Mouth (oral) cancer is a major neoplasm worldwide and accounts for most head and neck cancers. It theoretically should be largely preventable or detectable at an early stage. Approximately 90% of oral cancers are squamous cell carcinoma (SCC), which is seen typically on the lip or lateral part of the tongue usually as a lump or ulcer that is white, red, or mixed white and red. Note the image below. Any single lesion persisting for more than 3 weeks should be regarded with suspicion. The mnemonic RULE (Red, Ulcerated, Lump, Extending for 3 or more weeks) is an aid to diagnosis.
Oral SCC (OSCC) is particularly common in the developing world, mostly in older males. There is concern about an ongoing increase in younger patients and in women, as well as in the oropharynx. The etiology of SCC appears to be multifactorial and strongly related to lifestyle, mostly habits and diet (particularly tobacco alone or in betel, and alcohol use).Other factors such as infective agents may also be implicated, particularly in oropharyngeal cancer. Immune defects or immunosuppression, defects of carcinogen metabolism, or defects in DNA-repair enzymes underlie some cases of SCC. Sunlight exposure predisposes to lip cancer.
Findings from the history and clinical examination by a trained diagnostician are the primary indicators of OSCC, but the diagnosis must always be confirmed histologically with repeated biopsies if the clinical picture is consistent with SCC.
In oral squamous cell carcinoma (OSCC), modern DNA technology, especially allelic imbalance (loss of heterozygosity) studies, have identified chromosomal changes suggestive of the involvement of tumor suppressor genes (TSGs), particularly in chromosomes 3, 9, 11, and 17. Functional TSGs seem to assist growth control, while their mutation can unbridle these control mechanisms.
The regions most commonly identified thus far have included some on the short arm of chromosome 3, a TSG termed P16 on chromosome 9, and the TSG termed TP53 on chromosome 17, but multiple other genes are being discovered.
As well as damage to TSGs, cancer may also involve damage to other genes involved in growth control, mainly those involved in cell signaling (oncogenes), especially some on chromosome 11 (PRAD1 in particular) and chromosome 17 (Harvey ras [H-ras]). Changes in these and other oncogenes can disrupt cell growth control, ultimately leading to the uncontrolled growth of cancer. H-ras was one of the oncogenes that first caught the attention of molecular biologists interested in cell signaling, cell growth control, and cancer. It and the gene for epidermal growth factor receptor (EGFR) are involved in cell signaling.
The genetic aberrations involve, in order of decreasing frequency, chromosomes 9, 3, 17, 13, and 11 in particular, and probably other chromosomes, and involve inactivated TSGs, especially P16, and TP53 and overexpressed oncogenes, especially PRAD1.
The molecular changes found in OSCC from Western countries (eg, United Kingdom, United States, Australia), particularly TP53 mutations, are infrequent in Eastern countries (eg, India, Southeast Asia), where the involvement of ras oncogenes is more common, suggesting genetic differences that might be involved in explaining the susceptibility of certain groups to OSCC.
The rare Li-Fraumeni syndrome is associated with defects in TP53.
Carcinogen-metabolizing enzymes are implicated in some patients. Alcohol dehydrogenase oxidizes ethanol to acetaldehyde, which is cytotoxic and results in the production of free radicals and DNA hydroxylated bases; alcohol dehydrogenase type 3 genotypes appear predisposed to OSCC. Cytochrome P450 can activate many environmental procarcinogens. Ethanol is also metabolized to some extent by cytochrome P450 IIEI (CYP2E1) to acetaldehyde. Mutations in some TSGs may be related to cytochrome P450 genotypes and predispose to OSCC. Glutathione S transferase (GST) genotypes may have impaired activity; for example, the null genotype of GSTM1 has a decreased capacity to detoxify tobacco carcinogens. Some GSTM1 and GSTP1 polymorphic genotypes and GSTM1 and GSTT1 null genotypes have been shown to predispose to OSCC. N -acetyltransferases NAT1 and NAT2 acetylate procarcinogens. N -acetyl transferase NAT1*10 genotypes may be a genetic determinant of OSCC, at least in some populations.
