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The tumours of oral cavity can be classiﬁed as follows:
1. Benign tumours
2. Premalignant lesions
3. Malignant lesions
(b) Nonsquamous malignant lesions
I. BENIGN TUMOURS
1. Papilloma. Papillomas are common in the oral cavity.
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. Fibroma (ﬁbroepithelial polyp). It is a smooth, 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
3. Haemangioma. Mucosal haemangiomas can occur 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 pres-
ent 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 differenti-
ate 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 preop-
erative adjunct to surgery has been found very useful.
4. Lymphangioma. Lymphangiomas mostly involve anterior
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 spon-
taneously. Small lesions can be excised surgically. Symptom-
atic large lesions can be partially excised to reduce the bulk.
Total excision of these lesions is not possible.
5. Torus. It is a submucosal bony outgrowth. It may involve
the hard palate or mandible. Palatine torus is more com-
mon 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 inter-
fere with speech, mastication or ﬁtting of dentures.
6. Pyogenic granuloma (Figure 44.3). It is a reactive granu-
loma usually occurs in response to trauma or chronic irrita-
tion. 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. Pregnancy granuloma. It is clinically and histologically
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.
8. Granular cell myoblastoma or granular cell tumour. Most
of these tumours occur in the oral cavity and the site of pre-
dilection is tongue. Earlier they were thought to arise from
the muscle (hence called myoblastoma) but are now consid-
ered to be derived from Schwann cells. The tumour pres-
ents 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.
9. Minor salivary gland neoplasms. Pleomorphic adenoma
is the most common. Site of predilection is soft or hard pal-
ate 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.
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, sinona-
sal 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 pre-
sentation is 49 years with female preponderance.
44Tumours of Oral Cavity
224 SECTION III — DISEASES OF ORAL CAVITY AND SALIVARY GLANDS
It arises from the mesenchyme and is histologically com-
posed of spindle cells arranged in haphazard manner with
thick collagen bundles between the cells. It may show capil-
lary proliferation and pericystic pattern and thus need to
be differentiated from haemangiopericytoma. Immunohis-
tochemistry helps to differentiate them from neuroﬁbroma,
leiomyoma and other spindle cell tumours.
Treatment is complete surgical excision.
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 push-
ing the tongue up. It arises from the sublingual salivary
gland due to obstruction of its ducts. Some ranulae extend
into the neck (plunging type).
Treatment is complete surgical excision if small, or mar-
supialization, if large. Often it is not possible to excise 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 ran-
ula. 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 pathologi-
cally as any other disease. It is a clinical deﬁnition and does
not take pathology into consideration. Other white lesions
of oral mucosa, i.e. lichen planus, discoid lupus erythema-
tosus, white spongy nevus and candidiasis are excluded.
(a) Aetiological factors include smoking, tobacco chewing,
alcohol abuse particularly, if combined with smok-
ing. Chronic trauma can also occur due to ill-ﬁtting
dentures or cheek bites. It may also be associated
with submucous ﬁbrosis, hyperplastic candidiasis or
(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 (Figure 44.6).
(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
Figure 44.2 (A) Haemangioma on the lateral border of tongue. (B) Multiple haemangioma involving both lips, buccal mucosa and tongue in a
32-year-old man. He complained of bleeding when haemangioma was traumatized during chewing food.
Figure 44.3 Pyogenic granuloma.Figure 44.1 Fibroepithelial polyp left cheek.
225CHAPTER 44 — TUMOURS OF ORAL CAVITY
associated with malignancy. (ii) Nodular (speckled)
variety presents as white patches or nodules on ery-
thematous base. (iii) Erosive (erythroleukoplakia) 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 severe.
Higher the grade of dysplasia more are the chances
of its going into malignant change.
(f) Malignant potential. The chances of leukoplakia
becoming 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 leu-
koplakia, and the duration of follow-up.
(i) Many of the lesions will disappear spontaneously
if causative agent is removed.
(ii) In lesions with higher potential for malignant
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 kerati-
nization and as a result the red vascular connective tissue
of the submucosa shines through. There is no sex predi-
lection. Most common sites are lower alveolar mucosa,
gingivobuccal sulcus and the ﬂoor of the mouth. Most
of lesions of erythroplakia show severe dysplasia, carci-
noma in situ or a frank invasive carcinoma when ﬁrst
seen. Malignant potential is 17 times higher than in leu-
koplakia. Grossly, the lesion may be of three varieties—
homogenous, speckled or granular, and erythroplakia,
interspersed with areas of leukoplakia (often indistin-
guishable from erythroleukoplakia, type of leukoplakia).
