Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4416_Библиотеки_им_академика_М_И_Перельмана
.pdf
Section 6 Systemic Disorders/Surrounding Structures Involving PNS336
Fig. 24.4: Dentigerous cyst. Panoramic radiograph. Unilocular expansile lytic lesion within
left upper alveolus (asterisk). Unerupted left upper molar tooth (arrow). Left maxillary sinus is
not seen separately, right maxillary sinus is normal.
A B
Figs. 24.5A and B: Dentigerous cyst (same patient as in Fig. 24.4). (A) Unilocular expansile
cystic lesion within left upper alveolus (asterisk). Unerupted left upper molar tooth (arrow);
(B) Well-dened margins of the lesion. Left maxillary sinus is displaced anteriorly (arrow).
■ Imaging (Figs. 24.4 and 24.5):
• Cystic, unilocular, and expansile lesion
• Well-dened border, may be sclerotic
• Ill-dened margin with spread beyond the lesion suggests secondary
infection
• Solid component with or without bony erosion suggests an intramural
ameloblastoma.
Keratocystic Odontogenic Tumor
■ Previously referred to as odontogenic keratocyst, it is now recognized
and classied as a tumor.
■ Imaging:
• Unilocular/multilocular, lucent (on OPG) and high-density cyst (on
CT) lesion (Figs. 24.6A and B).
• Due to the presence of keratin it is intermediate SI/hyperintense
on T1-weighted images (WIs), shows hyperintensity on T2WI, and
restricted diusion. Characteristic low signal intensity—“T2 fall out” is
seen at the center of the lesion in few cases (Figs. 24.7A to D).
• It is locally aggressive and may show solid component.
A B
Figs. 24.6A and B: Keratocystic odontogenic tumor (KOT). NCCT. (A) Unilocular
expansile high density cystic lesion within right upper alveolus (asterisk); (B) Thinning of
inferior margin with bone erosion (arrow). Difcult to differentiate from dentigerous cyst,
though KOT is associated with root resorption and bone erosion with milky uid on aspiration.
337Chapter 24 Imaging of Dental Lesions and Sinonasal Cavity
A B
C D
Figs. 24.7A to D: Keratocystic odontogenic tumor (KOT) magnetic resonance imaging
(MRI). Multiple unilocular cystic lesions, bilateral maxilla (asterisks in A), and angle of
mandibles (arrowheads in D). (A) Intermediate signal intensity on T1WI; (B) Hyperintense on
T2WI; (C) Restricted diffusion; and (D) Minimal peripheral enhancement. Restricted diffusion
and T1 hyperintensity is characteristic for this lesion.
Section 6 Systemic Disorders/Surrounding Structures Involving PNS338
A
C
B
Figs. 24.8A to C: Multiple keratocystic
odontogenic tumor (KOT) (Gorlin-Goltz
syndrome). (A) Multiple unilocular cystic
lesions, left maxilla (asterisk), and right
mandible (arrow) s/o multiple KOT; (B) Fusion
of C7 and D1 vertebral bodies and posterior
elements (arrowhead); and (C) Bid ribs with
fusion anomalies of right 2–6 ribs (arrow) and
left 5–7 ribs.
■ e tumor may also exist with squamous cell carcinoma in up to
one-fourth of cases.
■ In view of high recurrence rates postsurgery follow-up with CT is required.
■ Gorlin-Goltz syndrome:
• Rare autosomal dominant inherited disorder
• Multiple odontogenic keratocysts and basal cell carcinomas, skeletal
(bid ribs, Sprengel’s deformity, vertebral anomalies), ophthalmic,
and neurological abnormalities (Figs. 24.8A to C).
Ameloblastoma
■ Ameloblastoma is the most common odontogenic tumor.
■ It is a benign epithelial tumor but shows locally aggressive behavior,
metastases are rare.
3,4
339Chapter 24 Imaging of Dental Lesions and Sinonasal Cavity
A
C
B
Figs. 24.9A to C: Ameloblastoma. (A)
Pericoronal mixed solid-cystic (asterisk)
expansile lesion; (B) Thinning of cortex
(arrowhead) and bone erosion (posterior,
inferior and lateral margins); (C) Lesion
in relation to left upper 4 tooth (arrow) and
retained secretions in left maxillary sinus
(asterisk).
■ Imaging: More frequent in the mandible. Common site in maxillapremolar/rst molar.
