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SECTION III — Diseases of Oral Cavity and Salivary Glands
Figure 43.2. A large exophytic mass with ulceration at the top on the left
side of tongue in a 58-year-old male, habituated to chewing tobacco and
“pan.” It was due to sharp gagged teeth; healed on extraction of teeth.
Figure 43.1. Multiple aphthous ulcers on the uvula and faucial pillars
(arrowheads).
B. IMMUNE DISORDERS
1. aphthous ulcers. They are recurrent and superficial,
usually involving movable mucosa, i.e. inner surfaces of
lips, buccal mucosa, tongue, floor of mouth and soft palate,
while sparing mucosa of the hard palate and gingivae. In
the minor form, which is more common, ulcers are 2-10 mm
in size and multiple with a central necrotic area and a red
halo (Figure 43.1). They heal in about 2 weeks without leaving a scar. In the major form, ulcer is very big, 2-4 cm in size
and heals with a scar but is soon followed by another ulcer.
Aetiology of aphthous ulcers is unknown. It may be an
autoimmune process, nutritional deficiency (vitamin B12,
folic acid and iron), viral or bacterial infection, food allergies or due to hormonal changes or stress.
Aphthous ulcers can be differentiated from viral ulcers
by their frequent recurrence, involvement of movable
mucosa as on the soft palate or cheek, and the absence of
constitutional symptoms like fever, malaise and enlargement of cervical nodes.
Treatment consists of topical application of steroids
and cauterization with 10% silver nitrate. In severe cases,
250 mg of tetracycline dissolved in 50 mL of water is given as mouth rinse and then to be swallowed, four times
a day. Local pain can be relieved with lignocaine viscous.
2. behçet syndrome (oculo-oro-geNitAl syNdrome).
It is characterized by a triad of (i) aphthous-like ulcers in
the oral cavity, (ii) enital ulcerations and (iii) uveitis. The
edge of the ulcer is characteristically punched out. There
may also be lesions of the skin, joints and central nervous
system.
C. TRAUMA
Traumatic ulcer. A traumatic ulcer on the lateral border
of tongue may be due to jagged tooth or ill-fitting denture, on the buccal mucosa due to cheek bite and on the
palate due to injury with a foreign object such as pencil
or toothbrush (Figures 43.2 and 43.3).
Similarly, acute ulcerative lesions of oral and oropharyngeal mucosa can result from accidental ingestion
of acids or alkalies or hot fluids.
Aspirin burn is seen in the buccal sulcus when a tablet
of aspirin is kept against a painful tooth to get relief from
toothache.
D. NEOPLASMS
Malignancies of the oral cavity or oropharynx may present as chronic ulcers. Though most commonly it is squamous cell carcinoma, it could be carcinoma of minor salivary glands or non-Hodgkin lymphoma.
E. SKIN DISORDERS
1. erythema multiForme. It is a disease of rapid on-
set involving the skin and mucous membranes, either of
which may be involved alone. The aetiology is unknown
but may be associated with drug allergy (sulfonamides) or
recent herpes simplex infection. Oral mucosal lesions consist of vesicles or bullae which soon rupture to form ulcers
covered with pseudomembrane. Any area of oral mucosa
is involved but the common sites are lips, buccal mucosa
and tongue. The lesions bleed easily. The distinctive feature is to form haemorrhagic crusts on the lips. Skin lesions consist of erythematous patches on the palms, soles
and extensor surfaces of the extremities. Oral lesions may
occur without skin involvement in 25% of patients. The
disease is self-limiting and management is mainly supportive. Steroids are used to treat the severe form.
2. pemphigus Vulgaris. It is an autoimmune disorder
affecting older age group (50-70 years). Oral lesions are
seen in 50% of the cases and may precede skin lesions.
Oral ulcerations are superficial and involve palate, buccal mucosa and tongue. Treatment consists of systemic
steroids and cytotoxic drugs.
3. benign mucous membrane pemphigoid (bmmp).
It is also an autoimmune disorder. Mucosal lesions involve cheek, gingivae and palate. Conjunctiva is the next
important site. Lesion starts as a bulla filled with clear
or haemorrhagic fluid which ruptures to form superficial
Chapter 43 — Common Disorders of Oral Cavity
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Figure 43.3. Ulcer on lateral border of tongue simulating carcinoma (arrowheads). It was caused by a sharp jagged tooth (A) and healed completely following tooth extraction (B).
ulceration covered with shaggy collapsed mucosa. Skin
lesions may be absent. Treatment consists of steroids.
