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A. Fry and L. Vassiliou
Segmental mandibulectomy is indicated in several
situations:
• Invasion of the mandibular marrow space
• Edentulous mandible with tumour xation on the alveolar
crest
• Edentulous, atrophic mandible with less than 1cm height.
• Tumours arising in a previously irradiated eld, in cases
of recurrent or metachronous disease. The route of tumour
spread in this situation is unpredictable because of aberrant lymphatic drainage.
If there are overt signs of mandibular involvement, then a
oor of mouth resection should be performed en bloc with
anterior mandibulectomy. Anterior mandibulectomy poses a
reconstructive challenge, as a composite microvascular free
ap will be required to restore the mandibular continuity, facilitate laryngeal suspension, and provide adequate soft tissue
cover and sealing to avoid oral-cervical or oral- cutaneous stula. In the case of an anterior segment mandibulectomy, a
reconstruction plate can be pre-plated before the resection, or
(now most commonly) pre-bent in the laboratory using a
three-dimensional CAD-CAM model and sterilised. This
technique can be even supplemented with 3D printed cutting
guides that t on the mandible and guide the exact position
and direction of the osteotomies and the drill holes for the xation of the reconstruction plate. These guides are paired with
cutting guides for raising the osseous microvascular free ap,
in order to achieve precise tting and accurate reconstruction.
To facilitate full function, including dental reconstruction,
dental implants may be placed on the osseous part of the
microvascular free ap at the time of the reconstruction.
In cases of extensive tumours with deeply invasive front
or involvement of the skin, dual ap reconstruction could be
required. A composite osseocutaneous ap is used to reconstruct the mandibular continuity and the skin defect, and a
bulkier myocutaneous ap from the latissimus dorsi, abdominal rectus, or anterolateral thigh (ALT) is used to reconstruct
the oor of the mouth and glossectomy.
Suggested Reading
Balasubramanian D, Thankappan K, Kuriakose MA, Duraisamy S,
Sharan R, Mathew J, etal. Reconstructive indications of simultane-
ous double free aps in the head and neck: a case series and litera-
ture review. Microsurgery. 2012;32(6):423–30.
Deleyiannis FW, Dunklebarger J, Lee E, Gastman B, Lai S, Ferris R,
et al. Reconstruction of the marginal mandibulectomy defect: an
update. Am J Otolaryngol. 2007;28(6):363–6.
Genden EM, Rinaldo A, Jacobson A, Shaha AR, Suárez C, Lowry J,
etal. Management of mandibular invasion: when is a marginal man-
dibulectomy appropriate? Oral Oncol. 2005;41(8):776–82.
Montero PH, Patel SG.Cancer of the oral cavity. Surg Oncol Clin N
Am. 2015;24(3):491–508.
Nammour S, Zeinoun T, Namour A, Vanheusden A, Vescovi
P.Evaluation of different laser-supported surgical protocols for the
treatment of oral leukoplakia: a long-term follow-up. Photomed
Laser Surg. 2017;35(11):629–38.
Shah J, Patel S, Singh B, Wong R.Jatin Shah’s head and neck surgery
and oncology. 5th ed. Philadelphia: Elsevier; 2019.
Excision ofPalatal Neoplasms
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AllisonA.Slijepcevic, DanielPetrisor, andMarkK.Wax
28
28.1 Introduction
The palate is an anatomic structure that is integral to normal
physiological functions of the upper aero digestive tract. It is
composed of two parts: the hard and soft palate, each with
their own unique anatomic characteristics. The hard palate
separates the oral cavity from the nasal cavity and maxillary
sinuses, while the soft palate separates the oropharynx from
the nasopharynx. The palate is involved in the physiologic
processes of eating, drinking, and articulation. Anatomically,
it is a relatively simple structure with a mucosal lining and
minor salivary glands. Bone is a component of the hard palate. Neoplasms affecting the palate can be divided into those
focused on either the hard palate or the soft palate. Treatment
of these lesions requires reconstruction, as defects in this
area have a signicant effect on deglutition and articulation.
Primary lesions in this area are relatively rare with the palate
usually involved by contiguous structures and pathology.
This chapter will discuss the anatomy and histopathology
of neoplasms affecting the hard and soft palate. The principles of surgical excision will be discussed. Methods of
reconstruction in order to rehabilitate the patient and obtain
good functional outcomes will be demonstrated. While obturators have been utilized for many decades, the ability to
obtain excellent functional outcomes with signicantly high
A. A. Slijepcevic
Department of Otolaryngology, Wake Forest University,
Winston Salem, NC, USA
e-mail: slijepcevica@wustl.edu
D. Petrisor
Department of Oral Maxillo Facial Surgery, Oregon Health and
Science University, Portland, OR, USA
e-mail: petrisord@ohsu.edu
M. K. Wax (*)
Department of Otolaryngology, Wake Forest University,
Winston Salem, NC, USA
Département Otolaryngology, OHSU,
Portland, USA
e-mail: waxm@ohsu.edu
quality of life using free tissue transfer and complete oraldental rehabilitation is now possible.
