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CHAPTER

45Nonodontogenic Tumors
Benign Tumors of the Jaws
Christopher M. Harris1 and Robert M. Laughlin2
1
Department of Oral and Maxillofacial Surgery, Naval Medical Center Portsmouth, Portsmouth, Virginia, USA
2Department of Oral and Maxillofacial Surgery, Naval Medical Center San Diego, San Diego, California, USA

radiopaque structures within the lesion (later). The


lesions can be well defined or poorly defined. The lesions
Nonodontogenic tumors include connectivetissue often have a radiolucent rim associated with them. Teeth
tumors, vascular lesions, reactive lesions, and neurogenic may be displaced, and/or resorption of roots may be
tumors. The clinical presentation and treatment of these seen.Histologically, the osteoblastoma is similar to the
lesions vary. This section will describe the general classifi- osteoid osteoma. These are differentiated mainly by clin-
cation of common nonodontogenic tumors and highlight ical features and size. Osteoblastomas demonstrate oste-
standard treatments. All lesions should be treated individ- oid tissue and interconnected trabeculae of woven bone.
ually based on their unique histopathology, aggressive- These trabeculae are surrounded by a single layer of
ness, and clinical and radiographic presentation. Please osteoblasts referred to as osteoblastic rimming. A fibro-
refer to Appendix 3 for further treatment guidelines. vascular stroma and osteoclasts are also seen. Aggres-
sive osteoblastomas and lowgrade osteosarcomas can
Tumors of Connective Tissue look similar histologically. Treatment of osteoblastomas
Osteomas is with excision or aggressive curettage. Recurrence is
uncommon with appropriate treatment. Recurrence is
Osteomas are benign tumors of bone. They are commonly
believed to arise from incomplete removal rather than
found within the skull, jaws, and sinuses. Osteomas are
inherent properties of the lesion. Aggressive osteoblasto-
composed of cortical and cancellous bone in varying pro-
mas, however, have been reported to have higher recur-
portions. These lesions typically present as an asympto-
rence rates and often require resection with definitive
matic mass, which can produce asymmetry of the jaw
margins.
bones. Radiographically, these lesions appear as dense
radiopaque projections of bone. Gardners syndrome Chondromas
should be suspected in patients presenting with multiple Chondromas are benign cartilaginous lesions of the
osteomas. Gardners syndrome is associated with multiple jaws. They may occur centrally or peripherally. They
osteomas, polyps of the large intestine, multiple epider- are exceedingly rare in the head and neck. They are
mal skin cysts, and multiple impacted teeth. The colon thought to arise in areas where embryonic cartilaginous
polyps in Gardners syndrome are considered premalig- cell rests are present. Therefore, the condyle, coronoid
nant, and a referral to a colon and rectal surgeon is rec- process, base of skull, and anterior maxilla are com-
ommended due to the certain malignant transformation monly involved sites. Radiographically, chondromas are
of these lesions. Treatment is with tumor excision. Recur- welldemarcated radiolucencies. Local bone destruction
rence is rare. should raise suspicion for malignancy. Chondromas have
Osteoblastomas a peak incidence within the third and fourth decades
of life and demonstrate an equal sex predilection. His-
Osteoblastomas are rare, benign tumors of bone. They
tologically, they demonstrate mature hyaline cartilage.
commonly occur in the long bones and spinal column.
Treatment should be directed at total tumor excision due
They have a peak incidence within the third to fourth
to the similarities of lowgrade chondrosarcomas histo-
decades of life and occur more frequently in males. The
logically.
mandible is the most commonly affected craniofacial
bone. Osteoblastomas may be asymptomatic and found Vascular and Reactive Lesions
on routine exam. However, localized pain and swelling
are commonly seen. Pain is unique in that in many cases Central Giant Cell Granulomas (CGCGs)
it is relieved by aspirin. Radiographically, the osteoblas- CGCGs are generally accepted to be nonneoplastic enti-
toma can resemble other benign and malignant tumors. ties that behave like neoplasms. Whether these lesions are
Osteoblastomas are typically radiolucent (early) with inflammatory, reactive, or true neoplasms is still debated.

