Malignant Tumors of the Palate

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.

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.[2] 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 (see Staging).

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.

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, as depicted in the image below, 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.

Pseudoepitheliomatous hyperplasia and necrotizing sialometaplasia are benign self-limited lesions that can mimic SCC and need to be distinguished histologically. Torus palatina (ie, bony hyperplasia of the palate) are hard midline masses that produce no symptoms and should not be confused with tumors.

A study by Zhurakivska et al found that two of eight patients with necrotizing sialometaplasia of the minor salivary glands of the palate had associated tumors (pleomorphic adenoma and adenoid cystic carcinoma), indicating that previous reports may have underestimated the frequency with which such neoplasms occur in relation to the condition. The investigators also suggested that the obscurement of minor salivary gland tumors by necrotizing sialometaplasia may cause treatment delays.[3]

The palate separates the oral cavity from the nasal cavity and the maxillary sinuses. The mucosa of the palate is a keratinizing pseudostratified squamous epithelium. However, the submucosa has numerous minor salivary glands, especially in the hard palate. The periosteal covering of the hard palate becomes a relative barrier to the spread of cancer into the palatine bone.

The neurovascular supply to the palate comes from the palatine foramina, located medial to the third molar teeth. These foramina provide a pathway for the tumor to spread. Descending palatine arteries from the internal maxillary artery provide the blood supply. Vessels pass anteriorly through the nasopalatine foramen to the nose. Sensory and secretomotor fibers from the maxillary (V-II) branch of the trigeminal nerve and pterygopalatine ganglion traverse to the hard palate via the greater and lesser palatine nerves.

Anatomically, the soft palate is part of the oropharynx. It consists of mucosa on both surfaces. Intervening between the 2 mucosal surfaces are the connective tissue, muscle fibers, aponeurosis, numerous blood vessels, lymphatics, and minor salivary glands. Functionally, the soft palate serves to separate the oropharynx from the nasopharynx during swallowing and speech. The soft palate approximates with the posterior pharyngeal wall during swallowing to prevent nasopharyngeal regurgitation and approximates during speech to prevent air escape into the nose.

Contraindications to surgical correction of malignant palate tumors are based on the patient's comorbidities and his or her ability to tolerate surgery. Coexisting medical conditions may put the patient at risk during anesthesia. Additionally, tumors may be deemed inoperable because of their size or extent of involvement. Tumors that have intracranial extension are considered inoperable if they involve the brain parenchyma. Radiation therapy is a treatment option in these rare cases. See the Treatment section for recommended treatments for various types and stages of palate cancer.

Radiologic evaluation helps to increase the accuracy of staging. Computed tomography (CT) scanning and magnetic resonance imaging (MRI) are the imaging modalities of choice.

Perform CT scanning in axial and coronal planes. Coronal images, as seen in the image below, are best for assessing bony invasion of the palate and extension into the nasal fossa or maxillary sinus.

CT scanning aids in assessing skull-base extension. Enlargement of skull-base foramina is indicative of tumor invasion. Axial images aid in assessing extension in the horizontal plane along the soft palate, pterygoid plates and muscles, infratemporal fossa, and masticator space.

CT scanning with intravenous contrast infusion should include the neck to assess for cervical node involvement. This is especially important for SCC and high-grade mucoepidermoid carcinoma.

A study by Ju et al found through multivariate logistic analysis that among patients with palatal tumors and intact mucosa, older age and enlargement of the greater palatine foramen on CT scan independently predict that the tumors are adenoid cystic carcinomas.[4]

MRI, as seen in the images below, is more accurate for assessing perineural extension along the foramina. This is especially important in adenoid cystic carcinoma with the propensity for perineural invasion.

In advanced tumors with paranasal sinus involvement, MRI is superior to CT scanning in distinguishing inflammatory disease from a neoplasm.

For extensive lesions with intracranial involvement, MRI aids in assessing dural invasion.

A study by Zheng et al indicated that MRI can be used to differentiate benign from malignant palatal tumors, with partially defined or ill-defined margins and lack of a capsule, as well as older patient age, being indicative of malignancy. The investigators found their evaluation method to have a sensitivity and specificity of 92.8% and 85.6%, respectively, in determination of malignancy.[5]

Perform chest radiography to assess for pulmonary metastasis, a second primary site, or both.

