5.  Oral cancer

Q. 2. Describe clinical features of carcinoma of tongue.

Ans.

In most countries, the tongue is the most common site of intraoral carcinoma.

Of all potential aetiologic factors, use of tobacco products is correlated as the closest cause to the carcinoma of the tongue.

Squamous cell carcinoma is the most common malignancy of the tongue, typically having three gross morphologic growth patterns: exophytic, ulcerative and infiltrative.

The infiltrative and ulcerative types are most common on the tongue. Lateral margins and ventral surface of the tongue are more frequently affected sites.

The most common finding is an indurated, ulcerated area of the tongue. The induration may extend deep into the tongue musculature and root of the tongue.

Before causing symptoms malignancies of the tongue may grow to significant size. Because of the relative laxity of the tissue planes separating the intrinsic tongue musculature, the cancer may spread easily and become symptomatic only when its size interferes with movement.

Squamous cell carcinoma of the tongue may arise in apparently normal epithelium, in areas of leukoplakia, or in an area of chronic glossitis.

These lesions are usually larger than 2 cm at presentation, with the lateral border being the most common subsite of origin. At this point, the patient may develop speech and swallowing dysfunction. Pain occurs when the tumour involves the lingual nerve, and this pain may also be referred to the ear.

Carcinomas of the tongue base are clinically silent until they deeply infiltrate the tongue musculature.

They are usually less differentiated. Because of the difficulties with direct visualization, they may extend into the oral tongue or have lymph node metastases before the diagnosis is established.


Q. 3. Pathogenesis and management of osteoradionecrosis.

Ans.

Osteoradionecrosis is necrotic tissue and bone that fails to heal spontaneously and does not respond to local care over a period of 6 months following radiotherapy.

Radiotherapy causes endarteritis obliterans resulting in obliteration of fine vasculature, progressive fibrosis, loss of normal cellular elements, fibrous and fatty degeneration of the bone marrow. These factors predispose to the development of osteoradionecrosis if exposed or injured and also increased vulnerability to trauma and infection.

The pathophysiologic characteristic is a nonhealing hypoxic wound in the bone.

It develops most commonly after local trauma such as dental extractions, biopsies, related cancer surgery and periodontal procedures.

Radiation induces tissue hypoxia in normal cells resulting in an imbalance where cell death and collagen lyses exceed the homeostatic mechanism of cell replacement and collagen synthesis, resulting in a wound that will not heal, in which the metabolic demands exceed the oxygen and vascular therapy.

Clinical features

Clinical manifestations include pain, foul taste, paraesthesia or anaesthesia, orocutaneous fistula’s, exposed necrotic bone, pathological fracture and suppuration.

It is more common in mandible than in maxilla due to decreased vascularity and density of the mandible.

On physical examination, missing hair follicles, change in surface texture of skin and colour are important findings that assist the clinicians in finding the area of radiation injuries.

Irradiated mandible, periosteum and overlying soft tissue undergo hyperaemia, inflammation, endarteritis, periarteritis, hyalinization, fibrosis and thrombosis of the vessels. These conditions ultimately lead to cellular death and progressive hypovascularity. The result is aseptic necrosis of the portion of the bone directly in the beam of radiation.

There is minimal localization of the infection, and there may be necrosis of considerable amount of bone, periosteum and overlying mucosa. Finally sequestration occurs.

Prophylactic therapy

Prior to beginning of radiotherapy, all patients should undergo a thorough dental evaluation including full mouth radiographs, dental and periodontal diagnosis and prognosis for each tooth.

Patient education regarding the need for meticulous oral hygiene and frequent follow-up must be stressed. The dentist should perform periodontal scaling, caries control and fabrication of fluoride trays.

Teeth that are infected/nonvital and cannot be salvaged with conservative endodontic therapy should be extracted. Ideally, extraction should be done 3 weeks prior to radiation therapy.

Prophylactic antibiotic therapy (penicillin) should be given in patients who are undergoing any extraction of teeth.

To prevent radiation caries, patient should be begin daily fluoride treatment with 1% neutral sodium fluoride gel in prefabricated trays for 5 minutes each day, for life time.

Postradiation dental care

Dentures should be avoided in the irradiated arch for one year after therapy.

A saliva substitute should be used to lubricate the mouth to replace diminished flow from irradiated mucous and salivary glands.

If postirradiation pulpitis develops and involved tooth is restorable, endodontic therapy should be undertaken.

There should be an interval of at least 3−9 months before undertaking extraction or osseous surgery, unless indicated.

Necessary extractions should be limited to 1−2 teeth per appointment. Removal of teeth should be performed as atraumatically as possible.

Management

Medical therapy in the treatment of osteoradionecrosis is primarily supportive involving nutritional support along with superficial debridement and oral saline irrigation for local wounds.

Antibiotics are indicated only for definitive secondary infection and as well use of hyperbaric oxygen therapy.

Minimal resection or in some cases mandibulectomy may be required for management of sequestrated bone.

Short essays

Q. 1. Rodent ulcer.

Or

Basal cell carcinoma.

Ans.

Basal cell carcinoma is also known as rodent ulcer. It is the most common cutaneous malignancy, which typically affects the sun-exposed surfaces of the skin.

It arises from the basal cells of the surface epidermis or external root sheath of the hair follicle.

These are slow growing tumours. On long standing they can cause local destruction of tissues.

Metastasis is seldom encountered. It is estimated that less than 0.1% of tumours metastasize. The most common sites of metastasis are the lymph nodes, bones and lungs.