Treatment is excision biopsy and follow-up.
3. Melanosis and mucosal hyperpigmentation. Benign pig-
mented lesions of oral mucosa may transform into malig-
nant melanomas; however, the incidence of this change
is not known. About one-fourth of mucosal melanomas
may resemble benign lesions and hence biopsy may
III. MALIGNANT LESIONS
CARCINOMA ORAL CAVITY
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 respon-
sible. (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.
Figure 44.4 Mucocele of the lower lip.
Figure 44.5 Ranula. Note a translucent swelling under the tongue.
Figure 44.6 Leukoplakia on lateral border of tongue.
226 SECTION III — DISEASES OF ORAL CAVITY AND SALIVARY GLANDS
2. Tobacco chewing. Powdered tobacco, mixed with lime, is
placed in some part of the vestibule of the mouth. Carci-
noma 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 dentures.
All these cause chronic irritation and may lead to devel-
opment of cancer.
SITES OF CANCER IN THE LIP AND ORAL CAVITY
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 sur-
face 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.
8. Retromolar trigone.
Clinical presentation and treatment of cancer of the oral
cavity at different sites are described below:
1. Carcinoma Lip (Figure 44.7)
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 44.8)
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
Carcinoma of buccal mucosa is very common. Its inci-
dence is next only to tongue cancer. Equally seen in both
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,” carci-
noma may be multicentric.
Gross appearance. Lesion may be exophytic or ulceroinﬁl-
trative; 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 mas-
seter 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 gingivobuc-
cal 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.
Figure 44.7 Carcinoma upper lip and oral commissure. Note associ-
Figure 44.8 Carcinoma buccal mucosa.
227CHAPTER 44 — TUMOURS OF ORAL CAVITY
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
(a) Stage I (T1 N0). 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
3. Carcinoma Oral Tongue (Table. 44.1)
Carcinoma involving anterior two-thirds of tongue is com-
monly 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 44.9). Vast majority are
squamous cell type.
Site. Most common site is middle of the lateral border or
the ventral aspect of the tongue. Uncommonly, the tip or
the dorsum may be involved.
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 metas-
tases 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 con-
tralateral nodal involvement can also occur.
Clinically, cancer of the oral tongue presents as:
(a) An exophytic lesion like a papilloma (Figure 44.10).
(b) A nonhealing ulcer with rolled edges, greyish white
shaggy base and induration (Figure 44.11).
(c) A submucous nodule with induration of the surround-
Table 44.1 Incidence of cancer per 10,000
population in India in year 2000a
Males Females Average
relative to all
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%
aNational Cancer Registry Programme (Indian Council of Medical
Research), Bangalore, published, April 2005.
Figure 44.9 Carcinoma lateral border of the tongue (arrow). Note
associated leukoplakia of ﬂoor of mouth (double arrows).
Figure 44.10 Exophytic growth on the right lateral border of tongue
in a 60-year-old male. It was squamous cell carcinoma.
Figure 44.11 Ulcerative type of squamous cell carcinoma of tongue
in a 40-year-old female.
228 SECTION III — DISEASES OF ORAL CAVITY AND SALIVARY GLANDS
(a) Early lesions are painless and remain asymptomatic for
a long time.
(b) Pain in the tongue locally at the site of ulcer.
(c) Pain in the ipsilateral ear; it is due to common nerve
supply of the tongue (lingual nerve) and ear (auriculo
temporal) from the mandibular division of the trigemi-
(d) A lump in the mouth.
(e) Enlarged lymph node mass in the neck.
(f) Dysphagia, difﬁculty to protrude the tongue, slurred
speech and bleeding from the mouth are late features.
For staging, see TNM classiﬁcation (Tables 44.2 and 44.3).
Treatment. Aim of treatment is to treat primary tumour
in the tongue, control neck disease (nodal metastasis) and
preserve function of the tongue as much as possible.
Small tumours (T1N0) give equal results if treated with
radiotherapy or surgery.
T2N0 tumours can also be treated by radiotherapy includ-
ing the neck nodes to eliminate micrometastases. They can
also be treated by surgical excision with prophylactic neck
Stage III or IV tumours require combined treatment
with surgery and postoperative radiotherapy. It gives better
results than either modality alone. Block dissection neck is
Depending on the size and extent of the primary lesion of
the tongue, surgery may consist of hemiglossectomy includ-
ing a portion of the ﬂoor of mouth, segmental or hemi-
mandibulectomy and block dissection of neck nodes—the
so-called “commando operation.”