A liver function test is adequate to assess for liver metastasis. Consider CT scanning of the abdomen and chest if distant metastasis is highly probable.

Biopsy of an ulcerative lesion may be easily obtained in the office transorally using biopsy forceps, with the patient under local anesthesia. Alternatively, fine-needle aspiration cytology studies may be performed if an experienced cytopathologist is available.

For ulcerative lesions, obtaining a biopsy specimen from closer to the edge of the tumor is important to avoid the necrotic central component.

In large, nonulcerated palatal lumps, an incision through the intact mucosa may be required prior to biopsy. Place the biopsy incision in a manner that allows for subsequent removal of the biopsy scar in continuity with the tumor.

Smaller submucosal lesions may be managed with excisional biopsy. If the pathology results indicate malignancy, further treatment is initiated.

Perform staging of the tumor according to the American Joint Committee on Cancer staging protocol because this is of critical importance to the patient's prognosis. Tumor and nodal status for oral cavity and oropharynx tumors are used for staging. Staging for cancer of the oropharynx and oral cavity, adapted from the 2002 American Joint Committee on Cancer, is as follows:

• Staging of primary tumor (T)

  • TX - Primary tumor not assessable

  • T0 - No evidence of primary tumor (T is carcinoma in situ.)

  • T1 - Tumor 2 cm or smaller in greatest dimension

  • T2 - Tumor larger than 2 cm but not larger than 4 cm in greatest dimension

  • T3 - Tumor larger than 4 cm in greatest dimension

  • T4 - Tumor invades adjacent structures (eg, through cortical bone, soft tissues of neck, deep [extrinsic] muscle of tongue)

• Staging of regional lymph nodes (N)

  • NX - Regional lymph nodes not assessable

  • N0 - No regional lymph node metastasis

  • N1 - Metastasis in a single ipsilateral lymph node, 3 cm or smaller in greatest dimension

  • N2 - Metastasis in a single ipsilateral lymph node, larger than 3 cm but not larger than 6 cm in greatest dimension; in multiple ipsilateral lymph nodes, none larger than 6 cm in greatest dimension; or in bilateral or contralateral lymph nodes, none larger than 6 cm in greatest dimension

  • N2a - Metastasis in a single ipsilateral lymph node larger than 3 cm but not larger than 6 cm in greatest dimension

  • N2b - Metastasis in multiple ipsilateral lymph nodes, none larger than 6 cm in greatest dimension

  • N2c - Metastasis in bilateral or contralateral lymph nodes, none larger than 6 cm in greatest dimension

  • N3 - Metastasis in a lymph node larger than 6 cm in greatest dimension

• Staging of distant metastasis (M)

  • MX - Presence of distant metastasis cannot be assessed

  • M0 - No distant metastasis

  • M1 - Distant metastasis

Examination under anesthesia

Approximately 10-15% of patients with head and neck squamous cell carcinoma (SCC) have a synchronous second primary cancer in the upper aerodigestive tract, lung, or esophagus. Patients with soft palate cancer have an even higher prevalence (approaching 25%) of synchronous and metachronous lesions. Hence, perform panendoscopy, including esophagoscopy, bronchoscopy, and laryngopharyngoscopy, on these patients. Alternatively, a complete flexible nasopharyngolaryngoscopy, chest radiography, and barium esophagography may suffice for synchronous tumor assessment.

The results of one study found that the use of panendoscopy may help identify synchronous second primary tumors in patients with a history of tobacco use but not in nonsmoking patients.[6]

Examination under anesthesia is required for tumor mapping in most patients with SCCs of the soft palate, except for those with very small lesions. Patients with small tumors confined to the soft palate, with all boundaries visible, do not require examination under anesthesia. In these patients, a complete flexible nasopharyngolaryngoscopy and transoral inspection and palpation are adequate for tumor mapping.

Treatment

Specific treatment of palate cancer depends on the location of the tumor (hard vs soft palate), stage of the tumor (see Staging), and pathologic type of the cancer. For this reason, management of SCC and carcinomas of minor salivary gland origin are discussed separately.

Treatment of T1-T2 squamous cell carcinoma 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.[7]

Treatment of the neck in T1-T2 squamous cell carcinoma 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. Recently, a 27% rate of occult cervical metastasis was reported in a series of 26 patients with maxillary alveolar ridge and hard palate squamous cell carcinoma. The authors thus suggest an elective neck dissection for such cancers with clinically N0 neck.[8] Other authors have suggested the use of sentinel lymph node biopsy in such situations.[9]

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

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

Treatment of T3-T4 squamous cell carcinoma 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.