28.2 Anatomy andPhysiology
The hard and soft palate forms distinct subsites in the oral
cavity, which are relevant to the development of palatal neoplasms [1, 2]. The hard palate extends from the incisive foramen anteriorly, alveolar ridges laterally, and junction of the
hard and soft palate posteriorly [3]. The soft palate extends
from the junction of the hard and soft palate anteriorly, the
palatopharyngeal walls laterally, and uvula posteriorly.
Figure28.1 demonstrates the anatomy of the hard and soft
palate.
The hard palate provides a barrier between the oral cavity
and nasal cavity/maxillary sinuses, preventing reux of oral
contents into the sinonasal cavity. The hard palate is also
involved in articulation. Patients with hard palate stulas
secondary to neoplasm or post-surgical complications may
experience reux of food contents from the oral cavity into
the nose with air escape during speech, producing a whistling sound [4]. The soft palate has important functions during speech and deglutition. It provides a sphincteric function
with the posterior pharyngeal wall and assists in moving
food boluses from the oral cavity to the oropharynx. The soft
palate also prevents the production of hypernasal speech by
preventing air escape from the oral cavity to the nose [3].
The palate forms during the fth and sixth weeks of gestation from neural-crest cells and epithelium during embryogenesis. The anterior and posterior aspects of the palate are
formed separately. The anterior hard palate, along with the
upper lip, and teeth are formed from an intermaxillary segment, while the posterior palate is formed by palatal shelves
[5–8].
Mucosal lining of the hard and soft palate is formed from
keratinized stratied squamous epithelium, lamina propria,
and mucinous palatal glands [3, 9]. This unique histopathol-
© Springer Nature Switzerland AG 2024
R. Simo et al. (eds.), Atlas of Head and Neck Surgery, Springer Surgery Atlas Series,
https://doi.org/10.1007/978-3-031-36593-5_28
257
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Fig. 28.1 The anatomy of
the hard and soft palate.
Figure (a) shows the
boundaries of the hard palate
including the incisive foramen
anteriorly, the alveolar ridges
laterally, and the junction of
the hard and soft palate
posteriorly. Figure (b) shows
the soft palate, which extends
from the oral cavity at the
junction of the hard and soft
palate, to the uvula in the
oropharynx
A. A. Slijepcevic et al.
ogy predisposes the palate to a diverse range of malignancies
arising from both squamous cells and glandular pathologies
[1, 10, 11]. The minor salivary glands carry benign and
malignant tumour pathology similar to other salivary glands
[12, 13].
The anatomic tissues of the hard and soft palate are different for each subsite. The palatine processes of the maxillary
bone and horizontal plates of the palatine bones form the
underlying structure of the hard palate, and the oor of the
maxillary sinuses. The soft palate is comprised of ve muscles, including the tensor veli palatine, mucsulus uvulae,
levator veli palatine, palatopharyngeus, and palatoglossus
lump or an ulcer on the soft or hard palate. Primary tumours
of the hard and soft palate are relatively rare as the surface
area and structures are small compared to other anatomic
structures in the oral cavity and oropharynx [1, 18, 19]. More
commonly, these anatomic structures are affected by spread
from a contiguous structure, the soft palate from carcinomas
arising in the tonsil, and the hard palate from tumours arising
in the maxillary sinuses [20, 21].
Surgical excision of palatal neoplasms is well documented in the past since the primary treatment of tumours in
the oral cavity and oropharynx is by surgery [20, 22].
Transoral excision is the most common approach.
[3].
The vascular supplies to the hard and soft palate are
provided by the greater and lesser palatine artery, branches
of the descending palatine artery, a branch of the internal
28.4 Indications forPalatal Neoplasm
Excision
maxillary artery. These arteries travel to the palate through
the greater and lesser palatine foramen. Sensation is supplied to the palate by branches of the second division of
the trigeminal nerve, the greater and lesser palatine nerves
[3].
The lymphatic drainage of the palate ows to the cervical
lymph node basins, notably levels I and II [14, 15].
