BAGIAN BEDAH REFERAT

FEBRUARI 2023
FAKULTAS KEDOKTERAN
UNIVERASITAS MUHAMMADIYAH MAKASSAR

AMELOBLASTOMA MANDIBULA

NURANISA
105101100321

PEMBIMBING :
dr. Asdar, Sp.B

FAKULTAS KEDOKTERAN
UNIVERSITAS MUHAMMADIYAH MAKASSAR
2023
 HALAMAN PENGESAHAN

Yang bertanda tangan di bawah ini menyatakan bahwa:

Nama : Nuranisa
NIM : 105101100321
Judul Referat : Ameloblastoma Mandibula

Telah menyelesaikan tugas dalam rangka kepaniteraan klinik pada bagian Ilmu Bedah
Fakultas Kedokteran Universitas Muhammadiyah Makassar.

Makassar, Februari 2023

Pembimbing,

dr. Asdar, Sp.B

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 KATA PENGANTAR

Assalamualaikum Warahmatullahi Wabarakatuh

Alhamdulillah, puji syukur atas kehadirat Allah SWT yang telah memberikan
rahmat dan karunia-Nya, sehingga penulisan referat ini dapat diselesaikan. Shalawat
serta salam semoga selalu tercurahkan kepada Baginda Besar Nabi Muhammad SAW.
Karena beliaulah sebagai suritauladan dalam kehidupan dunia ini.

Referat dengan judul “Ameloblastoma Mandibula” ini dapat terselesaikan

dengan baik dan tepat pada waktunya sebagai salah satu syarat dalam menyelesaikan
Kepaniteraan Klinik di Bagian Bedah Secara khusus penulis menyampaikan terima
kasih yang mendalam kepada dr. Asdar,Sp.B selaku pembimbing yang telah banyak
meluangkan waktu dengan tekun dan sabar dalam membimbing, memberikan arahan
dan koreksi selama proses penyusunan tugas ini hingga selesai.

Penulis menyadari bahwa penyusunan referat ini belum sempurna adanya dan
memiliki keterbatasan tetapi berkat bantuan dan dorongan dari berbagai pihak,
sehingga dapat berjalan dengan baik. Akhir kata, penulis berharap agar referat ini dapat
memberi manfaat kepada semua orang.

Makassar, Februari 2023

Penulis

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 DAFTAR ISI

HALAMAN PENGESAHAN ....................................................................................... 1

KATA PENGANTAR .................................................................................................. 2

DAFTAR ISI ................................................................................................................. 3

BAB I INTRODUCTION ............................................................................................. 4

BAB II LITERATURE REVIEW ................................................................................. 6

2.1 Anatomy ........................................................................................................ 6

2.2 Ameloblastoma ............................................................................................. 10

2.2.1 Definition and Etiology ................................................................................ 10

2.2.2 Epidemiology ............................................................................................... 10

2.2.3 Classification ................................................................................................ 11

2.2.4 Diagnosis ...................................................................................................... 13

2.2.5 Differential Diagnosis .................................................................................. 16

2.2.6 Treatment ...................................................................................................... 17

2.2.7 Complications ............................................................................................... 20

2.2.8 Prognosis ...................................................................................................... 21

DAFTAR PUSTAKA .....................................................................................................

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 I. INTRODUCTION

The word ameloblastoma derives from the early English word “amel,” meaning
enamel and the Greek word “blastos,” meaning germ. They are rare, odontogenic
tumors, thought to be composed of the epithelium of ectodermal origin, which means
they are tumors arising from the cells around the tooth root, or in close approximation,
derived from the ectoderm germ layer. Ameloblastomas represent about 1% of all jaw
tumors, but they are the second-most common odontogenic tumor. They are much more
common in the lower jaw than in the upper jaw, and more common in the posterior
mandible as compared to the anterior. The vast majority of the time, they are a benign
tumor with aggressive behavior; however, rarely they can develop into, or be associated
with, a malignancy (malignant ameloblastoma or ameloblastic carcinoma). It is
extremely rare to find ameloblastomas outside the maxilla and mandible due to the
association with teeth and their structures.1

It accounts for about 1% of all oral tumors and about 9-11% of odontogenic
tumors. It is generally a slow-growing but locally invasive tumor.Its peak incidence is
in the third to fourth decades of life and the male: Female ratio is 1:1. Its incidence was
0.6 cases/million, and of 0.31 cases/million in a white population of South Africa.
Ameloblastoma accounted for 60.3% of all odontogenic tumors in Indian population,
with a mean age of presentation of 30.2 years. A slight male predilection and major
occurrence in the mandibular molar-ramus area were elicited.They are classified as
unicystic, multicystic or solid, 86% of cases are multicystic ameloblastomas.
Ameloblastoma in the mandible can progress to great size and cause facial asymmetry,
displacement of teeth, malocclusion, and pathologic fractures.2 This tumour is thought
to arise from the remaining cells of the dental lamina, the epithelial cell rests of
Malassez, or the basal cell layer of the epithelial surface. Most patients with
ameloblastoma are between the ages of 30 and 50 years, and this tumour occurs with
equal frequency in men and women, with 80% occurring in the mandible