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4. lichen planus. Oral lesions are seen with or without
skin lesions. Skin lesions are pruritic, purple, polygonal
papules. They are seen on the forearms and medial side of
thigh. Oral lesions occurs in two forms:
(a) Reticular. White striae forming lace-like pattern are
seen on the buccal mucosa on both sides. They are
asymptomatic and require no treatment.
(b) Erosive. It is characterized by painful ulceration on the
buccal mucosa, gingiva or lateral tongue. Each ulcer is
surrounded by a keratotic periphery. Treatment consists of topical steroids.
5. chronic discoid lupus erythematosus. Oral
lesions are almost always associated with skin lesions. Oral
lesions are similar to those of erosive form of lichen planus.
F. BLOOD DISORDERS
Blood dyscrasias cause ulcerations in the oral cavity and pharynx. Due to lack of defence mechanism, e.g. granulocytes,
infections quickly supervene causing ulcers. Acute leukaemia
is mainly of two types-acute lymphoblastic type, which occurs in young children and acute myeloid type, occurring in
the middle aged or the elderly. Both cause hypertrophy of
gums with ulceration and bleeding. Agranulocytosis is characterized by ulcerations in throat with severe neutropenia
(Figure 43.4). Cyclical neutropenia is a condition with periodic
falls in neutrophil count when the person becomes prone
to infections and oral ulceration. In pancytopenia, there is a
drop in RBC count, white cell count and platelets.
When suspected, blood dyscrasias are investigated by
peripheral blood film, blood counts and bone marrow aspiration.
G. DRUG ALLERGY
Systemic administration of drugs like penicillin, tetracycline, sulfa drugs, barbiturates, phenytoin, etc.
Figure 43.4. A 58-year-old man developed ulcerations on the palate
when white cell count fell to 2500 per cubic mm on cancer chemotherapy with cisplatin and 5-fluorouracil.
may cause erosive, vesicular or bullous lesions in the
oral cavity. Contact stomatitis may occur due to local
reaction to mouth washes, lozenges, chewing gum,
toothpastes or to prosthetic dental materials. Oral lesions may vary from erythema to vesicles and bullae
formation.
H. VITAMIN DEFICIENCIES
Vitamin B12 and folic acid deficiency may cause ulcers.
I. MISCELLANEOUS
Radiation mucositis. It follows radiation of oral cavity or
oropharynx for cancer. At first, the mucosa becomes red
and then forms spotty areas of mucositis which coalesce
to form large ulcerated areas covered by slough.
Mucositis of cancer chemotherapy can be caused by
drugs like methotrexate, 5-FU and bleomycin. It manifests as erythema, oedema and ulceration.
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SECTION III — Diseases of Oral Cavity and Salivary Glands
MISCELLANEOUS LESIONS OF TONGUE
AND ORAL CAVITY
1. median rhomboid glossitis. It is red rhomboid
area, devoid of papillae, seen on the dorsum of tongue in
front of foramen caecum. It is a developmental anomaly
that occurs due to persistence of tuberculum impar, which
fails to invaginate. Recent studies reveal this condition
to be due to chronic candida infection. The condition is
asymptomatic and no treatment is necessary.
2. geographical tongue. It is characterized by ery-
thematous areas, devoid of papillae, surrounded by an irregular keratotic white outline (Figure 43.5). The lesions
keep changing their shape and hence the condition is
also called “migratory glossitis.” The condition is asymptomatic and may not require any treatment.
3. hairy tongue. Due to excessive formation of kera-
tin, the filiform papillae on the dorsum of the tongue
become elongated. They get coloured, brown or black,
due to chromogenic bacteria and look like hair. Smoking seems to be one of the factors. Treatment consists of
scraping the lesions with a tongue cleaner, application of
half-strength hydrogen peroxide and improving the general nutritional status of the patient by vitamins. Causative factors, if known, should be removed.
4. Fissured tongue. It may be congenital or seen in
cases of syphilis, deficiency of vitamin B complex or anaemia. Congenital fissuring associated facial palsy is seen in
Melkersson-Rosenthal syndrome.