Tobacco is a potent risk factor for oral cancer. An interaction occurs between redox-active metals in saliva and the low reactive free radicals in cigarette smoke. The result may be that saliva loses its antioxidant capacity and instead becomes a potent pro-oxidant milieu.
DNA repair genes are clearly involved in the pathogenesis of some rare cancers, such as those that occur in association with xeroderma pigmentosum, but, more recently, evidence of defective DNA repair has also been found to underlie some OSCCs.
Immune defects may predispose to OSCC, especially lip cancer. OSCC is also now being reported with increased frequency in association with diabetes and systemic sclerosis.
Intraoral OSCC primarily affects the posterior lateral part of the tongue. Spread is local, especially through muscle and bone, and metastasis initially is to the anterior cervical lymph nodes and later to the liver and skeleton.
The oral cavity is 1 of the 10 most frequent sites of cancer internationally, with three quarters of cases affecting people in the developing world, where, overall, oral cancer is the third most common cancer after stomach and cervical cancer. An estimated 378,500 new cases of intraoral cancer are diagnosed annually worldwide.
Unfortunately, the parts of the world where oral cancer is most common are also those where descriptive information (ie, incidence, mortality, prevalence) is least available. In certain countries, such as Sri Lanka, India, Pakistan, and Bangladesh, oral cancer is the most common cancer. In parts of India, oral cancer can represent more than 50% of all cancers. OSCC is also common in Brazil.
In developed countries, oral cancer is less common but is the eighth most common form of cancer overall; however, the ranking varies a great deal among countries. For example, in areas of northern France, oral cancer is the most common form of cancer in men. Estimates show that in 1980, more than 32,000 new cases of oral cancer were diagnosed throughout the European community. The prevalence of lip cancer appears to be decreasing, but the prevalence of intraoral cancer appears to be rising in many countries, especially in younger people. This is especially true in Central and Eastern Europe, especially Hungary and Northern France.
The prevalence of tongue cancer is consistently found to be higher (by approximately 50%) in blacks compared with whites within the same regions of the United States. The prevalence of oral cancer is also generally higher in ethnic minorities in other developed countries.
Oral cancer affects males more frequently than females, although the ratio is equalizing.
Oral cancer is predominantly found in middle-aged and older persons.
Symptoms and Signs
Oral lesions are asymptomatic initially, highlighting the need for oral screening. Most dental professionals carefully examine the oral cavity and oropharynx during routine care and may do a brush biopsy of abnormal areas. The lesions may appear as areas of erythroplakia or leukoplakia and may be exophytic or ulcerated. Cancers are often indurated and firm with a rolled border. As the lesions increase in size, pain, dysarthria, and dysphagia may result.
Lip and Oral Cavity Cancer Treatment .
Staging of Head and Neck Cancer) lesions (greatest dimension 2 to 4 cm) and most T1 lesions with a depth of invasion about ≥ 4 mm.
Routine surgical reconstruction is the key to reducing postoperative oral disabilities; procedures range from local tissue flaps to free tissue transfers. Speech and swallowing therapy may be required after significant resections.
Radiation therapy is an alternative treatment. Chemotherapy is not used routinely as primary therapy but is recommended as adjuvant therapy along with radiation in patients with advanced nodal disease.
Treatment of squamous cell carcinoma of the lip is surgical excision with reconstruction to maximize postoperative function. When large areas of the lip exhibit premalignant change, the lip can be surgically shaved, or a laser can remove all affected mucosa. Mohs surgery can be used. Thereafter, appropriate sunscreen application is recommended.
Combined clinics that include surgeons, oncologists, and support staff usually have an agreed treatment policy and offer the best outcomes. Oral squamous cell carcinoma (OSCC) currently is treated largely by surgery and/or irradiation, although few unequivocal controlled trials of treatment modalities have been conducted. Photodynamic and chemotherapy have occasional applications, and there is an increased use of chemotherapy, [general anesthesia is not needed, and (3) salvage surgery is available if radiotherapy fails.