4
Ameloblastoma develops invasively, and recurrence rates are higher if they are not
adequately resected during surgery. Extended resection of the jaw is effective in
controlling recurrence, but it presents significant aesthetic and functional problems.3

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 II. LITERATURE REVIEW
2.1 Anatomy
The mandible is the bone of the lower jaw. It consists of a body of right and left
parts, which are fused anteriorly in the midline (mandibular symphysis), and two rami.
The site of fusion is particularly visible on the external surface of the bone as a small
vertical ridge in the midline. The upper surface of the body of mandible bears the
alveolar arch, which anchors the lower teeth, and on its external surface on each side
is a small mental foramen Posterior to the mandibular symphysis on the internal surface
of the mandible are two pairs of small spines, one pair immediately above the other
pair. These are the superior and inferior mental spines (superior and inferior genial
spines), and are attachment sites for a pair of muscles that pass into the tongue and a
pair of muscles that connect the mandible to the hyoid bone.4

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 Figure 1. Mandible. A. Superior view. B. Lateral view. C. Medial view. 4
Extending from the midline and originating inferior to the mental spines is a raised
line or ridge (the mylohyoid line), which runs posteriorly and superiorly along the
internal surface of each side of the body of the mandible to end just below the level of
the last molar tooth. Above the anterior one- third of the mylohyoid line is a shallow
depression (the sublingual fossa), and below the posterior two- thirds of the mylohyoid
line is another depression (the submandibular fossa). Between the last molar tooth and
the mylohyoid line is a shallow groove for the lingual nerve. Immediately posterior to
the last molar tooth on the medial upper surface of the body of mandible is a small
triangular depression (retromolar triangle). The pterygomandibular rapheattaches just
medial to the apex of this triangle and extends from here to the tip of the pterygoid

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hamulus above. The ramus of mandible, one on each side, is quadrangular shaped and
oriented in the sagittal plane. On the medial surface of the ramus is a large mandibular
foramen for transmission of the inferior alveolar nerve and vessels. 4
The teeth are attached to sockets (alveoli) in two elevated arches of bone on the
mandible below and the maxillae above (alveolar arches). If the teeth are removed, the
alveolar bone is resorbed and the arches disappear. The gingivae (gums) are specialized
regions of the oral mucosa that surround the teeth and cover adjacent regions of the
alveolar bone. The different types of teeth are distinguished on the basis of
morphology, position, and function. In adults, there are 32 teeth: 16 in the upper jaw
and 16 in the lower jaw. On each side in both maxillary and mandibular arches are two
incisor, one canine, two premolar, and three molar teeth. 4
₋ The incisor teeth are the “front teeth” and have one root and a chisel- shaped
crown, which “cuts.”
₋ The canine teeth are posterior to the incisors, are the longest teeth, have a
crown with a single pointed cusp, and “grasp.
₋ The premolar teeth (bicuspids) have a crown with two pointed cusps, one
on the buccal (cheek) side of the tooth and the other on the lingual (tongue)
or palatal (palate) side, generally have one root (but the upper first premolar
next to the canine may have two), and “grind.”
₋ The molar teeth are behind the premolar teeth, have three roots and crowns
with three to five cusps, and “grind.”
Two successive sets of teeth develop in humans, deciduous teeth (“baby” teeth) and
permanent
Teeth (“adult” teeth). The deciduous teeth emerge from the gingivae at between 6
months and 2 years of age. Permanent teeth begin to emerge and replace the deciduous
teeth at around age 6 years, and can continue to emerge into adulthood. The 20
deciduous teeth consist of two incisor, one canine, and two molar teeth on each side of
the upper and lower jaws. These teeth are replaced by the incisor, canine, and pre-

8
molar teeth of the permanent teeth. The permanent molar teeth erupt posterior to the
deciduous molars and require the jaws to elongate forward to accommodate them. 4

Figure 2. Teeth. A. Adult upper and lower permanent teeth. B. Deciduous

(“baby”) teeth. 4
All teeth are supplied by vessels that branch either directly or indirectly from the
maxillary artery. Veins from the upper and lower teeth generally follow the arteries. 4

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 Figure 3. Arteries and veins of the teeth. 4

2.2 Ameloblastoma
2.2.1 Definition and Etiology
Ameloblasts are of ectodermal origin and derived from oral epithelium. The cells
are only present during tooth development that deposit tooth enamel, which forms the
outer surface of the crown. Ameloblasts become functional only after odontoblasts
form the primary layer of dentin (the layer beneath enamel). The cells eventually
become part of the enamel epithelium and eventually undergo apoptosis (cell death)
before or after tooth eruption. There exist deposits of these cells in the structures in and
around the tooth, termed cell rests of Malessez and cell rests of Serres. Current thought
is that ameloblastomas can arise from either the cells mentioned above or other cells of
ectodermal origin, such as those associated with the enamel organ. Approximately 80%
occur in the mandible and the other 20% in the maxilla.1