Figure 43.6. Tongue-tie.
seen with equal frequency in both males and females and
are considered normal.
7. nicotine stomatitis. This disorder is seen in smokers
particularly those in the habit of reverse smoking. Palatal
mucosa shows pin-point red spots in the centre of umbilicated papular lesions. They are due to inflammation
of the minor salivary glands and their duct openings as a
reaction to the heat of the smoke. The nicotine stomatitis
is a misnomer as nicotine is not the cause. Management
is elimination of smoking.
5. ankyloglossia (tongue tie) (Figure 43.6). True
tongue tie which produces symptoms is uncommon. If
tongue can be protruded beyond the lower incisors, it is
unlikely to cause speech defects. A mobile tongue is important to maintain orodental hygiene-to clean the debris and prevent formation of dental plaques. Treatment
of any significant tongue tie is transverse release and vertical closure. Thin mucosal folds can be simply incised.
6. Fordyce spots. They are aberrant sebaceous glands
present under the buccal or labial mucosa and shine
through it as yellowish or yellow-brown spots. They are
Figure 43.5. Geographical tongue.
SUBMUCOUS FIBROSIS
Oral submucous fibrosis (OSF) is a chronic insidious process characterized by juxtaepithelial deposition of fibrous
tissue in the oral cavity and pharynx. The condition was
first described in India by Joshi in 1953. The disease is
widely seen in India, Pakistan, Taiwan, Sri Lanka, Nepal
and Thailand due to habit of betel-nut chewing.
AETIOLOGY
1. Socioeconomic status. In India, poor socioeconomic
status has been associated with higher risk of precancerous lesions like leukoplakia, erythroplakia and
submucous fibrosis. This is related to education, diet,
lifestyle and access to medical care.
2. Tobacco chewing. It is a major risk factor in submucous fibrosis as it is in lesions of leukoplakia and
erythroplakia.
3. Areca nuts. Areca nuts are chewed alone, with tobacco or in the form of pan (containing lime, catechu and
other ingredients on a betel leaf). Betel quid without
tobacco also increases the risk of oral precancerous
lesions, but causes higher risk for oral submucous fibrosis relative to leukoplakia, erythroplakia or multiple precancerous lesions. International agency for
research on cancer has classified betel quid without
tobacco also as a carcinogen for humans.
4. Alcohol. It is observed that drinking increases the risk
of leukoplakia by 1.5-fold, OSF by 2-fold and that of
erythroplakia by 3-fold.
5. Nutritional. Deficiency of vitamins and micronutri-
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ents has been suggested. Therapy of OSF with vitamin
A, zinc and antioxidants has shown some beneficial
effect. Lesser intake of fruits and vegetables has been
associated with oral premalignant lesions.
6. Immune process. OSF is considered a cell-mediated
immune reaction to arecoline in areca nuts. It may
also reflect a localized collagen disorder or an autoimmune process in the oral cavity.
7. Multifactorial. Several factors may operate together
in the causation of OSF. Habit of betel-nut chewing,
drinking or smoking tobacco coupled with dietary deficiencies may have synergistic effect.
PATHOGENESIS
Histopathology in early cases of OSF shows presence of
polymorphonuclear leukocytes, eosinophils and a few
lymphocytes while advanced cases show lymphocytes
and plasma cells. Immunochemistry of inflammatory
cells showed higher population of activated T-lymphocytes especially the T-helper/inducer lymphocytes but
minor population of B-cells and macrophages. Later
studies also showed significant increase in number of
T-lymphocytes, macrophages and high CD4+ to CD8+
lymphocyte ratio in the subepithelial connective tissue
suggesting that OSF is a cellular immune response. Small
number of B-lymphocytes suggests minor role of humoral
immunity in OSF. In advanced stages, there was severe
fibrosis and loss of vascularity in the lamina propria and
submucosa. The process may extend deeper into muscle
layers also. Activated macrophages and T-lymphocytes
produce fibrogenic cytokines which act on mesenchymal
cells to produce fibrosis. Also certain cytokines liberated
by T-lymphocytes upregulate synthesis of collagen but
downregulate collagenase production further promoting
fibrosis. It is thus believed that OSF is due to increased
production of collagen and its decreased degradation in
subepithelial layers of the oral mucosa (Figure 43.7).
