19.

Lip cancer

• Most common malignant lesion of the oral cavity

• Can be recognised and removed easily.
✓ Etiology
 Pipe/cigarette smoke
 Pipe= more local effect → lip carcinoma
 Chewing of betel nut
 Sun (UV)
 Poor hygiene
 better prognosis than cancers of the oral cavity
 Other Factors → Frequency decreased by vitamin A, C, E carotenoids

Growth Patterns

Expansive front

Invasive front → Worst prognosis → Tumorous islands infiltrate

Metastasis

 Usually, low metastasizing capacity

 Submental, submandibular
 Oral cancer typically gives lymph node metastasis to regional lymph nodes!!
 Very rare for distant metastasis → Mainly lung if it happens.
 Level of lymph nodes are also important.
 Level 1 → submental/submandibular
 Level 2,3,4 → jugular
 Level 5 → supraclavicular
 Level 6→ pretracheal/prelaryngeal

Types

1) Squamous cell carcinoma (90%)

 Polymorphous epithelial cells
 Enlarged cells
 N/C ratio
 No identical cells
 Nuclei almost fill entire cytoplasm
 Keratinizing or non-keratinizing
 Vermillion border
 Grades
 Well
 Moderately
 Poorly differentiated → Keratinization absent
 More common in Males
  TNM staging system High
 Most common on tongue and floor of the mouth
 Causes 
 Smoking and alcohol
 Diet nutrition
 Viruses (eg. HPV 16 and 18, HSV)
 Chronic candida infection 
 Speckled leukoplakia’s – prone to undergo malignant transformation
 Can have premalignant potential
 Immunosuppression
 Dental factors
 Poor oral hygiene, in combination with above
 Occupational risks 
➢ Outdoor workers (forestry, agriculture etc.) increase incidence.
➢ Sunny climates like Australia, lip cancer can account for over 50% of oral cancers.
➢ Lip (vermillion border) caner occurs much more frequently in the lower than the upper lip
 More common in men than women
 Particularly associated with outdoor occupations
 Rare in dark skin races (increase in melanin pigment)
 Sq. cell carcinoma of lip may be preceded by hyperkeratotic and dysplastic changes – solar keratosis.

• Early diagnosis important, many forms

Early lesions – asymptomatic 

▪ White patch, a small exophytic growth which in early stages shows no ulceration or erythema, as small indolent ulcer,
or area of erythroplakia

▪ Pain rare

▪ Clinical signs arising suspicion of carcinoma

 Persistent ulceration, induration and fixation of affected tissue to underlying structures

 Induration → rubbery hardness caused by invasion of the carcinoma resulting in the loss of normal elasticity
and compliance of normal mucosa
 Fixation →caused by the carcinoma infiltrating through and binding together different natural tissue planes
 Underlying bone destruction can be detected if carcinoma arises from alveolar mucosa
 Early involvement of lymph nodes
• Carcinoma developing on the vermilion border of the lip is clearly visible and noticed early stage
• Slightly raised swelling or a crusty, inconspicuous lesion resembling delayed healing of herpes labialis
Advanced or late lesion
 A broad based exophytic mass, with a rough, nodular, warty haemorrhagic or necrotic surface,
or a s a deeply destructive and craterlike ulcer with raised, rolled everted edges
 Infiltration of the oral musculature may result in functional disturbances esp. if tumor
 involves the tongue or floor of the mouth
 Due to reduced mobility of the tongue
➢ Complains of impaired speech or difficulty in swallowing
➢ Pain
 Bone invasions see on x-rays, clinically by movement of teeth and in mandible – altered sensation over the
distribution of the mental nerve or pathological fracture
 Size of surface lesion does not correspond to the underlying invasion

Pathology (of the squamous cell carcinoma)

Clinically

 presents in a variety of ways

 local invasion leads to 
 induration and fixation of tissues
 destruction of tissues
 distortion of tissues
 dysfunction of tissues
 metastatic spread to regional lymph nodes
 enlarged, firm nodes.
 may be mobile or fixed.
 Invasion and destruction of local tissues, causing induration and tethering or fixation.
 Grade – well -, moderately – and poorly differentiated.
 Well differentiated →squamous cells, prickle cells, keratin, intercellular bridges
 Moderately differentiated.
 Less keratinization
 Still readily identified as squamous in type
 Poorly differentiated.
 Keratinization is absent.
 Cells show prominent nuclear and cellular pleomorphic and abundant mitosis.
 Some epithelia unnoticeable
 Variable lymphocytic and plasma cell infiltration in the stroma supporting the invasive malignant
epithelium → Response of hosts immune system to tumour antigens and tumour necrosis and ulceration.
 Most are very locally destructive.
 Variable infiltration of adjacent tissues
 Spread in lymph nodes → Progressive involvement of more inferior groups in the chain as metastic disease
spreads.
 Blood borne metastases occur later in clinical course of the disease.
2) Basal cell Carcinoma (10%)
 Common neoplasm of the skin of the face, especially in elderly patients
 Occasionally present on the lips, particularly the upper lip
 Many are skin tumours that have spread to involve the vermilion.
 Nevoid basal cell carcinoma syndrome → Multiple nevoid basal cell carcinomas arising at a younger age
and non-sun exposed sites.
 Typical form presents as
 Slow growing nodule that eventually ulcerates centrally
 HISTO – cytologically malignant basaloid cells, arranged in a variety of patterns, invading adjacent tissues.
3) Carcinoma In Situ (CIS)
 Whole thickness of epithelium is carcinomatosis BUT basement membrane intact.