A study by Givi et al indicated that in patients with SCC of the maxillary alveolus/hard palate who are clinically node negative (cN0), elective lymph neck dissection is linked to lower recurrence rates and improved survival. The neck recurrence rate was 6% in those study patients who underwent dissection and 21% in those who did not, with occult nodal metastases found in 29% of necks in the dissection group. (T3 and T4 tumors were more prevalent in the dissection group than in the nondissection patients [62% vs 34%, respectively].) Five-year recurrence-free survival was 68% in patients who underwent dissection versus 45% in the nondissection group, while overall survival was 86% vs 62%, respectively.[10]

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. However, use of vascularized free flaps, such as the scapular osteocutaneous flap or free fibula osteocutaneous flap, are highly effective in functional as well as aesthetic reconstruction and restoration of maxillary buttresses.[11, 12, 13]

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

Treatment of squamous cell carcinoma of the soft palate

Size, location, and contiguous spread of the primary tumor are important factors in the prognosis. Extension outside the palatine arch, especially to the base of the tongue, adversely affects patient survival. Patients with midline tumors and tumors that extend across the palatine arch have poorer survival rates. This is because of a higher incidence of regional metastasis. Absence of the soft palate results in velopharyngeal insufficiency, affecting both speech and swallowing.

Because of difficulties in adequate reconstruction, radiation therapy has been the recommended treatment for soft palate cancers in the past. Although advances in reconstructive techniques and prosthetic reconstruction have allowed for more effective surgical resection and rehabilitation for patients with soft palate cancers, radiation therapy remains the primary treatment modality in many centers for T1, T2, and T3 lesions, with results comparable with those of surgery.

Using radiotherapy as the primary treatment, control of the primary lesion is achieved in 80-90% of T1 lesions, 60-70% of T2 lesions, and 55-65% of T3 lesions. This rate drops to less than 50% for T4 lesions. Effective treatment for the primary lesion requires a dose of approximately 70 Gy.

Potential complications of radiotherapy include severe xerostomia, muscular fibrosis and resultant trismus, osteoradionecrosis of the mandible, and soft tissue ulceration. Complications of radiotherapy are volume dependent and dose dependent.

More recently, some centers prefer interstitial brachytherapy using iridium Ir 192 to boost the initial external beam of radiotherapy. The primary tumor is given 40-60 Gy of external beam radiation, followed by 20-40 Gy of brachytherapy. Boosting the primary tumor site to high doses allows improved locoregional control of the tumor, while reducing complications by avoiding wide-field, high-dose radiation.

Both radiotherapy and surgery are adequate for controlling early lesions. For advanced T3 and T4 lesions, traditional external beam radiotherapy alone is associated with poor survival rates. As a result, for advanced stage III and IV tumors, a planned combined treatment, including surgical resection followed by radiation therapy to the primary tumor and the neck, is the recommended treatment.

An alternative is the use of chemotherapy combined with radiotherapy, followed by surgical resection. Cisplatin and 5-fluorouracil are the chemotherapeutic agents used. Chemotherapy may be given in 2-3 cycles to assess the patient's response and to reevaluate. If the patient responds to chemotherapy, radiation is given for a full course of 70 Gy; surgery is reserved for salvage. Surgery is considered if the patient responds poorly to the chemotherapy.

Chemotherapy may be given concomitantly with radiotherapy, reserving surgery for salvage. Administration of 5-fluorouracil can be performed as an intravenous bolus or continuous infusion over 72-120 hours. Doses range from 800-1200 mg/m2. For cisplatin, the usual dose is 60-100 mg/m2 every 3 weeks. Accelerated fractionation radiotherapy has provided comparable disease-specific survival when compared with concomitant chemoradiation (cisplatin) for locally advanced oropharyngeal stage III and IVA/B cancers, while yielding a lower rate of long-term dependency on gastric-tube feeding. Standard fractionation (hypofractionation) radiation is inferior to both accelerated fractionation and to chemoradiation in this group.[14]

Combined external beam radiation followed by brachytherapy is an alternative to surgery for the management of advanced lesions, reserving surgery for salvage.

