They comprise eight incisors, four canines, eight
molars. Notation is by quadrant and capital letter
starting at the midline.
Permanent teeth
These start to erupt from 6 years of age, usually completed by the late teens. There are 32 adult teeth,
made up of 8 incisors, 4 canines, 8 premolars and
12molars. Notation is by quadrant and number starting at the midline.
The nerve supply of each tooth lies within the rich
neurovascular complex of the pulp, which is
by layers of hard tissue (dentine and enamel). It is
responsible for the proprioception of the dentition
and for the sensation of odontalgia – commonly
known as toothache.
protected
Dental caries
This is the most common disease of the oral cavity
and poses a major health burden. It can affect both
the permanent and deciduous dentition and is the
most common indication for a general anaesthetic in
the paediatric population.
Pathogenesis
Dental caries is bacteria- mediated breakdown of the
hard tissues of the teeth. Bacteria, usually Streptococcus
mutans found in plaque, will break down dietary sugars to produce acid. These acids dissolve the mineral
content of the hard tissues, resulting in caries. The caries will progress through the layers of the tooth causing cavities and eventually pulp death.
Clinical features
Presence of plaque, dark discolouration of teeth,
cavities, pain in response to eating, drinking and temperature changes, and unprovoked toothache. Risk
factors include poor oral hygiene, high sugar diet, dry
mouth secondary to medications, autoimmune disease and radiotherapy.
Special investigations
• Dental radiography: the scanning dental/
orthopantomogram (OPG) is used for a broad
assessment but if caries is suspected an intraoral
dental radiograph should be used to assess the
extent of the disease.
• Pulp test: sensitivity to hot, cold or electricity may
be used to assess if the pulp of the tooth is alive.
Differential diagnosis
Includes erosion, abrasion, enamel hypoplasia,
amelogenesis imperfecta, dentinogenesis imperfecta,
fluoride/tetracycline staining.
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Treatment
Removal of caries and dental restoration, extraction
of affected tooth. Future prevention by improvement
in oral hygiene.
Dental abscess
Pathogenesis
A dental abscess is a mixed bacterial infection
bacteroides, streptococci) that can develop subse-
(
quent to caries (necrotic pulp), but also with periodontal disease and unerupted wisdom teeth
(pericoronitis). Although the majority of abscesses are
self- limiting and localized, they can progress to lifethreatening Ludwig’s angina
dibular swelling can threaten to occlude the airway.
3
, where large subman-
Clinical features
Initially:
•
Pain on biting onto a tooth.
• Bad taste in mouth.
• Visible discharging sinus through gingiva (gums).
Subsequently:
•
Buccal, palatal or lingual swelling adjacent to
tooth.
Extraoral swelling in submandibular region or
•
cheek.
•
Difficulty opening mouth (trismus) or swallowing.
Symptoms may progress to an airway, sight and/or
threatening emergency if spread to the fascial
lifespaces within head and neck, as indicated by extreme
trismus, drooling and stridor (Ludwig’s angina). Signs
of systemic infection including pyrexia, tachycardia
and raised white cell count. This will require urgent
incision and drainage under general anaesthetic.
Special investigations
• Dental radiography, usually OPG to identify causative tooth.
Computed tomography (CT) or ultrasound scan of
•
large swellings to identify position and extent of
abscess.
Differential diagnosis
Infected cyst of sebaceous, dermoid, or branchial origin, or an oral cancer or other skin infection (e.g.
actinomycosis).
Treatment
Depending on the extent of the abscess, this may range
from removal of dental pulp and root canal treatment,
to removal of tooth and drainage of any associated
abscess via tooth socket, intraoral incision or extraoral
incision together with broad spectrum antibiotics.
Cysts andtumours ofdental origin
Odontogenic tumours
These are not common and usually benign in nature.
•
Odontomes: hamartomas of odontogenic tissue,
which may contain dental tissues or odontomas.
Ameloblastoma: derived from ameloblasts
•
(epithelial cells which produce enamel for the developing tooth). It can be locally invasive in nature but
can rarely undergo malignant transformation; it
rarely metastasizes. Usually multilocular and commonly found at the angle of the mandible. Any age
may be affected, but the majority present in the second and third decades with equal sex distribution.
Treatment of both conditions is surgical resection.
Odontogenic cysts:
Present as asymptomatic radiolucencies on radiographs.
•
Dentigerous cyst: occurs around the crown of
unerupted teeth.
• Radicular (apical periodontal) cyst: occurs in
association with root apex of non- vital teeth.
• Keratocysts or keratinizing odontogenic tumours
are potentially aggressive cysts that can act as a
locally invasive tumour and will mimic other cysts.
High chance of recurrence with resection due to
presence of daughter/ satellite cysts. Multiple
cysts and basal cell carcinomas characterize the
autosomal dominant Gorlin- Goltz syndrome
4
.
3
Wilhelm Frederick von Ludwig (1790–1865). A prisoner of
war in the Napoleonic wars, he later practised in Stuttgart
and was personal Physician to King Wilhlem I.
4
Robert J Gorlin (1923–2006), Pathologist, University of
Minnesota School of Dentistry. Robert W Goltz (1923–2014),
Dermatologist at the same institution, and co- author of the
1960 paper describing the syndrome.
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