Oral cancer is a subtype of head and neck cancer, is any cancerous tissue growth located in the oral cavity.

It may arise as a primary lesion originating in any of the oral tissues, by metastasis from a distant site of origin, or by extension from a neighboring anatomic structure, such as the nasal cavity. Alternatively, the Oral cancers may originate in any of the tissues of the mouth, and may be of varied histologic types: teratoma, adenocarcinoma derived from a major or minor salivary gland, lymphoma from tonsillar or other lymphoid tissue, or melanoma from the pigment-producing cells of the oral mucosa. There are several types of oral cancers, but around 90% are squamous cell carcinomas

[1]

Causes and risk factors

Oncogenes are activated as a result of mutation of the DNA. The exact cause is often unknown. Regardless of the cause, treatment is the same: surgery, radiation with or without chemotherapy. Risk factors that predispose a person to oral cancer have been identified in epidemiological (epidemiology) studies. India being member ofInternational Cancer Genome Consortium is leading efforts to map oral cancer's complete genome. In many Asian cultures chewing betel, paan and Areca is known to be a strong risk factor for developing oral cancer. In India where such practices are common, oral cancer represents up to 40% of all cancers, compared to just 4% in the UK. Some oral cancers begin as leukoplakia a white patch (lesion), red patches, (erythroplakia) or non-healing sores that have existed for more than 14 days. In the US oral cancer accounts for about 8 percent of all malignant growths. Men are affected twice as often as women, particularly men older than 40/60. In Indian subcontinent Oral submucous fibrosis is very common. This condition is characterized by limited opening of mouth and burning sensation on eating of spicy food. This is a progressive lesion in which the opening of the mouth becomes progressively limited, and later on even normal eating becomes difficult. It occurs almost exclusively in India and Indian communities living abroad. [edit]Tobacco Smoking and other tobacco use are associated with about 75 percent of oral cancer cases,[3] caused by irritation of the mucous membranes of the mouth from smoke and heat of cigarettes, cigars, and pipes. Tobacco contains over 60 known carcinogens, and the combustion of it, and by products from this process, is the primary mode of involvement. Use of chewing tobacco or snuff causes irritation from direct contact with the mucous membranes. Tobacco use in any form by itself, and even more so in combination with heavy alcohol consumption, continues to be an important risk factor for oral cancer. However, due to the current trends in the spread of HPV16, as of early 2011 the virus is now considered the primary causative factor in 63% of newly diagnosed patients. [edit]Alcohol Use of alcohol and other toxic liquids is another high-risk activity associated with oral cancer. There is known to be a very strong synergistic effect on oral cancer risk when a person is both a heavy smoker and drinker. The risk is greatly increased compared to a heavy smoker, or a heavy drinker alone. Recent studies in Australia, Brazil and Germany point to alcohol-containing mouthwashes as also being etiologic agents in the oral cancer risk family. Constant exposure to these alcohol containing rinses, even in the absence of smoking and drinking, lead to significant increases in the development of oral cancer. However, studies conducted in 1985, [4] 1995,[5] and 2003[6] summarize that alcoholcontaining mouth rinses are not associated with oral cancer. In a March 2009 brief, the American Dental Association said "the available evidence does not support a connection between oral cancer and alcohol-containing mouthrinse".[7] A 2008 study suggests that acetaldehyde (a break-down product of alcohol) is implicated in oral cancer.[8][9] This study specifically focused on abusers of alcohol and made no reference to mouthwash. Any connection between oral cancer and mouthwash is tenuous without further investigation. [edit]Human