Disadvantages mainly include the facts that (1) adverse effects are common; (2) cure is uncommon, especially for large tumors; and (3) subsequent surgery is more difficult and hazardous and survival is reduced further.
Radiotherapy can be performed by external beam radiation (teletherapy), which is commonly accompanied by adverse effects, or interstitial therapy (eg, brachytherapy, plesiotherapy). Implants of iridium Ir 192 for a few days are often used, supplying a radiation dose equivalent to teletherapy but one that is confined to the lesion and immediate area. Plesiotherapy causes fewer complications but is suitable only for tumors that are smaller than 2 cm and located in selected sites.
Of short-term complications, the oral mucositis that invariably follows external beam radiotherapy involving the oral tissues or cancer chemotherapy can be the most distressing and may have significant effect on the quality of life. Occasionally, oral mucositis is so severe that cancer therapy needs to be curtailed. As many as 40% of patients can be affected.
Longer-term complications of radiotherapy, such as dry mouth (xerostomia), loss of taste, osteoradionecrosis (ORN) (less commonly), and other problems also may be distressing. Radiotherapy also complicates further surgery, because in particular, the endarteritis impoverishes healing. Prevention and treatment of oral complications whenever possible are important and should be performed by an oncologic team including a dental practitioner and an oral hygienist.
Prevention and treatment planning before cancer therapy
Prevention of oral disease and careful treatment planning are essential to minimize oral disease and the need for, and possible adverse consequences of, operative intervention. Adults with malignant head and neck disease unfortunately often have poor oral hygiene and care and are poorly compliant with oral health care. Most (97%) need oral health care before radiotherapy or chemotherapy for cancer. Almost one third of patients need oral care before bone marrow transplantation.
Extremely important, but often overlooked, is the need for psychosocial counseling; patients must be counseled carefully to ensure they can adjust, at least partially, to the complications of cancer therapy.
Many patients undergoing head and neck cancer surgery, particularly of the neck, can have life-threatening postoperative complications. These can often be predicted by preoperative assessment using a specific activity scale questionnaire, an assessment of alcohol abuse, and a platelet count, because thrombocytosis identifies patients at risk for wound infection.
Fruits and vegetables appear to offer some protective effect. The potential of topical gel formulations for local delivery of chemopreventive plant anthocyanins is being investigated.
Oral health and disease in cancer therapy
Complications of cancer therapy depend on the type of malignancy and location, the treatment modality used (ie, agents, sequencing, rate of delivery, dosage), and host factors. For example, the severity of oral mucositis following radiation therapy depends on the ionizing radiation used, the rate at which it is delivered, and the total dose given.
Manifestations of cancer therapy may include mucositis and oral ulceration, infections, bleeding, pain, xerostomia, ORN, taste loss, trismus, and caries. These require prevention and management.
Mucositis can be induced either by chemotherapy or by radiotherapy. Mucositis appears from 3-15 days after cancer treatment, earlier with chemotherapy than with radiotherapy. Pain can be so intense that it interferes with eating and quality of life. Occasionally, therapy must be stopped for several days to allow healing. In addition to causing local pain and ulceration, mucositis can provide a portal for microbial entry and thus, can result in local and, sometimes, systemic infection.
The acute mucosal reaction to radiotherapy results from mitotic death of cells in the epithelium. The cell cycle time of basal epithelial cells is approximately 4 days, and because this epithelium is 3-4 cells thick, radiation changes begin to appear at approximately 12 days after the start of irradiation, independently of the dose, fractionation, or radiation technique.
Initial mucosal erythema is followed after a few days by the appearance of a patchy fibrinous exudate. If a high dose of radiation is given over a short time, ulceration may supervene, with a thick fibrinous membrane covering the denuded surface.
Surviving epithelial cells respond to radiation damage by dividing more rapidly; therefore, complete healing is the rule. The duration mucositis takes to heal depends on the dose intensity of the radiotherapy, but usually, healing is complete within 3 weeks after the end of treatment. Tobacco smoking delays resolution.
