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Chapter
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3
Oral Cavity
C hapter Outline
·
Ranula
·
Sublingual Dermoids
·
Stomatitis
·
Cancrum Oris
·
Syphilitic Lesions of
Oral Cavity
·
Leukoplakia
·
Erythroplakia
·
Oral Submucosal
Fibrosis
·
Premalignant Conditions
of Oral Cavity
·
Oral and Upper
Aerodigestive Cancers
·
Cheek
·
Carcinoma Cheek/Buccal
Mucosa
·
Lip
·
Neoplasm of Lip
·
Carcinoma Lip
·
Tongue
·
Tongue Ulcers
·
Benign Tumours of
Tongue
·
Tongue Fissure
·
Glossitis
·
Tongue Tie
·
Carcinoma Tongue
·
Carcinoma of Posterior
One-Third/Base of the
Tongue
·
Nasopharyngeal
Carcinoma
·
Maxillary Tumours
·
Malignant Tumours of
Tonsil
·
Carcinoma Hard Palate
·
Laryngeal Tumours
·
Malignant Tumours of
Larynx
·
Trismus
causes rupture of the acini due to increased pressure leading into
extravasation cyst. Cyst contains saliva. The paired sublingual
salivary glands are located beneath the mucosa of the anterior
part of the floor of the mouth, anterior to the submandibular
ducts and above the mylohyoid and geniohyoid muscles. It
is closely related to lingual nerve and submandibular salivary
gland duct.
A
B
Oral cavity includes lips, buccal mucosa, alveolar margins
(gingiva), retromolar trigone, hard palate, floor of the mouth,
anterior 2/3rd of the tongue (oral/mobile tongue).
RANULA
(Rana = Frog, Ranula looks like belly of frog, hence the name—
Latin).
Ranula is an extravasation cyst arising from sublingual gland.
It is actually a pseudocyst. Occasionally, it can arise from
submandibular salivary gland also. Initially, there is blockage
of the duct (of sublingual gland) causing retention cyst, which
C
Figs. 3.1A to C: Ranula. Note the bluish discolouration, brilliantly
transilluminant and the location.
Features
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Presents as a bluish smooth, soft, fluctuant, brilliantly transil-
luminant swelling in the lateral aspect of the floor of the mouth.
Plunging ranula: Ranula often extends into the submandib-
ular region through the deeper part of the posterior margin
of mylohyoid muscle and is called as plunging ranula. It is
intraoral ranula with cervical extension. It is cross fluctuant
across mylohyoid. It can arise from both submandibular
and sublingual salivary glands as a mucus retention cyst
initially, which reaches neck by passing across the mylohyoid muscle presenting as soft, fluctuant, non-tender,
dumbbell-shaped swelling in the submandibular region. It
is bidigitally palpable.
Differential diagnosis: Lymph cyst; sublingual dermoid;
retention cysts arising from glands of Nuhn and Blandin or
from ducts of Rivinus.
Investigations: US neck or MRI neck and oral cavity is
diagnostic.
357
CHAPTER 3 Oral Cavity
A B
Figs. 3.2A and B: Sublingual dermoid. It lies usually in midline. It is not
transilluminant. Note the extension into the neck in submental region.
Excised specimen is also shown.
Types
Treatment
Marsupialisation (unroofing) can be done initially, and
later once the wall of the ranula is thickened it is excised
completely (Marsupial means pouch where baby is kept,
carried and sucked on the mother’s belly, like in Kangaroo).
If ranula is small it can be excised without marsupia lisation.
Excision of sublingual salivary gland is often needed. In
plunging ranula, submandibular salivary gland needs to be
excised occasionally.
Note:
• Ranula has a delicate fibrous capsule and is lined by macrophages. It
contains clear fluid/saliva. It is thin walled.
• It may get infected; it may get infected; occasionally, it may extend
posteriorly along parapharyngeal space and may cause dysphagia.
• It may interfere with speech and swallowing. It may damage Wharton’s duct.
• Only Marsupialisation even though often is sufficient but has got higher
recurrence rate than sublingual gland excision.
• Usually transoral route is sufficient; one should avoid injuring the lingual
nerve and submandibular salivary duct.
SUBLINGUAL DERMOIDS
They are sequestration dermoids lined by squamous epithe-
lium containing keratin.
It is smooth, soft, fluctuant, non-transilluminant bidigitally
palpable swelling.
