Malignant Tumors of the Palate

The palate is divided anatomically into the hard palate (part of the oral cavity) and the soft palate (part of the oropharynx). Cancer of the soft palate accounts for approximately 2% of head and neck mucosal malignancies. Half of all hard palate cancers are squamous cell carcinomas (SCCs). Nonsquamous cell cancers, including minor salivary gland cancers, sarcomas, and melanomas, account for the other half . However, in the soft palate, 80% of cancers are SCCs. Nonsquamous malignancies account for the other 20%. The prevalence of oral cavity and oropharyngeal cancer has geographic variations, with the highest rate reported in India, accounting for 50% of all cancer cases in that country.

Histologic distribution of hard palate malignant neoplasms

Histologic types and frequencies of minor salivary gland neoplasms of the palate

Etiology: Although a strong correlation is established between tobacco and alcohol consumption and SCC of the oral cavity and soft palate, the relationship to hard palate cancer is not as clear. Reverse smoking is a specific etiologic factor for SCC of the hard palate. In reverse smoking, the lit end of the cigarette is placed in the mouth so that an intense heat is generated during smoking. Other factors, including ill-fitting dentures, poor oral hygiene, mechanical irritation, and mouthwash, are implicated in oral cavity SCC; however, the evidence is less convincing.

Pathophysiology: A thorough history and physical examination help to assess the extent of tumor.

SCC extension beyond the hard palate occurs in up to 70% of lesions. Posterior extension involves the soft palate, with possible velopharyngeal insufficiency and hypernasal speech. Palatal hypesthesia indicates trigeminal nerve involvement in the sphenopalatine foramen or pterygopalatine fossa extension.

An absent corneal reflex is indicative of skull-base extension through the foramen rotundum, foramen ovale, or inferior orbital fissure.

Dental numbness may indicate perineural invasion. Middle ear effusion is suggestive of nasopharyngeal extension or invasion of the tensor veli palatini muscle.

Involvement of the mandibular division of the trigeminal nerve may manifest as hypesthesia along the mandible or wasting of the temporalis or masseter muscles. This is indicative of infratemporal fossa involvement. Trismus, malocclusion, and pain are symptoms of invasion of the pterygoid muscles. Extension to the gingiva requires assessment. Dental sockets provide a pathway of invasion to the alveolar process of the maxillary bone and into the maxillary sinus. Nasal floor involvement may occur by direct extension through the palate.

Lymph node involvement is of special concern in SCC and high-grade mucoepidermoid cancer. It is rare in other salivary gland carcinomas. Approximately 30% of patients have cervical node metastasis at the time of presentation. The submandibular nodes (level I) and upper deep jugular lymph nodes (level II) are the first echelon of nodal drainage. However, in tumors with posterior soft palate extension, retropharyngeal nodes may be involved. Soft palate carcinomas are staged as oropharyngeal cancers according to the American Joint Committee on Cancer

Almost half of patients present with extension of the tumor beyond the soft palate. Common sites of extension include the tonsils, retromolar trigone, inferior or superior alveolar process, hard palate, and base of tongue. Extension into the sphenopalatine foramen may result in palatal hypostasis. In extensive lesions extending into the nasopharynx, middle ear effusion is common. The tumor may extend anterosuperiorly into the pterygomaxillary and infratemporal fossa.

Clinical: SCCs of the palate manifest as ulcerative surface lesions. Often, patients are asymptomatic in the early stages, but they may experience pain in advanced stages. A palate mass, bleeding, a foul odor, ill-fitting dentures in edentulous patients, or loose teeth may be the presenting symptoms for patients with hard palate cancer. In persons with advanced-stage soft palate cancers, velopharyngeal insufficiency, altered speech, difficulty swallowing, referred otalgia, trismus, or a neck mass may be present. Because the area is easily visualized, tumors are often found at early stages incidentally by the patient or the physician.

On the other hand, minor salivary gland tumors manifest as submucosal lesions with a smooth, normal mucosal covering. Melanomas are smooth, black lesions but may be brown or brownish gray. Kaposi sarcomas are bluish lesions that are commonly seen in patients with HIV infection.

Treatment of T1-T2 SCC of the hard palate

Surgery is the preferred treatment for SCC of the hard palate. However, megavoltage radiation has also been used with some success as a viable alternative in treating patients with these tumors.

Small T1 and T2 lesions can be managed with either surgery or radiation therapy. Radiation therapy is given to a total dose of 60-70 Gy. The proximity of the tumor to the bone and potential complications of osteoradionecrosis make radiation therapy less desirable for managing these lesions. On the other hand, surgery for these lesions is simple, with low morbidity and no loss of function.

For tumors that do not involve the periosteum or bone, through-and-through excision of the palate, opening the sinonasal fossa, is not necessary. For these lesions, a simple transoral excision into and including the periosteum is sufficient. A 1-cm margin is taken with the tumor. The periosteum serves as the superior margin. The periosteum may be spared only in very superficial tumors that are not close to the periosteum. This is an intraoperative decision. With surgical management, the 5-year survival rates are 75% for stage I and 50% for stage II tumors.

In most cases, the defect from such lesions may be left open to heal by secondary intention and granulation. Skin grafting is discouraged. Consider placing a palatal acrylic prosthesis (healing plate), which can be fabricated by a dentist or prosthodontist prior to resection. This helps protect the palate wound during the healing process. In some cases, palatal and/or buccal mucosal flaps are necessary to restore tissue deficiency, especially when dealing with patients postradiation therapy and/or those with larger soft palate defects.

Treatment of the neck in T1-T2 SCC of the hard palate

Clinical and radiological N0 necks in these patients do not require elective treatment. When occult neck metastasis is suggested, staging functional neck dissection (including levels 1, 2, and 3) is performed.

Treatment of an N1 neck is controversial. A pathological N1 node is considered adequately treated with neck dissection alone when no extracapsular extension is present. However, in many centers, any pathological N1 node is treated with postoperative radiotherapy; this is recommended. Definitely initiate postoperative radiation therapy for patients with extracapsular extension.

If the pathological stage of the neck is N2 or higher, initiate postoperative radiotherapy.

Treatment of T3-T4 SCC of the hard palate

T3 and T4 lesions frequently require combined oncologic treatment, including surgery and radiation therapy to both the primary site and the neck. N1 necks may be treated with radiotherapy or neck dissection. Necks that are N2 or higher are treated with planned combined surgery and radiotherapy. Larger palatal cancers have a poor prognosis and require multimodality oncologic therapy. Radiation is given using high-voltage equipment to a total of 60-70 Gy.

Importantly, when planning surgery for lesions that extend beyond the hard palate, determine the deficit that will result from resection. Resection of the soft palate can cause significant velopharyngeal insufficiency. Because the soft palate is a dynamic structure, it is difficult to reconstruct. Lesions that invade the palatine bone require partial palatectomy, with resulting oroantral and oronasal fistula. Invasion into the nasal cavity or the maxillary sinus requires inferior maxillectomy, partial maxillectomy, or total maxillectomy, depending on the extent of the lesion. Prosthetic rehabilitation is highly effective in these patients.

Extension into the pterygopalatine and infratemporal fossa requires skull-base approaches to effectively extirpate the tumor.