Brachytherapy for tumors with bony invasion or in proximity of the mandible results in a high rate of osteoradionecrosis. These patients are best treated with planned surgical excision followed by external beam radiotherapy, as are patients with tumor extension beyond the palatine arch into the base of the tongue.

Treatment of neck metastasis in soft palate squamous cell carcinoma

SCCs of the soft palate and uvula have a high rate of occult regional metastasis, as high as 20-30% at presentation, even in early primary tumors. Therefore, definitive treatment must encompass regional lymphatics in all SCCs of the soft palate. In midline lesions or in those that cross the midline, the rate of bilateral metastasis is high, requiring treatment of both necks.

Tumor thickness is an excellent predictor of nodal metastasis in soft palate cancers. In one study, all patients with tumors thicker than 3.12 mm had cervical metastasis, with tumor thickness correlating more directly with nodal metastasis than with T stage.

Clinical regional metastasis at presentation reduces the 5-year survival rate by half, from 80% in N0 necks to 40% in necks with clinically evident metastasis. For small tumors treated primarily with radiotherapy, N0 and N1 necks can be controlled adequately with radiotherapy alone. For N2 and greater neck metastasis, 74% of patients still have residual SCC following radiotherapy. Hence, treat N2 and greater regional metastasis with planned combined therapy, including neck dissection followed by radiotherapy.

Treatment of minor salivary gland cancers of the palate

Seventy-four percent of minor salivary gland tumors are malignant (see the histologic types and frequencies of minor salivary gland neoplasms of the palate in the Introduction section). The palate is the most common site for minor salivary gland carcinomas. Most of these occur in the hard palate. Minor salivary gland malignancies are divided into high- and low-grade tumors. High-grade tumors include adenoid cystic carcinoma, high-grade mucoepidermoid carcinoma, high-grade adenocarcinoma, malignant mixed tumor, and carcinoma ex pleomorphic adenoma. Low-grade malignancies include low-grade mucoepidermoid carcinoma, polymorphous low-grade adenocarcinoma (with its propensity to occur in the hard palate), acinic cell carcinoma, and other rare tumors.

The most important poor prognostic factors for malignant minor salivary gland tumors of the palate are grade 3 histology, tumor size larger than 3 cm, and positive margins.

Surgery is the mainstay of treatment for minor salivary gland tumors of the palate. For minor salivary gland tumors of the palate in which perineural invasion is suggested, identify and evaluate the greater palatine nerve by frozen section. If the nerve is involved, follow it with proximal resection until negative margins are attained. If negative margins cannot be attained at the foramen rotundum, postoperative radiation therapy must include the trigeminal ganglion.

Postoperative radiotherapy with or without chemotherapy is indicated for high-grade tumors, large T3 or T4 lesions, positive margins, tumors showing perineural invasion, and cervical lymph node metastasis.

Radiotherapy, possibly combined with chemotherapy, is used as the primary treatment if the patient refuses surgery or is not a candidate for surgery because of extensive unresectable disease.

Cervical node metastasis is a rare event for salivary gland tumors of the palate, occurring in approximately 3% of cases. Therefore, elective neck dissection is not indicated in these tumors in the absence of clinical or radiological signs of nodal metastasis.

For adenoid cystic carcinoma, surgery followed by radiation therapy is the treatment of choice. Wide surgical margins are taken because this tumor is known for microscopic extension beyond the gross tumor margins. The propensity for perineural extension requires resection along the greater palatine nerves with frozen section control to achieve negative margins. Postoperative radiation is preferred because preoperative radiation therapy increases surgical complications.

Transoral approach

The transoral approach, as seen in the image below, provides adequate exposure for superficial tumors of the hard palate that do not invade the bone. General anesthesia aids exposure and provides comfort for the patient. The patient is placed in a supine position with the head extended.

A Dingman or Crockard mouth gag provides attachable cheek retractors to facilitate exposure as depicted in the image below.

Alternatively, a hard rubber bite block or a Denhardt gag may be used to retract the mouth open for exposure. The lesion is mapped with an adequate margin of 1 cm. A soft tissue incision is made with a knife or electrocautery device. Electrocautery reduces blood loss. Alternatively, the carbon dioxide laser provides adequate hemostasis and causes less tissue damage. The incision includes the periosteum if it is to be taken as the superior margin. Using a periosteal elevator, the periosteum is elevated under direct vision, and the tumor is removed.

