Tumors of the mouth

From Otolaryngology Online


Tumors of oral cavity can be classified as:

1. Benign tumors

  a. Solid
  b. Cystic

2. Premalignant lesions

3. Malignant lesions

  a. Carcinoma
  b. Nonsquamous malignant lesions

Benign tumors:


This is rather common in the oral cavity. The incidence of these lesions are known to peak in the 3rd and 5th decades. Common sites affected include:

Soft and hard palate




These tumors are mostly 1 cm in size and are usually soft to firm in consistency. It is usually pedunculated and white in color. The surface is irregular.

These lesions are caused by Human papilloma virus infections. These lesions are usually benign and are asymptomatic. These lesions may persist or relapse spontaneously. These lesions are postulated to be induced by HPV 6 or 11.

Types of papilloma:

Verruca vulgaris:

This is also known as the common wart. This is the most common HPV associated skin lesion. This lesion can also be found in the oral cavity. This lesion is usually associated with HPV2 and 4. In the mouth these lesions are commonly found on the keratinized surfaces of gingiva and palate.

These lesions are considered to be contagious, and some lesions can occur following autoinoculation. These lesions are typically found in children but can also be seen in any age group. These lesions often rapidly enlarge (average size about <5mm). It then becomes stable.

Focal epithelial hyperplasia:

This is also known as Heck disease. Focal epithelial hyperplasia is associaterd with HPV 13 and 32. Heck disease commonly affects children, and is increasingly seen in HIV positive population. This lesion is located in thelabial, buccal and lingual mucosa.

Condyloma accuminatum:

Normally these lesions are seen in the genital area and are considered to be a sexually transmitted disease. Oral cavity condylomas are associated wtih HPV2,6, and 11. Clinically these lesions are usually large in size and are similar in appearance to papillomas. They are also more clustered. Condylomas are more diffuse and deeply rooted than papillomas.


This is usually by complete excision at the base with 1 mm margin up to the depth of the submucosa. Removal is usually considered tobe the cure. Recurrence of these lesions suggests the possibility of retransmission of infection.


This is also known as fibroepithelial polyp. These lesions are also referred to as irritation fibroma. This is by far the most common of the oral fibrous tumor like growths. Majority of these lesions represent focal fibrous hyperplasia due to trauma or local irritation. These lesions are usually 1 cm in size and are soft to firm in consistency. The surface is similar in color to the surrounding mucosa, but they could be hyperkeratotic or ulcerated owing to trauma. They can occur anywhere in the oral / oropharyngeal mucosa. Recurrence after complete surgical removal is possible if the offending irritation still persists.


Fibromas are unencapsulated solid, nodular mass of dense fibrous connective tissue, sometimes the fibrous tissue could be hyalinized.

Unusual subtypes of fibromas:


This is actually a rare dermatologic pseudotumor and can be seen in oral cavity of aged adults. These lesions present as asymptomatic submucosal and nodular masses involving the floor of the mouth and hard palate. Histologically these lesions consists of collagen fibers and coarse elastic fibers. These elastic fibers can be demonstrated with elastin stain. Surgical excision is the treatment of choice.

Sclerotic fibroma:

This was first described as a component of Cowden syndrome. This is a rare benign fibrous neoplasm. It is very rarely seen in the oral cavity involving the buccal and labial mucosa. This tumor is well delineated, but is unencapsulated. It is formed by a mass of densely collagenized, hypocellular fibrous tissue. The fibrous tissue forms a storiform pattern and prominent cleft can be seen between the collagen bundles. These tumors are CD 34 and vimentin positive.

Giant cell fibroma:

It appears as asymptomatic sessile / pedunculated nodule which is smaller than 1 cm in diameter. Majority of these lesions are diagnosed in persons aged 10-30 years. No sex predilection has been reported. Common sites of oral involvement happens to be the mandibular gingiva, followed by maxillary gingiva, tongue and palate.

Peripheral cemento-ossifying fibroma:

This is a reactive gingival lesion that arises from cells of the periodontal ligament / periosteum. Most commonly it is located in the gingival papilla between adjacent teeth. This condition may occur in persons of any age, but are often seen in persons aged 10-20 years. Females are affected more commonly than males.