4. Carcinoma Hard Palate
It is either squamous cell or glandular variety; the latter being
more common. Glandular variety arises from minor salivary
glands of the palate and may be adenoid cystic, mucoepider-
moid or adenocarcinoma. It is common in India especially
in people who have the habit of reverse smoking, i.e. keep-
ing the burning end of bidi or cigar in the mouth. Both men
and women are affected.
Cancer starts as a superﬁcial ulcer with rolled out edges
and gives no symptoms except painless irregularity on the
palate felt by the tongue. It may spread to the gingiva,
lip, soft palate or invade the bone of hard palate, ﬂoor of
the nasal cavity or the antrum. Lymphatic metastases may
spread to the submandibular and upper jugular nodes. Can-
cer palate should be differentiated from cancer of maxillary
antrum or nose which has spread to the palate.
Treatment. Small tumours are resected along with the
underlying bone, larger ones require partial maxillectomy.
If nodes are enlarged, block dissection is also combined. Sur-
gical defect in the palate, left after excision of the growth, is
closed by a suitable prosthesis.
5. Carcinoma of Alveolar Ridges
It is also called gingival carcinoma; it is mostly seen in
men. Usual site of involvement is lower jaw behind the ﬁrst
molar. Tumour may spread to the cheek, ﬂoor of mouth,
retromolar trigone or the hard palate. Gingival cancer may
invade the underlying bone and then spread rapidly along
the neurovascular bundle. Nodal metastases go to subman-
dibular and upper jugular nodes.
Treatment. Radiotherapy is avoided because of the risk
of radio-osteonecrosis. Surgery is the treatment of choice.
Early mucosal lesion on the lower alveolus is treated by local
excision with marginal resection of the mandible. Extensive
lesions require wide excision which may necessitate seg-
mental or hemimandibulectomy. Block dissection may be
Table 44.2 TNM classiﬁcation (AJCC, 2002)
of cancers of lip and oral cavity
Primary tumour (T)
Tumour 2 cm or less in greatest dimension
Tumour > 2 cm but not more than 4 cm in greatest
Tumour > 4 cm in greatest dimension
Tumour invades adjacent structures (e.g. cortical
bone, inferior alveolar nerve, ﬂoor of mouth,
skin of face).
Tumour invades adjacent structures (e.g. cortical
bone, deep (extrinsic) muscles of tongue,
maxillary sinus, skin. Superﬁcial erosion alone
of bone/tooth socket by gingival primary is not
sufﬁcient to classify as T4.
Regional lymph nodes (N)
Metastasis in a single ipsilateral lymph node
3 cm or less in greatest diameter.
Metastasis in a single ipsilateral lymph node
> 3 cm but not more than 6 cm in greatest
dimension (N2a); or multiple ipsilateral lymph
nodes none more than 6 cm in greatest
dimension (N2b) or bilateral or contralateral
lymph nodes none more than 6 cm in greatest
Metastasis in lymph node more than 6 cm in
Distant metastasis (M)
No distant metastasis
Source: AJCC, Cancer Staging Manual, Chicago, 2002.
Table 44.3 Staging of carcinoma lip and oral cavity
Stage I T1 N0 M0
Stage II T2 N0 M0
Stage III T3
Stage IV A T4
Stage IV B Any T N3 M0
Stage IV C Any T Any N M1
229CHAPTER 44 — TUMOURS OF ORAL CAVITY
combined if nodes are also palpable. Upper alveolar lesions
may require partial maxillectomy.
6. Cancer Floor of Mouth
Squamous cell carcinoma is the most common. It affects
males more than females in ratio of 4:1. Typically, lesions
start anteriorly near the opening of submandibular duct
which may get obstructed, leading to enlargement of sub-
mandibular gland (Figure 44.12).
Usually, the lesion is ulcerative or inﬁltrative type and
spreads locally into the adjoining areas such as ventral aspect
of the tongue, lingual gingiva, mandibular periosteum or
deeply into the ﬂoor of mouth and submental space. Lym-
phatic metastases go to submandibular nodes. Lesions of
the ﬂoor of mouth remain asymptomatic for a long time or
cause soreness or irregularity in the ﬂoor of the mouth. A
swelling in the submandibular region may be either due to
obstructive enlargement of submandibular salivary gland or
lymph node metastases and this may require differentiation.