Lesions of the palate require surgical pathologic diagnosis,
usually with incisional biopsy. Benign lesions may bother
the patient from an appearance perspective or produce clinical symptomatology. The symptoms may be secondary to
issues with eating or speaking. Pain, bleeding, slurring and
problems with nutritional intake can all be secondary to
lesions on the soft or hard palate. Removal of the benign or
clinically bothersome lesions is relatively straightforward. It
28.3 History ofPalatal Neoplasm Excision
usually does not result in through and through defects and
thus structural integrity is maintained. Occasionally bony
Historically, surgery on the soft and hard palates was rst
described in the early 1800s. This was done primarily for
treatment of cleft lip and palate [16]. Plastic surgery was at
the forefront of technical and reconstructive developments to
correct this devastating issue in children [17]. Lesions in this
area cause symptoms early and most patients will detect a
growths that are benign may interfere with dental rehabilita-
tion and require removal. Any lesion on the hard palate
mucosa that is suspicious for malignancy should be biopsied.
The majority of hard palate lesions are managed with surgical
excision as the ability to obtain pathologically clear margins
and provide a single modality treatment is excellent [23].
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28.5 Neoplasms ofthePalate
The most common lesions of the hard palate are bony torus
palatini. Figure28.2 shows a torus palatine of the bony hard
palate. These are osseous exophytic lesions of the hard palate
[24]. Between the periosteum and the mucosa is a thin subcutaneous layer that contains numerous small minor salivary
glands [25].
Any benign or premalignant lesion that can affect the
mucosa of the oral cavity or oropharynx can present on the
mucosa of the soft or hard palate. Malignant lesions are most
often squamous cell carcinoma [26]. The most common
benign salivary gland tumour is the pleomorphic adenoma
[27]. As expected the majority of minor salivary gland
tumours are malignant [28]. Minor salivary gland tumours
have an afnity for the posterior hard palate and soft palate
due to the distribution of salivary tissues in these areas [29].
They mostly occur as well-circumscribed dome-shaped
smooth surfaced non-movable swellings [12]. Pain and
ulceration are rare and usually seen in the adenocarcinomas
[30].
28.5.1 Benign Neoplasms ofthePalate
Benign neoplasms of the hard and soft palate encompass
varying pathologies of the oral cavity mucosa and underlying bone. Pathologies include inammatory and autoimmune disorders, infectious lesions, cysts, and premalignant
lesions. Recognizing benign palate pathology may guide
practitioners in the clinical work-up and treatment of palatal
lesions, allowing differentiation of lesions that require biopsy
and possible resection.
Autoimmune disorders affect the mucosa of the palate,
causing mucosal lesions which often require biopsy to deter-
Fig. 28.2 A torus palatine of the hard palate, which is a benign exostosis of the hard palate bone that may require excision to t palatal prostheses and dentures
mine the underlying aetiology of the lesion and to rule out
the presence of malignancy. Pemphigus vulgaris is an autoimmune condition associated with auto-antibodies which
attacks desmin in the mucosa. The oral lesions of pemphigus
appear blistering and ulcerative, and treatment includes systemic immunosuppression [31, 32]. A related condition, bullous pemphigoid or mucous membrane pemphigoid, is an
autoimmune condition which causes subepidermal blistering
of the oral mucosa from antibody deposition in the mucosal
basement membrane. Similar to pemphigus vulgaris, treatment consists of immunosuppressive therapy [32, 33].
Lichen planus causes reticulated, lace-like lesions of the oral
mucosa, which may be related to a genetic predisposition,
trauma, hepatitis C, and graft-versus host disease [34, 35].
Treatment of oral lichen planus with topical and systemic
immunotherapy is necessary to limit the chronic inammatory lesions produced by the disease, which are associated
with development of malignancy [33, 36]. Erythema multiforme is an inammatory mucosal condition that causes target and bullous lesions associated with delayed medication
reactions and viruses. The lesions may cause diffuse epidermyl necrolysis, which require systemic treatment with
immunosuppressive agents and cessation of the offending
drug [32, 37].
Reactive lesions may appear similar to autoimmunerelated mucosal lesions; however, their aetiology is related to
chronic inammation and trauma. Aphthous ulcers are common lesions of the hard and soft palate, and may be idiopathic or related to local trauma, while recurrent aphthous
ulcers are associated with medications including NSAIDs
and systemic conditions including Crohn’s disease and
Bechet’s. Lesions are most often small mucosal ulcerations,
and treatment is limited to analgesics and mouthwashes [32,
38]. Necrotizing sialometaplasia is a benign necrotizing dis-
order of the minor salivary glands, which causes lesions that
resemble malignancy [39]. The lesions are submucosal and
appear raised and edematous. Biopsy may shows necrotizing
minor salivary tissue with no dysplasia [39, 40]. Pyogenic
granuloma is a benign, reactive lesion of the gingiva formed
with pathology consistent with capillary haemangioma. The
lesions are maxillary gingiva, and are associated with pregnancy. The granulomas appear as lobulated and polypoid,
and treatment includes excision or observation with involution [34, 41].