The maxillary gingiva is involved often than the mandibular gingiva. The anterior region is commonly affected. Mobility / migration of adjacent teeth can occasionally be observed.

Microscopic studies reveal fibrous proliferation accompanied by increased cellularity with plump immature fibroblasts with variable amounts of calcified material. This calcified material could be osteoid, cementoid or dystrophic.

These lesions can be managed by surgical excision down up to the periosteum followed by elimination of local irritants. A recurrence rate of 15% have been reported. In these cases reexcision could be successful. Associated dentition can always be retained.

Peripheral odontogenic fibroma:

This is an uncommon neoplasm which is considered to arise from odontogenic epithelial cell rests present in the periodontal ligament or in the attached gingiva itself. These lesions should not be confused with that of perepheral cementoossifying fibroma. These lesions are considered to be the extraosseous counterpart of the central odontogenic fibroma of WHO type.

These lesions manifests as firm, slowly growing sessile and nodular growth of fingiva, more often seen on the mandibular buccal / labial aspect causing displacement of teeth. In rare cases there may be associated external root resorption. It can occur in a variety of age groups with a slight female predlection.

Microscopically these tumors show an unencapsulated mass of interwoven cellular fibrous connective tissue that contains scattered nests / strands of odontogenic epithelium. The surface generally is not ulcerated.

Treatment is conservative excision taking care to maintain gingival architecture and periodontal integrity.


These lesions represent a group of infiltrating fibrous proliferations with a biological behavior and histologic appearance ranging between those of benign fibrous lesions and fibrosarcomas.

In the head and neck region these lesions are sometimes referred to as aggressive juvenile fibromatoses. These lesions are also known as extraabdominal desmoids. These lesions could involve patients of any age group. Majority of these lesions are identified in patients younger than 10 years of age.

The frequent site of involvement is the soft tissues adjacent to the mandible. These lesions appear as firm, painless, poorly demarcated mass lesions with variable growth rates. These lesions are locally aggressive and often cause resortpion of underlying bone if present.

Myofibroma / Myofibromatosis:

Myofibroblasts are spindle shaped cells with features of both fibroblasts and smooth muscle cells. If these cells happens to be the predominant cell type in a tumor then it is known as myofibromas. Myofibroma is used to describe solitary lesion while the term myofibromatosis is used to describe multicentric lesions if present. These tumors are benign and less aggressive than that of fibromatosis. Even though these tumors can occur in either sex, it demonstrates a slight male predilection.

Solitary myofibromas commonly involve the mandible. Treatment of these lesions is by conservative excision.


Hemangiomas involving the mucosa can occur in the oral cavity and oropharynx. These lesions are commonly seen in children. Hemangiomas are of three types: capillary, cavernous and mixed varieties.

When these hemangiomas are present at birth or in young children they must be observed for some period of time as spontaneous regression of these lesions are known to occur. Hemanigomas that continue to grow are really problematic.

These tumors can be identified by rapid endothelial cell proliferation during early infancy. This is followed by involution over time. Other allied abnormalities are the resultant of anomalous development of vascular plexus. The malformations have normal endothelial cell growth cycle that affects the veins, capillaries or the lymphatics. They do not involute.

These lesions commonly manifest within the first month of life. These lesions exhibit a rapid proliferative phase and could involute slowly at a later date. These lesions could also undergo complete involution. The associated vascular malformations are more stable and often fail to regress.

Hemangiomas can be associated with the following syndromes:

Osler-Rendu-Weber syndrome:

This syndrome is characterised by multiple telangiectasis, rare GI involvement, and occasional CNS involvement. This syndrome is of autosomal dominant inheritance.

Sturge-Weber syndrome:

This syndrome is characterised by portwine stain and leptomeningeal angiomas. This lesion is noninherited and nonfamilial.

Maffucci syndrome:

This syndrome is associated with hemangiomas of mucous membranes and dyschondroplasia.


These lesions should be understood in terms of their embryology and development. The sequence of events falls into 3 stages:

Undifferentiated capillary network stage

Retiform developmental stage

Final developmental stage

In the undifferentiated capillary network stage the primitive mesenchyme is nourished by an interlacing system of blood spaces without distinguishable arterial and venous channels.

Separate venous and arterial stems appear on either side of the capillary network in the retiform developmental stage. This stage begins at about 48 days of embryonic development.