Atlas of Operative Oral and Maxillofacial Surgery, First Edition. Edited by Christopher J. Haggerty and Robert M. Laughlin
2015 John Wiley & Sons, Inc. Published 2015 by John Wiley & Sons, Inc.

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PART SEVEN Pathology and Reconstructive Surgery

The lesions have been described as nonaggressive and aggres- appearance. Root resorption and cortical expansion with
sive. Aggressive lesions can cause pain, root resorption, thinning may be seen, and phleboliths may be noted.
cortical expansion and perforation, mucosal involvement, There is no absolute pathognomonic radiographic finding
and higher recurrence rates after treatment. Nonaggressive for central hemangiomas; therefore, all lesions within the
lesions tend to be asymptomatic and do not have the above jaws should be initially treated as if they have a vascular
features. CGCGs have a peak incidence within the third, component. Lesions that are suspicious for hemangiomas
fourth, and fifth decades of life and have a higher predilec- should undergo needle aspiration prior to biopsy. Aspira-
tion in females. Radiographically, these lesions can appear tions that reveal frank blood are nearly pathognomonic
as unilocular or multilocular radiolucencies with noncorti- for a vascular lesion. Angiography is required prior to any
cated borders. Histologically, CGCGs demonstrate multinu- surgical manipulation of these lesions due to the potential
cleated giant cells (osteoclasts) scattered within a spindle cell for lifethreatening hemorrhage and airway embarrass-
background. Hemosiderin and erythrocytes may be seen. ment. Angiography can demonstrate the borders of the
Fibrosis, osteoid, and bone may also be seen. Histological lesion and afferent feeding vessels, and can be utilized for
similarities to Brown tumors and aneurysmal bone cysts are selective embolization prior to surgical removal. Emboli-
noted. Hyperparathyroidism should be ruled out in these zation therapy with surgical removal (curettage or resec-
patients. Aneurysmal bone cysts may be a cystic variant of tion) the surgical ligation of afferent vessels, followed by
CGCGs. Cherubism also has similar histologic findings, but surgical removal (curettage or resection), are the pre-
can usually be ruled out with clinical findings. ferred therapies. Recurrence rates are low with complete
Various treatment modalities have been described in removal of the lesion.
the current literature. Surgical curettage has a nearly
20% recurrence rate. Intralesional steroid injections have Fibrous Dysplasia (FD)
been used with mixed results. The protocol typically used FD is a benign, nonencapsulated neoplasm character-
includes a 50/50 mixture of lidocaine and triamcinolone, ized by cellular fibrous connective tissue and irregu-
injecting 2 mL per 1 cm of lesion. Intralesional steroid lar islands of metaplastic bone replacing normal bone.
injections are typically performed weekly for a total of FD occurs by mutations of the gene GNAS1 (guanine
6 weeks. Calcitonin injections (100 /day) have been nucleotidebinding protein, stimulating activity pol-