Clinical features

Basal cell carcinoma is usually seen in individuals over the fourth decade of life.

Men are affected twice as commonly as women and the fair complexioned individuals are relatively more prone to develop basal cell carcinoma compared to dark complexioned individuals.

Basal cell carcinoma can have various clinical appearances. Some of the relatively common varieties are as follows:

a. Noduloulcerative type (most common variety)

b. Superficial spreading type

c. Pigmented

d. Morphea-form (sclerosing)

e. The cystic type.

Ulceronodular type

In the initial stages, it appears as a large nontender papule which slowly enlarges and exhibits a central depression, which over a period of time reveals ulceration associated with some bleeding and crusting.

The pathognomonic feature of basal cell carcinoma is a waxy, translucent or pearly appearing ulcer with a raised pale border. Telangiectasias are common.

Pigmented form

It resembles melanomas and appear as bluish-black or brown coloured macules.

Cystic variety

This form of basal cell carcinoma is rare and appears as a bluish to grey-coloured, mucin filled cyst-like lesions.

Sclerosing type

This form of basal cell carcinoma is uncommon and typical lesion mimics a scar.

It appears as a white or yellow waxy sclerotic plaque.

The tumour cells initiate the proliferation of fibroblasts within the dermis and an increased collagen deposition, i.e., sclerosis.

Superficial type

It is seen as an erythematous, well-circumscribed patch or plaque.

The lesion may be associated with the formation of a white coloured scales mimicking lesions of psoriasis.

Surgical excision for basal cell carcinoma is still the most popular modality of treatment. Mohs micrographic surgery offers high cure rates for basal cell carcinoma.


Q. 2. Squamous cell carcinoma.

Or

Treatment of squamous cell carcinoma.

Ans.

Squamous cell carcinoma is defined as ‘a malignant epithelial neoplasm exhibiting squamous differentiation as characterized by the formation of keratin and/or the presence of intercellular bridges’.

The epidermoid carcinoma is the most common malignant neoplasm of the oral cavity.

Aetiology

Tobacco.

HIV infected and as well as immunosuppressed individuals.

Low consumption of vitamin A and C.

Prolonged exposure to UV light.

History of syphilis, chronic irritation/trauma.

Leukoplakia.

Poor oral hygiene.

Clinical features

Presents as painless mass or ulcer.

The tumour may begin as a superficially indurated ulcer with slightly raised borders and may proceed either to develop a fungating, exophytic mass or to infiltrate the deep layers of the tongue, producing fixation and induration without much surface changes.

Typical lesion develops on the lateral border or ventral surface of the tongue.

The lesion is red white in colour.

It can appear as leukoplakia, exophytic or ulcerated, some lesions will be indurated firm on palpation, indicative of tumour cells infiltrating muscle fibres of the tongue.

Diagnosis is based on clinical examination of head and neck followed by a fibre-optic examination of the laryngopharynx and then a TNM staging and incisional biopsy for confirmation.

Treatment

The tumour can be treated through surgery and radiation.

Generally, the primary tumour is excised with 1.5 cm margins for T1N0M0 lesions and for T2N0M0 and more advanced stages, treating the neck prophylactically with either an incontinuity functional neck dissection or radiotherapy in a dose of 5,000–6,500 cGy is recommended if the incisional biopsy shows greater than 3-mm depth of invasion.

For nodal invasion disease of N1, functional neck dissection is recommended for nodal disease of N2 or N3-modified radical neck dissection is preferred by postoperative radiotherapy from 5,000–6,500 cGy.


Q. 3. Clinical features and radiographic appearance of osteosarcoma.

Or

Osteogenic sarcoma.

Ans.

Osteosarcomas are primary malignant bone tumours in which mesenchymal cells produce osteoid.

Predisposing factors

The exact pathogenesis for the tumour is unknown.

Various predisposing factors proposed are trauma, virus, genetic mutations, preexisting bone cyst, osteogenesis imperfecta, Paget disease, fibrous dysplasia and previous history of radiation.

Clinical features

Osteosarcomas of the jaw bones are usually seen in the third and forth decades of life.

Males are slightly more commonly affected than females.

The mandible and maxilla are equally affected.

The common sites affected are the symphysis, ramus and posterior parts of the body of the mandible. In the maxilla, the alveolar ridge, antrum and the palate are frequently affected.

The common symptoms of this lesion in jaws are swelling and pain, paraesthesia/anaesthesia, loose teeth and trismus.

When the tumour extends to involve the nasal cavity, maxillary sinus and orbit, clinical signs and symptoms such as epistaxis, nasal obstruction, haemorrhage, exophthalmos and blindness may be apparent.

The earliest radiographic changes consists of a symmetric widening of the periodontal ligament space around a tooth or several teeth as a result of tumour infiltration along the ligament space. This radiographic feature is referred to as Garrington sign. Occasionally lamina dura may be lost.

The irregular widening of the mandibular canal, with areas of narrowing and loss of fine parallel cortical margins of the walls of the mandible. In some individuals spiking resorption of the teeth are seen.

Other radiographic findings include ill-defined ‘moth-eaten’ destruction of bone, honey-comb—like appearance, granular appearance, sunray appearance, Codman’s triangle and onion peel appearance.

The typical features seen on radiograph are as follows:

i.

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Apr 11, 2016 | Posted by in Orthodontics | Comments Off on 5.  Oral cancer
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