The final developmental stage begins at 2 months development and it involves the gradual replacement of the immature plexiform network by the mature vascular channels.

Capillary hemangioma is rather common and it represents an arrest in the development of the mesenchyme primordia in the undifferentiated capillary network stage. As the differentition progresses primitive vessels penetrate deeper into the subcutaneous layer, the muscle or the bone tissue giving rise to capillary hemangiomas.

The proliferating hemangiomas have been shown to have estradiol -17 beta receptors in the cytoplasm. Steroid therapy has been theorized to block these receptors, hence steroid therapy has become the first line of treatment for proliferating lesions.

Growth factors involved in the enlargement of hemangiomas:

Vascular endothelial growth factor

Basic Fibroblast growth factor

Transforming growth factor beta

Interleukin 6

One theory suggests that the endothelial cells of hemangiomas are derived from a distant population of endothelial precursors carried by existing vascular pathways to a receptive environment. Potential such sources include the bone marrow and the placenta. This explains the three fold increased risk of hemangiomas observed in infants subjected in utero to chorionic villous sampling, since local placental injury could predispose to shedding of cells into the fetal circulation.



In the proliferating phase steroids / beta blockers are of much use. Propranolol at a dose of 2-3 mg /kg/day in 2-3 divided doses can be used for a period ranging from 2-10 months.

Prednisolone can be used in doses of 3mg/kg/day for 3 days, followed by 5 weeks of every other day dosing of prednisolone at 1.5 mg/kg/day and then one week of every other day dosing of prednisolone at 0.75 mg/kg/day.

Stabilised lesions can be surgically removed. Intralesional triamcinolone injections have also been used with success.


These lesions commonly involve anterior 2/3 of tongue. They may involve the tongue diffusely and could cause macroglossia or may present as a soft tissue swelling which can be compressed.

These lesions do not undergo spontaneous regression. Small lesions can be managed by surgical excision. Complete excision of these lesions is not possible.

These lesions are rare, benign congenital malformations of unknown etiology. They originate from the lymph vessels.

Theories of lymphangioma:

Two theories have been proposed to explain the origin of lymphangiomas. The first one considers the lymphatic system to develop from five primitive sacs arising from the venous system. In the head and neck region, endothelial outpouching from the jugular sac spreads centrifugally to form the lymphatic system.

Another theory proposes that the lymphatic system develops from mesenchymal clefts in the venous plexus reticulum and spreads centripetally towards the jugular sac. Lymphangiomas could develop from congenital obstruction / sequestration of the primitive lymphatic enlargement.


Small lesions can be managed by surgical excision. When present in the tongue, laser photocoagulation has been found useful in controlling the tongue size.

OK-432 a lyphophilized incubation mixture of streptococcus pyogenes and penicillin G potassium has been used in treating these conditions by local infiltration.


The word “tori” is derived from the latin word torus which means “to stand out” / “lump”.

Synonyms: Exostosis of oral cavity, Buccal exostosis.


Torus palatinus is a sessile nodule of bone occuring commonly in midline of hard palate. It can also occur over the lingual surface of the maxilla (torus mandibularis). Torus mandibularis is a bony protruberance located on the lingual aspect of the mandible (commonly between the canine and premolar areas). These are bony masses, begining their development during early teens and gradually progresses to adult hood. These masses are slow growing and painless.

These masses are usually self limiting, rarely they may cause periodontal diseases. Periodontal disease is usually caused by the mass forcing food towards the teeth while being chewed instead of away from it. Too large torus may interfere with dentures.


Masticatory hyperfunction

Genetic factors (common in females)

Environmental factors


Age of occurrence:

It is very rare during the first decade of life. Its increase in size occur during the second and third decades of life. According to Bruce etal the average age of presentation of tori is 34. Since there is very little literature available on this subject very little knowledge regarding age of occurrence is available.

Rate of growth:

The rate of growth of these bony masses is very slow and gradual. Studies have shown that maximum increase in size occurs during the second and third decades of life. Role of imaging:

CT scan is virtually diagnostic.


Oral exostosis was first classified by Haugen. He classified oral cavity exostosis according to their sizes as small, medium and large.