Torus palatinus are benign bone exostosis of the hard palate that occur at the midline lateral aspect of the hard palate.
They consist of cortical bone and are covered by thin mucosa.
Tori have a congenital and genetic association, and may
require removal for tting of dental prosthetics [24, 25, 42,
43].
Infection-related lesions of the palate include viral and
fungal pathologies. Herpes simplex virus, most commonly
HSV-1, may cause limited stomal ulcers to fulminant acute
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A. A. Slijepcevic et al.
herpetic gingivostomatitis. Herpetic gingivostomatitis manifests as raised red lesions, which ulcerate with brinous exudate [44]. Treatment includes oral acyclovir [45]. Oral
papillomas, or condyloma acuminatum, are benign epithelial
tumours caused by human papillomavirus (HPV) strains 6
and 11, which are considered low risk for malignant transformation [9, 46]. Oral condylomas caused by HPV are sexually transmitted. Treatment includes surgical excision with
cold instrumentation or lasers [47]. Oral candida, or thrush,
affects adults with underlying oral pathologies related to
immunocompromise, autoimmune disease, a history of
radiation therapy, xerostomia, denture use, and antibiotic use
[48–50]. Supercial thrush lesions appear white and are easily removed from underlying mucosa, which may appear
erythematous. Treatment includes topical antifungals [50].
Benign tumours of the minor salivary glands may be identied on the hard palate as non-tender areas of mucosal
swelling [12]. The most common benign minor salivary
gland tumours include pleomorphic adenoma and myoepithelioma [12, 51]. Pleomorphic adenomas of the minor salivary glands may appear as palatal ulcerations. Pathology
shows mixed myoepithelial and salivary ductal elements
which may inltrate local tissues with pseudopodia [52].
Myoepithelioma tumours may occur on the hard or soft palate. Masses may present as nodular palate lesions of the submucosa [53, 54]. Treatment of pleomorphic adenoma and
myoepithelioma consists of wide local excision [51].
Figure 28.3 shows a large mucoepidermoid tumour
originating from a minor salivary gland of the hard palate.
Odontogenic pathology may affect the hard and soft palate. Amalgam tattoos are dark lesions on the oral mucosa
caused by pigment deposition from prior dental work.
Odontogenic cysts may present as palatal lesions. Dental
cysts can be categorized as developmental, inammatory, or
cystic neoplasms. Dentigerous cysts are asymptomatic,
developmental cysts associated with unerupted and impacted
third molars. These cysts appear as unilocular radiolucent
cysts surrounding the crowns of maxillary canines [55–57].
Dentigerous cysts carry a risk of transformation to ameloblastoma [57]. Treatment includes dental extraction and cyst
enucleation. Care should be taken to avoid creating a stula
to the maxillary sinus during cyst enucleation [55].
Nasopalatine duct cysts, also known as median palatine
cyst or incisive canal cysts, are cysts located in the anterior
maxilla near the incisors, just posterior to the incisive papilla.
The result from failed resorption of the fetal nasopalatine
duct, and may proliferate to a cystic lesion [58, 59]. Cysts are
associated with infectious complications, and may be enucleated [59].
28.5.2 Premalignant andMalignant
Neoplasms ofthePalate
Premalignant mucosal lesions of the palate include leukoplakia and erythroplakia. Leukoplakia is a benign lesion of the
oral mucosa, with a white, plaque appearance and irregular
borders [60]. Development of leukoplakia is associated with
cigarette smoking, alcohol consumption, and areca nut [60,
61]. Pathology may show dysplastic changes with hyperker-
atosis, parakeratosis with dysplasia, or epithelial carcinoma
[61]. The risk of malignant transformation is broad, ranging
from less than 1% to 30%. Higher risk of transformation is
associated with alcohol use, heterogeneous lesions, and
pathology with high-risk dysplasia [62–65]. Treatment of
leukoplakia includes observation for new lesions associated
with trauma, excisional biopsy, and laser ablation [60, 66].
Erythroplakia is an erythematous plaque-like lesion of the
oral mucosa, and is associated with a higher risk of malignant transformation than leukoplakia [67, 68]. Lesions frequently involve the soft palate, and may appear atrophic [67,
69]. Similarly to leukoplakia, erythroplakia is associated
with smoking, alcohol, and betel nut use. Pathology may
show epithelial dysplasia, carcinoma in situ, or invasive carcinoma [67]. The rate of malignant transformation of erythroplakia with known carcinoma in situ ranges from 14% to
50% [67, 70–76]. Erythroplakia is treated by surgical excision [67–69].