They are congenital in origin; commonly occurs as midline
swelling; lateral dermoid can occur but rare.
Swelling may often attain large size presenting both sublin-
gually, intraorally and midline submentally on external side.
Occasionally it can cause trismus, dysphagia, pain, odynophagia.
Differential diagnoses are—haemangioma, lymphangioma,
sublingual dermoid, lipoma and Ludwig’s angina.
MRI is useful investigation.
Excision is done through intraoral approach usually; large
cyst extending under geniohyoid muscle may require external
approach.
1. Median sublingual dermoid:
¾
It is derived from epithelial cell rests at the level of fusion
of two mandibular arches. It may be supramylohyoid
or inframylohyoid. It is located between two genial
muscles, in relation to mylohyoid muscle. It is a midline
swelling which is smooth, soft, cystic, nontender, nontransilluminant.
¾
Treatment is excision through oral approach.
¾
Complication is abscess formation.
2. Lateral sublingual dermoid:
¾
It develops in relation to submandibular duct, lingual
nerve and stylohyoid ligament. It is derived from first
branchial arch. It forms a swelling in the lateral aspect
of the floor of the mouth.
¾
Treatment: Small one is removed per orally. Larger one,
through submandibular incision.
STOMATITIS
It is inflammation of oral mucosa by trauma, radiotherapy,
chemicals, nutritional deficiency or infection.
Traumatic stomatitis may be due to dentures, teeth bite,
and brushing of teeth harshly which presents as painful thin
covering of furr with increased salivation. Proper mouth wash
will cure the condition.
Aphthous stomatitis is seen in malnutrition, debility, steroid
usage. Present as multiple hyperaemic painful vesicles later
forming deep round painful ulcers. It is treated with mouth
wash and if needed by antibiotics. Recurrent aphthous stoma-
titis with ulcers is often familial, more common in women,
common in lip, cheek, tongue which are very painful with
more salivation. It heals spontaneously. But during active
period, it interferes with speech, swallowing distressfully. It
is treated by many drugs like levamisole, antibiotics, vitamin
B and C, local applications of anaesthetics (xylocaine)/choline
salicylate/benzalkonium chloride.
If you think you are right all the time, you learn nothing from life. —Sir Henry T Buutlin
358
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Candida stomatitis (Monilial thrush) is due to fungal infec-
tion, Candida albicans which is seen in diabetics, individuals
on steroid therapy, long-term antibiotics, patients who are
bedridden, on prolonged ICU care, in infants, and debilitated patients. Initially multiple red spots which are painful
appear in the tongue and buccal area which later turn into
curdy white patches. Often it extends into pharynx and
oesophagus causing dysphagia. It is treated with antifungal
drugs like clotrimazole or fluconazole. Rhagades occur at
corners of mouth in congenital syphilis leaving radiating
scar and furrow.
Vincent’s ulcerative stomatitis (Vincent’s angina/trench
SRB's Manual of Surgery
mouth) is due to infection by Gram –ve anaerobic bacteria
Borrelia vincentii and Fusiformis. It is common in adoles-
cents and young adults below the age of 35 years. Presents
with fever, excessive salivation, red swollen gums with
painful ulcers covered with yellow slough (pseudomem-
brane) which can be removed like membrane—ulcerative
gingivitis. From the gums it spreads to cheek, palate, and
It is an infective gangrene, a severe form of Vincent’s acute
ulcerative gingivitis and stomatitis.
Seen in poorly nourished, ill-child due to Borrelia vincentii
and Fusiformis bacteria.
It starts in lips later extends to gums, spreads into cheek,
bone, soft tissues and skin causing extensive tissue loss
with severe toxaemia.
Extensive necrosis of the mucus membrane of the oral cavity
with destruction of deeper soft tissue and often bone.
In children it may follow after an attack of measles, gastro-
enteritis, typhoid, bronchopneumonia. Malnutrition is a
predisposing factor.
Excessive salivation, fetid odour with destruction, discharge
and toxic features.
Borrelia vincentii can be cultured.
X-ray part shows bone destruction.
Condition has got high mortality.
Secondary infections may also coexist.
pharynx. Tongue involvement is uncommon. Tender neck
lymph nodes are palpable. Musty foetor oris is typical. Edentulous patients will not develop this infection. Infection in
tonsillar crypts is called as Vincent’s angina. It is confirmed
by swab culture. It is treated by antibiotics (penicillin group);
peeling of membrane, mouth wash, supportive measures,
vitamin B and C.