Less than 2 mm in their largest diameter – small

2 – 4 mm in their largest diameter – medium

More than 4 mm in their largest diameter

According to Haugen majority of oral cavity exostosis belonged to the small and medium categories.

Reichart in his modification of Haugen's classification suggested few changes:

Grade I – Tori up to 3 mm in their largest dimension

Grade II – Tori up to 6 mm in their largest dimension

Grade III – Tori above 6 mm belong to this group


Torus palatinus occur in varying shapes. It can be flat, nodular, lobular or spindle shaped. Small tori are invariable nodular and they are the most common variety encountered. Lobular shapes are pretty rare.

Indications for surgical removal:

The mucosa over torus is ulcerated

When it interferes with placement of dentures

When there is associated periodontal disorder

Where torus can be used as graft material

Phonatory disturbances

Sensitivity of the overlying mucosal layer

Disturbances involving masticatory apparatus

Esthetic reasons

Surgical removal:

Torus palatinus can be removed either under local / general anesthesia. If the surgery is tobe performed under local anesthesia the following nerves should be anesthetised using 2 % xylocaine mixed with 1 in 100,000 units adrenaline.

Nasopalatine nerve should be anesthetised as it exits through the anterior palatine foramen

Anterior palatine nerves should be anesthetised through posterior palatine foramen

Anesthetic solution should also be infiltrated over the mass to detach the oral mucosa from the mass

To surgically remove torus mandibularis infiltration anesthesia is used over the mass. Nerve block anesthesia blocking inferior alveolar, mental and lingual nerves can also be used.


To remove torus palatinus a double Y incision is preferred. This incision prevents damage to the nasopalatine and anterior palatine blocks of the hard palate. The incision should involve the full thickness of the muco periosteal lining.

Surgery to remove torus mandibularis involve incision over the mandibular ridge. If the incision is made above the torus it provides a good operating field. In rare cases scalloped inter dental incisons can be used.

Fissure burr is used to remove the bony torus. After removal of torus the flap could be found to be redundant and the same may also be trimmed. The flaps may be sutured back in place using absorbable suture material.

Surgical complications of torus palatinus:

Perforation into the nasal cavity

Secondary anesthesia due to damage to palatine nerve

Palatine artery hemorrhage

Laceration of palatine mucosa

Fracture of palatine bone

Surgical complications of torus mandibularis:

Mandibular fracture

Devitalisation of teeth

Injury to salivary ducts

Injury to lingual nerve

Flap laceration

Post op complications:


Wound infection

Flap necrosis

Pyogenic granuloma:

This is a reactive granuloma occurring in response to trauma / chronic irritation. These lesions commonly involve anterior gingiva, but other sites like tongue, buccal mucosa, lips can also be involved. These lesions are usually smooth, soft, reddish purple in color and bleeds on touch.

Some authors regard pyogenic granuloma as an infectious entity. According to Kerr staphylococci and botryomycosis infection in the walls of blood vessels act as contributing factors in the develpment of these lesions.

These lesions can be treated by surgical excision.

Granular cell tumor (Granular cell myoblastoma):

Majority of these lesions occur in the oral cavity. Among the structures of the oral cavity tongue happens to be commonly involved. These lesions presents as a painless submucosal nodule. These lesions can ideally be managed by wide surgical excision.

Congenital epulis is a granular cell tumor involving the gums of future incisors in female infants.

Neoplasms involving minor salivary glands:

Oral cavity mucosa is richly endowed by minor salivary glands. Tumors involving these glands could present as oral cavity masses. Pleomorphic adenoma is the most common tumor involving the minor salivary glands. Common areas involved include the hard and soft palate. Of course it could involve any portion of the oral cavity.

Solitary fibrous tumor:

These tumors are most common in the pleura, but can also be seen involving the tongue and buccal mucosa. These lesions present as a painless slow growing well demarcated mobile submucosal tumor. Females are commonly involved.

Histologically these lesions are composed of spindle cells arranged in an haphazard manner with thick collagen bundles between these cells. It may also show capillary proliferation and need to be differentiated from hemangiopericytoma.

Treatment is by surgical excision.

Cystic lesions involving oral cavity:


This is a mucous retention cyst involving minor salivary glands of the lip. Most common site is in the lower lip. These lesions appear as a soft and cystic mass of bluish color.

