223

CLASSIFICATION

The tumours of oral cavity can be classifi ed 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. Papilloma. Papillomas are common in the oral cavity. Peak incidence is in the third to fi fth 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 (fi broepithelial polyp). It is a smooth, mucosa-covered pedunculated tumour, usually about 1 cm in size and soft to fi rm 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. 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 diffi cult 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 fi tting 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 fi rst 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 fi rm 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 fi brous 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.

44 Tumours 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 neurofi broma, leiomyoma and other spindle cell tumours.

Treatment is complete surgical excision.

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 fl oor 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 ramifi cations 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 defi ned leukoplakia as a clinical white patch that cannot be characterized clinically or pathologi-cally 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 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-fi tting dentures or cheek bites. It may also be associated with submucous fi brosis, hyperplastic candidiasis or Plummer – Vinson syndrome.

(b) Sites involved. Buccal mucosa and oral commissures are the most common sites. It may however involve fl oor 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

A B 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.

225 CHAPTER 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 fi ssures. 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.

(g) Management (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 fl oor of the mouth. Most of lesions of erythroplakia show severe dysplasia, carci-noma in situ or a frank invasive carcinoma when fi rst 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 become mandatory.

III . MALIGNANT LESIONS

CARCINOMA ORAL CAVITY

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 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 defi ciencies . Their role in genesis of cancer has not been defi nitely established. Ribofl avin defi ciency may be responsible for cancer in alcoholics. Paterson – Brown – Kelly syndrome also called Plummer – Vinson syndrome (iron defi ciency anaemia) is responsible for cancer of the oral cavity and hypopharynx.

5. Dental sepsis, jagged sharp teeth and ill-fi tting dentures . All these cause chronic irritation and may lead to devel-opment of cancer.

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 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 fi rst 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 lower one.

Carcinoma of buccal mucosa is very common. Its inci-dence is next only to tongue cancer. Equally seen in both sexes.

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 ulceroinfi l-trative; the latter may infi ltrate 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-ated leukoplakia.

Figure 44.8 Carcinoma buccal mucosa.

227 CHAPTER 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 fossa.

Treatment

(a) Stage I (T 1 N 0 ) . Surgical excision. (b) Stage II (T 2 N 0 ) . (i) Radiotherapy to primary lesion and

also nodes if bone is not involved. (ii) If bone (maxilla/mandible) is involved or growth infi ltrates 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 fl aps.

(c) Stage III and IV . Surgical resection, reconstruction with skin and/or myocutaneous fl aps 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 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 infi ltrate deeply into the lingual musculature causing ankyloglossia or may spread to the fl oor 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-

ing tissue.

Table 44.1 Incidence of cancer per 10,000 population in India in year 2000 a

Males Females Average

Proportion relative to all body cancers

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 44.9 Carcinoma lateral border of the tongue (arrow). Note associated leukoplakia of fl oor 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

Symptomatology

(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-nal nerve.

(d) A lump in the mouth. (e) Enlarged lymph node mass in the neck. (f) Dysphagia, diffi culty to protrude the tongue, slurred

speech and bleeding from the mouth are late features.

For staging, see TNM classifi cation ( 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 (T 1 N 0 ) give equal results if treated with radiotherapy or surgery.

T 2 N 0 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 dissection.

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 always done.

Depending on the size and extent of the primary lesion of the tongue, surgery may consist of hemiglossectomy includ-ing a portion of the fl oor 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 superfi cial 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, fl oor 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 fi rst molar. Tumour may spread to the cheek, fl oor 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 classifi cation (AJCC, 2002) of cancers of lip and oral cavity

Primary tumour (T)

T 1 T 2 T 3 T 4 (lip) T 4 a (oral

cavity)

Tumour 2 cm or less in greatest dimension Tumour > 2 cm but not more than 4 cm in greatest

dimension Tumour > 4 cm in greatest dimension Tumour invades adjacent structures (e.g. cortical

bone, inferior alveolar nerve, fl oor of mouth, skin of face).

Tumour invades adjacent structures (e.g. cortical bone, deep (extrinsic) muscles of tongue, maxillary sinus, skin. Superfi cial erosion alone of bone/tooth socket by gingival primary is not suffi cient to classify as T 4 .

Regional lymph nodes (N)

N 1 N 2 N 3

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 (N 2 a); or multiple ipsilateral lymph nodes none more than 6 cm in greatest dimension (N 2 b) or bilateral or contralateral lymph nodes none more than 6 cm in greatest dimension (N 2 c).

Metastasis in lymph node more than 6 cm in greatest dimension.

Distant metastasis (M)

M 0 M 1

No distant metastasis Distant metastasis

Source: AJCC, Cancer Staging Manual, Chicago, 2002.

Table 44.3 Staging of carcinoma lip and oral cavity

Stage I T 1 N 0 M 0 Stage II T 2 N 0 M 0 Stage III T 3

T 1 T 2 T 3

N 0 N 1

M 0 0

Stage IV A T 4 T 4 Any T

N 0 N 1 N 2

M 0 M 0 M 0

Stage IV B Any T N 3 M 0 Stage IV C Any T Any N M 1

229 CHAPTER 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 infi ltrative type and spreads locally into the adjoining areas such as ventral aspect of the tongue, lingual gingiva, mandibular periosteum or deeply into the fl oor of mouth and submental space. Lym-phatic metastases go to submandibular nodes. Lesions of the fl oor of mouth remain asymptomatic for a long time or cause soreness or irregularity in the fl oor 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 N 0 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, fl oor 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 sites.

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 fl oor 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 defi ciency 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 fl oor 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).

CHEMOPREVENTION

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 benefi cial 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 signifi cant 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.