Surgery chapters
Oral cavity malignancy
Risk factors for mouth cancer in Pakistan, premalignant lesions (leukoplakia, erythroplakia, submucous fibrosis), clinical features, investigation, TNM staging, neck node levels and treatment of oral squamous cell carcinoma.
In 30 seconds
- Over 90% of mouth cancers are squamous cell carcinoma; the main causes are tobacco (smoked and chewed, including naswar), betel quid (pan, areca nut, gutka) and alcohol, which act together; South Asia has one of the highest rates.
- Erythroplakia has the highest malignant risk; leukoplakia (especially speckled) and oral submucous fibrosis are also premalignant, so biopsy red or mixed lesions.
- Treatment is mainly surgery with clear margins plus neck dissection (elective even in many N0 necks), with postoperative radiotherapy for adverse features.
On this page
Overview
Oral cancer is a major cancer in Pakistan and the rest of South Asia, driven by chewing tobacco, betel quid and areca nut products (pan, gutka, mainpuri, naswar) as well as smoking. Most cases present late.
For PGET, learn the risk factors, the premalignant lesions, the sites and spread, and the principles of treatment. One MCQ usually comes from this topic.
Anatomy of the oral cavity
- Extends from the vermilion border of the lips to where the hard palate meets the soft palate above and the circumvallate papillae (junction of anterior two-thirds and posterior third of tongue) below.
- Subsites: lips, anterior two-thirds of the tongue (oral tongue), floor of mouth, buccal mucosa, upper and lower gingiva (alveolus), retromolar trigone (mucosa behind the last molar over the ascending ramus), hard palate.
- The base of tongue and tonsil are oropharynx, not oral cavity. HPV matters mainly in the oropharynx; it has little role in oral cavity cancer.
Aetiology and risk factors
| Factor | Points |
|---|---|
| Tobacco | Smoked (cigarettes, bidi, huqqa) and smokeless: chewed with pan, gutka, naswar (placed in the lower lip or buccal sulcus, common in KP and Balochistan). Reverse smoking (lit end inside the mouth) causes palatal cancer |
| Betel quid / areca nut | Pan (betel leaf, areca nut, slaked lime, often tobacco); the main carcinogen in South Asia; causes submucous fibrosis |
| Alcohol | Acts synergistically with tobacco |
| Poor oral hygiene, sharp teeth, ill-fitting dentures | Chronic irritation |
| Nutrition | Iron deficiency (Plummer-Vinson syndrome), low fruit and vegetables |
| Sunlight (UV) | Lower lip cancer |
| Others | Immunosuppression, syphilis (historically), Fanconi anaemia, Li-Fraumeni |
Memory hook
The "6 S" causes of tongue cancer: Smoking, Spirits, Spices (betel), Syphilis, Sharp tooth, Sepsis (poor hygiene).
Premalignant lesions and conditions
| Lesion | Description | Malignant risk |
|---|---|---|
| Leukoplakia | White patch that cannot be rubbed off and cannot be called any other disease | Low to moderate; higher if non-homogeneous, on the floor of mouth / ventral tongue, large, or dysplastic |
| Speckled (erythroleukoplakia) | White patch on a red base | Higher than plain leukoplakia |
| Erythroplakia | Bright red, velvety plaque, may bleed on contact | Highest; often already in situ or invasive carcinoma |
| Proliferative verrucous leukoplakia | Multifocal warty white lesions, often older women without the usual risk factors | Very high (over half) |
| Oral submucous fibrosis | Fibrous bands under the mucosa, pale and stiff mucosa, progressive trismus, burning with spicy food; almost entirely in South Asians | Premalignant; due to areca nut |
| Chronic hyperplastic candidiasis | White patch (often at commissures) | Some risk |
| Lichen planus (erosive) | Lace-like white striae, erosions | Small risk |
| Plummer-Vinson (sideropenic dysphagia) | Iron deficiency, web, glossitis | Post-cricoid and oral cancer |
Exam trap
A white patch that rubs off is usually candida (thrush); leukoplakia does not rub off.
Management of premalignant lesions
- Stop the cause (tobacco, pan, naswar, alcohol), correct deficiencies.
- Biopsy all erythroplakia and speckled leukoplakia urgently, sampling more than one area if large.
- Dysplastic lesions: excision (scalpel or laser) and long-term follow-up with photographs.
- Submucous fibrosis: stop chewing, mouth-opening exercises, intralesional steroids; surgery to release bands in severe trismus.
Field change and second primaries
- Long exposure of the whole upper aerodigestive mucosa to carcinogens damages it all (field cancerisation).