Cytotoxic drugs, which have a selective action on cells in the mitotic cycle, kill regenerating epithelial cells; therefore, the simultaneous use of chemotherapy and radiotherapy results in more severe and prolonged mucosal toxicity.
Frank oral ulceration may be a portal for infection and septicemia. Preventing or ameliorating mucositis may be possible not only by minimizing exposure to radiation, but also by taking active measures. For example, radiotherapy radically increases oral gram-negative enterobacteria and pseudomonads. The presence of gram-negative bacilli may contribute to the mucositis. In addition, these microorganisms release powerful endotoxins that themselves cause both systemic and local effects on the host.
If gram-negative bacilli have a role in the etiology of irradiation mucositis, preventing, treating, or ameliorating mucositis may be possible by abolishing the gram-negative florae. Promising results have been reported in 2 clinical trials using polymyxin E and tobramycin applied locally 4 times daily. This regimen has not been evaluated fully for the treatment of existing irradiation mucositis. Oral hygiene should be maintained with brushing the teeth. Advise the patient to eat a soft, bland diet and avoid irritants such as smoking, spirits, or spicy foods. Topical analgesics (eg, aspirin, benzydamine, lignocaine, dyclonine, diphenhydramine) may provide symptomatic relief. Topical chlorhexidine gluconate and sucralfate may reduce the frequency and severity of mucositis.
Levels of Streptococcus mutans, Lactobacillus species, and candidal species significantly increase after radiotherapy. These changes are maximal from 3-6 months after radiotherapy, after which no further change or a partial return towards the baseline florae occurs.
The frequency and severity of oral infections with virus, bacteria, and fungi significantly increase after cytotoxic chemotherapy and radiochemotherapy. The primary symptomatic viral infections affecting the mouth in patients with cancer include herpes simplex virus (HSV) and herpes varicella-zoster virus infections. Acyclovir remains the primary treatment, but new agents, such as famciclovir, penciclovir, sorivudine, foscarnet, and other agents, may be needed in cases of acyclovir resistance.
Homeostatic microbial communities are protective in health by preventing or interfering with the colonization of exogenous pathogens (colonization resistance). When oral tissues are irradiated, colonization resistance is practically abolished, and alteration of the oral microflora occurs, with increases in yeasts and some gram-negative organisms.
The possible role of yeasts in irradiation mucositis has garnered considerable interest because the number of candidal subspecies, in particular, appears to increase. Candidosis is the most common oral fungal infection in patients with cancer and may cause soreness and, occasionally, may be responsible for dissemination of infection. Xerostomia, dental prostheses, alcohol use, and tobacco smoking predispose patients to oral candidosis. A meta-analysis of numerous studies has shown the prophylactic value of clotrimazole or fluconazole.
Salivary tissue, particularly serous acini, is highly vulnerable to radiation damage, and the parotid glands are damaged most readily. A radiation dose as small as 20 Gy can cause permanent cessation of salivary flow if given as a single dose, and with the conventional treatments for oral carcinoma (60-70 Gy), a rapid decrease in flow occurs during the first week of radiotherapy, with an eventual approximate 95% reduction.
Salivary flow begins to diminish. After 5 weeks of radiotherapy, the flow virtually ceases and rarely completely recovers. Both resting and stimulated salivary flow are inhibited. Nevertheless, the sensation of dryness of the mouth tends to diminish after a few months to a year, partly as a result of compensatory hypertrophy of unirradiated salivary glandular tissue. After 1 year, little further improvement occurs.
The degree of hyposalivation depends on the degree of exposure of the salivary tissue. Hyposalivation occurs when the upper border of the radiation field is above the submental area, particularly when the parotid glands are involved. Partially irradiated glands have resultant higher flow rates than fully irradiated glands. Mantle, unilateral, and bilateral fields of radiation can be associated with a reduction in salivary flow of 30-40%, 50-60%, and approximately 80%, respectively.