Treatment. Small lesions without involvement of tongue,
lingual gingiva or nodes can be treated by surgical excision
or radiotherapy with equal results. Larger lesions with exten-
sion to the tongue, gingiva or mandible require wide exci-
sion including marginal or segmental mandibular resection.
Block dissection is indicated when cervical nodes show clini-
cal evidence of metastases. Prophylactic neck dissection or
irradiation is advised for N0 neck in stage II cancer because
of high incidence of micrometastases (40%), stage III and
IV cancers require surgery and radiotherapy.
7. Carcinoma Retromolar Trigone
Involvement of retromolar trigone may be primary or sec-
ondary to extension of growths from the gingiva, ﬂoor of
mouth, buccal mucosa or the palatine arch.
Treatment depends on the extent of lesion. Wide surgical
excision often combined with block dissection is required.
MULTIPLE PRIMARY CANCERS
About 15% of patients with carcinoma of the oral cavity have
multiple primary cancers affecting the upper aerodiges-
tive tract. This is because of the common risk factors such
as smoking and alcohol simultaneously operating at various
NONSQUAMOUS MALIGNANT LESIONS
In addition to carcinoma, other malignant lesions that
involve the oral cavity are:
1. Minor salivary gland tumours. In one series, 80–90% of all
minor salivary gland tumours were malignant. Palate is the
most common site but can involve tongue, cheek, lip, gums
and ﬂoor of mouth (Figure 44.13).
Adenoid cystic variety is the most common (40%). Next in
frequency are the adenocarcinoma (30%) and mucoepider-
moid carcinoma (20%). Treatment is wide surgical excision
along with block dissection, if the neck nodes are positive.
2. Melanoma. Mucosal melanomas of oral cavity and oro-
pharynx are rare. Peak age incidence is the sixth decade;
males are affected more (2:1). Palate and gingiva are the
most common sites. They appear as areas of higher pigmen-
tation and later may ulcerate and bleed. Amelanotic variety
is also seen. Both cervical nodal and distant metastases are
seen. Treatment of choice is wide surgical excision includ-
ing underlying bone. Local recurrence is common. Progno-
sis is poor with 5-year cure rate of only 15%.
3. Lymphoma. Lymphomas can involve oral cavity or oro-
pharynx, majority of them occurring in the palatine ton-
sils. Males are affected more. Usual presentation is that
of a smooth, submucosal bulky mass which is occasionally
ulcerated. They are mostly of non-Hodgkin variety. Cervical
nodes may be involved in 40–70% of the patients. Treatment
is radiation, alone or in combination with chemotherapy.
4. Kaposi sarcoma. It is a vascular tumour, multifocal in ori-
gin, primarily affecting skin but may occur in the oral cavity.
Its incidence is high in AIDS (acquired immune deﬁciency
syndrome) patients. The lesion appears as a reddish purple
nodule or a plaque mostly on the palate. Microscopically, it
Figure 44.12 Ulcerative squamous cell carcinoma in the ﬂoor of oral
cavity (arrow) in a 55-year-old male.
Figure 44.13 Mixed salivary tumour palate.
230 SECTION III — DISEASES OF ORAL CAVITY AND SALIVARY GLANDS
consists of spindle cells with haemorrhagic cleft-like spaces.
Treatment is not satisfactory. Kaposi sarcoma in non-AIDS
patients may respond to chemotherapy but its response in
patients suffering from AIDS is poor (see also p. 371).
It is the use of certain pharmacological agents to halt, delay
or reverse the process of carcinogenesis. It has been used to
prevent oral premalignant lesions to develop into cancer
or to prevent the development of second primary cancers
after the main primary cancer has been treated. Agents used
have been vitamin A, beta carotene, alpha tocopherol (vita-
min E), selenium and natural or synthetic retinoids such as
13-cis retinoic acid. Beta carotene and vitamin A induced
remission of oral leukoplakia is seen in 25–50% of patients.
Similarly, in a controlled trial, 13-cis retinoic acid reduced
the incidence of second primary lesions in the aerodigestive
tract. The beneﬁcial effect of these agents may be limited to
the duration of treatment only.
In addition to their use in head and neck, retinoids have
shown signiﬁcant chemopreventive activity in cancers of
lung, skin, cervix, bladder and ovary. Trials are also being
conducted in Cox-2 inhibitors (e.g. celecoxib) in the pre-
vention of oral premalignant lesions.