- About 15% of patients with a mouth or oropharynx cancer develop a second primary, usually later (metachronous), and often within the first 2 years. A tumour within 6 months is called synchronous.
- Hence lifelong follow-up and stopping tobacco.
Pathology and spread
- Over 90% are squamous cell carcinoma. Others: verrucous carcinoma (slow, exophytic, well differentiated, rarely spreads to nodes, linked to chewing tobacco), minor salivary gland tumours, melanoma, sarcoma, lymphoma.
- Common sites: worldwide the lateral border of the tongue and the floor of mouth; in Pakistan and India, the buccal mucosa and gingivobuccal sulcus (where the quid is held).
- Lymphatic spread is the main route: first to levels I and II, then III. Tongue tumours may skip directly to levels III or IV and can spread to the opposite side (the tongue drains across the midline).
- Distant spread is uncommon (lungs most often).
Neck node levels
| Level | Nodes |
|---|---|
| I | Submental (Ia) and submandibular (Ib) |
| II | Upper deep cervical (jugulodigastric) |
| III | Middle deep cervical |
| IV | Lower deep cervical |
| V | Posterior triangle |
| VI | Central (anterior) compartment |
Clinical features
- Non-healing ulcer (more than 3 weeks) with raised, rolled, everted, indurated edges, which bleeds on touch; or an exophytic growth.
- Pain, often referred to the ear (lingual and auriculotemporal nerves).
- Loosening of teeth, ill-fitting dentures, numbness of the lower lip (mental nerve involvement by mandibular invasion).
- Trismus (pterygoid involvement), dysphagia, slurred speech (tongue fixation), foul breath, weight loss.
- Hard, painless neck nodes, which may be fixed.
- Many patients in Pakistan present with advanced (stage III-IV) disease.
High-yield
Any oral ulcer that persists more than 3 weeks, especially in a tobacco or pan user, needs a biopsy to exclude cancer.
Investigations
| Test | Purpose |
|---|---|
| Incisional (wedge) biopsy from the edge, including some normal tissue | Diagnosis; avoid necrotic centre |
| MRI (or CT) of primary and neck | Depth of invasion, soft-tissue spread, nodes. MRI is less spoilt by dental fillings; ideally before biopsy |
| CT | Best for bone (mandible) invasion; CT chest for all patients (metastases, second primary) |
| Orthopantomogram (OPG) | Dental assessment |
| Ultrasound + FNAC of neck nodes | Nodal staging |
| PET-CT | Unknown primary, suspected recurrence |
| Examination under anaesthesia / panendoscopy | Map the tumour, look for second primary |
Staging (TNM, simplified)
| T | Size (greatest dimension) |
|---|---|
| T1 | 2 cm or less |
| T2 | More than 2 cm up to 4 cm |
| T3 | More than 4 cm |
| T4 | Invades adjacent structures (bone of mandible or maxilla, skin, deep muscle, maxillary sinus) |
- The newer (AJCC 8th) system also uses depth of invasion (5 mm and 10 mm cut-offs) to set T stage, and extranodal extension for N stage.
| N (classic) | Nodes |
|---|---|
| N1 | Single same-side node, 3 cm or less |
| N2a | Single same-side node over 3 cm and up to 6 cm |
| N2b | Multiple same-side nodes, none over 6 cm |
| N2c | Both sides or opposite side, none over 6 cm |
| N3 | Any node over 6 cm |
- Stage I = T1N0; stage II = T2N0; stage III = T3N0 or any N1; stage IV = T4, N2, N3 or M1.
Treatment
Management is decided by a multidisciplinary head and neck team. Surgery is the main treatment for oral cavity cancer.
Primary tumour
- Wide excision aiming for about 1 cm of normal tissue in all directions so that the final pathological margin is clear (over 5 mm).
- Tongue: partial glossectomy or hemiglossectomy (laser or diathermy).
- Mandible: rim (marginal) mandibulectomy if tumour abuts bone without deep invasion; segmental mandibulectomy if bone is invaded.
- Access: transoral for small tumours; lip-split and mandibulotomy for posterior or large tumours.
Reconstruction
- Small defects: primary closure, healing by secondary intention, or a skin graft.
- Larger defects: local or pedicled flaps (nasolabial, pectoralis major myocutaneous flap, temporalis).
- Microvascular tissue transfer (vessels rejoined in the neck): radial forearm flap for tongue and floor of mouth; fibula, scapula or iliac crest (DCIA) flaps to rebuild the mandible.