PATHOLOGY
The basic change is fibroelastotic transformation of connective tissues in lamina propria associated with epithelial atrophy, sometimes preceded by vesicle formation. In
later stages, when fibrosis is marked, there is progressive
trismus and difficulty to protrude the tongue.
Leukoplakia and squamous cell carcinoma may be
associated with submucous fibrosis possibly because of
common aetiological factors involved.
It is a premalignant condition and malignant transformation has been seen in 3-7.6% of cases.
Chapter 43 — Common Disorders of Oral Cavity
Figure 43.7. Cellular immune response to areca nuts in oral submucous fibrosis and possible pathogenesis. (Based on CP Chiang et al. in
Oral Oncology 2002;38:56-63.)
(c) Repeated vesicular eruption on the palate and
pillars.
(d) Difficulty to open the mouth fully.
(e) Difficulty to protrude the tongue.
3. Findings. Changes of submucous fibrosis are most
marked over (i) soft palate, (ii) faucial pillars and (iii) buccal mucosa (Figure 43.8). In initial stages, there is patchy
redness of mucous membrane with formation of vesicles
which rupture to form superficial ulcers.
In later stages, when fibrosis develops in the submucosal layers, there is blanching of mucosa with loss of suppleness. Fibrotic bands can be seen and felt in the affected
areas. Fibrosis and scarring has also been demonstrated in
the underlying muscle leading to further restrictive mobility of soft palate, tongue and jaw. Trismus is progressive, so much so that patient may not be able to put his
finger in the mouth or brush his teeth. Orodental hygiene
is affected badly and teeth become carious. Examination
of oral cavity is difficult particularly to rule out other associated premalignant lesions or malignancy.
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TREATMENT
CLINICAL FEATURES
1. age anD Sex. No age or sex is immune but the dis-
ease mostly affects age group of 20-40 years.
2. SyMPtoMS. Patient often presents with:
(a) Intolerance to chillies and spicy food.
(b) Soreness of mouth with constant burning sensa-
tion; worsened during meals particularly of pungent spicy type.
Medical
1. Steroids. Topical injection of steroids into the affected
area is more effective than their systemic use as it also
has the advantage of fewer side effects. It may be com-
bined with hylase. Dexamethasone 4 mg (1 mL) com-
bined with hylase, 1500 IU in 1 mL is injected into
the affected area biweekly for 8-10 weeks. This brings
marked improvement in symptoms and relieves tris-
mus.
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Figure 43.8. Submucous fibrosis. (A) Note the blanched appearance of the soft palate and faucial pillars. (B) Marked trismus due to submucous
fibrosis.
SECTION III — Diseases of Oral Cavity and Salivary Glands
2. Avoid irritant factors, e.g. areca nuts, pan, tobacco,
pungent foods, etc.
3. Treat existent anaemia or vitamin deficiencies.
4. Encourage jaw opening exercises.
Surgical
It is indicated in advanced cases to relieve trismus. Various surgical techniques used are:
1. Simple release of fibrosis and skin grafting. There is
high recurrence rate due to graft contracture.
2. Bilateral tongue flaps. Requires flap division at a second stage.
3. Nasolabial flaps. They are small to cover the defect
completely, cause facial scar and require division of
flaps at second stage.
4. Island palatal mucoperiosteal flap. It is based on
greater palatine artery. Possible only in selected cases.
Requires extraction of second molar for the flap to sit
without tension. Not suitable for bilateral cases.
5. Bilateral radial forearm free flap. It is bulky and hair
bearing. May require debulking procedure, third molar may require extraction.
6. Surgical excision and buccal fat pad graft.
7. Superficial temporal fascia flap and split-skin graft.
8. Coronoidectomy and temporal muscle myotomy.
Chapter 44
papilloma.
Fibroma (Fibroepithelial polyp).
haemangioma.
lymphangioma.
5. torus.
pyogenic granuloma (Figure 44.
pregnancy granuloma.
8. granular cell myoblastoma or granular cell
tumour.
9. minor saliVary gland neoplasms.