papillomavirus

Main article: HPV-positive oropharyngeal cancer Infection with human papillomavirus (HPV), particularly type 16 (there are over 120 types), is a known risk factor and independent causative factor for oral cancer. (Gilsion et al. Johns Hopkins) A fast growing segment of those diagnosed does not present with the historic stereotypical demographics. Historically that has been people over 50, blacks over whites 2 to 1, males over females 3 to 1, and 75% of the time people who have used tobacco products or are heavy users of alcohol. This new and rapidly growing sub population between 20 and 50 years old is predominantly non smoking, white, and males slightly outnumber females. Recent research from Johns Hopkins indicates that HPV is the primary risk factor in this new population of oral cancer victims. HPV16 (along with HPV18) is the same virus responsible for the vast majority of all cervical cancers and is the most common sexually transmitted infection in the US. Oral cancer in this group tends to favor the tonsil and tonsillar pillars, base of the tongue, and the oropharynx. Recent data suggest that individuals that come to the disease from this particular etiology have some slight survival advantage.

Chronic exposure to actinic radiation. Chronic exposure to the sun is a significant factor in the development of
cancer of the lower lip, the most common form of oral cancer. The high inci dence of oe_Farmer's lipand oe_Sailor's lip, as well as epidermoid carcinomaof the lip in hot climates attests to the etiologic significance of long-term expo

sure to sunlight. Apparently, repeated exposure to ultraviolet solar rays over a period of 15-30 years results in atrophic alterations of the exposed aspect of the lower lip, which may develop into carcinoma. The carcinogenic action of solar rays varies according to intensity

Ionizing radiation at therapeutic, not diagnostic, dosage levels. Fortunately,because of stricter radiotherapeutic guidelines, few patients are today exposed to sufficient quantities of ionizing radiation to produce cancers of the oral cavity.
[edit]Hematopoietic

stem cell transplantation

Patients after hematopoietic stem cell transplantation (HSCT) are at a higher risk for oral squamous cell carcinoma. Post-HSCT oral cancer may have more aggressive behavior with poorer prognosis, when compared to oral cancer in non-HSCT patients.[10] This effect is supposed to be owing to the continuous lifelong immune suppression and chronic oral graft-versus-host disease.[10]

Oral Cavity The oral cavity consists of the lip, floor of mouth, oral tongue (the anterior two thirds of the tongue), buccal mucosa, upper and lower gingiva, hard palate, and retromolar trigone.
Signs and symptoms
Skin lesion, lump, or ulcer that do not resolve in 14 days located:

On the tongue, lip, or other mouth areas Usually small Most often pale colored, be dark or discolored Early sign may be a white patch (leukoplakia) or a red patch (erythroplakia) on the soft tissues of the mouth Usually painless initially May develop a burning sensation or pain when the tumor is advanced Behind the wisdom tooth Even behind the ear

Additional symptoms that may be associated with this disease:

Tongue problems Swallowing difficulty Mouth sores Pain and paraesthesia are late symptoms

Lip The ratio between men and women with cancer of the lip is approximately 15:1.208 Persons with light-colored skin or with prolonged exposure to sunlight are most prone to develop lip carcinoma. Anatomy The lips are composed of the orbicular muscle with skin on the external surface and mucous membrane on the internal surface. The transition from skin to mucous membrane of the oral cavity is the lip vermilion. The blood supply is by way of the labial artery, a branch of the facial artery. The motor nerves are branches of the seventh cranial nerve. The sensory nerve to the