Nutritional stomatitis is due to—(1) vitamin B deficiency like
nicotinic acid (pellagra), riboflavin deficiency. It is common
in tongue presenting as red area with atrophy of papillae. (2)
Vitamin C deficiency is commonly seen as bleeding gums
and loosening of teeth. (3) Iron deficiency anaemia causes
superficial glossitis mainly in females.
Angular stomatitis is superficial lengthy red brown
fissures/ulcers in and around the angle of the mouth with
cracks. Candida and streptococci infections are common.
It is often called as cheilosis/perleche. It is treated with
vitamin B, C, iron and protein supplements with adequate
oral hygiene. Perleche is seen in children who suck their
finger.
Note:
Phagedena is a destructive ulceration with gangrene seen in cancrum oris,
chancroid. (Phagedena is destruction without proliferation but malignancy
is destruction with proliferation).
Fig. 3.3: Severe infection of lip.
CANCRUM ORIS (NOMA)
‘Noma’ means—‘to devour’ in Greek—‘eat greedily’ or
‘consume destructively’.
It is a rapidly spreading, progressive, mutilating, gangre-
nous devastating stomatitis, beginning in the mucous
membrane of the corner of the mouth or cheek, progressing
rapidly to involve the entire thickness of the lips or
cheek or both, with necrosis and sloughing of the entire
tissue; usually observed in poorly nourished children and
debilitated adults caused by polymicrobial, opportunistic
infection caused by components of the normal oral flora
that become pathogenic during periods of compromised
immune status. It is also common in HIV patients. Noma
pudendi involves genitals.
Treatment
Systemic antibiotics, high dose penicillins, metro nidazole.
High protein and vitamin rich diet, through naso gastric tube.
Wound irrigation and liberal excision of the dead tissue.
Blood transfusion, TPN.
Later patient requires flaps to cover the defect.
SYPHILITIC LESIONS OF ORAL CAVITY
Chancre in lip: It is highly contagious primary chancre,
presents as painless macule later forming painful superficial
ulcer. Ulcer eventually heals with a scar. It can be on both
upper and lower lip—primary syphilis.
Mucous patches which are greyish white contagious patches
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seen on lip, cheek and fauces. Mucous patches fuse together
to form linear snail track ulcers in fauces, pillars—secondary
syphilis. Hutchinson’s contagious condyloma in midline
tongue can occur.
Gummatous painless ulcer is seen in anterior 2/3rd of tongue,
palate and nasal septum (causes perforation and collapse of
nasal bridge).
Syphilitic chronic glossitis is seen in tertiary syphilis which
is a precancerous condition.
COMMON CAUSES
B
x Smoking Susceptibility, vitamin deficiencies
x Spirit Pan chewing using areca, tobacco,
slaked lime
x Sepsis Chronic hypertrophic candidiasis
(long-standing candida infection)
x Superficial glossitis Human papilloma virus, a possible
cause
x Syphilis
x Spices
x Sharp tooth
359
CHAPTER 3 Oral Cavity
LEUKOPLAKIA
It is a white patch in the mucosa of the oral cavity that cannot
be characterised clinically or patho lo gi cally to any other
disease. It is a premalignant condition.
It is hyperkeratotic, irreversible patch which is most common
premalignant lesion of the oral cavity. It is persistent and
adherent patch.
Types
1. Homogenous—uniform white patches with less malignant
potential; most common type; prevalent in buccal mucosa.
2. Nodular—fine nodules on the surface; more malignant
potential.
3. Speckled leukoplakia—white flecks with fine nodules with
an atrophic erythematosus base; much higher potentiality for
malignancy. But it is less common.
¾
Proliferative verrucous leukoplakia is rare but aggressive with 85% malignant potential; is common in elderly
women; not associated with tobacco use.
FEATURES OF HIGHER RISK POTENTIAL IN LEUKOPLAKIA
B
x Speckled type Hard and indurated type
x Nodular type Presence of epithelial dysplasia
x Erosions, ulcerations
Incidence of leukoplakia in those who smoke or chew pan is
20%, whereas incidence in non-smokers is 1%.
Incidence of its turning into malignancy is 4–10%. It
increases with age, duration of the pan chewing, smoking.
Buccal mucosa and oral commissures are most common
sites. Common in males (3:1).