performed for up to 24 months with reported success. ypeptide1). Postnatal mutations will cause localized
Subcutaneous interferon therapy has also been utilized. monostotic disease. Mutations affecting stem cells in
Nonsurgical treatments modalities frequently do not embryonic stages will cause systemic conditions (i.e.,
resolve the CGCG, but may allow for surgical intervention JaffeLichenstein or McCuneAlbright syndromes)
with less morbidity and cosmetic deformity and should be characterized by defects in multiple cell lines resulting
considered for large lesions. CGCGs that exhibit aggres- in multiple bone and cutaneous lesions, as well endo-
sive behavior, are recurrent or are refractory to intrale- crine abnormalities.
sional steroid injections may be treated with peripheral FD commonly is discovered within the second decade
ostectomy or resection with 510 mm margins. of life. Sex predilection is equal. The lesions are typi-
cally nonpainful and expansile. Displacement of adjacent
Central Hemangiomas structures is common. Maxillary involvement is more
Hemangiomas are benign proliferations of vascular tis- prevalent than mandibular involvement. With maxil-
sues. It is debated whether hemangiomas are a prolifera- lary involvement, other adjacent facial bones may be
tion of endothelium (true neoplasm) or a hamartomatous involved. This is described as craniofacial fibrous dyspla-
proliferation of mesoderm, which undergoes endothelial sia. Growth generally ceases with skeletal maturation.
differentiation. Regardless of the etiology, they are poten- Radiographs demonstrate an expansile groundglass
tially lifethreatening entities. They are most commonly lesion with poorly defined borders. Histologically, the
identified within the posterior mandible, but are other- lesion is characterized by a cellular fibrous tissue with
wise rare within the jaws. They have a peak incidence woven bone trabeculae that do not connect interspersed
within the first and second decades of life and a female throughout this background. The bone trabeculae have
predilection. Hemangiomas typically present as pain- been classically described as resembling Chinese charac-
less, firm swellings of the underlying bone. Patients may ters. The edges of the lesion fuse with the normal bone
report a pulsation over the lesion. Teeth may be mobile without a capsule. Treatment involves resection of small
with bleeding around the gingival margins. A bruit and lesions. Surgical reduction and contouring are performed
thrill may be present. However, many hemangiomas are with larger lesions that cause functional or aesthetic con-
asymptomatic and present with none of the above find- cerns. In up to 50% of cases, repeated debulking pro-
ings. Radiographically, the lesions may be unilocular or cedures are necessary until growth ceases. Longterm
multilocular radiolucencies. The multilocular variant has surveillance is needed due to the possibility of malignant
been described as the classic soap bubble or honeycomb transformation.