In cases in which the tumor involves the periosteum or the bone, the bone must be taken as the margin. This can be achieved using a cutting burr. If possible, preserve the superior mucoperiosteal coverage to prevent oronasal fistula, although this may be difficult. A prosthetic device is highly effective for swallowing and speech rehabilitation.

In cases in which the tumor is lateral and involves the alveolar ridge, a partial alveolectomy is included with palate resection. To improve exposure, a buccogingival sulcus incision is made to the level of the anterior maxillary wall. A facial degloving approach is used to improve exposure. The infraorbital nerve is preserved. An opening is made into the maxillary antrum to expose the superior surface of the palate. Following soft tissue incisions, bony cuts are made as needed using a Stryker saw, and the tumor is removed. Exposed soft tissue surfaces are covered with a split-thickness skin graft, except for closed cavities. Immediate prosthetic rehabilitation is performed with the aid of the prosthodontist who preoperatively prepared the temporary prosthetic device.

For extensive tumors of the hard palate involving the hard palate bilaterally, a total palatectomy and inferior bilateral maxillectomy is required. These resections leave the patient with extensive midfacial defects involving the palate, upper jaw, and sinuses. Flap and graft reconstruction of these defects is fraught with difficulty, often resulting in breakdown, which leads to oroantral or oronasal fistula. A total midfacial prosthetic rehabilitation is highly effective for restoring deglutition, speech, and facial contour and for making the postoperative surgical bed easier to monitor.

In cases of soft palate cancer, very small mucosal lesions may be resected transorally with preservation of the superior mucosa. If the defect is close to the hard palate, an advancement rotation flap from the hard palate may be used to close the defect. Small defects at the posterior margin of the soft palate may be closed by approximating the superior and inferior mucosa. The resulting velopharyngeal insufficiency corrects over time. A superiorly based pharyngeal flap may be used to close the defect.

Mandibulotomy

A mandibular approach provides wide exposure for resection of T4 soft palate cancers extending to the hard palate, lateral pharynx, tonsil, base of tongue, and/or mandible. A visor flap or lip-splitting neck incision may be used. A horizontal incision is made from the mastoid tip to the submentum. The lip is split with a stair-step cut along the vermilion to prevent lip notching, and a Z incision is carried over the mentum to join the submental incision. The periosteum is raised on either side of the incision. A parasymphysial stair-step osteotomy is made in a way that preserves the anterior muscular attachments of the mandible in the opposite side.

Once the position of the osteotomy is determined, mandibular miniplates are bent to adapt to the contour of the mandible for mandibular plating at the end. An incision is made in the floor of the mouth from the labiogingival sulcus to the anterior resection margin. The mylohyoid muscle is cut. This allows the mandible to swing open. Excellent exposure is provided to the entire soft palate and oropharynx.

If no mandibular bony invasion is noted based on preoperative imaging studies, the periosteum is raised as the margin. Relevant soft tissue cuts are made around the tumor, and it is removed. If invasion of the hard palate or the upper alveolus is noted, osteotomies are made using a Stryker saw following adequate soft tissue cuts. This exposure allows for an inferior maxillectomy. Give attention to assessing invasion of the medial pterygoid muscle, and, if invaded, take adequate deep margins. In irradiated patients or when a chance for composite resection of the mandible exists, a lateral mandibulotomy is preferred. The site of the cut varies depending on the exact extent of the tumor. A visor flap can be used, obviating the need for lip splitting.

Reconstruction of the palate

A basic hard palate prosthesis can be designed with extension into the oropharynx. When a posterior functioning band of soft palate is preserved, the obturator extension sits in the defect. During swallowing, the posterior band raises against the obturator. For total soft palate defects, the posterior extension of the obturator sits in the oropharynx anterior to the pharyngeal constrictor. During swallowing, the superior constrictor is raised against this static prosthesis to achieve velopharyngeal closure.