Leukoplakia of long duration; leukoplakia in elderly; leuko-
plakia in younger females; leukoplakia in floor of the mouth
and tongue; leukoplakia with induration, cracks and fissures
are more likely to turn into malignancy.
Biopsy confirms the diagnosis as well as rules out the
carcinoma. Tissue study for p53 mutation, inappropriate
expression of oncogenes, DNA aneuploidy, reduction in
epithelial cadherin adhesive protein (reduction indicates
higher malignant potential).
Histology: Parakeratosis with widening of rete pegs.
HISTOLOGICAL STAGING
B
x Acanthosis—elongation of
rete pegs—smooth, white,
dry patch
x Parakeratosis
x Widening of rete pegs
x Dyskeratosis—keratin cell
layer formation deep to
epidermis
x Dysplasia
x Carcinoma in situ
Features
White or greyish, well-localized patch which is adherent,
firm or hard or indurated. It is often multifocal, bilateral or
occurs in many areas like cheek, tongue, gums. Ulcerations
are often seen.
It is usually painless and non-tender.
80% occur after the age of 40 years.
Hairy leukoplakia is dense pigmented friable lesion seen
commonly in the tongue; it is common in AIDS patients;
there are no hairs (misnomer). Surface looks like hairy due
to thickening, corrugation by severe hyperkeratosis and
acanthosis. Epstein Barr Virus (EBV) is the comon cause.
Do not try hard to learn all things in life; life itself teaches you everythings at right time.
Fig. 3.4: Leukoplakia cheek.
Note:
Leukoplakia tongue looks as though it has been covered with white paint
that had hardened, dried and cracked—Sir Henry T Buutlin.
Treatment
Pan chewing and smoking has to be stopped.
Excision, if required skin grafting has to be done.
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Regular follow-up is necessary.
Isotretinoin is helpful. Beta-carotene, tocoferol are also used.
CO
laser excision.
2
cosa epithelial atrophy and dysplasia. Arecoline stimulates
collagen synthesis; tannin stabilizes the collagen fibrils and
makes them resistant for collagen degradation by collagenase.
4.5–7.6% of oral submucosal fibrosis turns into malignancy.
ERYTHROPLAKIA
It is red velvety appearance of the mucosa which cannot
characterise any recognised condition.
It is 17–20 times more potentially malignant than leukoplakia.
Malignant transformation occurs in more than 50% of cases.
Histologically parakeratosis with severe epithelial dysplasia
is the typical feature.
SRB's Manual of Surgery
Red colour is due to decreased keratin causing shining and
prominence of submucosal red vascularised connective
tissue.
It is equal in both sexes.
It is common in lower alveolar mucosa, gingivobuccal sulcus,
floor of the mouth, tongue, vestibule and soft palate.
It can be homogenous/speckled/granular or erythroplakia
interspersed with leukoplakia.
Diagnosis is done by biopsy.
Treatment: Biopsy and surgical excision.
Treatment
Precipitating factors should be avoided—spices, chilli,
alcohol, tobacco.
Maintaining oral hygiene.
Local injection of dexamethasone (4 mg) with hyalase (1500
units) biweekly for 10 weeks; vitamin and iron supplements.
Chewable hydrocortisone tablets.
Submucosal injection of human chorionic gonadotrophin; IFN
gamma, colchicine tablets (0.5 mg); lycopene 16 mg a day.
Surgical excision of the lesion with coverage of raw area using
skin graft or tongue flap.
Multiple release incisions with ‘Z’ plasties; tongue flap
coverage can be done.
Stem cell therapy.
Fig. 3.5: Erythroplakia of cheek.
ORAL SUBMUCOSAL FIBROSIS
(In 1952, J Schwartz coined the term atrophica idiopathica
mucosa oris to describe an oral fibrosing disease which he
discovered in five Indian women from Kenya. S.G. Joshi subsequently coined the termed oral submucous fibrosis in 1953).
It is a progressive fibrosis deep to the mucosa of the oral
cavity which causes trismus and ankylo glossia.
The mucosa of cheek, gingivae, palate and tongue shows a
mottled/marbled pallor.
It is common among Asians and Indians.
Aetiology: Hypersensitivity to chilli, betelnut, tobacco and vitamin
deficiencies probably alter the collagen metabolism leading to
juxtaepithelial progressive inflammatory fibrosis of the submu-
Fig. 3.6: Submucosal fibrosis of right cheek. Note the stiff fibrotic
bands and scarring.