A high initial salivary flow rate is associated with higher flow rates after radiotherapy. Radiotherapy to the nasopharynx damages both of the parotid glands and causes severe and permanent hyposalivation. Radiotherapy to a salivary tumor may avoid the contralateral gland and not cause severe hyposalivation. Radiotherapy fields used in the treatment of oral cancer normally avoid at least part of the parotid glands; therefore, hyposalivation tends not to be as severe as it would be if both glands were irradiated in their entirety.
Hyposalivation leads to discomfort and loss of taste and appetite. In addition to minimizing unnecessary glandular irradiation, stimulating the salivary glands prior to radiotherapy has been suggested as valuable for reducing glandular damage. The use of pilocarpine during radiotherapy has shown encouraging results. In hyposalivation, residual salivary tissue may be stimulated by gustatory or pharmacologic stimuli.
Sugar-free chewing gum may be a useful stimulus, is inexpensive, and has no adverse effects. Drugs that may be effective particularly include various cholinergic agents such as pilocarpine, given as ophthalmic drops placed intraorally or as tablets, is effective in relieving symptoms and in improving salivation when used in doses of up to 5 mg administered 3 times daily.
Individuals with dry mouth frequently sip water, particularly during eating, and they often need to keep water by their bedsides. Several saliva substitutes or mouth-wetting agents are currently marketed. Most contain carboxymethylcellulose, although some that contain animal mucins and some also contain constituents that may facilitate enamel remineralization. Some patients find these products useful, but clinical experience suggests that they are not always well accepted. Some studies have suggested that mucin-containing preparations are accepted better by patients and may promote the establishment of normal oral florae; however, when cost and convenience are taken into consideration, many patients prefer to simply sip water frequently or to use an aerosol pump of water.
Advise xerostomic patients to avoid agents such as medications, tobacco, and alcohol that may further impair salivation.
Although periodontal disease is not usually a problem, patients who undergo cancer therapy may be predisposed to caries because of hyposalivation, foods with a high sucrose content, and, possibly, a shift to more cariogenic oral microflora. Several types of carious lesions have been identified, most involving the incisal edges and cervical areas. The direct effect of radiation on tooth structure is probably less than the indirect effect (eg, xerostomia).
Patients must achieve a good level of oral hygiene before radiotherapy or chemotherapy commences. Dietary control and topical fluoride therapy are essential and must be continued for life. Fluoride is applied best to the entire surface of all teeth to have the maximal protective effect. This is achieved best by providing custom-built carriers for each patient. A gel containing 1% sodium fluoride is put into the carrier and applied to the teeth for 5 min/d. Fluoride mouth rinses are also useful. Sodium fluoride mouth rinses with chlorhexidine diacetate may be particularly effective. Amorphous calcium phosphate preparations are also protective.
Patients receiving radiotherapy to the mouth invariably experience some disturbance or loss of taste sensation. The taste receptor cells are relatively radioresistant, and the mechanism of this loss of taste has not been elucidated. Xerostomia probably contributes because disturbance of taste is common after irradiation of the parotid glands.
Taste loss can be a distressing symptom and contributes to poor nutrition in patients receiving radiotherapy. Fortunately, taste perception usually recovers slowly within a few months after the end of radiotherapy, although sometimes loss is permanent. Zinc sulphate may help improve taste sensation in some patients.
ORN, although uncommon, is potentially the most serious oral complication of radiation therapy. Radiation results in thrombosis of small blood vessels; fibrosis of the periosteum and mucosa; and, damage to osteocytes, osteoblasts, and fibroblasts. The damaged osteoclasts and osteoblasts survive until they attempt to divide, at which time mitotic death occurs. An individual bone cell may not divide for months or years after irradiation, or it may not divide unless stimulated by trauma. Therefore, a slow protracted loss of bone cells occurs after radiotherapy, with a consequent slowing of remodeling, which eventually may result in thinning and reduced bone strength. The mandible consists of more compact bone with a higher density than the maxilla; therefore, it absorbs more radiation than the maxilla.
The predisposition to ORN occurs because the blood supply of the mandible in the age group that develops cancer is poor and is almost entirely via the periosteum (which also becomes less vascular). The maxilla, with its lower density and rich vasculature, is rarely the site of ORN.