A study by Ye et al indicated that the buccal fat pad can be effectively used in immediate palate reconstruction after cancer surgery, even if the patient subsequently undergoes radiotherapy. The study involved 18 patients, with the buccal fat pad employed as a pedicled flap to reconstruct palate defects ranging from 7.5-19.2 cm2 and radiotherapy administered 4-5 weeks after surgery. The investigators reported that the flaps provided adequate defect closure, that epithelialization of all flaps occurred within 3 weeks postoperatively, and that no radiotherapy-related complications affected the flaps.[15]

For extensive defects of the soft palate and lateral pharyngeal wall with an exposed mandible, vascularized soft tissue reconstruction is mandatory. This is especially important for patients who are irradiated. The temporalis muscle or musculofascial flap is reliable and readily available for reconstruction. It allows complete reconstruction of the soft palate and provides coverage for the lateral pharyngeal defect and exposed mandible. It may be combined with a superiorly based pharyngeal flap for a double-layer closure of the palate. A dermal graft is used to cover the muscle if it is not covered by fascia.

Microvascular radial forearm fasciocutaneous free-flap reconstruction is another alternative for total soft palate reconstruction.

For excellent patient education resources, visit eMedicineHealth's Cancer Center. Also, see eMedicineHealth's patient education article Cancer of the Mouth and Throat.

Complications of surgical resection of the soft palate may include (1) velopharyngeal insufficiency (most common), (2) hypernasal speech, (3) dysphagia, and (4) middle ear effusion from scarring at the eustachian tube opening or loss of function of tensor and/or levator palatini muscles.

Obviously, the extent of and potential for these complications depend on the extent of resection, the size of the defect, and the method of reconstruction. The larger the resection and the defect, the greater the chance for these complications. The soft palate is a dynamic structure; optimal functioning requires muscular action to elevate and tense it during deglutition and relax it during nasal respiration. Therefore, any reconstruction of the soft palate with flaps and prosthetics does not reproduce its function; it will be limited in function in the best of circumstances.

Complications from hard palate resection depend on the extent of resection. For soft tissue resection with preservation of the bony palate and soft palate only, the resulting defect heals with granulation and epithelialization, and no complications are expected. If patients had previous radiation therapy to the area, healing may be delayed.

For more extensive resection that results in oroantral or oronasal defects, oronasal and oroantral fistulas may develop. Small defects may be closed with local flaps from the rest of the hard palate or from the buccal mucosa. Larger defects are managed adequately and effectively with obturators. Because the organ is not dynamic, obturators are very effective and well tolerated.

In the last 5 years, inclusion of quality of life (QOL) measures in the treatment decisions for head and neck cancer have become important. Oropharyngeal cancers that include the soft palate are an area of active clinical research, using QOL as an outcome measurement. With combined modalities of treatment including surgery and radiotherapy or chemoradiation, both being comparable in cure rates for advanced cancers, predicted QOL becomes an important consideration to help make treatment decisions.[16]

A retrospective study by Yang et al determined the 3- and 5-year survival rates for a cohort of 62 patients with SCC of the maxillary gingiva and hard palate to be 66.6% and 57.3%, respectively, with the survival rate found to be associated with tumor grade, T classification, margin status, cervical lymphatics, and local recurrence. The study also reported that in patients within this cohort, postoperative radiotherapy improved the prognosis in those with lesions located after the first premolar plane area.[17]

A study by Rapp et al found that in patients with SCC of the soft palate, survival rates were comparable for patients with stage I, II, or III disease who were treated with radiotherapy (either alone or in combination with adjuvant chemotherapy and/or neck dissection for residual disease). However, these rates were lower in patients with stage IV SCC. Five-year local control rates for patients with T1, T2, T3, or T4 SCC were 90%, 90%, 70%, and 59%, respectively. Five-year cause-specific survival rates for stage I, II, or III disease were 88%, 86%, and 88%, respectively, while the rate for stage IVA/B disease was 58%. Five-year overall survival rates for stage I, II, or III SCC were 50%, 57%, and 54%, respectively, compared with just 26% for stage IVA/B disease.[18]

A retrospective study by Trabrizi et al indicated that T stage, sex, and bony and perineural involvement, as well as close superior and posterior surgical margins (< 2mm), are associated with the recurrence of adenoid cystic carcinomas. However, neither age nor histopathologic type was found to be linked to recurrence.[19]

Elective treatment of the clinically negative neck in head and neck cancer versus observation and subsequent treatment of those who develop neck metastasis remains a subject of controversy. Recent retrospective data suggest that the rate of occult neck disease (pN1) in N0 patients receiving meticulous workup is low. Close observation with later treatment reserved for subsequent neck disease produces statistically similar survival rates to the elective prophylactic treatments and may be a valid form of treatment. Current literature, however, lacks clinical evidence to answer this question.