Common malignant lesions of the palate mucosa include
squamous cell carcinoma and melanoma. Squamous cell car-
Fig. 28.3 A mucoepidermoid
tumour of the hard palate.
Figure (a) shows a CT scan of
the tumour that erodes
through the horizontal bony
processes of the maxillary and
palatine bones. Figure (b)
shows protrusion of the right
hard palate caused by the
exophytic tumour
ab
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261
cinoma is found on both the hard and soft palate. Lesions are
often noted in males in the sixth decade, and are associated
with smoking and alcohol use [1, 77, 78]. Soft palate lesions
develop from leukoplakia and erythroplakia, and carry a
poor prognosis related to high rate of locoregional relapse
with over 50% reported cancer related deaths [78, 79]. Hard
palate lesions are also associated with aggressive features
and tendency to spread to the cervical lymph nodes, with a
20% rate of occult cervical metastases associated with higher
stage lesions [2, 80]. Pathology shows ulcerated and necrotic
lesions with dysplastic keratinocytes [81, 82].
Treatment of palatal squamous cell carcinoma is based on
tumour stage. Lower stage tumours may be treated with surgery or radiation, while advanced stage tumours require multimodal therapy including neck dissection [1, 2, 80]. Oral
cavity mucosal melanoma occurs most frequently on the palate, and can appear as a darkly pigmented irregular lesion
[10, 83]. The disease has a male predominance occurring in
the sixth decade [10, 18]. Pathology may show epithelial
hyperplasia with nests of dysplastic melanocytes [83].
Treatment focuses on surgical excision of lesions followed
by post-operative radiation [18].
Minor salivary glands of the oral cavity have a much
higher risk of malignant pathology than larger glands in the
head and neck. The most common minor salivary gland
malignancy is mucoepidermoid carcinoma [11]. Adenoid
cystic carcinoma and polymorphous low-grade adenocarcinoma are also common in the minor salivary glands [84].
Mucoepidermoid carcinoma may affect both the hard and
soft palate, and inltrate into the paranasal sinus cavities and
adjacent oral cavity subsites [85]. Tumour pathology shows
heterogenous submucosal lesions of the minor salivary
glands composed of cystic structures with mucous producing
cells and strands of squamous cells [86]. Surgical excision is
the primary treatment of mucoepidermoid carcinoma,
although radiation therapy may be used for locoregional disease control and inoperable tumours [85, 87, 88]. Adenoid
cystic carcinoma is a highly inltrative tumour that may
invade local nerves and into the sinus cavities [52]. Treatment
includes tumour resection and post-operative radiation [86].
Polypmorphous low-grade adenocarcinoma is an indolent,
slow-growing tumour of the palatal minor salivary glands
[52]. While tumours demonstrate an inltrative behaviour
with tendency to recur, surgical excision alone is the
recommended treatment [89].
lesions are treated with surgical techniques that spare surrounding tissue and underlying anatomic structures [90]. The
morbidity of surgical excision of a benign lesion is
minimal.
Excision of malignant tumours entails the same surgical
principles that one uses for any mucosal cancer, complete
excision of the tumour with a wide margin [23, 91]. The
issue with hard palate lesions is the periosteum and bone.
Small supercial tumours can be removed by peeling the
periosteum from the hard palate. This simplies reconstruction, as mucosal granulation will lead to complete healing
[92]. Minor salivary gland tumours arising in the submucosa
or more extensive squamous cell tumours will attach to the
bone of the hard palate. This necessitates a through and
through resection of the hard palate bone and overlying sinus
or nasal mucosa. Figure28.4 shows a full-thickness defect of
the hard palate following excision of a malignant palate
lesion. Rehabilitation should be by either a prosthesis or surgically due to the signicant morbidity of the oro-nasal stula [93–95].
Soft palate tumours require a wide surgical margin. The
thinness of the soft palate means anything other than a small
lesions will involve a through and through defect of the soft
palate. Rehabilitation by reconstruction is required to separate the nasopharynx from the oropharynx.
In the majority of primary palate neoplasms surgical excision should be a single modality treatment with a high cure
rate [23]. Tumours that extend beyond the palate extend into
the hard palate or have perineural invasion will require combined modality treatment [96, 97].
28.6 Principles ofPalatal Neoplasm
Excision
Surgical approaches must take into account the underlying/
adjacent structures to assess what the defect will be and the
potential need for rehabilitative reconstruction. Benign
Fig. 28.4 Full-thickness defect of the hard palate following resection
of a malignant neoplasm. Through-and-through defects create stulas
between the oral and nasal cavity, which require reconstruction with
prostheses or surgery with local and free tissue aps
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28.7 Surgical Approaches forHard
andSoft Palate Neoplasm Resection
The excision of oral cavity neoplasms ranges from limited
transoral approaches to robotic technology for more extensive lesions. While early palatal lesions may remain conned
to the oral cavity, aggressive lesions may spread into the
maxillary sinus, oropharynx, and the pterygopalatine fossa.