Mucocele is classically defined as a mucous filled cyst. Two types of mucoceles can occur i.e extravasation and retention types. In children extravasation types are common and retention types are very rare in them. Extravasation mucocele results from broken salivary gland duct causing spillage of saliva into the soft tissues. These extravasation mucocele undergoes three phases in their development. In phase I mucous spills diffusely from the excretory duct into the connective tissues. In phase II which is also known as phase of resorption. In this phase there is foreign body reaction and granuloma formation occurs. In phase III there is formation of pseudocapsule around the mucosa.

Blockage of salivary gland ducts can cause decrease / absence of glandular secretion leading on to the formation of retention mucocele.

Clinical appearance of both extravasation and retention mucoceles is almost similar. Mucoceles usually present as bluish, soft and transparent cystic swelling which could resolve spontaneously.

Extravasation mucoceles appear frequently in the lower lip followed by tongue, buccal mucosa and palate. This is rarely seen in the retromolar region. Retention mucoceles can occur at any site of the oral cavity. When it is located in the floor of the mouth it is kown as the Ranula.

Ranula was reported even during the period of Hippocrates and Celsius. The word ranula has been derived from the latin word “Rana” which means the frog. This is because it resembles the translucent belly of a frog. Ranula is formed by rupture of excretory duct of the salivary gland, which is followed by rupture of saliva into the surrounding tissues . This accumulation lacks a true epithelial capsule and hence is a pseudocyst . Biochemical studies reveal that fluid within the ranula is rich in protein and amylase. Salivary secretions from sublingual gland is also rich in protein and amylase and hence it has been suggested that ranulas are commonly caused by ruptured sublingual excretory ducts. The high protein content of the fluid in the ranula stimulates inflammatory reaction causing pseudocyst formation . There are two different types of ranulas. These two types of ranula are caused by differing pathogenesis. True cyst: This type of ranula has an epithelial lining. This type of ranula is usually caused due to obstruction of ducts of sublingual gland or ducts of one of the minor salivary glands. Pseudocyst: This type of ranula does not have an epithelial lining. This is caused due to ductal injury of commonly the sublingual salivary gland, extravasation of saliva and accumulation into the submucous tissue. Sometimes this type of ranula is surrounded by granulation tissue or condensed connective tissue . Clinical classification of ranula: Clinically ranula has been classified into two types: 1. Intra oral ranula 2. Plunging ranula Intraoral ranula: This type of ranula is confined to the floor of the mouth. It is known to slowly enlarge in size into painless fluctuant swelling. Plunging ranula: In this type the extravasating pseudocyst breaches the mylohyoid to present as neck swelling. Plunging ranulas commonly arise from sublingual salivary gland 4 . Rarely it can pass behind the posterior edge of mylohyoid muscle to present in the neck. The possibility of cervical / plunging ranula should be considered in a patient with painless swelling in the neck that gradually increases in size. Histroy of truma to oral cavity / surgical procedures involving the oral cavity should be sought.

Anatomy of sublingual salivary gland: Sublingual salivary gland is paired. These glands are located below the mucosa of the anterior part of the floor of the mouth. These glands lie anterior to the submandibular ducts, above the mylohyoid and geniohyoid muscles. These glands drain their saliva into submandibular duct via 8-20 excretory ducts known as ducts of Rivinus. Salivary drainage from these glands can also occur directly into the floor of the mouth on an elevated crest of mucous membrance known as plica fimbriata located on either side of the frenulum of the tongue.

Important structures related to sublingual salivary gland in the floor of the mouth: Lingual nerve crosses deep to the submandibular duct in the lateral floor of the mouth. In the anterior part of the floor of the mouth this nerve is located posterior to the duct. Submandibular duct is located deep to the mucosa of the anterior and lateral floor of the mouth. It opens into the oral cavity on either side of the frenulum.

Clinical features:

Bluish mass could be seen occupying the anterior portion of the floor of the oral cavity pushing the tongue backwards. It appeared cystic in nature. Dilated veins could be seen over the swelling. On palpation the mass was soft and cystic. It was not bidigitally palpable.

In a CT scan uncomplicated ranulas appear as thin walled cystic lesion with central fluid attenuation (10-20 HU). If this cyst gets infected / has been drained / sclerosing agents used will appear with increased attenuation values and thickened lining . It may sometimes under these circumstances appear as non-enhancing soft tissue mass.