upper lip is the infraorbital branch of the maxillary nerve, and the mental nerve supplies the lower lip. Pathology The most common neoplasms are squamous cell carcinomas. Basal cell carcinomas start on the skin of the lip and may secondarily invade the vermilion. Keratoacanthoma occurs on the skin of the lips and may be mistaken grossly and histologically for squamous cell carcinoma. Leukoplakia and carcinoma in situ are common problems on the lower lip and may precede the appearance of carcinoma by many years. Primary lesions arising from the moist mucosa of the lip are considered under the section Buccal Mucosa. American Joint Committee on Cancer Staging for Oral Cavity Primary Tumors TX Primary tumor cannot be assessed T0 No evidence of primary tumor Tis Carcinoma in situ T1 Tumor 2 cm or less in greatest dimension T2 Tumor more than 2 cm but no more than 4 cm in greatest dimension T3 Tumor more than 4 cm in greatest dimension T4a (Lip-vermillion border) Tumor invades through cortical bone, inferior alveolar nerve, floor of mouth, or skin of face (i.e., chin or nose) T4a (Oral cavity) Tumor invades adjacent structures (e.g., through cortical bone, into deep [extrinsic] muscle of tongue [genioglossus, hyoglossus, palatoglossus, and styloglossus], maxillary sinus, skin of face) T4bTumor invades masticator space, pterygoid plates, or skull base and/or encases internal carotid artery Clinical Picture The vermilion is the most common site of origin. Squamous cell carcinoma may present as an enlarging discrete lesion that is not tender until it ulcerates. Some lesions develop very slowly on a background of leukoplakia or carcinoma in situ and present as superficially ulcerated lesions with little or no bulk. Erythema of the adjacent skin suggests dermal lymphatic invasion. Palpation of the lip will reveal the extent of induration. Paresthesia of the skin of the lip indicate nerve invasion.
Treatment

Surgical Treatment Surgical treatment for early lesions (0.5 to 1.5 cm) involves a W or V excision. V excisions may be used for very small lesions but do not give as good a margin for the lower lip defect. If the vermilion is diffusely involved with little or no involvement of the muscle, a vermilionectomy may be done and the mucosa from the oral cavity advanced to cover the defect. Irradiation Technique Lip cancer may be successfully treated by external beam, interstitial brachytherapy, or a combination of both. Interstitial brachytherapy may be accomplished with removable sources such as iridium-192 (192Ir). External beam techniques use orthovoltage (55.8 Gy at 1.8 Gy per fraction) or electrons (60 to 66 Gy at 2 Gy per fraction) with lead shields behind the lip to limit exit irradiation. IMRT is not indicated except for the occasional patient with advanced neck disease and/or clinical perineural invasion where it is necessary to extend the dose distribution to the skull base and reduce the dose to the contralated parotid.

Floor of the Mouth

Anatomy The floor of the mouth is a U-shaped area bounded by the lower gum and the oral tongue; it terminates posteriorly at the insertion of the anterior tonsillar pillar into the tongue. The paired sublingual glands lie immediately below the mucous membrane; the paired genioglossus and geniohyoid muscles separate them. Bony protuberances, the genial tubercles, occur at the point of insertion of these two muscle groups at the symphysis and may interfere with the placement of interstitial sources. The mylohyoid muscle arises from the mylohyoid ridge of the mandible and is the muscular floor for the oral cavity; it ends posteriorly at about the level of the third molars. The submandibular gland rests on the external surface of the mylohyoid muscle between the mandible and the insertion of the mylohyoid. The submandibular duct (Wharton's duct) is about 5 cm long. It courses between the sublingual gland and the genioglossus muscle and exits in the anterior floor of the mouth near the midline. Pathology Most neoplasms are squamous cell carcinoma, usually of moderate grade. Clinical Picture On physical examination, the earliest lesions appear as a red area, slightly elevated, with illdefined borders and very little induration. As the lesion enlarges, the edges of the tumor become distinct, elevated, and rolled, with a central ulceration and induration. Some lesions start with a background of leukoplakia. Bimanual palpation will determine the extent of the induration and the degree of fixation to the periosteum. Large lesions bulge into the submental space and rarely grow through the mylohyoid muscle into the soft tissues of the neck. Gross invasion of the mandible may be detected, especially when the anterior teeth have been removed. A tumor may grow through the mandible to involve the gingivolabial sulcus and lip. The submandibular duct and gland are evaluated by bimanual palpation. Treatment Selection of Treatment Modality Early Lesions Operation or radiation therapy is equally effective treatment for T1 or T2 lesions. Most patients are treated surgically because of the risk of soft tissue or bone necrosis after irradiation. A few patients are seen after excisional biopsy of a tiny lesion, and the only finding is a surgical scar with varying degrees of induration or nodularity under the scar (TX). The margins are often equivocal. These patients are sometimes treated with an interstitial implant or, more commonly, re-excision. Moderately Advanced Lesions The usual recommendation for moderately advanced anterior midline lesions is rim resection or segmental mandibulectomy and osteomyocutaneous free flap reconstruction; postoperative irradiation is added as dictated by the findings in the specimen. The neck with clinically negative nodes are usually managed by bilateral functional neck dissection for midline lesions. Advanced Lesions Massive lesions have a small chance of cure with combined surgery and radiation therapy; only palliation can be offered in some cases. Surgical Treatment Wide Local Excision Small lesions (5 mm or less in size) may be excised transorally with a 1-cm margin with primary closure or a skin graft. If the duct is involved, the submandibular gland and duct are removed in continuity. Rim Resection