28.7.1 Transoral Resection
Transoral surgery can be used to excise small lesions of the
hard and soft palate. Access to lesions of the hard and soft
palate includes use of a bite block and Crowe-Davis retractor
to approach the oral cavity, this allows for full oral opening
and exposure of the palate from the incisive foramen to the
uvula.
Tumour excision using a transoral approach and CO2
laser has been described to fully resect limited lesions amenable to primary closure [23, 91]. TLM is associated with
low complication rates and short in-patient stays [23]. While
patients undergoing TLM resection may experience speech
and swallowing difculty following surgery, the overall morbidity is low [98].
28.7.2 Resection ofPalatal Neoplasms
Involving theSoft Palate
andOropharynx
Malignant neoplasms of the soft palate may extend to oropharyngeal structures: tonsillar fossae and parapharyngeal
space [78, 99, 100]. The extension of soft palate tumours into
the oropharyngeal spaces requires advanced excision techniques for tumour clearance and preservation of speech and
swallowing function.
Transoral robotic surgery (TORS) can be used to access
tumours extending to the lateral pharyngeal wall, which
involve musculature of the soft palate (palatglossal and palatopharyngeal muscles) [20]. TORS provides a minimally
invasive approach for tumour resection surrounding important neurovascular structures, and is associated with minor
complications including post-operative haemorrhage and
dysphagia [20, 22, 84]. TORS has been used to specically
resect minor salivary gland tumours of the soft palate and
oropharynx with effective tumour clearance [101].
Figure28.5 shows the operative suite arrangement required
for TORS resection of palatal neoplasms.
Key anatomic structures encountered during TORS excision of palatal lesions with lateral pharyngeal wall extension
A. A. Slijepcevic et al.
Fig. 28.5 The surgical approach required for transoral robotic surgery
(TORS) resection of palate neoplasms. The robotic system has multiple
arms used for surgical instrumentation of the oropharynx, including
cautery and cold-steel instruments. A surgical assistant at the patient’s
head provides frequent suctioning of the surgical site and removal of
free tissue specimens, while the surgeon controls the robot arms
remotely while performing the procedure
includes the muscles of the palate, the palatopharyngeus and
palatoglossus muscle, and the tonsillar fossae. Reconstruction
of the palate and lateral pharyngeal wall defects may require
local or free ap reconstruction to preserve speech and swallowing and protect underlying vasculature.
28.7.3 Resection ofPalatal Neoplasms
Involving theMaxillary Sinus
Neoplasms involving the hard palate may cause erosion
through the bony hard palate with invasion into the maxillary
sinus [102, 103]. Excision of these lesions requires resection
of the hard palate tissues and some form of maxillectomy
[103]. Various approaches may be taken: transoral, transfacial, or endoscopic.
A range of resections are possible through a transoral
approach including small lesions of the alveolus, partial or
complete palatectomy, and maxillectomy [104, 105].
Extensive palatectomy procedures that include hemimaxillectomies may be facilitated using a combined tran-
ab
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Fig. 28.6 The resection of a
hemi-maxillectomy specimen
using a LeFort I osteotomy
approach. Figure (a) shows
the resection specimen that
includes the entire hard palate
and bilateral medial maxillary
walls. Figure (b) shows the
resection site with exposure
of the bilateral nasal cavities
and maxillary sinuses
263
soral and endonasal endoscopic resection approach. While a
transoral approach allows for palatectomy, endoscopic endonasal maxillectomy may be needed to fully visualize the
28.7.4 Resection ofPalatal Neoplasms
Involving theMaxillary Sinus Using
Transfacial Approaches
maxillary sinus cavity, and facilitate tumour clearance [96].
Using this approach, intraoral dissection of the hard palate
with osteotomies and cautery of the soft palate musculature
may be completed, while endoscopic medial maxillectomy
provides a large antrostomy to access tumour in the oor of
the maxillary sinus [97]. Figure 28.6 shows a hemimaxillectomy defect made with a LeFort I osteotomy to
resect a lrage hard palate malignancy that involved the maxillary sinuses.
Aggressive palatal lesions that involve the maxillary sinus
may extend to the pterygopalatine or infratemporal fossae
[106–108]. Combined transoral and endoscopic approaches
can be used to a complete subtotal maxillectomy and access
these tumours. Lesions invading the pterygopalatine and
infratemporal fossae may be accessed through completion of
a medial maxillectomy, and dissection of the posterior max-
Transfacial approaches for tumours that involve the maxillary sinus are less commonly used in current practice, as
minimally invasive endoscopic techniques are favoured.
