Detecting Oral Detecting Oral CancerCancer

What is cancer?

• Cancer is a loss of growth regulation

– Cells grow when they shouldn’t tumour

– Cells grow where they shouldn’t invasion, metastasis

Cancer is a genetic disease of somatic cells

• Mutations in specific genes can cause a normal cell to become cancerous

What are these genes that lead to cancer when

mutated?• Proto-Oncogenes

– Gas pedal for cell proliferation – Mutation Oncogene Gas pedal stuck down

• Tumour suppressor genes– Brakes for cell division– Mutation Brakes don’t work

• Care taking (DNA repair) genes

Carcinogenesis

• Carcinogensis is a multistep process involving mutation in multiple genes

Angiogenesis

• Without blood supply tumour can grow 2mm (106 cells)

• Produce growth factors to stimulate angiogenesis

• Blood vessels around tumour is a bad sign!

Cancer is a loss of growth regulation induced by:

• Environmental factors

• Genetic factors

Oral Cancer-Introduction

• The 6th most common malignancy within the EC although the 3rd in men (4th in women) of developing countries

• The most common malignant tumour in south east asia.

• 40% of all malignancies in parts of India

• Commoner in males

Introduction

• The prognosis for cure improves the earlier the diagnosis is made and appropriate treatment started

• treatment for a small early lesion is likely to be less mutilating and have a lower morbidity than treatment for a large advanced lesion

Introduction

Unlike many malignant lesions occurring elsewhere in the body oral scc can be readily observed in its early stages. There are few

places in the oral cavity that a lesion can genuinely progress

unnoticed by patient and clinician.

Introduction

The fact that so many patients still continue to present late with advanced disease is a sad

indictment of the state of medical and dental care in the UK!

Incidence and Survivalof Oral or Pharyngeal Cancer

• 5410 new cases diagnosed yearly

– Males 3594

– Females 1816

• 5 year survival rate: 50%

UK 2007

Epidemiology

Squamous cell carcinoma (scc) accounts for about 90% of all oral malignancy the remainder include

salivary gland neoplasms, lymphomas and sarcomas.

Epidemiology

The rate of new oral cancers would appear to be falling from its peak in

1920 to the present levels. However, there is disturbing evidence that

cancers of all types including oral cancer are on the increase.

Epidemiology

• there is a strong clinical impression as yet unsubstantiated that we are

seeing a rise in incidence of aggressive oral scc in young patients

with no accepted risk factors

Aetiology

• Actinic Radiation

• Epithelial atrophy

• Viruses

• Immunosuppression

• Candida infection

• Smoking

• Chewing habits

• Alcohol

• Poor diet

• Industrial hazards

• Dental factors

Aetiology

• Smoking:Cigar and pipe smoking Vs cigarette smokingReverse smoking

• Chewing habits:Pan chewing → Leukoplakia → SCC

• Alcohol:Unclear mechanismType and quality more important than quantity

Aetiology

Smoking and Alcohol synergism

• Smoking alone: 9 times greater risk

• Alcohol alone: 8 times greater risk

• Smoking and alcohol consumption:

9+8=40!!

Aetiology

• Industrial hazards:Higher incidence in textile workers

• Dental factors• Actinic Radiation:

SCC more common in lower lip than upper lipLip cancer is rare in dark-skinned people

• Epithelial atrophy:May enhance the absorption of carcinogens

Aetiology

• Viruses:

HPV particularly types 16 & 18

• Immunosuppression:

Increased incidence of certain cancers in patients with renal transplants or HIV

• Candidal infection:

Chronic hyperplastic candidosis is premalignant

Your average oral SCC patient!

• Male with carious teeth

• Rarely attends dentist!!!!!!

• Smokes 40-60 since ???

• Drinks cheap alcohol

• Eats “junk food” on the road whilst running around in his delivery van!

Indications for urgent referral

• Any unhealed ulcer for more than two weeks

• Any unexplained oral bleeding

• Any area of induration

• Any unexplained white patch

• All-red or red/white patches

• Cervical nodes

Clinical presentation

• Can affect any part of the oral mucosa

• Sites particularly at risk vary according to aetiological factors:

Europe: Tongue and lip

India: Buccal mucosa

Clinical presentation

• Early lesions are usually asymptomatic

• May present as:

a white patch

a red patch

an ulcer

an exophytic growth

Clinical presentation

• Pain may be a late feature

• Advanced lesions have a very variable presentation

• Bone destruction may be evident on radiographs

• Teeth may become mobile

• There may be altered sensation

Our Role

• Patient education

• Elimination of risk factors

• Thorough examination

• Be safe.. refer if in doubt

Examination Overview

• Head and neck exam should be a routine part of dental and medical check-ups.