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Tumours of Oral Cavity
CLASSIFICATION
The tumours of oral cavity can be classified as follows:
1. Benign tumours
(a) Solid
(b) Cystic
2. Premalignant lesions
3. Malignant lesions
(a) Carcinoma
(b) Nonsquamous malignant lesions
I. BENIGN TUMOURS
SOLID TUMOURS
1.
ity. Peak incidence is in the third to fifth decades. Most of
them appear on the soft and hard palate, uvula, tongue
and lips. Mostly they are less than 1 cm in size, pedunculated and white in colour. Their surface is irregular but
sometimes smooth. Treatment is excisional biopsy. Recurrence is rare.
2.
mucosa-covered pedunculated tumour, usually about
1 cm in size and soft to firm in consistency. It can occur anywhere in the oral or oropharyngeal mucosa
(Figure 44.1). The usual cause is chronic irritation. It is
easily treated by conservative surgical excision.
3.
in the oral cavity or oropharynx (Figure 44.2). They are
mostly seen in children. Three types of haemangiomas
are known: capillary, cavernous and mixed. When haemangiomas are present at birth or in young children, they
should be observed for some period as spontaneous regression can occur.
In patients of 40–50 years, haemangioma-like dilated
veins (phlebostasis) may occur on the oral or lingual
mucosa.
An infected haemangioma may be difficult to differ-
entiate from a pyogenic granuloma. Haemangiomas that
are large and persistent or those which continue to grow
are problematic. Use of cryosurgery or laser is not possible in large diffuse lesions. Sclerotherapy has also not
been found effective. However, microembolization alone
or as a preoperative adjunct to surgery has been found
very useful.
Papillomas are common in the oral cav-
It is a smooth,
Mucosal haemangiomas can occur
4.
terior two-thirds of tongue. They may involve the tongue
diffusely and cause macroglossia or may present as localized soft swelling which is compressible. They do not
involute spontaneously. Small lesions can be excised surgically. Symptomatic large lesions can be partially excised
to reduce the bulk. Total excision of these lesions is not
possible.
volve the hard palate or mandible. Palatine torus is more
common and presents as a narrow ridge, solitary nodule
or a lobulated mass in the midline of the hard palate.
Mandibular tori project from the lingual aspect of the
gingiva, near the bicuspid area and are bilateral. Tori are
innocuous and resection is indicated only when they interfere with speech, mastication or fitting of dentures.
6.
tive granuloma usually occurs in response to trauma or
chronic irritation. It mostly involves anterior gingivae
but sometimes the other sites such as tongue, buccal mucosa or lips. Usually it is soft, smooth, reddish to purple
mass which bleeds on touch. Treatment is surgical excision. Recurrence is unlikely after complete excision.
7.
tologically similar to pyogenic granuloma. It usually
starts in the first trimester of pregnancy and regresses
once pregnancy has ended. It is excised only if it persists
after pregnancy. It is likely to recur if operated during
pregnancy.
and the site of predilection is tongue. Earlier they were
thought to arise from the muscle (hence called myoblastoma) but are now considered to be derived from
Schwann cells. The tumour presents as a firm submucosal
nodule. Treatment is conservative surgical excision. Recurrence is uncommon.
Congenital epulis is also a granular cell tumour involving the gums of future incisors in female infants.
adenoma is the most common. Site of predilection is soft
or hard palate but can occur anywhere in the oral cavity.
It presents as a painless submucosal nodule. Treatment is
wide surgical excision because of the high incidence of
recurrence.
It is a submucosal bony outgrowth. It may in-
Most of these tumours occur in the oral cavity
Lymphangiomas mostly involve an-
3). It is a reac-
It is clinically and his-
Pleomorphic
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SECTION III — Diseases of Oral Cavity and Salivary Glands
Figure 44.1. A fibroepithelial polyp in the left cheek.
10. solitary Fibrous tumour. Though most common in the pleura, this tumour has been seen in the oral
tongue and buccal mucosa, and rarely also in the nasopharynx, sinonasal tract, soft palate, retromolar trigone,
salivary gland and thyroid. It is a benign tumour.
Clinically it presents as a painless, slow-growing, well
demarcated, mobile, submucosal tumour. Mean age at
presentation is 49 years with female preponderance.