• Orthopantogram:
‒ Unilocular/multilocular, expansile lytic lesion causes root
resorption.
‒ It may be pericoronal or may replace a tooth.
• Computed tomography:
‒ Mixed solid cystic lesion, either component may predominate.
inning of cortex with scalloped margins (Figs. 24.9A to C).
‒ Multilocular lesions have a honeycomb/bubbly appearance.
‒ Solid component is enhancing and may cause bone erosion and
soft tissue extension (Figs. 24.10A and B).
• Magnetic resonance imaging:
‒ T1-weighted image: Isointense, T2WI—hyperintense signal
intensity.
‒ Contrast-enhanced magnetic resonance imaging: Heterogeneous
enhancement, nonenhancing foci seen within.
‒ Diusion-weighted imaging: Cystic component shows free
diusion while solid component may show restriction.
Section 6 Systemic Disorders/Surrounding Structures Involving PNS340
A B
Figs. 24.10A and B: Ameloblastoma. (A) Large expansile (arrow) lesion with bone erosion;
(B) Mixed solid cystic lesion (arrowhead). Solid component and erosions is more common
in ameloblastoma.
■ Dierential diagnosis:
• Dentigerous cyst:
‒ e closest dierential diagnosis.
‒ In fact it is thought that about half of ameloblastomas arise from
the lining of a dentigerous cyst.
‒ Both are more frequent in the mandible than maxilla.
• Keratocystic odontogenic tumor:
‒ It is the other close dierential diagnosis.
‒ Characteristically cystic lesion, hyperintense on T1WI.
Odontogenic Myxoma
■ Uncommon benign but locally aggressive odontogenic tumor.
■ Pathology: Nonencapsulated tumor with spindle cells/collagen bers
within a mucoid matrix.
■ Occurs in young patients, in 2nd or 3rd decade of life, and is more
frequent in females.
■ e predominant site in the maxilla (or mandible) is in the posterior
aspects. Can grow as a large, painless mass in the maxillary sinus.
■ Imaging:
• Plain radiographs: Expansile radiolucent tumors. Often with
expansion. inning of the cortex and perforation at places. Teeth
displacement is frequent, while resorption is infrequent.
• Internal architecture is variable ranging from no trabeculation to ne
to thick trabeculations within. Variants with thin and straight septa
gives the characteristic “tennis racket” appearance, curved or coarse
5
A B
Figs. 24.11A and B: Odontogenic myxoma. (A) Expansile lytic lesion right maxilla with
few thin septations (arrow) and erosion of the anterior cortex (arrowhead); (B) Erosion of the
lateral (black arrow) cortex and thin, lace like trabeculations (asterisk).
septae give a “soap bubble” or “honeycomb pattern”, while ne septae
produce a “sh net” appearance.
• Computed tomography (Figs. 24.11A and B): e density compared
to muscle is hypodense/isodense. Presence of thin lace-like
trabeculations is characteristic. Cortical thinning/perforation is often
seen but tumor margins are well-dened, not inltrative.
• Magnetic resonance imaging: Tumors show variable signal intensity
and contrast enhancement.
341Chapter 24 Imaging of Dental Lesions and Sinonasal Cavity
NONODONTOGENIC OSSEOUS LESIONS
■ Nonodontogenic lesions which involve the maxillary alveolus and
expand the bone or are associated with a soft tissue component can also
protrude into/involve the maxillary sinus.
■ ese include lesions, such as central giant cell granuloma, simple bone
cyst, aneurysmal bone cyst, and bro-osseous lesions like ossifying
broma and dysplasia. ese lesions are frequent in the maxilla/
mandible but can less commonly arise within the sinonasal cavity
(see Chapter 12).
Giant Cell Reparative Granuloma
■ Common sites are mandible/maxilla, infrequently seen involving
sinonasal cavity.
■ Age: Young adults, females more than males.
■ Imaging ndings (also see Chapter 12):
6
Section 6 Systemic Disorders/Surrounding Structures Involving PNS342
A
C
B
Figs. 24.12A to C: Giant cell reparative
granuloma. (A) Large, heterogeneous,
expansile mixed density mass in right
upper alveolus (arrow); (B) Maxillary sinus
displaced postero superiorly (arrowhead); and
(C) Heterogeneous postcontrast enhancement
(asterisk).
• Expansile lesions with bone erosion (Figs. 24.12A to C)
• Cystic/hemorrhagic foci may be seen within with heterogeneous
signal intensity on magnetic resonance imaging (MRI).