Several transfacial approaches are available for resection of
palatal tumours with maxillary sinus extension if endoscopic
approaches cannot be completed. The Weber Ferguson
approach is a transfacial approach that requires external
facial incisions beneath the lower eyelid, along the lateral
nasal wall, and through the columella and upper lip through
a lip-split incision. The approach allows access to the entire
maxillary sinus; however, the approach is associated with
lower lid ectropion and skin scarring [113, 114]. Intranasal
incisions, including full septal transxion and intercartilaginous incisions, and an upper sublabial incision, are used to
access the midface bony skeleton [114, 115].
illary wall which houses the sphenopalatine artery just
beneath the ethmoidal crest. Once the medial maxillary wall
is fully resection, the bone posterior maxillary may be
removed to access the soft tissues of the both fossae [107].
28.8 Reconstruction oftheHard andSoft
Palate
Key anatomic structures in the pterygopalatine fossa include
the maxillary artery and nerve, sphenopalatine ganglion, and
the vidian nerve [109, 110]. The major structures of the
infratemporal fossa are more extensive, and include the muscles of mastication, including the pterygoid and temporalis
muscles, and the third division of the trigeminal nerve.
Structures of the infratemporal fossa near the soft palate
include tensor veli palatine and levator veli palatine, and the
Eustachian tube [110].
Palate reconstruction requires a range of reconstructive
options depending on the extent of tissue loss. Lesions with
limited tissue loss may be repaired with primary closure.
Various local tissue aps can reconstruct hard and soft palate
tissue defects to prevent oronasal stulas, and restore the
function of the soft palate for speech and swallowing. Full
palatal defects with associated maxillary sinus resections
may require free ap tissue reconstruction.
Extensive tumours of the soft palate may invade the lateral oropharyngeal wall to involve the parapharyngeal space
[111]. Multiple surgical approaches have been described
28.8.1 Local Tissue Reconstruction
given the location of tumours in the parapharyngeal space,
including the endoscopic transmaxillary, transoraltranspharyngeal, and transcervical approaches [112].
The goal of hard and soft palate reconstruction includes prevention of oronasal stulas, which occur most frequently at
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the junction of the hard and soft palate. Adequate tissue is
needed to prevent tension, which predisposes tissues to stula formation. Soft palate repair focuses on preventing velopharyngeal insufciency, which is associated with nasal
regurgitation of food boluses and hypernasal speech [116,
117].
Small full-thickness palate defects can be repaired with
local tissue rotational aps. A posteriorly based U-shaped
ap can be designed to transpose intact hard palate mucosa
to cover small full-thickness palatal defects, while donor site
bone and mucopereosteum granulate. Full-thickness midline
palatal defects may be repaired using mucoperiosteal
bipedicle aps that are elevated from the lateral palatal walls
and advanced to cover the midline defect. The associated lateral donor sites are left open to granulate [92].
Soft palate defects have a broad range of reconstructive
options. For soft palate lesions, the hard palate can be used to
create a palatal island ap. Figure28.7 shows a palatal island
ap used to reconstruct a soft palate defect. This axial rotation ap is based on the greater palatine artery. The mucoperiosteum of the hard palate is elevated and rotated on a
posterolateral axis to reconstruct the uvula [118]. For larger
soft palate defects, the paraspinal musculature including the
longus capitis muscle, may be used as a pedicled rotational
ap [119]. The reconstruction of subtotal soft palate defects
using a layered approach with rotational aps from the superior pharyngeal and palatoglossal muscles has also been
described [120, 121].
Large hard and soft palate defects with associated maxillectomy sites may be repaired using buccal advancement
aps. Most buccal aps require simple elevation of the tissue
bordering the palate defect, undermining of the buccal
mucosa, and advancement for defect closure [92, 122]. When
reconstruction is focused on preventing velopharyngeal
incompetence, musculature of the oral cavity can be used to
restore palate function.
The buccinator myomucosal ap may be used to reconstruct both hard and soft palate defects. The ap is based
on the facial artery and the buccinator branch of the maxillary artery, and can be anteriorly or posteriorly based. The
posteriorly based ap contains a neurovascular bundle
containing the buccinator muscle, artery, and nerves,
which is advantageous when restoring the function of the
soft palate. The anteriorly based ap is an axial artery
based ap which can be used to reconstruct the hard palate
[123, 124]. A similar ap, the facial artery musculomucosal ap (FAMM) ap, is an axial ap based on the facial
artery. Figure28.8 shows the design of a FAMM ap. The
ap contains buccal mucosa, submucosal tissue, and a portion of the buccinators muscle, along with the facial artery
for blood supply. The ap may be inferiorly based to allow
transposition and advancement to the soft palate defect
[125, 126].