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Odontogenic Tumors debated. Typically, these lesions occur in young adults


within the posterior mandible. They are frequently associ-
Odontogenic tumors arise from structures involved with ated with impacted third molars and can be mistaken for a
tooth formation. Benign odontogenic tumors encompass cystic lesion (i.e., a dentigerous cyst or odontogenic kerato-
a variety of lesions within the jaws. Odontogenic tumors cyst). Clinically, they may be asymptomatic or demonstrate
vary significantly both histologically and with their clinical a painless jaw swelling. Pain and neurosensory disturbance
behavior. Many odontogenic tumors are true benign neo- are not typical. Radiographically, unicystic ameloblasto-
plasms, whereas others are extremely aggressive, locally mas present as a unilocular radiolucency with or without
destructive lesions. Malignant variants of these lesions expansion. The unicystic ameloblastoma varies in treat-
are also encountered. This section will describe the gen- ment depending on the histological findings of the tumor.
eral classification of these tumors and highlight commonly Three histological types are seen with unicystic amelo-
encountered lesions. All lesions should be treated individ- blastomas. These are the luminal, intraluminal, and mural
ually based on their unique histopathology, aggressive- ameloblastoma. These ameloblastic changes tend to sup-
ness, and clinical and radiographic presentation. Please port the concept of an evolving spectrum of neoplastic
refer to Appendix 3A for further treatment guidelines. transformation of odontogenic cysts. Luminal unicystic
Benign odontogenic tumors can be characterized by ameloblastomas have ameloblastoma tumor confined
the embryonic tissue of origin. Classifications include within the cystic lining itself. Intraluminal variants have
(i) odontogenic epithelium, (ii) odontogenic ectomesen- projections of ameloblastoma into the cystic lumen. Mural
chyme (primarily), and (iii) mixed odontogenic epithe- ameloblastomas have tumor that is within the cystic lin-
lium and ectomesenchyme. Ectomesenchymal tumors ing and invades the surrounding noncystic regions of the
may have odontogenic epithelium histologically, but they surrounding tissue. Treatment of the luminal and intralu-
are not believed to play a significant role in the patho- minal unicystic ameloblastoma is typically complete with
genesis. The classic odontogenic epithelial tumors are enucleation of the cyst. Marginal or segmental resections
the ameloblastoma and the calcifying epithelial odonto- may be warranted for mural unicystic ameloblastomas
genic tumor (CEOT). Ectomesenchymal tumors include due to the invasion of surrounding tissue. Longterm
the odontogenic myxoma and cementoblastoma. Mixed followup is recommended for all variants.
tumors include the ameloblastic fibroma and fibro The peripheral ameloblastoma is histologically identical
odontoma or odontoma lesions. to the intraosseous ameloblastomas; however, they are
Odontogenic Epithelial Tumors alveolar mucosal lesions. They are typically small (<2.0
cm), nonulcerated, nonpainful, and located within the
Ameloblastomas posterior mandibular alveolar mucosa. Treatment consists
Ameloblastomas are one of the most commonly encoun- of local excision with longterm followup as the recur-
tered benign odontogenic tumors. There are several histo- rence rate is approximately 15%.
logical variants and three major clinical variants. The major
clinical variants include the multicystic or solid variant, the Calcifying Epithelial Odontogenic
unicystic variant, and the peripheral ameloblastoma. Tumors (Pindborg Tumors)
The multicystic or solid variant can be locally invasive and Calcifying epithelial odontogenic tumors (CEOT) behave
destructive. These lesions are typically slow growing and as aggressive, benign lesions arising from odontogenic
show little tendency to become aggressive (i.e., malignant). epithelium. Like the ameloblastoma, these lesions can
The most common location is within the posterior mandi- be locally destructive and invasive. They are commonly
ble, but they can occur in other locations of both jaws. One identified within the posterior mandible, but can be found
exception is the desmoplastic variant, which tends to occur in other regions. Patients typically present with a painless
within the anterior maxilla. Most cases occur in adulthood expansion of the posterior mandible. Radiographically,
and are typically asymptomatic, exhibiting no neurosensory CEOTs are typically multilocular and expansile, and dem-
changes. Radiographically, these lesions are typically multi- onstrate calcifications. Histologically, amyloid deposits
locular and expansile in nature. Radiopacities are not seen with calcified ringlike structures called Liesgang rings are
with ameloblastomas. The standard treatment is resection noted. Treatment of the CEOT is similar to the ameloblas-
with 1 to 1.5 cm bony margins. For lesions that have perfo- toma with marginal or segmental resection with 1.0 cm
rated through the cortical plate and/or extended into adja- margins. Recurrence rates have been reported at approxi-
cent areas, an intact anatomical boundary (i.e., periosteum) mately 15%. Enucleation and curettage procedures are
is included with the specimen. Recurrence is rare with defin- associated with higher recurrence rates.
itive negative margins. Longterm followup is required.
The unicystic ameloblastoma is less common than the Odontogenic Adenomatoid Tumors (OATs)
solid variant. The tumors origin and whether it arises OATs are nonaggressive benign neoplasms arising from
de novo or from neoplastic cystic transformation are still odontogenic epithelium. OATs occur more frequently in

