Oral Cancer
Cancer begins in cells, the building blocks that make up tissues. Tissues make up the organs of the body.

Normally, cells grow and divide to form new cells as the body needs them. When cells grow old they die, and new cells take their place.

Sometimes this orderly process goes wrong. New cells form when the body does not need them, and old cells do not die when they should. These extra cells can form a mass of tissue called a growth or tumour. Tumours can be benign or malignant:

Benign tumours
  • Are not cancerous.
  • Are rarely life-threatening.
  • Generally, once removed and they usually do not grow back.
  • Cells from these do not invade the tissues around them nor spread to other parts of the body.
Malignant tumours
  • Are cancerous.
  • Are generally more serious than begin tumours. They may be life-threatening.
  • Often can be removed, but sometimes they grow back.
  • Cells from malignant tumours can invade and damage nearby tissues and organs.
  • Cells from malignant tumours can spread to other parts of the body. The cells spread by breaking away from the original cancer (primary tumour) and entering the bloodstream or lymphatic system. They invade other organs, forming new tumours and damaging these organs. The spread of cancer is called metastasis.
Oral Cavity
The oral cavity is the first portion of the digestive tract. It is a complex structure with nutritional, respiratory and communicative functions. Bound by hard and soft tissues, it includes the upper and lower teeth, the tongue, the salivary glands, mucosal glands, the various freni and the rugae over the hard palate. The mouth is bound anteriorly by the lips, on the lateral aspect by the cheeks. Its roof is formed by the hard palate and inferiorly by the mucosa covering the superior surface of the tongue and the sheet of muscles attaching to the inner side of the mandible. The oral cavity is continuous with the pharyngeal cavity, a more complex and somewhat irregular space.
Oral Cancer
Oral cancer is part of a group of cancers called head and neck cancers. Oral cancer can develop in any part of the oral cavity or oropharynx. Most oral cancers begin in the tongue and in the floor of the mouth. Almost all oral cancers begin in the flat cells (squamous cells) that cover the surfaces of the mouth, tongue, and lips. These cancers are called squamous cell carcinomas.

When oral cancer spreads (metastasizes), it usually travels through the lymphatic system. Cancer cells that enter the lymphatic system are carried along by lymph, a clear, watery fluid. The cancer cells often appear first in nearby lymph nodes in the neck.

Cancer cells can also spread to other parts of the neck, the lungs, and other parts of the body. When this happens, the new tumour has the same kind of abnormal cells as the primary tumour. For example, if oral cancer spreads to the lungs, the cancer cells in the lungs are actually oral cancer cells. The disease is metastatic oral cancer, not lung cancer. It is treated as oral cancer, not lung cancer. Doctors sometimes call the new tumour "distant" or metastatic disease.

Risk Factors for Oral Cancer

Two groups of risk factors - those that are well-established as causes of oral cancer and a second group of possibly relevant contributory factors. Age is included as an established risk factor because exposure to the risks listed increases with age but age on its own is not a risk factor. Also, oral cancer is not always a disease of old age. Clinicians treating oral cancer are concerned that its incidence appears to be increasing in younger age groups.

Established risk factors
  • Smoking tobacco – cigarettes, cigars, pipes, bidis
  • Chewing tobacco – betel quid/paan/gutkha/pan masala
  • High alcohol consumption (synergistic with tobacco)
  • The presence of potentially malignant oral lesions and conditions
  • Prior history – of oral cavity or other aero-digestive tract cancer
  • Age, in conjunction with other risks listed
Other possible risk factors
  • Dietary deficiencies, particularly of vitamins A, C and E and iron, trace elements.such as selenium and zinc.
  • Viral infections, e.g. certain types of human papilloma viruses (HPVs).
  • Candida infection.
  • Excessive exposure to sunlight or radiation (for lip cancer).
  • Immune deficiency disease or immune suppression.
  • Familial or genetic predisposition.
  • Air pollution and environmental exposure to the burning of fossil fuels.
  • Chronic sepsis in the mouth.
Tobacco use, however, remains the most widely believed risk factor for oral cancer.
  • Oral cancer most often occurs in those who use tobacco in any form.
  • Although other lifestyle and environmental factors also have been identified as risk factors for oral cancer, tobacco use remains the single most important and preventable cause of this disease.
  • Although oral cancer undoubtedly has a multifaceted aetiology, tobacco use and alcohol consumption are widely considered to be its major risk factors.
  • It has been conclusively established that tobacco use, especially cigarette smoking, is causally related to at least eight major cancer sites and increases the mortality rate for several others.
  • Cigarette smoking is a major cause of cancers of the oral cavity. Individuals who smoke pipes or cigars experience a risk for oral cancer similar to that of the cigarette smoker.
  • Scientific evidence shows that use of snuff can cause cancer in humans, particularly cancers of the cheek and gum. The evidence for causality is strongest for cancer of the oral cavity, wherein cancer may occur several times more frequently in snuff dippers as compared to non- tobacco users.
  • Smoking, combined with alcohol use greatly increases risk.
It has been found that most patients with oropharyngeal cancer drink alcohol. However, the problems with identifying alcohol as an independent risk factor for oral cancer are:
  • Heavy drinkers usually are also heavy users of tobacco products.
  • Consumption of alcohol together with a poor diet may be an enhancing factor for oral cancer.
  • Alcohol intake and often- episodic nature of usage is often underreported. This makes it difficult for a patient to estimate ‘average’ use.
According to various studies, all three forms of alcohol (beer, hard liquor, and wine) have been associated with oral cancer, though hard liquor and beer have a higher associated risk. The studies have also found that the level of consumption was also a deciding risk factor. For example, one study found increased risk only if 56 or more glasses of wine per week were consumed. Another study noted a significant increase only if the average daily consumption of alcohol exceeded 120 grams. That evidence contradicts about the role of alcohol in oral cancer and may relate to the difficulty in measuring intake or to alcohol's effect on other variables (or both). But it is reasonable to assume that any form of alcohol taken in excess may promote oral cancer.
Though there is insufficient evidence to establish that mouthwashes can cause oral cancer, this might be a cause if used frequently, because they have high alcohol content as high as 26 percent.
Dietary factors have been identified as having a possible association with oral cancer. But, accumulated scientific evidence shows that use of tobacco and alcohol increases oral cancer risk and far outweighs any evidence linking a deficient diet to increased risk.