Rim resection of the mandible in continuity with excision of the primary lesion preserves the arch and may be combined with postoperative radiation therapy .Invasion of the periosteum is often an indication for this procedure. Patients who have been edentulous for a long time may have an atrophic mandible and are not suitable because the mandible is likely to fracture. Segmental Mandibulectomy In the lateral floor of mouth, a modified neck dissection is performed and the specimen remains attached to the mandible. Irradiation Technique Superficial T1 cancers are treated with either brachytherapy or intraoral cone irradiation to approximately 65 Gy and the neck is observed. Larger lesions are treated with external beam irradiation of 45 to 50 Gy over 5 weeks followed by an interstitial implant for an additional 20 to 30 Gy. Combined Treatment Policies Postoperative irradiation is preferred, because the risk of bone complications and fistulae is higher with preoperative irradiation. Preoperative irradiation may be used if the patient has a large fixed node. Management of Recurrence Radiation failures are treated by an operation. The salvage rate is good for patients with T12 lesions and poor for those with more advanced lesions. Surgical treatment failures may be treated by a repeat operation and postoperative irradiation. Oral Tongue Anatomy The circumvallate papillae locate the division between oral tongue and base of tongue. The arterial supply is mainly by way of paired lingual arteries that are branches of the external carotid. The sensory pathway is by way of the lingual nerve to the gasserian ganglion. Clinical Picture Mild irritation of the tongue is the most frequent complaint. As ulceration develops, the pain worsens and is referred to the external ear canal. Extensive infiltration of the muscles of the tongue affects speech and deglutition and is associated with a foul odor. Extent of disease is determined by visual examination and palpation. The tongue protrudes incompletely and toward the side of the lesion as fixation develops. Posterior oral tongue lesions may grow behind the mylohyoid and present as a mass in the neck at the angle of the mandible. Invasion of the hypoglossal nerve is rare Excisional Biopsy (TX) Excisional biopsy of a small lesion may show inadequate or equivocal margins. An interstitial implant or re-excision will produce a high rate of local control. Early Lesions (T1 or T2) A partial glossectomy with primary closure or a skin graft may be done transorally and is usually the preferred therapy. Depending on the depth of invasion, an elective neck dissection may be indicated. Postoperative radiation therapy would only be added for indications previously discussed in Selection of Treatment Modality. Moderately Advanced Lesions (T2 or T3) The preferred treatment for the majority of these patients is partial glossectomy, neck dissection, and postoperative radiotherapy. Advanced Lesions (T4) Combined treatment with surgery and radiation therapy will cure very few patients. Most patients in this category will receive palliative therapy.