Ultrasound neck: Revealed thin walled cystic lesion involving the floor of the mouth.


This patient was managed by total excision of ranula along with sublingual salivary gland. Excision was performed under general anesthesia. Patient was placed in a supine position with a slight elevation of head end. The oral cavity is kept open using bite blocks. Tongue is held out using tongue holding forceps.

The mucosa over the ranula was incised taking care not to enter the sac. A dissection plane in the submucosa is established over the wall of the ranula. The cyst was excised along with sublingual salivary gland taking care not to damage submandibular duct and lingual nerve.

Surgical resection is invariably curative. Surgery should include not only removal of the ranula but also the sublingual salivary gland from which it has arisen. If ranula is removed along with sublingual salivary gland it does not recur that commonly.

Other methods include: 1. Incision and drainage – This procedure is like any other abscess drainage. It has a very high recurrence rate about 80%. 2. Marsupialization – In this procedure the cyst is opened up and drained. The cyst wall is everted and sutured to the oral cavity mucosa. This has a recurrence rate of about 40%. 3. The best results are achieved by total resection of the cyst along with sublingual salivary gland.

Sclerotherapy: Currently this is holding out lots of promise. The sclerosing agent used is OK-432 7 . This is actually a lyophilized mixture of low virulence strain of streptococcus pyogenes incubated with benzyl penicillin. This acts by stimulating inflammatory lesion with destruction of cyst lining if present and cicatricial contraction of the lesion by scar tissue formation. Patients who have been treated with sclerotherapy have mild elevation of temperature and pain and tenderness over the lesion. The hither to painless lesion becomes rather painful due to inflammatory reaction.

Caution: Before proceeding with sclerotheapy, it should be ensured that the patient is not abnormally sensitive to Benzyl Penicillin which is commonly known to produce anaphylactic reaction. This procedure is performed under ultrasound guidance. Angio catheter is used for this purpose. A catheter with 21 guage needle is preferred. The cyst is punctured and the needle is placed at the centre of the cyst. About 10m of cyst fluid is aspirated. The same amount of OK-432 solution is injected into the cyst. The needle is withdrawn and pressure dressing is applied. It is ideal to puncture the ranula via the neck because if done orally the sclerosing agent tended to leak into the oral cavity. This is more beneficial in treating plunging ranula. Ultrasonic screening is performed at 3 month, 6 month and 1 year intervals following sclerotherapy.


A sublingual dermoid is a median / laterally situated mass above the level of mylohyoid. It shines through the mucosa as a whitish mass in contrast to that of mucocele. A submental dermoid develops below the mylohyoid and presents as a submental swelling behind the chin.

Premalignant lesions:


This is defined by WHO as a white patch that cannot be characterized clinically / pathlogically as any other disease.


Smoking, tobacco chewing, alcohol use, trauma to oral cavity mucosa due to ill fitting denture or sharp tooth.

Histologically these lesions may show some level of epithelial dysplasia. Higher the grade of dysplasia greater are the chances of these lesions transforming into malignancies.

These lesions have a tendency to resolve spontaneously, provided the causation is removed. Biopsy can be taken to rule out malignant transformation. Small suspicious lesions can be excised and subjected to histopathological examination.

Common sites of involvement:

Buccal mucosa, and oral commissures are commonly involved. In india buccal mucosa is commonly involved.

Common in persons above the fourth decade. Males are affected thrice as common than females.

Clinical types of leukoplakia:

Oral cavity leukoplakia is classified into two main types:

Homogenous type:

This lesion appears as a flat white lesion. This lesion is uniform, and appears as thin white area.

Non homogenous type:

This type includes speckled, nodular and verrucous leukoplakia. The speckled type of leukoplakia appears as white and red lesion, which appears predominantly with a white surface. Verrucous leukoplakia appears as elevated, proliferated / corrugated surface appearance. Proliferative verrucous leukoplakia is characterised by an aggressive evolution, multifocal appearance, resistance to treatment. These lesions have a high degree of recurrance rates. A higher percentage of these lesions could lead to malignant transformation.

Nodular leukoplakia appears as small polypoidal outgrowths, rounded predominantly white excrescences.