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PART SEVEN Pathology and Reconstructive Surgery

females with a peak incidence within the second decade radiolucent border is seen. The involved teeth will typi-
of life, and they frequently involve an unerupted canine. cally test as vital with pulp testing. Areas of noncalcified
OATs have been coined the twothirds tumor: twothirds tissue in the area of the radiolucent rimming are also seen.
occur in females, twothirds occur in the maxilla, two Histologically, cementumlike proliferation continuous
thirds are associated with unerupted teeth, and twothirds with the tooth root is noted. Root resorption may be seen.
are associated with canines. OATs can produce swelling if Treatment consists of excision of the lesion and removal of
they are large; however, most are small, asymptomatic, the tooth. Recurrence is not expected.
and incidentally found on routine imaging. Radiographi-
Ossifying Fibromas (Cemento Ossifying Fibroma)
cally, these lesions can be radiopaque or have small radio-
paque structures within the lesion. The entire structure of Ossifying fibromas are a type of benign fibroosseous
an unerupted tooth is frequently involved. This differs from tumor. These lesions can arise in both jaws, but they have
the dentigerous cyst, which tends to involve only the crown a predilection for the mandible. These lesions are thought
of the involved tooth. Large lesions may cause tooth dis- to arise from the periodontal ligament. The premolar
placement. Histologically, odontogenic epithelium is seen and molar regions are commonly affected. The lesions
with ductlike structures possessing a lumen lined with a are slow growing, expansile, and typically not painful.
single row of low columnar cells with reverse polarization. Facial asymmetry is noted with larger lesions. Women
Intraluminal eosinophilic material and scattered calcifica- are affected more frequently than men. Early lesions may
tions may also be seen. Clinically, OATs have a wellformed appear completely radiolucent. With maturation, radi-
capsule with excision. Treatment is enucleation with the opacities appear, and the lesion will eventually become
removal of the involved tooth. Recurrence rates are low. completely radiopaque with a radiolucent rim. The lesions
are expansile in all directions and are therefore typically
spherical in shape. Treatment is with enucleation and
Ectomesenchymal Tumors
curettage for most lesions. Clinically, these lesions easily
Odontogenic Myxomas shell out of the affected bone. Larger lesions, which have
Odontogenic myxomas are aggressive lesions that can significant expansion or aggressive growth features, may
arise in both jaws; however, mandibular involvement is require resection. Recurrence is uncommon, but lifelong
more common. Patients may be asymptomatic or have a surveillance is recommended.
painless jaw swelling depending on the size of the lesion.
Odontogenic myxomas have a peak incidence within Mixed Odontogenic Tumors
the second and third decades of life and appear to have
no sexual predilection. Radiographically, the lesions are Ameloblastic Fibromas
typically multilocular with thin bone trabeculae noted. Ameloblastic fibromas can be classified as either a neo-
Expansion, cortical thinning, and tooth resorption or plasm or a hamartoma. The lesions typically arise within
displacement are common. Impacted teeth are not nec- the posterior mandible, may be expansile, and are typi-
essarily seen with the lesion. Histologically, the lesion cally nonpainful. Radiographically, the lesion presents as
resembles dental pulp due to the mesenchymal tissue ori- a unilocular or multilocular radiolucent mass. Tooth dis-
gin. Randomly arranged spindle cells within a loose myx- placement and/or root resorption may be seen. Patients
oid stroma with minimal collagen fibrils scattered within are typically children between the ages of 6 and 10; how-
are typical. Odontogenic epithelial rests and bone trabec- ever, lesions may be seen in older children and young
ulae are also noted. The lesions are not encapsulated and adults. Histologically, the tumors demonstrate mesen-
tend to penetrate bone further than their radiographic chymal and epithelial components. Strands or islands of
depiction. Due to this, the recommended treatment is odontogenic, ameloblasticappearing epithelium within
marginal or segmental resection with 1.5 cm margins and a background connective tissue and myxoid stroma and a
an uninvolved anatomic boundary. Enucleation or curet- fibrous capsule are present. Treatment involves enuclea-
tage is reserved for only easily accessible and small lesions. tion and curettage for all but very large lesions, which
Routine followup is recommended for enucleated lesions may require resection. Recurrence is rare with proper
due to their propensity to recur. treatment. If recurrence occurs, ameloblastic fibrosarcoma
should be considered within the differential diagnosis.
Cementoblastomas
The cementoblastoma is a benign tumor of hamartoma- Odontomas
tous cementoblasts, which form a tumor of disorganized Odontomas are hamartomas of tissues of the develop-
cementum. The lesion develops around the apical half ing tooth. Two types exist: compound and complex.
of premolar and molar teeth, typically mandibular. Pain Compound odontomas appear to be small, toothlike
may be associated with the lesions. Radiographically, a structures. Complex odontomas present as a calcified
radiopaque mass involving the roots of the teeth with a mass not resembling teeth. These lesions are generally

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CHAPTER 45 Benign Tumors of the Jaws