It arises from the mesenchyme and is histologically
composed of spindle cells arranged in haphazard manner with thick collagen bundles between the cells. It may
show capillary proliferation and pericystic pattern and
thus need to be differentiated from haemangiopericytoma. Immunohistochemistry helps to differentiate them
from neurofibroma, leiomyoma and other spindle cell
tumours.
Treatment is complete surgical excision.
Figure 44.3. A pyogenic granuloma.
CYSTIC LESIONS
1. mucocele. Most common site is the lower lip
(Figure 44.4). It is a retention cyst of minor salivary glands
of the lip. The lesion appears as a soft and cystic mass of
bluish colour. Treatment is surgical excision.
2. ranula (Figure 44.5). It is a cystic translucent lesion
seen in the floor of mouth on one side of the frenulum
and pushing the tongue up. It arises from the sublingual
salivary gland due to obstruction of its ducts. Some ranulae extend into the neck (plunging type).
Figure 44.4. A mucocele of the lower lip.
Treatment is complete surgical excision if small, or mar-
supialization, if large. Often it is not possible to excise
Figure 44.2. (A) A haemangioma on the lateral border of the tongue. (B) Multiple haemangiomas involving both lips, buccal mucosa and
tongue in a 32-year-old man. He complained of bleeding when the haemangioma was traumatized during chewing of food.
Chapter 44 — Tumours of Oral Cavity
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Figure 44.5. A ranula. Note a translucent swelling under the tongue.
the ranula completely because of its thin wall or ramifications in various tissue planes.
Dermoid. A sublingual dermoid is median or lateral,
situated above the mylohyoid. It shines through the mucosa as a white mass in contrast to the translucent nature
of the ranula. A submental dermoid develops below the
mylohyoid and presents as a submental swelling behind
the chin.
II. PREMALIGNANT LESIONS
1. Leukoplakia. WHO defined leukoplakia as a clinical
white patch that cannot be characterized clinically or
pathologically as any other disease. It is a clinical defi-
nition and does not take pathology into consideration.
Other white lesions of oral mucosa, i.e. lichen planus,
discoid lupus erythematosus, white spongy nevus and
candidiasis are excluded.
(a) Aetiological factors include smoking, tobacco chew-
ing, alcohol abuse particularly, if combined with
smoking. Chronic trauma can also occur due to
ill-fitting dentures or cheek bites. It may also be
associated with submucous fibrosis, hyperplastic
candidiasis or Plummer–Vinson syndrome.
(b) Sites involved. Buccal mucosa and oral commissures
are the most common sites. It may however involve
floor of mouth, tongue, gingivobuccal sulcus and
the mucosal surface of lip. Buccal mucosa is the
most common site in India (Figures 44.6 and 44.7).
(c) Age and sex. Mostly, it is seen in the fourth decade,
males are affected two to three times more often.
(d) Clinical types. (i) Homogenous variety presents with
a smooth or wrinkled white patch. It is less often
associated with malignancy. (ii) Nodular (speckled)
variety presents as white patches or nodules on
erythematous base. (iii) Erosive (erythroleukopla-
kia) variety where leukoplakia is interspersed with
erythroplakia and has erosions and fissures. The
latter two varieties have higher incidence of malignant transformation.
(e) Histology. About 25% of leukoplakias may show
some form of epithelial dysplasia from mild to
Figure 44.6. Leukoplakia on the lateral border of the tongue.
Figure 44.7. Leukoplakia at the site of ‘quid’ (of tobacco and lime).
severe. Higher the grade of dysplasia more are the
chances of its going into malignant change.
(f) Malignant potential. The chances of leukoplakia be-
coming malignant are cited from 1 to 17.5%. On
an average about 5% become malignant. Malignant potential varies according to the site and type
of leukoplakia, and the duration of follow-up.
(g) Management
(i) Many of the lesions will disappear spontane-
ously if causative agent is removed.
(ii) In lesions with higher potential for malig-
nant change, a biopsy is taken to rule out
malignancy.
(iii) In suspicious small lesions, surgical excision
or ablation with laser or cryotherapy can be
done.