SUBMUCOSAL FIBROSIS
B
x Due to:
– Prolonged local irritation by chilies, tobacco (pan/quid), areca
due to arecoline
– Dietary causes—deficiencies of vitamin A, B complex (ribo-
flavin) and iron
– Localised collagen disorder
x Racial: It is common among Indians/Asians and people of Indian
origin
x Prevalence in India is 5 per 1000
x Incidence is 4–7%
x Common in middle age; equal in both sexes
x Soreness and burning in mouth which is more during meals;
vesicular eruptions; trismus; difficulty in protruding the tongue.
Initial red area turns into superficial ulcers which later forms stiff,
fibrotic bands and scarring
x Common in soft palate, faucial pillars; buccal mucosa
x Disease is progressive, even after cessation of causative factor
like areca use/smoking
x It shows epithelial atrophy, hyperplasia, dysplasia and fibrosis
PREMALIGNANT CONDITIONS OF ORAL CAVITY
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High risks—lesions with definite risk of malignant change
Leukoplakia.
Erythroplakia.
Chronic hyperplastic candidiasis: It is common in commis-
sures of the mouth and tongue. Dense plaque of leukoplakia
is common with curdy white patches due to Candida albicans
infection. It often may not respond to drugs, surgery or laser.
Immunodeficiency is often associated with this. It is treated
by topical or systemic antifungal drugs/surgical excision or
laser therapy.
Fig. 3.7: Extensive leukoplakia on the dorsum of the tongue with
carcinoma on the lateral margin. Leukoplakia is high risk premalignant.
Medium risks—premalignant but not associated with higher
incidence of carcinoma
Oral submucosal fibrosis.
Syphilitic glossitis.
Sideropenic dysphagia (Sideropenia is iron deficiency without
anaemia); or Plummer-Vinson syndrome. Sideropenia is
common in Scandinavian females. It causes atrophy of
epithelium and becomes potentially malignant. Proper iron
therapy controls the disease and reduces the risk.
Equivocal risk lesions
Oral lichen planus.
Dyskeratosis congenital—reticular atrophy, nail dystrophy,
leukoplakia in oral cavity.
Discoid lupus erythematosus.
Note:
• Oropharyngeal cancer is one of the most common cancers —40% in
Indian subcontinent. In western countries, it accounts for 4% only.
• Risk factors—tobacco and related products; alcohol; areca
nut; human papilloma virus; Epstein Barr virus; Paterson-
Kelly syndrome; nutritional deficiency.
• Patient may develop a second primary (15%) in the oropharynx in
different site at same time or within 6 months of the existing primary
(synchronous—4% prevalence; 20% of second primaries) or after 6
months of first primary (metachronous—80% of second primaries).
Metachronous second primary is more common than synchronous
second primary and it usually occurs in 2 years.
PREMALIGNANT CONDITIONS OF ORAL CAVITY
B
x Leukoplakia
x Erythroplakia
x Chronic hyperplastic candidi-
asis
x Oral submucosal fibrosis
x Syphilitic glossitis
x Sideropenic dysphagia
x Oral lichen planus
x Discoid lupus erythematosus
x Dyskeratosis congenita
ORAL AND UPPER AERODIGESTIVE CANCERS
It is one of the commonest cancers in Asian countries and
India (40%).
All ‘S’ mentioned probably are the causative agents. Smoking,
quid of chewing pan are important causes. Tobacco, betel
nut, alcohol, human papilloma virus (present in 80% of
oral cancers; present in 40% normal individuals), EB virus,
vitamin A deficiency, Plummer-Vinson syndrome, bad dental
hygiene, denture irritation—are etiologies. Risk is 8 times in
tobacco chewers; 10 times with quid users; 30 times with
night quid users.
Known risk factors Possible risk factors
Tobacco, alcohol, betel quid and
areca nut
Human papilloma virus
Precancerous conditions
Previous cancer (oral or other)
Family history of SCC
Sun exposure
Diet low in vegetables and fruits
Weakened immunity
Graft versus host reaction
Lichen planus
Alcohol increases the solubility of carcinogens and suppresses
the DNA repair.
Incidence of oral cancer in India is 28 per 1, 00,000 popula-
tion. Commonest oral cancer in India is of buccal mucosa
(more than 70%).