Ossifying Fibroma
■ Ossifying broma (OF) is a relatively common lesion in the mandible/
maxilla.
■ It is classied under the benign odontogenic and maxillofacial bone
tumors.
■ Imaging ndings:
• Computed tomography (Figs. 24.13A and B): Well-dened mixed
• Expansile lesion, occasionally bone erosion seen.
• Well-dened margins of the lesion aids in its distinction from brous
3,7
density lesion with soft tissue component, matrix mineralization, and
calcication along the periphery. e amount of soft tissue versus
mineralized matrix is variable.
dysplasia.
A B
Figs. 24.13A and B: Ossifying broma. (A) Large well-dened mixed density expansile mass
lesion in left nasal cavity and maxillary sinus; and (B) Thinning of bony margins and extension
into upper alveolus (asterisk). Erosion of turbinates and medial maxillary wall (arrow).
• Magnetic resonance imaging: e soft tissue component of the lesion
shows heterogeneous enhancement, while the mineralized matrix/
rim appear as signal voids.
Fibrous Dysplasia
■ Fibrous dysplasia is not a neoplastic disorder, but a benign disorder
involving multiple bones wherein the medulla is replaced by immature
brous tissue and eventually osseous tissue.
■ Craniofacial bones are a frequent site of involvement, may be part of the
polyostotic form.
■ Imaging ndings (Figs. 24.14A and B):
3,7
343Chapter 24 Imaging of Dental Lesions and Sinonasal Cavity
A B
Figs. 24.14A and B: Fibrous dysplasia. (A) Narrowing of right optic canal (arrowhead)
and inferior orbital ssure (arrow); and (B) Expanded left frontal, maxillary, zygomatic, and
sphenoid bones with intact contour. Ground-glass density (asterisk).
Section 6 Systemic Disorders/Surrounding Structures Involving PNS344
• CT: Involved bone is expanded but basic shape and contour intact.
• Its margins with the adjoining bone are ill dened, i.e. it merges
imperceptibly.
• Matrix may initially appear lucent, then assume a “cotton wool”
appearance, and nally evolves into “ground glass” density.
• MRI: Intermediate signal on T1WI, intermediate or low signal intensity
on T2WI with signicant contrast enhancement in brous tissues.
MUCOSAL LESIONS
■ Primary mucosal malignancies such as carcinoma buccal mucosa or
carcinoma palate can erode into the maxillary sinus.
■ Imaging ndings (Figs. 24.15A and B):
• Enhancing soft tissue mass causing permeative bone destruction and
erosion with extension into the maxillary sinus.
A B
Figs. 24.15A and B: Carcinoma palate eroding into maxillary sinus. (A) Erosion of oor
of left maxillary sinus with soft tissue extension (arrow); and (B) Enhancing soft tissue density
mass palate (squamous cell carcinoma) (asterisk).
OSTEONECROSIS OF MAXILLA
■ Osteonecrosis is characterized by bone destruction of the maxillary
alveolus.
■ In an immunocompromised patient, the cause is usually osteomyelitis
(bacterial/fungal). e infection can have a dental origin and spread
along the sinus walls, pterygoid plates, and skull base (see Chapter 7).
8
Fig. 24.16: Osteonecrosis of maxilla. Panoramic computed tomography (CT) reconstructed
image. Osteolysis of left half of maxilla with absent teeth (arrow). Unilateral involvement in
herpes zoster.
345Chapter 24 Imaging of Dental Lesions and Sinonasal Cavity
A B
Figs. 24.17A and B: Osteonecrosis of maxilla (unilateral involvement in herpes zoster).
(A) Irregular lysis of left alveolar arch (arrow); and (B) Osteolysis of left half of maxilla with
absent teeth (arrowhead) and adjacent soft tissue.
■ In an immunocompetent patient, aseptic necrosis occurs with an
appearance similar to osteomyelitis. is is reported to be due to small
vessel occlusion. Causes include radiotherapy, bisphosphonate use,
sickle cell anemia, hemoglobinopathies, postviral infection, and electric
shock.
■ Unilateral involvement is seen in cases of herpes zoster infection with
distribution along the same dermatome of the nerve (Fig. 24.16).
■ Clinical presentation is with pain, mucosal swelling, and progressive
loosening of teeth.
Соседние файлы в папке Библиотека им академика М.И. Перельмана