asymptomatic and found on routine radiographic 9. A reconstruction plate may be prebent using a stere-
examinations. Compound odontomas have a predilec- olithic model prior to surgical resection (Figures 45.6
tion for occurring in the anterior jaws, and complex and 45.8).
odontomas in the posterior jaws. The lesions are typi- 10. Osteotomies are performed using a reciprocating,
cally found in patients younger than 25 years of age. oscillating, or giggly saw at the predetermined
Radiographically, they most often present as radiopaci- proximal and distal margins of the lesion (Figures
ties, but they may be radiolucent or mixed depending 45.3, 45.10, and 45.11). The lesion is removed in
on the progression of calcification of the lesions with its entirety and sent for final pathology (Figures
time. Histologically, enamel, dentin, cementum, and 45.12 and 45.13). A small amount of cancellous
pulpal tissue are seen. Treatment involves enucleation bone may be harvested from the distal and proxi-
and curettage, and recurrence is rare. mal ends of the native bone and sent to pathology
as frozen sections to identify atypical cells within
Technique: Mandibular Resection the marrow.
1. One must determine first if a transcutaneous (larger 11. Primary or secondary reconstruction (Figures 45.16
mandibular lesions with resultant continuity defects) and 45.17) is performed based upon the surgeons
or transoral (smaller mandibular lesions not resulting preference and the anticipated recurrence rate of the
in continuity defects, and maxillary lesions) approach lesion.
will be utilized. 12. The fourlayer closure is performed to include the
2. The patient is placed in a supine position. After ptyergomasseteric slingperiosteum, platysma, sub-
endotracheal intubation, the patient is prepped and cutaneous tissues, and skin. A suction or passive
draped in a sterile fashion. drain may be inserted and secured to the overlying
3. Local anesthetic containing a vasoconstrictor is infil- skin.
trated within the area of the lesion, and regional
blocks may also be utilized. Key Points
4. If performing a transcutaneous approach, the pro-
posed incision should be placed within a natural skin- 1. A definitive diagnosis must be made prior to any defin-
fold, 1.5 to 2.0 cm below the inferior border, to mini- itive surgical procedure as lesions have different levels
mize damage to the marginal mandibular branch of of aggressiveness and recurrence rates.
the facial nerve. 2. Adequate surgical exposure is necessary for both
5. If performing a transoral approach, a sulcular incision the resection and the reconstruction of pathological
with or without vertical releasing incisions is per- lesions.
formed. 3. Plain films may be utilized in the operating room for
6. Transcutaneous incisions will follow sharp dissection en bloc resection of bony lesions to evaluate peripheral
through the skin, subcutaneous fat, and platysma margins.
muscle to the superficial layer of the deep cervical fas- 4. Margins of the final specimen need to be evaluated on
cia (SLDCF). Within the region of the premasseteric a microscopic level to ensure complete resection.
notch, the marginal mandibular branch of the facial 5. En bloc resections require a passively adapted recon-
nerve and the facial artery and vein will be encoun- struction plate with at least three (preferably four or
tered deep to the SLDCF. Care is taken to isolate the more) fixation screws on each side of the defect (Fig-
marginal mandibular branch of the facial nerve. Once ure 45.15).
isolated, dissection can proceed either superior or 6. Teeth within or near the line of the planned osteotomy
inferior to the nerve. should be extracted in anticipation of 35 mm of bone
7. Once the nerve is protected within the flap, dissection dieback from the osteotomy site.
continues to the inferior border of the mandible. The 7. All pathologic resections should be planned with the
facial vein and artery will be encountered. These ves- final reconstruction (soft tissue, hard tissue, and pros-
sels may be preserved depending upon the location thetic rehabilitation) in mind.
of the lesion. In the event the vessels do not allow
adequate surgical access, the vein and artery should
Case Report
be ligated and divided.
8. Wide exposure of the entire lesion (Figures 45.9, 45.10, Case Report 45.1. A 54yearold presents with a chief
and 45.11) through subperiosteal or supraperiosteal complaint of leftsided mandibular pain, swelling, tris-
dissection is necessary. Depending on the type of mus, and weight loss for the past several months. On clin-
the lesion and if cortical perforation has occurred, a ical examination, a significant swelling could be palpated
supraperiosteal dissection may be required to allow extraorally along the left posterior aspect of the mandi-
for resection with an intact anatomical barrier. ble, a maximum vertical opening of 5 mm was recorded,