In oral cavity, in West, it is common in tongue (50%), buccal
mucosa (25%), floor (15%), gums and others (10%).
Leukoplakia (commonest), erythroplakia, chronic hyper-
plastic candidiasis are precancerous lesions; submucosal
fibrosis, syphilitic glossitis, sideropenic dysphagia are
precancerous conditions. Oral lichen planus, discoid lupus,
dyskeratosis congenita are doubtful associated lesions.
Precancerous lesion is one where cancer is more likely to
occur; precancerous condition is one where there is increased
risk of cancer.
Upper aerodigestive cancers include that of oral cavity, larynx
and pharynx. Depending on anatomical location they present
with different features other than common features—trismus,
ear pain, hoarseness of voice, dysphagia, ankyloglossia.
Usually they are locoregional disease with high affinity to
involve regional lymph nodes. Distant spread is rare except in
nasopharyngeal carcinoma. Tongue has highest incidence of
Poor oral and dental health
Poor fitting dentures
Secondary smoking (second
hand smoke)
361
CHAPTER 3 Oral Cavity
We are weaving the future on the loom of today.
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SRB's Manual of Surgery
A
B
Figs. 3.8A to C: Nasolabial flap–used to cover the defect in the lower alveolus.
nodal spread, then floor of the mouth, lower alveolus, cheek,
upper alveolus, palate.
Multiple synchronous (at same time, 10%) de novo sites and
or metachronous (at different periods, 15%) multiple sites.
Cancers in posterior third of tongue and floor of the mouth
is often missed on clinical examination—coffin corner or
sump area.
Primary may be very small to be detected clinically in places
like fossa of Rosenmuller, pyriform fossa, nasopharynx,
posterior third tongue but present clinically as hard lymph
node secondaries in neck called as secondaries with unknown
primary. Hard secondaries in neck confirmed by FNAC but
all investigations including blind biopsies, CT head and neck
region and endoscopies could not identify primary lesion
creates a situation called as secondaries in neck nodes with
an occult primary (30%).
Trismus (pterygoid muscle involvement), ear pain due
to auriculotemporal nerve involvement, eye pain in
nasopharyngeal carcinoma, dysphagia due to tongue
involvement mainly the posterior third, hearing loss due to
spread to Eustachian tube can occur.
Bronchopneumonia, aspiration are common problems.
Biopsy, endoscopy, CT neck, MRI, chest X-ray are different
investigations needed depending on anatomical location of
lesion.
Staging will help to plan the treatment and predict prognosis.
Surgical wide excision and radiotherapy are main modalities
of treatment. Chemotherapy is used as an adjuvant. Curative
treatment in early growth with preservation of functions like
swallowing, speech, cosmesis; but with adequate oncological
clearance is the principle of surgical approach. Radiotherapy
is also used as curative therapy.
Palliative chemotherapy, radiotherapy and surgery can be
done depending on location of the lesion.
Involvement of mandible, neck nodes—number, size and
fixity alters the prognosis and treatment schedule.
Outcome also depends on the anatomical location of the
malignancy. Lip carries better prognosis; tongue has poor
prognosis.
C
General principles used in approaching oral cancers are as
follows (however it depends on grading and staging of the
tumour):
¾
If only primary is present which is mucosal with size less
than 2 cm without nodal spread, then wide local excision with supraomohyoid block dissection of same side
is done (N0); primary may also be treated with curative
brachytherapy or external beam teletherapy. If nodes are
histologically positive then radical neck dissection is done.
¾
Larger mucosal primary with similar features are also
treated similarly; but post-operative RT or/and chemotherapy is added depending on grading of the tumour.
¾
In all these types of lesions, if there are positive mobile
neck nodes which is confirmed by FNAC, then radical
neck dissection should be done.
¾
If primary lesion extends into adjacent soft tissue
with mandibular involvement then mandibular resection (marginal mandibular/segmental/partial/hemimandibulectomy) is needed. Part is reconstructed using
plates or bone graft taken from iliac crest or opposite
11th rib. 2.4 mm reconstruction plate with PMMF or
non-vascularised bone graft (iliac crest cancellous
chips) or vascularised bone graft from fibula/iliac
crest/scapula are the present recommendations. Skin
covering is done by split skin graft inside to mucosa
or by appropriate flaps depending on the need and
feasibility of donor area (PMMF/DP flap/forehead
flap). Neck is addressed similarly. Post-operative
EBRT and chemotherapy is needed either concurrent
or sequential.