This is a premalignant condition involving the oral cavity mucosa. These lesions are similar to leukoplakia but show a red patch / plaque on the mucosal surface. The red color has been attributed to decreased keratinization which causes the red vascular connective tissue of the submucosa to shine through.

Commonly involved sites include lower alveolar mucosa, gingivobuccal sulcus and the floor of the mouth.

Treatment is by excision of the lesion and repeated follow up.

Melanosis / mucosal hyperpigmentation:

These benign lesions involving the oral cavity mucosa can transform into malignant melanomas. Excision biopsy is the accepted management modality.

Carcinoma oral cavity:

Cancers involving the oral cavity is one of the most common malignancies. Commonest histology of these lesions happens to be squamous cell carcinoma.

Common etiological factors include use of tobacco and alcohol. Oral cancers are six times more common in smokers than in non smokers.

Tobacco chewing is another important cause for carcinoma involving oral cavity mucosa.

Alcohol conusmption in combination with smoking plays an added effect on the carcinogenic effects of both these substances since alcohol is an excellent solvant which dissolves various carcinogenic chemical found in the tobacco. This facilitates permeation of carcinogens into the oral cavity mucosa.

Dietary deficiencies eg. Riboflavin has been postulated as one of the factors for malignacy. Plummer vinson syndrome which is a combination of iron deficiency anemia and oesphageal web can also present with oral cavity carcinoma.

Sites of oral cavity cancers:

1. Mucosal lip

2. Buccal mucosa

3. Anterior two thirds of tongue

4. Hard palate

5. Lower alveolar ridge

6. Upper alveolar ridge

7. Floor of themouth

8. Retromolar trigone

Carcinoma lip:

Squamous cell carcinoma of lip constitutes nearly a quarter of all oral cancers. These lesions commonly begin as a premalignant ulcerative lesion of the lip. These lesions go by the name actinic cheilosis.

Lower lip is commonly involved. The site commonly involved lies between the midline and commissure of the lip. These lesions could appear as exophytic or ulcertive type. Nodal metastasis in these lesions develop rather late. Submental and submandibular nodes are the first to be involved. Other components of deep cervical nodes may get involved later.

Squamous cell carcinoma can be easily detected at an early stage because it happens to be involving the highly visible area of the body.


Surgical excision with adequate safety margin of healthy tissue is ideal. The defect needs to be repaired. Nodal metastasis should be managed by block neck dissection.

Carcinoma buccal mucosa:

Buccal mucosa covers a large area. This extends from the meeting point of both lips in front to the pterygomandibular raphe behind. Carcinoma involving this area is equal in both sexes.

Common site of origin in this area is the angle of the mouth, followed by the line of occlusion of the upper and lower teeth. It may also arise from the buccal sulcus where pan / tobacco quid is kept.

These lesions may be exophytic or ulceroinfiltrative. These lesions could infiltrate to involve deeper planes. Exophytic type of lesions could be associated with erythroleukoplakia. Buccal mucosa is also a common site for verrucous carcinoma which is characterized by white papillar growth with considerable keratinization.

Local spread:

From the site of origin these lesions could spread deeper involving submucosa, muscle, subcutaneous fat and skin. Involvement of buccinator muscle / masseter muscle could lead to trismus.

Nodal involvement usually occurs in about nearly half of these cases. Submandibular nodes are involved first followed later by the upper jugular nodes.

Clinical features:

Early lesions are asymptomatic. Pain and bleeding could be seen when these lesions are ulcerative and invde deeply. Involvement of muscles of mastication could cause trismus. Fungating mass over the cheek and fould smelling bleeding mass in the oral cavity are rather late features.

Histological types:

Squamous cell carcinoma is the most common malignancy. Tumors can also arise from minor salivary glands.

Biopsy is diagnostic.

Wide excision with adequate surgical margin is the treatment of choice. Nodal metastasis needs block excision.

Carcinoma of anterior two thirds of tongue:

These lesions are common in men of the age group of 50-70 years. It could also occur in individuals of younger age group and in females.

These lesions can develop from pre-existing leukoplakia, long standing dental ulcer, syphilitic glossitis. Majority of these lesions are of squamous type.