The neck
| Neck status | Management |
|---|---|
| Clinically node-positive | Therapeutic neck dissection with the primary |
| Node-negative (N0), early tumour | Elective (selective) neck dissection of levels I-III (supraomohyoid) is now preferred over watching, because occult nodes are common; sentinel node biopsy is an option in some centres |
| Midline tumours (floor of mouth, tongue reaching midline) | Consider both sides |
Types of neck dissection
| Type | What is removed |
|---|---|
| Radical (Crile) | Levels I-V plus the internal jugular vein, spinal accessory nerve, sternocleidomastoid (and submandibular gland) |
| Modified radical | Levels I-V but one or more of those three structures kept |
| Selective | Only some levels removed (e.g. supraomohyoid I-III for oral cancer); all three structures kept |
High-yield
The main disability after a radical neck dissection is shoulder drop and weak abduction from accessory nerve sacrifice (trapezius paralysis).
Radiotherapy and chemotherapy
- Postoperative radiotherapy for adverse features: close or involved margins, perineural or lymphovascular invasion, multiple nodes, large tumours. Chemoradiotherapy (cisplatin) if margins are involved or there is extranodal extension.
- Primary radiotherapy (external beam or brachytherapy) for patients unfit for surgery.
- Side effects: mucositis, xerostomia, dental decay, trismus, and osteoradionecrosis of the mandible (dental assessment and extractions before radiotherapy reduce the risk).
Lip cancer
- Usually SCC of the lower lip (about 95%) from sunlight; in outdoor workers and fair-skinned men. Basal cell carcinoma is commoner on the upper lip skin.
- Visible early, so it is often caught small. Node spread (submental and submandibular) is uncommon.
- Small lesion (up to one-third of the lip): V- or W-shaped (wedge) excision with three-layer closure, aligning the vermilion border.
- Larger defects (one-third to two-thirds): local flaps (Abbe, Karapandzic, Johansen step). Total lip loss: microvascular radial forearm flap.
- Surgery and radiotherapy each cure the large majority of early lip cancers.
- Lip shave (vermilionectomy) for widespread premalignant change of the lower lip.
Prognosis and follow-up
- Prognosis depends mainly on neck node status (the most important factor), stage, depth of invasion and margins.
- Recurrence is most likely in the first 2 years; close follow-up for recurrence and second primaries.
- Stop smoking and chewing; speech and swallowing therapy and dental care are part of rehabilitation.
Exam focus
Expect: the commonest histology (SCC), the premalignant lesion with highest risk (erythroplakia), areca nut and submucous fibrosis with trismus, naswar and pan as local causes, buccal mucosa as the common site in South Asia, lower lip cancer and wedge excision, spread to level I-II nodes and skip metastasis from the tongue, the contents of a radical neck dissection and accessory nerve palsy, 1 cm surgical margins, rim versus segmental mandibulectomy, MRI versus CT, postoperative radiotherapy indications and osteoradionecrosis.
Quick revision
- Oral SCC: tobacco (smoked and smokeless), betel quid/areca nut, alcohol.
- Erythroplakia > speckled leukoplakia > homogeneous leukoplakia for cancer risk.
- Submucous fibrosis: areca nut, trismus, premalignant.
- Non-healing ulcer over 3 weeks with indurated everted edge: biopsy.
- Spread to levels I-II first; tongue can skip and cross midline.
- T1 up to 2 cm, T2 2-4 cm, T3 over 4 cm, T4 invades bone or skin.
- Excise with 1 cm margins; elective selective neck dissection for many N0 necks.
- Radical neck dissection removes IJV, accessory nerve and SCM.
- Lip cancer: lower lip, sunlight, wedge excision.
Written by The House Job from standard references (Bailey & Love).
FAQ
Which oral lesion is most likely to become cancer?
Erythroplakia carries the greatest risk, followed by speckled leukoplakia; both must be biopsied.
Why are the buccal mucosa and gingivobuccal sulcus common sites in Pakistan?
People hold betel quid, gutka or naswar in the cheek pouch or sulcus for long periods, so that mucosa receives the greatest carcinogen exposure.
Why is the neck often treated even when no nodes are felt?
Oral cancers, especially of the tongue, often have hidden nodal deposits, and elective neck dissection improves outcome compared with waiting for nodes to appear.
What is lost in a classical radical neck dissection?
All five node levels with the internal jugular vein, spinal accessory nerve and sternocleidomastoid; losing the accessory nerve causes shoulder drop.
How is a small lower lip cancer treated?
By a full-thickness V or W wedge excision of up to one-third of the lip, closed in three layers with careful alignment of the vermilion border.