2. Erythroplakia. Similar to leukoplakia, which is a
white patch, erythroplakia is a red patch or plaque on
the mucosal surface. Red colour is due to decreased
keratinization and as a result the red vascular connective tissue of the submucosa shines through. There is
no sex predilection. Most common sites are lower alveolar mucosa, gingivobuccal sulcus and the floor of
the mouth. Most of lesions of erythroplakia show severe dysplasia, carcinoma in situ or a frank invasive
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3. Melanosis and mucosal hyperpigmentation. Benign
SECTION III — Diseases of Oral Cavity and Salivary Glands
carcinoma when first seen. Malignant potential is 17
times higher than in leukoplakia. Grossly, the lesion
may be of three varieties—homogenous, speckled or
granular, and erythroplakia, interspersed with areas of
leukoplakia (often indistinguishable from erythroleukoplakia, type of leukoplakia). Treatment is excision
biopsy and follow-up.
pigmented lesions of oral mucosa may transform into
malignant melanomas; however, the incidence of this
change is not known. About one-fourth of mucosal
melanomas may resemble benign lesions and hence
biopsy may become mandatory.
III. MALIGNANT LESIONS
CARCINOMA ORAL CAVITY
Figure 44.8. Carcinoma of the upper lip and oral commissure. Note
associated leukoplakia.
Aetiology
Compared to western countries, India has high incidence
of oral cancers. Age adjusted incidence rate in India is
44.8 and 23.7 in males and females, respectively, compared to 11.2/100,000 in USA. Several aetiological factors
are responsible. (6-S aetiology, i.e. smoking, spirits, sharp
jagged tooth, sepsis, syndrome of Plummer–Vinson and
syphilitic glossitis.)
1. Smoking. Incidence of oral cancer is six times more
in smokers than in nonsmokers. In certain parts of India, there is an unusual habit of reverse smoking where
burning end of the “churat” (rolled tobacco leaf) is put
in the mouth. This gives high incidence of cancer of
the hard palate.
2. Tobacco chewing. Powdered tobacco, mixed with
lime, is placed in some part of the vestibule of the
mouth. Carcinoma develops at the site of the quid.
Chewing “pan” and keeping the quid in the vestibule
is largely responsible for oral cancer in India.
3. Alcohol. Cancer of upper aerodigestive tract occurs
six times more in heavy drinkers as compared to nondrinkers.
4. Dietary deficiencies. Their role in genesis of cancer
has not been definitely established. Riboflavin deficiency may be responsible for cancer in alcoholics.
Paterson–Brown–Kelly syndrome also called Plummer–
Vinson syndrome (iron deficiency anaemia) is responsible for cancer of the oral cavity and hypopharynx.
5. Dental sepsis, jagged sharp teeth and ill-fitting den-
tures. All these cause chronic irritation and may lead
to development of cancer.
8. Retromolar trigone.
Clinical presentation and treatment of cancer of the
oral cavity at different sites are described below:
1. carcinoma lip (Figure 44.8). Mostly, it is squamous cell carcinoma, often seen in males in the age group
of 40–70 years. Lower lip is more often involved. Site of
predilection is between the midline and commissure of
the lip. Lesion is of exophytic or ulcerative type. Lymph
node metastases develop late. Submental and submandibular nodes are the first to be involved; other deep cervical
nodes may also get involved later.
Treatment is surgical excision with adequate safety
margin of healthy tissue and plastic repair of the defect.
Lymph node metastases require block dissection.
Radiotherapy also gives good results in early cases.
2. carcinoma buccal mucosa (Figure 44.9). Buccal
mucosa covers a large area. It extends from the meeting
point of lips in front to the pterygomandibular raphe behind and from upper gingivobuccal sulcus to the lower one.
Carcinoma of buccal mucosa is very common. Its incidence is next only to tongue cancer. Equally seen in both
sexes.
Sites of cancer in the lip and oral cavity
(AJCC, 2002)
1. Mucosal lip (from junction of skin—vermilion border
to line of contact of upper and lower lip).
2. Buccal mucosa (includes mucosa of cheek and inner
surface of lips up to line of contact of opposing lip).
3. Anterior two-thirds of tongue (oral tongue).
4. Hard palate.
5. Lower alveolar ridge.
6. Upper alveolar ridge.
7. Floor of mouth.
Figure 44.9. Carcinoma of the buccal mucosa.
Chapter 44 — Tumours of Oral Cavity
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Site of origin. Most common site is the angle of
mouth or the line of occlusion of upper and lower teeth.