Sites involved include:

Lateral border of tongue

Ventral aspect of tongue

Tip of the tongue

Dorsum of the tongue


These lesions infiltrate deep into the lingual musculature causing ankyloglossia. These lesions could also spreadto the floor of the mouth, alveolus and mandible.

Nodal metastasis could involve submandibular and upper jugular nodes.


These lesions could present as:

Exophytic lesion like a papilloma

Non healing ulcer with rolled edges, greyish white shaggy base and induration.

Submucous nodule with induration of the surrounding tissue.


Early lesions are painless and could remain asymptomatic.

Pain in the tongue

Pain in the ipsilateral ear since the nerve supply to the tongue and ear are related. The lingual nerve and auriculo temporal nerves are branches of the trigeminal nerve.

Lump in the mouth

Enlarged neck nodes

Slurred speech, difficulty in swallowing, difficulty in tongue protrusion.

Carcinoma hard palate:

This could be squamous cell carcinoma or glandular malignant tumor. Glandular adenocarcinomas arise from minor salivary glands which are present in the palate.

Squamous cell carcinoma is the commonest malignant lesion involving the palate. It is common in individuals who reverse smoke.

These lesions usually begin with a superficial ulcer with rolled out edges. Initially they are asymptomatic. They can only be felt as irregularity by the tongue. These lesions could spread to the gingiva, lip, soft palate or invade the bone of hard palate, floor of the nasal cavity or the antrum.

Nodal metastasis is usually to the submandibular and upper jugular nodes.

Small tumors can be resected along with underlying bone. Large lesions can be managed by maxillectomy followed by irradiation.

Carcinoma of alveolar ridges:

This is also known as alveolar carcinoma. These lesions are commonly seen in men. Common site of involvement is lower jaw behind the first molar. Tumor could spread to the cheek, floor of the mouth, retromolar trigone and hard palate.

These lesions can be managed by surgical excision. Radiotherapy is aovided as it could cause osteoradionecrosis.

Cancer floor of the mouth:

Squamous cell carcinoma is common in this area. It is common in males. These lesions typically begin start in the anterior portion of the floor of the mouth close to the opening of the duct of submandibular salivary gland.

This lesion could be ulcerative or infiltrative.

Small lesions involving only the floor of the mouth without tongue involvement can be treated by surgical resection / irradiation.

Carcinoma retromolar trigone:

Involvement of this area could be due to primary lesion involving this area or as extension from other areas of oral cavity.

Management depends on the extent of the lesion. Wide excision often combined with block neck dissection may be neede.

TNM classification of oral malignancy:

Primary tumor:

TX - Primay tumor cannot be assessed

Tis - Carcinoma in situ

T1 - Tumor 2 cm or less, 5 mm or less depth of invasion

T2 - Tumor size greater than 2 cm, but less than 4 cm. Depth of invasion is more than 5 mm but less than 10 mm

T3 - Tumor size more than 4 cm or any tumor with depth of invasion of more than 10 mm but less than 20 mm.

T4 - Moderately advanced or very advanced local disease

T4a - Moderately advanced local disease. Tumor invades adjacent structures or extensive tumor with bilateral tongue involvement or with depth of involvement of more than 20 mm.

T4b - Very advanced local disease. Tumor invades masticator space, pterygoid plates, or skull base or encase the internal carotid artery.

Nonsquamous malignant lesions involving oral cavity:

These lesions include:

Minor salivary gland tumors. Nearly 80% of tumors of minor salivary glands are malignant. Palate is the most common site. Adenoid cystic carcinoma is the most common variety.

Melanoma - Mucosal melanomas involving oral cavity mucosa is rare. Males are most commonly affected. Palate and gingiva are commonly involved. Cervical nodal metastasis / distant metastasis are also common. It can be managed by wide excision including the adjacent bone.

Lymphoma - Can involve oral cavity. They are mostly non-Hodgkin variety. Cervical nodes may be involved in half of these patients. Irradiation / chemotherapy or a combination of both can be used to manage these patients.

Kaposi sarcoma - This is a vascular tumor. Its incidence is high in HIV patients. These lesions appear as a reddish purple nodule / plaque mostly in the palate. Microscopically these lesions contain spindle cells with hemorrhagic cleft like spaces. Chemotherapy is ideal to treat these patients.