Various factors predispose patients to ORN, but generally, the risk is greatest in the mandible, in higher radiation doses, fraction size, number of fractions, and when teeth are extracted after radiotherapy. Nevertheless, ORN also may occur unrelated to trauma. Many patients with oral cancer abuse alcohol and tobacco and are in poor general condition, which together with poor nutritional status and oral hygiene, make them particularly prone to oral ulceration and ORN.
ORN is most unlikely with radiation doses below 60 Gy; in doses up to 70 Gy, the rate is 1.8%, and in doses higher than 70 Gy, the rate is approximately 9%. In modern series, 5-15% of patients who undergo radiotherapy to the head and neck region develop ORN. Radiation shields decrease the radiation dose received by the bone and minimize the risk of ORN.
Because infection or trauma (including surgical intervention) may result in local infection, delayed healing, and ORN, these should be kept to a minimum. The rate of ORN is 3 times higher in dentate than in edentulous patients as a result of infection from periodontal disease and trauma from tooth extraction.
Tooth loss after high-dose irradiation is by no means inevitable, and the prevalence of bone necrosis is lowest if extraction can be avoided altogether. The only teeth that need to be extracted before radiotherapy include those that are not vital, need root filling or elaborate restorative techniques, or are associated with active periodontal disease. Extractions of these teeth should be performed atraumatically, the tissues sutured to promote rapid healing, and antimicrobial therapy instituted. All other teeth should be cleaned and restored before radiotherapy begins.
If dental extraction is performed shortly after radiotherapy, when devascularization occurs in addition to damage to the osteoblasts, the risk of ORN is particularly high. The risk of ORN is less if dental extraction is performed well before radiotherapy, but, regardless, the risk remains as a consequence of the enhanced remodeling of bone that continues for some months after the extraction. Dental extractions typically are best performed judiciously and a minimum of 2-3 weeks before commencement of irradiation therapy.
If surgery later becomes necessary in the management of malignant disease, irradiated tissue should be handled as gently as possible. The highest rate of mandibular ORN occurs in patients who have dental extractions immediately prior to radiotherapy or immediately after. Many authors agree that postradiation extractions should be avoided if possible.
A conservative approach to the treatment of ORN is indicated because up to approximately 60% of cases of ORN resolve with conservative therapy. ORN is treated best in a progressive manner, depending on results and the healing of the lesion. Therapeutic approaches include local wound care, topical or systemic antibiotics, ultrasound, hyperbaric oxygen (HBO), and minor-to-extended surgery with reconstruction procedures.
Meticulous oral hygiene is essential, including the use of 0.02% aqueous chlorhexidine mouthwashes after meals. Irrigate away debris and allow sequestra to separate spontaneously because any surgical interference only encourages extension of the necrotic process. Any sequestrum that becomes loose should be removed gently along with any sharp edges of spicules of bone.
Antimicrobials are not especially effective because the tissues are avascular; therefore, prolonged treatment is necessary. Tetracyclines are useful because of their selective bone uptake, and a regimen of 250 mg of tetracycline 4 times a day for 10 days, followed by 250 mg twice daily continued for several months, is recommended. Add metronidazole at 200 mg 3 times a day in cases of severe infection or when anaerobes are implicated.
HBO therapy also has been shown to promote healing. HBO therapy at 2-2.5 atmospheres of pressure for 1.5-2 h/d for up to 84 sessions is recommended. Adverse effects with HBO therapy are uncommon but include transient myopia, seizures, and otic or pulmonary barotrauma; the latter potentially results in air embolism. Concern has been expressed that HBO therapy may exacerbate a variety of autoimmune and immunosuppressive disorders and viremia, although little evidence supports this concern.
Relative contraindications to HBO therapy include upper respiratory tract infection, chronic sinusitis, epilepsy, chronic obstructive airways disease, high fever, a history of spontaneous pneumothorax or thoracic or ear surgery, viral infections, congenital spherocytosis, and a history of optic neuritis. Untreated pneumothorax is the only absolute contraindication. Risks of HBO therapy may be minimized by a careful pretreatment assessment including chest radiography and electrocardiography. Some advise otolaryngologic and ophthalmologic assessment.