¾
If primary is advanced then chemotherapy with EBRT is
used. If lesion reduces in size and becomes operable it
is then operated accordingly.
¾
In fixed primary or secondary, RT with chemotherapy
is used for palliation to relieve pain, fungation, sepsis.
In advanced stage terminal events may be severe malnutri-
tion, bleeding, sepsis, and bronchopneumonia.
Posterior lesions has got poor prognosis than anterior
lesions. Lip carries best. Prognosis depends on anatomical
location, grading, lymph node status, soft tissue involvement
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and response of therapy.
Carcinoma of Gingivobuccal Complex
It is cancer (SCC) involving buccal mucosa and gingiva etiology
of which is keeping tobacco quid in gingivobuccal sulcus.
It is often called as Indian oral cancer as it is most com monly
seen in India.
Buccal mucosa extends from upper to lower alveolus; from
commissure in front to retromolar region behind.
Features, management are same. Marginal mandibulectomy/
segmental resection is commonly needed.
Adjuvant RT and chemotherapy is useful.
Retromolar Trigone
Retromolar trigone (coffin corner) is the attached mucosa on
the anterior surface of the ascending ramus of the mandible
posterior to the last lower molar tooth extending superiorly to
the maxillary tuberosity. It is triangular in shape with base is
superior behind the 3rd upper molar tooth and apex inferiorly
behind the lower 3rd molar tooth.
Carcinoma in this area commonly invades the ascending
ramus of the mandible and upward spread involves the pterygomandibular space. Tonsillar fossa, soft palate may also get
involved. Lymphatics from this area may communicate into
pharyngeal lymphatics.
SCC in this area can be treated with high voltage radiotherapy
or surgery. Lip split incision is required with mandibulotomy.
Marginal mandibulectomy is not possible; mandibulectomy
with reconstruction is required.
CARCINOMA CHEEK/BUCCAL MUCOSA
Squamous cell carcinoma is the most common type of carcinoma of the cheek.
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CHAPTER 3 Oral Cavity
Fig. 3.9: Carcinoma alveolus and gingiva—wide excision and
marginal mandibulectomy is done.
CHEEK
Anatomy of Cheek
They are fleshy flaps on either side of the face. The demarca-
tion between the lips and cheek is nasolabial fold.
It is composed of skin, superficial fascia with parotid duct,
buccinator muscle, submucosa with buccal glands and
mucous membrane.
Lymphatics: Submandibular and preauricular nodes.
Fig. 3.10: Haemangioma cheek.
Fig. 3.11: Carcinoma buccal mucosa with extensive necrosis.
It is the most common oral cancer in India.
Occasionally it can be adenocarcinoma arising from the
minor salivary glands or mucous glands. Rarely it can also
be melanoma.
MALIGNANCIES OF THE ORAL CAVITY
B
x Squamous cell carcinoma—commonest
x Minor salivary gland tumours
x Melanomas
x Adenocarcinomas—rare
x Sarcomas—rare (Sarcomatoid)
x Basaloid SCC
SITES OF CARCINOMA IN ORAL CAVITY IN ORDER
B
In India In Western countries
x Cheek—commonest x Tongue
x Tongue x Floor of the mouth
x Floor of the mouth x Lip
x Palate x Cheek
x Lips
All surgeries are major; there is no minor surgery.
364
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A
SRB's Manual of Surgery
Figs. 3.12A to C: Carcinoma cheek in different patients. Note the usage of tongue depressor for
B
C
proper visualisation of the lesion.
Precipitating Factors
All ‘S’—Smoking, spirit, syphilis, sharp tooth, sepsis, spices.
Incidence of oral cancer is six times more in smokers than
non-smokers.
PREMALIGNANT LESIONS AND CONDITIONS
B
x Leukoplakia x Oral submucosal fibrosis
x Erythroplakia x Sideropenic dysphagia
x Chronic hyperplastic candidiasis x Syphilitic glossitis
Betel nut chewing (Pan, with pan quid kept in cheek pouch for a
long time) is an important causative factor of carcinoma cheek.