While there is a broad range of local intraoral mucosal
aps for palatal reconstruction, the temporalis myofascial
ap serves as an alternative palatal reconstructive method to
reconstruct unilateral and bilateral palate defects [93]. The
ap is based on the deep temporal vasculature. Reconstruction
with this ap requires a pre-auricular, hemi-coronal scalp
incision to access the deep temporal fascia and zygomatic
arch; dissection in this plane protects the frontal branch of
the facial nerve which lies supercially. The temporalis mus-
Fig. 28.7 A palatal island
ap used for soft palate
reconstruction following
resection of a mucosal
malignancy. Figure (a) shows
the mucoperiosteum of the
hard palate being elevated and
rotated on the axis of the
ap’s blood supply, the
greater palatine artery. Figure
(b) shows the ap being used
to reconstruct a lateral
oropharyngeal wall defect.
The hard palate donor site
heals by secondary intention
a
b
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cle is identied and rotated beneath the zygomatic arch to
reach palatal defect in the oral cavity [127, 128].
28.8.2 Free Flap Reconstruction ofLarge
Palatal Defects
Hemi-palate and complete palate defects require free ap
reconstruction to replace extensive tissue loss. Depending on
patients’ preference for dental restoration, osteocutaneous
aps may be used for dental implant placement [129].
Hard and soft palate defects requiring soft tissue coverage
may be reconstructed with fasciocutaneous free aps. The
radial forearm has been used to repair soft palate defects, and
provides supple tissue to repair oropharyngeal defects. The
fasciocutaneous portion of the free ap may be modied to
t the unique shape of palatal defects to optimize repairs
[130]. Ulnar forearm free ap is an alternative to the radial
forearm free ap for soft palate reconstruction for patients
Fig. 28.8 A facial artery musculomucosal ap (FAMM) ap. This
superiorly based ap is pedicled on the facial artery. When elevated, the
ap will contain buccal mucosa, subcutaneous tissue, and the buccinator muscle, which are transposed to reconstruct the palate defect
with a hand donor site that is dependent on the radial artery
for perfusion [131, 132]. Figure 28.9 shows a soft palate
defect reconstructed with a fasciocutaneous radial forearm
free ap.
The anterolateral thigh (ALT) may be used to reconstruct
extensive and complex palate defects. The ap is based on
the descending branch of the lateral circumex femoral
artery, and offers a long vascular pedicle and abundant soft
tissue to repair full palate defects [133, 134]. The ALT free
ap has been used to repair palatal stulas to full defects of
the soft palate with improvement of velopharyngeal insufciency [94, 134].
Hard palate defects, involving the alveolar ridge, dentition, and maxillary sinus, require bone and soft tissue reconstruction to rehabilitate the facial and oral cavity contours,
and allow for dental restoration. The hard palate and maxillary oor may be reconstructed with an osteocutaneous ap.
The osteocutaneous radial forearm free ap may be used to
reconstruct hemi-defects of the hard palate that involve the
alveolar ridge. The radial bone of the free ap may be inset
into the palate along abutting alveolar bone, and secured
with plating. The oral mucosal defect is closed with the
cutaneous forearm skin [135].
The bula free ap may be used as a composite tissue
graft with bone and cutaneous tissue to reconstruct hard palate and alveolar ridge defects [95]. The ap is vascularized
by the peroneal artery and vein, which course posteriorly to
the bula bone and deep to the exor halluces longus muscle
during ap dissection. The ap pedicle provides perforator
vessels through an intermuscular septum to overlying skin
[136]. The goal of bula ap reconstruction of palate and
maxillary defects is to restore separation of the oronasal cavities, and allow for mastication as the bula bone is durable
enough to support dental implantation [129, 137].
Figure 28.10 shows a hard palate defect extending to the
bilateral maxillary sinuses that was reconstructed with a bula free ap, dental implants, and dentures. Patients with
Fig. 28.9 The reconstruction of a soft palate defect using a fasciocutaneous radial forearm free ap. Figure (a) shows the soft palate defect
extending to the junction of the hard and soft palate to the oropharyngeal walls. Figure (b) shows the radial forearm ap reconstruction of
a b
the soft palate. Free ap reconstruction treats velopharyngeal insufciency that is associated with hypernasal speech and nasal regurgitation
of food boluses. The ap also provides vascularized tissue coverage of
the neurovascular structures deep to the oropharyngeal walls
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