Irradiation Technique The ability to control the primary lesion is enhanced by giving all or part of the treatment by interstitial radiation therapy or by intraoral cone.215,220,221 Superficial T1 tumors may be treated with 192Ir brachytherapy alone using the plastic tube technique. Larger lesions that have an increased risk for subclinical neck disease may be treated with external beam radiotherapy and a brachytherapy boost or with brachytherapy combined with an elective neck dissection. Buccal Mucosa Epidemiology Squamous cell carcinoma is relatively uncommon in the United States. In southern India it is common and is related to chewing a combination of tobacco mixed with betel leaves, areca nut, and lime shell.225 Anatomy The buccal mucosa is the mucous membrane covering the inner surface of the cheeks and lips, ending above and below with a transition to the gingiva. It ends posteriorly at the retromolar trigone. The parotid duct opens into the buccal mucosa opposite the second upper molar. It is innervated by a branch of the mandibular nerve (V), which is sensory to the buccal mucosa, and the skin of the cheek that covers the buccinator muscle. Clinical Picture Small lesions produce the sensation of a lump that is felt with the tongue. Pain is minimal, unless there is posterior extension to involve the lingual and dental nerves. Pain may be referred to the ear. Obstruction of the Stensen's duct will produce parotid enlargement. Extension posteriorly, behind the pterygomandibular raphe or into the buccinator and masseter muscles, causes trismus

Treatment Selection of Treatment Modality Small lesions (1 cm or smaller) may be excised with primary closure; small lesions that involve the lip commissure are sometimes treated by radiation therapy. Lesions 2 to 3 cm in size can be treated with surgery or by radiation therapy, usually the former. Larger lesions are usually treated with surgery and postoperative radiotherapy. Surgical Treatment Lesions that invade the mandible or maxilla require bone resection along with the soft tissues. Repair may require a maxillary prosthesis. A myocutaneous flap repairs full-thickness removal of the cheek. Irradiation Technique Buccal mucosa lesions are suited for treatment with electrons, intraoral cone, and interstitial techniques to spare the contralateral normal tissues. When tumors extend into one of the gingivobuccal gutters or onto bone, treatment must be entirely by external beam. Gingiva and Hard Palate (Including Retromolar Trigone) Anatomy The lower gingiva includes the mucosa covering the mandible from the gingivobuccal gutter to the origin of the mucosa on the floor of the mouth. The retromolar trigone lies behind the third molar and is contiguous above with the maxillary tuberosity. Beneath the mucosa of the

retromolar trigone is the tendinous pterygomandibular raphe, which is attached to the pterygoid hamulus and the posterior mylohyoid ridge of the mandible and serves as the insertion of the buccinator, orbicular oris, and superior pharyngeal constrictor muscles. Behind the pterygomandibular raphe and between the medial pterygoid muscle and the ascending ramus is the pterygomandibular space, containing the lingual and dental nerves; it is related posteriorly to the deep lobe of the parotid and the parapharyngeal space. There are no minor salivary glands in the mucous membranes of the alveolar ridges. Clinical Picture The patient with squamous cell carcinoma may present to the dentist first with ill-fitting dentures, pain, loose teeth, or a sore that will not heal. A history of inappropriate dental extractions or root canal therapy is common. Invasion into the mandible may involve the inferior dental nerve and produce paresthesia of the lower lip. A background of leukoplakia is frequently present. Retromolar trigone lesions have pain referred to the external auditory canal and preauricular area. Invasion of the pterygoid muscle produces trismus. Surgical Treatment Rim Resection For discrete T12 carcinomas. Segmental Mandibulectomy For small lesions with minimal bone invasion, a short section of mandible is removed in continuity with the tumor. Partial Mandibulectomy The mandible and tumor are usually resected from the mental foramen to the coronoid process, usually leaving the head of the condyle. Reconstruction of the mandible is usually accomplished with an osteomyocutaneous flap. Hemimandibulectomy Extensive lesions may require removal of the mandible symphysis to the condyle on one side. Massive anterior lesions require removal of the mandible from angle to angle. This is reconstructed with a composite osteomyocutaneous flap. Irradiation Technique Small lesions of the lower gum and retromolar trigone may be treated by intraoral cone for all or part of their therapy. Well-lateralized lesions of the retromolar trigone and posterior gum may be treated by either an ipsilateral mixed beam or angled wedge pair technique; the latter is preferred