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PART SEVEN Pathology and Reconstructive Surgery

and there was severe pain to the area. On review of the Modeling Inc., Golden, CO, USA). The prebent recon-
cone beam computed tomography scan, a bony mass was struction plate was placed prior to creating the bone oste-
identified within the patients left posterior mandible. An otomies. An inferior alveolar nerve pullthrough was
incisional biopsy of the area was performed, and histo- performed, and the reanastamosed nerve was tagged to
pathological slides suggested an aggressive central giant the reconstruction plate with 20 Prolene sutures. Four
cell granuloma. The patient was initially treated with months after definitive resection, the patients continu-
serial steroid injections within the body of the mass to ity defect was reconstructed with an anterior iliac crest
no avail. Due to the patients trismus, pain, weight loss, bone graft performed through an extraoral approach. The
refractory intralesional steroid injections, and request, patient developed a partial return of sensation to the V3
an intraoral block resection was performed with 5 mm distribution on the left side after nerve anastomosis. (See
margins using Virtual Surgical Planning (VSP; Medical Figures 45.1 through 45.17.)

Figure 45.1. Radiograph demonstrating a multiloculated, aggressive, expansile hard tissue


lesion located within the left posterior mandible with root resorption, and involvement of the
inferior border of the mandible.

Figure 45.2. Virtual Surgical Planning workup demonstrating the Figure 45.3. Based on the location of the mass, a vertical ramus
anatomy of the craniofacial bones and teeth. The tumor and the osteotomy was outlined to resect the posterior margin.
inferior alveolar nerve are highlighted in red. Fivemillimeter resec-
tion margins are measured from the tumor periphery.

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CHAPTER 45 Benign Tumors of the Jaws

Figure45.4. An intraoral cut guide is virtually designed. The dental Figure45.5. The posterior cut guide will articulate with the angle
occlusion will stabilize the anterior cut guide during the osteotomy. of the posterior mandible. Predictive holes are marked in red.
Predictive holes are marked in red and represent fixation points for
both the guide and the prebent reconstruction plate.

Figure45.6. A reconstruction plate is virtual adapted to the virtual


postoperative mandibular anatomy.

Figure45.7. Sterile stereolithic model with cut guides in place. Figure45.8. Sterile prebent reconstruction plate.

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PART SEVEN Pathology and Reconstructive Surgery

Figure45.9. Occlusalbased anterior cut guide in place. The mental Figure45.10. The anterior resection is performed with a reciprocat-
nerve is retracted anteriorly with the cut guide. ing saw utilizing the custom anterior cut guide. The premolar tooth
anterior to the osteotomy is extracted in anticipation of 35 mm of
bone die back post-osteotomy.

Figure 45.11. An intraoral vertical ramus osteotomy is performed Figure45.12. En bloc resection compared to stereolithic model and
based on the Virtual Surgical Planning workup and utilizing the cut guides.
posterior cut guide. An inferior alveolar nerve pullthrough was per-
formed for this benign tumor.

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CHAPTER 45 Benign Tumors of the Jaws

Figure45.14. The transected inferior alveolar nerve was reapproxi-


Figure45.13. Due to the lingual cortical expansion of the mass, a
mated with 70 Nylon sutures and secured to the reconstruction
cuff of periosteum was removed to serve as an anatomical barrier.
plate with 20 Prolene sutures.

Figure 45.15. Immediate postoperative film depicting a wellposi- Figure 45.16. Four months after en bloc resection, an extraoral
tioned reconstruction plate with the condyle ideally seated within approach was utilized to expose the 4 cm mandibular continu-
the glenoid fossa. The postoperative film correlated well with the ity defect. The inferior alveolar nerve is identified and freed from
Virtual Surgical Planning workup. surrounding scar tissue.

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PART SEVEN Pathology and Reconstructive Surgery

References
Ellis, E. and Zide, M.F., 2006. Surgical approaches to the facial skel-
eton. 2nd ed. Philadelphia: Lippincott, Williams & Wilkins.
Marx, R.E. and Stern, D., 2003. Oral and maxillofacial pathology a
rationale for diagnosis and treatment. 2nd ed. Hnbover Park, IL:
Quintessence.
Neville, B., Damm, D.D., Allen, C. and Bouquot, J., 2009. Oral
and maxillofacial pathology. 3rd ed. Philadelphia: W.B. Saunders.

Figure 45.17. The defect was reconstructed with an anterior iliac


crest corticocancellous graft secured to the reconstruction plate with
fixation screws.

415