Betel/areca nut, betel leaf, slaked lime, and tobacco (often
with catechu and condiments) wrapped in betel leaf is
repeatedly chewed after putting into the mouth; and the
quid formed is kept for long duration in gingivolabial sulcus;
which is said to be highly carcinogenic. Tobacco is the main
carcinogenic component, followed by arecoline (stimulate
collagen synthesis and fibroblast proliferation) and tannin
(stabilizes collagen) alkaloids of areca.
B
Fi g. 3.13B
Figs. 3.13A and B: Betels commonly used to prepare quid which is kept
in gingivoalveolar groove. It is common cause for carcinoma oral cavity.
A
Fig. 3.14: Verrucous carcinoma of the cheek
extending into the lip.
Fi g. 3.13A
TYPES
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B
(1) Ulcerative; (2) Proliferative (exophytic)—commonest;
(3) Verrucous
Verrucous Carcinoma
It occurs as a superficial proliferative exophytic lesion with
minimal deep invasion, often multiple.
Lesion has white, dry, velvety or warty, keratinised surface.
It is common in females.
It is of low grade, very well-differentiated squa mous cell carci-
noma, which is locally malignant without any lymphatic spread.
It is a curable malignancy.
After biopsy treatment is wide excision. Radiotherapy is not
given as it may lead to poorly differentiated carcinoma.
Biological Behaviour of Carcinoma Cheek
Carcinoma is common in posterior half of cheek than anterior.
It spreads into the deeper plane to involve buccinator, ptery-
goids; into the retromolar trigone, base of the skull, pharynx.
It spreads outwards to involve the skin causing fungation,
ulceration, orocutaneous fistula formation.
Mandible is commonly involved either by direct extension or
through subperiosteal lymphatic plexus which communicates
freely with oral lymphatics.
Lymph nodes commonly involved are submental, subman-
dibular, deep cervical and often lateral pharyngeal groups.
Nodal spread is seen in 50% of cases.
Infection of the tumour area and soft tissues around is
common, causing fever, foul smelling ulcer, halitosis.
Respiratory infection is common in these patients.
Once tumour extends into the retromolar region, soft palate
and pharynx, dysphagia will occur.
Lesion will later spread to involve alveolus.
Clinical Features
Ulcer (painless to begin with) in the cheek which gradually
increases in size in a patient with history of chewing pan
and smoking is the commonest presentation and initially it
is painless.
Pain occurs when it involves the skin, bone or if secondarily
infected. Referred pain to the ear signifies involvement of
lingual nerve. Lingual and auriculotemporal nerves arise from
mandibular division of trigeminal nerve.
Halitosis which is bad odour breath is common in many oral
cancers. It is due to necrosis of tumour, release of mercaptan,
butyric acid and ammonia.
Involvement of retromolar trigone indicates that it is an
advanced disease, as the lymphatics here com municate freely
with the pharyngeal lymphatics.
Everted edge, induration are the typical features of the ulcer.
Mandible is examined bidigitally, for thickening, tender-
ness, irregularity and sites of fracture. Mandible may get
involved by direct extension, through mandibular canal,
or through periodontal membrane. Loss of central part of
mandible due to destruction by tumour will cause pouting
of lower lip with drooling of saliva—Andy Gump deformity.
Mandibular canal is close to occlusive alveolar surface in
elderly and edentulous patients to cause early mandibular
spread in carcinoma.
Trismus and dysphagia signify involvement of pterygoids or
posterior extension.
Fig. 3.15 : Advanced carcinoma cheek presenting as swelling outside.
There is an ulcer inside over the mucosa.
Fig. 3.16: Trismus in an advanced carcinoma of cheek.
Occasionally it may extend into the upper alveolus and to the
maxilla causing swelling, pain and tenderness.
Once involvement of soft tissue occurs, it may come out
through skin as fungating lesion often with orocutaneous
fistulas with saliva dribbling through fistula.
Submandibular lymph nodes and upper deep cervical lymph
nodes are involved which are hard and nodular; initially mobile
and later get fixed to each other and then to deeper structure.
¾
Once lymph nodes get fixed it may infiltrate into hypoglossal nerve (tongue will deviate towards the same side),
spinal accessory nerve (defective shrugging of shoulder)
and cervical sympathetic chain (Horner’s syndrome).
¾
Compression over external carotid artery leads to absence
of superficial temporal artery pulsation. Eventually it
causes fungation and bleeding from major vessels—-
carotid blow out.
Note:
Node involvement may be due to infection. So often trial antibiotic is given
initially.
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CHAPTER 3 Oral Cavity
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