• Take a history of alcohol and tobacco use.

• Follow up on suspicious signs.

Tools and Time

• Proper lighting

• Dental mouth mirror

• Gauze squares

• Gloves

• 5 minutes

Oral Lesions Suspiciousfor Oral Cancer

• Homogenous leukoplakia

• Leukoplakia with early squamous cell carcinoma

• Nodular leukoplakia with severe epithelial dysplasia

• Erythroleukoplakia with candida infection

Leukoplakia

• Idiopathic white patch that cannot be wiped off the mucosa

• Up to 4% risk of malignant change in 5 years• Very variable clinical presentation (homogeneous,

speckled, verrucous, nodular,..etc)

• Management include biopsy, conservative treatment, excision, and laser ablation

Erythroplasia (erythroplakia)

• Red velvety patches

• Idiopathic

• Very high risk of

malignant change

• 70% are carcinomas

in situ on first biopsy

• Same management as leukoplakias

Candidal leukoplakia

• Rough adherent

white plaque

• Typical site is buccal

mucosa behind the

commissures

• Variable risk of malignant change

• Management is with vigorous systemic antifungals

Lichen planus

• Chronic inflammatory mucocutaneous disease

• Unclear pathogenesis• Two distinctive clinical types

– (non-erosive and erosive)

• Usually bilateral distribution• Only erosive type is premalignant• Management includes biopsy and

steroids

Epithelial dysplasia

• Loss of tissue architecture

• The degree of dysplasia is widely believed

to be an important factor but there is little definitive evidence to support this assertion

Early stages may be reversible !

Precancerous lesions

• Risk of malignant transformation depends on:1. Site

2. Nature of lesion

• Can’t predict if the lesion will– Regress (15%)– Remain the same– Progress to cancer (4-8%)

Management of precancerous lesions

• Remove the apparent cause if possible (stop smoking, antifungals)

• Biopsy

• Long term review

Prognosis of oral cancer

STNMP system:

Site

Tumour size

Node involvement

Metastasis

Pathology

Staging• T1 <2cm. T2 >2cm<4cm. T3 >4cm.

T4 massive tumour with invasion

• N0: No nodes• N1: ipsilateral <3cm• N2a: ipsilateral >3cm<6cm• N2b: ipsilateral multiple <6cm• N2c: Bilateral/Contralateral: <6cm• N3: any node >6cm

Investigation

• Surgical biopsy, Incisional

• FNA, for neck and parotid lumps

• Radiographs

• CT

• Ultrasound esp for abdomen and liver mets.

Treatment

• CURATIVE

• LOCAL DISEASE CONTROL

• PALIATIVE ONLY

Team Approach

• Maxillofacial Surgeon• Plastic/Neuro surgery• Oncologist• Radiotherapist• Nutritionist• Speech therapist• Dentist• Maxillofacial prosthodontist

Treatment

Treatment modalities:

• Surgical excision

• Radiotherapy

• Chemotherapy??

• Surgery and radiotherapy

Surgery

• Excision of the tumour with a safety margin

• 1-2cm 3D margin for SCC• Intra-bony lesions require bigger

margin• Partial mandibulectomy or

maxillectomy with soft tissue and L.Ns

Management of the neck

• Therapeutic neck dissection: When disease is obviously present in the neck and the dissection is undertaken to ablate the disease

• Elective neck dissection; No obvious clinical disease in the neck but a high chance of occult disease or neck opened for access

Early Detection Saves Lives!

• 5-year survival for localized disease is

76%

• 5-year survival for metastatic disease is

19%

Radiation mucositis

• Generalized erythematous and ulcerative response of oral mucosa

• Starts the 2nd week of treatment with radiotherapy

• Very painful

• Secondary infection worsen the condition

• subsides after the course of radiation leaving atrophic epithelium and avascular submucosa

Treatment of radiation mucositis

• Sodium bicarbonate & camomile mouth-wash • Benzydamine hydrochloride MW (anti-inflammatory,

anti-microbial, analgesic)

• Miconazole for candidosis• Soft diet• Artificial saliva may help• PTA (polymyxin E, tobramycin, amphotericin) lozenges

(reduces duration and severity)

Osteoradionecrosis

• Radiation affects the vascularity of bone more susceptible to infection

• Painful necrosis with sloughing of overlying soft tissues

• Extraction with antibiotic cover

• ORN is more likely if extraction after a long period of radiotherapy treatment

Dental practitioner role

1. Early detection of suspicious lesions

2. Prevention (e.g. stop smoking advice)

3. Prophylactic treatment before radiotherapy

4. Lifelong monitoring after radiotherapy

5. Prostho. treatment as part of reconstruction