Therapeutic ultrasound at a frequency of 3 MHz pulsed 1 in 4 at an intensity of 1 W/cm2 applied to the mandible for 10 minutes daily for 50 days also may effectively improve ORN.
Surgical management also has played a role in the treatment of ORN and may include sequestrectomy, alveolectomy with primary closure, closure of orocutaneous fistulae, or hemimandibulectomy.
The goal of surgery for oral squamous cell carcinoma (OSCC) is to remove the primary tumor together with a margin of clinically normal tissue to ensure complete excision of malignant tissue. Surgery thus provides a one-stage definitive procedure, from which the patient normally recovers within 10-14 days. Although modern reconstructive techniques can produce good orofacial aesthetics and function, neither can be totally ensured. Cancer centers receive many patients with advanced disease, and many operations fail to remove the tumor completely, resulting in a poor outcome and recurrence of the tumor.
Ensuring that the patient is as prepared as possible for the major surgery required, particularly in terms of general anesthesia, potential blood loss, and ability to metabolize drugs, is important. In addition, address any potential dental or oral problems preoperatively in order to avoid later complications such as ORN.
Surgery provides complete tumor and lymph node excision. A full histologic examination can then be performed for staging purposes and to help predict prognosis and the need for adjuvant radiotherapy. Surgery also provides another option of treatment for radiotherapy-resistant tumors.
Disadvantages primarily are perioperative mortality and morbidity, but modern techniques have significantly decreased these risks, as well as the aesthetic and functional defects. When OSCC is fatal, it almost always is either because of failure to control the primary tumor or because of nodal metastases. Death resulting from distant metastasis is unusual.
Ablative surgery ideally excises the cancer with at least a 2-cm margin of clinically normal tissue. If at least 1 node has clinical signs of invasion, a reasonable presumption is that others may be involved and must be removed by traditional radical neck dissection.
Functional neck dissections (modified to preserve the jugular, sternomastoid, or accessory nerve, while ensuring complete removal of involved nodes) have gained popularity. Moderate-dose radiotherapy occasionally is used to "sterilize" such necks.
Reconstruction is tailored to the patient's ability to cope with a long operation and the risk of significant morbidity. For soft tissue reconstruction, tissue often must be brought into the region to close the defect using split skin grafts or flaps. Local flaps (eg, nasolabial flaps) provide thin, reliable flaps suitable for repairing small defects. Distant flaps required to repair larger defects include the following:
- Free flaps: Microvascular surgery facilitates excellent reconstruction in a single operation using, for example, forearm flaps based on radial vessels, which are particularly useful to replace soft tissue, or those based on the fibula when bone is required.
- Pedicle flaps: Myocutaneous or osteomyocutaneous flaps based on a feeding vessel to muscle and perforators to the skin paddle (eg, flaps based on the pectoralis major, latissimus dorsi, or trapezius) may be used in a one-stage operation to replace skin, and because they also contain muscle, they have adequate bulk to repair defects and may be used to import bone (usually rib). Forehead or deltopectoral pedicle flaps, once the mainstay, required a 2-stage operation, replaced only skin, and relied on a tenuous blood supply.
- Hard tissue: Hard tissue reconstruction ideally is performed at the time of tumor resection. Dental implants can be inserted at that point to carry a prosthesis. Bone is traditionally taken as free nonvascularized bone grafts from the iliac crest or rib but may survive poorly if contaminated or if the vascularity is impaired after irradiation. In such cases, or when a large defect is present, an osteomyocutaneous flap greatly improves the graft vascular bed. True free vascularized bone grafts (eg, fibula grafts) have great benefits but are time consuming and require considerable expertise. The benefits of bone grafting for maxillary defects are less certain, and maxillary reconstruction is usually with an obturator (bung), which has the advantage that the cavity can be readily inspected.
Specific complications from the surgery of OSCC may include infection and rupture of the carotid artery, salivary fistulae, and thoracic duct leakage (chylorrhea).