Low beta-carotene intake has been associated with an increased risk of lung, laryngeal, gastric, ovarian, breast, cervical and oral cancers.

Various studies have shown that a low intake of fruits and vegetables, which are the primary sources of beta- carotene, is also related to a generalized increased cancer risk and mortality.

At the same time, an increased consumption of fruits and/or vegetables has been associated with a decreased risk of oral or oropharyngeal cancer when compared with low intake levels.

Low intake of vitamin C has been associated with an increased risk of cancers of the stomach, oesophagus, oral cavity and larynx. Patients who consume high levels of vitamin C and fibre have half the risk of oral cancer as those with the lowest level of intake.

According to one study, patients with low serum levels of vitamin E had more than double the general risk of gastrointestinal cancers. In another study, which evaluated more than 2,000 cases, the use of vitamin E supplements showed a diminished risk for oral and pharyngeal cancer.

It has been found in dietary studies across multiple cultures that high fruit consumption has a protective effect and high alcohol consumption has a carcinogenic effect.

Actinic Radiation
Sunlight, through actinic radiation, is a factor that helps produce cancer along the vermilion border of the lip. One finds these ‘sunlight’ induced cancers are much more common in fair- skinned individuals exposed to the outdoor life than in individuals with darker pigmentation. That is because, darker pigmentation, it appears, protects against actinic radiation damage. (The wavelengths of the light thought to be responsible for the actinic damage are in the 2900-3200' range.)
Dental Factors
There is little evidence to suggest that poor oral hygiene, improperly fitting dental prostheses, defective dental restorations and misaligned or sharp teeth promotes oral cancer.
Viruses and their Interactions with Oncogenes
Alterations of cellular oncogenes, which lead to altered expression of their products, have been implicated in human cancers.

Cellular oncogenes, also known as proto- oncogenes, get their transforming properties or become activated by gene amplification, point mutations and gene rearrangements.

Oncogenes can encode growth factors and growth factor receptors. They act on internal signalling molecules and regulate DNA transcription factors. Other genes encode proteins that inhibit the cell cycle or promote programmed cell death (apoptosis).

Tumour suppressor genes may become inactivated or mutated with consequential loss of control over cell division. The retinoblast and gene products are examples.

It must be considered that many molecular events governing control of cell cycles are influenced by viruses.

The viruses most commonly implicated in oral cancer transformation have been the human papillomavirus (HPV), herpes group viruses, and the adenoviruses. Of these, HPV and herpes have been the most thoroughly studied. They are now considered to be the most likely "synergistic viruses" involved in human oral cancer. The herpes viruses most often linked to oral cancer are the Epstein-Barr virus (EBV) and cytomegalovirus (CMV).

Oral cancer does not appear to be a common consequence of systemic immunosuppression. This is even though, among HIV- positive immunocompromised individuals, HIV- associated oral malignancies have been reported. The most common are Kaposi's sarcoma (KS) and non- Hodgkin's lymphomas
Symptoms of Oral Cancer
Common symptoms of oral cancer include:
  • Patches inside your mouth or on your lips that are white, a mixture of red and white, or red
    • White patches (leukoplakia) are the most common. White patches sometimes become malignant.
    • Mixed red and white patches (erythroleukoplakia) are more likely than white patches to become malignant.
    • Red patches (erythroplakia) are brightly colored, smooth areas that often become malignant.
  • A sore on your lip or in your mouth that won't heal.
  • Bleeding in your mouth.
  • Loose teeth.
  • Difficulty or pain when swallowing.
  • Difficulty wearing dentures.
  • A lump in your neck.
  • An earache.
Anyone with these symptoms should be seen by the doctor or dentist, with care, so that any problem can be diagnosed and treated as early as possible. Most often, these symptoms do not mean cancer. An infection or another problem can cause the same symptoms.
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