It may also arise from the buccal sulcus where “pan” or
tobacco quid is kept. As the whole of buccal mucosa is
“condemned,” carcinoma may be multicentric.
Gross appearance. Lesion may be exophytic or ulceroinfiltrative; the latter may infiltrate deeply. Exophytic
type may be associated with erythroleukoplakia. Buccal
mucosa is also the most common site for verrucous carcinoma which is a white papillary growth with considerable keratinization.
Local spread. From its site of origin, the lesion may
spread deeply involving submucosa → muscle → subcutaneous fat → skin. Involvement of buccinator muscle or
anterior masseter causes trismus.
Tumour may spread radially from its site of origin
and involve angle of the mouth and lip anteriorly, retromolar trigone and medial pterygoid posteriorly, upper
gingivobuccal sulcus and maxilla superiorly, lower gingivobuccal sulcus and alveolar ridge and gums inferiorly.
Lymphatic spread. Nodal involvement occurs in about
50% of cases. Submandibular and later the upper jugular
nodes may get involved. Upper jugular nodes may also
be involved, directly skipping the submandibular group.
Clinical features. Early lesions are asymptomatic. Pain
and bleeding are seen when lesions are ulcerative and invade deeply. Involvement of the buccinator, masseter or
the pterygoid muscles causes trismus. Fungating mass
over the cheek, or a foul-smelling bleeding mass in the
oral cavity are late features.
Histological type: Squamous cell carcinoma is the most
common. Tumours can also arise from minor salivary
glands with histology as in salivary gland tumours.
Investigations. Biopsy of the lesion for histological
type of the growth. Computed tomography scan for involvement of bone (mandible or maxilla) and extension
into infratemporal fossa.
Treatment
(a) Stage I (T1N0). Surgical excision.
(b) Stage II (T2 N0). (i) Radiotherapy to primary lesion
and also nodes if bone is not involved. (ii) If bone
(maxilla/mandible) is involved or growth infiltrates
the muscle, surgery is the treatment of choice. It involves excision of the growth, marginal or segmental
mandibulectomy (or partial maxillectomy) and reconstruction of the area with skin or mucosal flaps.
(c) Stage III and IV. Surgical resection, reconstruction with
skin and/or myocutaneous flaps and postoperative radiotherapy to the site of lesion and nodes. Surgical
resection is combined with neck dissection if nodes
are clinically palpable.
3. carcinoma oral tongue (table 44.1). Carcinoma
involving anterior two-thirds of tongue is commonly
seen in men in the age group of 50–70 years. It may also
occur in younger age group and in females. It may also
develop on a pre-existing leukoplakia, long-standing dental ulcer or syphilitic glossitis (Figure 44.10). Vast majority are squamous cell type.
Site. Most common site is middle of the lateral border
or the ventral aspect of the tongue (Figure 44.11). Uncommonly, the tip or the dorsum may be involved.
TABLE 44.1 INCIDENCE OF CANCER PER 10,000
POPULATION IN INDIA IN YEAR 2000
Proportion
relative to all
Males Females Average
Lip 0.25 0.12 0.18 0.32%
Mouth 3.42 2.97 3.19 4.46%
Tongue 3.23 1.15 2.19 3.13%
a
National Cancer Registry Programme (Indian Council of Medical Research),
Bangalore, published, April 2005.
Figure 44.10. Carcinoma of the lateral border of the tongue (arrow).
Note associated leukoplakia of the floor of the mouth (double arrows).
Figure 44.11. Ulcerative type of squamous cell carcinoma of the
tongue in a 40-year-old female.
body cancers
a
Spread. Locally, it may infiltrate deeply into the lingual musculature causing ankyloglossia or may spread to
the floor of mouth, alveolus and mandible. Lymph node
metastases go to the submandibular and upper jugular
nodes (from the lateral border of tongue) and to the submental and jugulo-omohyoid group (from the tip). Bilateral or contralateral nodal involvement can also occur.
Clinically, cancer of the oral tongue presents as:
(a) An exophytic lesion like a papilloma (Figure 44.12).
(b) A nonhealing ulcer with rolled edges, greyish white
shaggy base and induration (Figure 44.13).
(c) A submucous nodule with induration of the sur-
rounding tissue.
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