2.2.2 Epidemiology
Ameloblastomas can occur over a broad age range, and most commonly affect
patients between the ages of 20 to 40 years. They are uncommon in children younger
than ten years. Males and females are equally affected. Ameloblastomas are located
most commonly in the posterior mandible, with fewer tumors arising in the maxilla.
Rizzitelli A et al. conducted a population-based study of malignant ameloblastoma to
determine it’s incidence rate and absolute survival. They looked at 293 patients across
the United States and found that the overall incidence rate of malignant ameloblastoma
was 1.79 per 10 million persons/year. The rate of incidence was higher in males than
females and also higher in the black versus white population. They also found that
malignant ameloblastoma, comprising the two types, metastasizing ameloblastoma,
and ameloblastic carcinoma, represents 1.6 to 2.2% of all odontogenic tumors. Their
findings confirmed previous epidemiologic research, which showed the male to female
ratio to be between 2.3 and 5. 1

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 There do exist variations that tend to arise in specific populations. The
ameloblastic fibroma is similar to ameloblastoma, but with a different histopathologic
presentation. They generally occur in the age group between 10 to 16 years of age.
Treatment involves simple enucleation and curettage as opposed to 10 mm margins
with ameloblastoma. The ameloblastic fibro-odontoma is another variation and
typically arise in patients aged 6 to 10. Treatment is enucleation and curettage.
Radiographs and demographics are vital in making these diagnoses. Malignant
variations of the ameloblastoma can occur between the teenage years up to older age.
1

2.2.3 Classification
The new version simplified classification into 3 types: conventional, unicystic
and peripheral. The solid/multicystic term was discarded, as it could be confused with
the unicystic type. Desmoplastic ameloblastoma was also reclassified as a histological
subtype and not as a clinical-pathological entity, based on the fact that it behaves like
any conventional ameloblastoma, although its clinical and radiographic characteristics
are peculiar.5,6

Figure 4. Flowchart with the new classification of ameloblastomas -

WHO2017

Out of these types, conventional ameloblastoma is the most common,

representing 85% of all ameloblastomas, and occurs mainly in the 3rd and 4th decades

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of life. Its biological behavior is considered more aggressive due to its higher incidence
of recurrence. Histologically it can be divided into follicular, plexiform, acanthomatous
and granular cell morphological patterns; other less common histological variants are
clear cell and desmoplastic cells. In general, one-third of the conventional type has a
plexiform pattern, one-third a follicular pattern, and the remaining third corresponds to
the other variants. It is currently accepted that there is no relationship between
histological pattern and tumor behavior or prognosis. In addition, it is not uncommon
for the same ameloblastoma to present different histological patterns. (Fig.4) 6

Figure 5. Conventional ameloblastoma presenting multiple patterns:

plexiform, follicular and acanthomatous (Original Magnification × 100) 6

Unicystic ameloblastomas (AU) are neoplastic entities characterized by a cystic

morphological appearance covered by an ameloblastic epithelium that may present
tumor growth to the lumen and the fibrous connective tissue. Based on its
histopathological characteristics, it presents 3 histological subtypes, characterized by
the proliferation pattern of the epithelial component into: luminal, intraluminal and
mural. Luminal and intraluminal variants respond satisfactorily to conservative
surgical approaches, whereas the mural variant presents higher rates of recurrence, and
is thus treated in the same manner as conventional ameloblastomas. 6

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 Figure 6. Unicystic ameloblastoma showing intraluminal proliferation in
follicular and acanthomatous pattern (Original Magnification × 100) 6

Peripheral ameloblastoma is the least common variant, accounting for only 1%

of cases. It primarily affects patients with a mean age of 52 years and occurs most
frequently in the gingiva of the mandible. It rarely presents recurrences, even when
treated conservatively. The histopathological aspect is represented by islands of
ameloblastic epithelium with a pattern similar to the conventional type. 6

2.2.4 Diagnosis
Ameloblastomas usually are asymptomatic until the patient notices intraoral or
facial swelling. Patients often present with progressive maxillary or mandibular
expansion and facial asymmetry. Pain and altered sensation are uncommon. Patients
may complain of a change in bite and loose teeth. Smaller tumors are usually detected
first on routine dental radiographic exams. Untreated tumors can grow to massive
proportions and cause facial deformity, as exhibited, especially in third world countries
where patients can go for long periods before seeking treatment or having access to
care. 1

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 Figure 7. (A) Axial CT with bone algorithm showing a kidney-shaped
odontogenic keratocyst in the left maxilla. (B)Axial CT displayed a circular-
shaped ameloblastoma occupying the right maxilla with a length of 29.27 mm
and a width of 27.30 mm

The diagnosis of ameloblastoma requires imaging (usually a CT scan) as well as

a biopsy. The CT scan most commonly shows a well-defined, uni- or multilocular
radiolucent expansile lesion. It is also good for the evaluation of any cortical
destruction or soft tissue extension. Although ameloblastoma originating within bone
is often detected on dental X-rays (orthopantomogram, OPG) or plain film, however,
the extent of soft tissue or bone invasion is often not accurately documented. On X-
ray, the unicystic ameloblastoma appears as a lytic lesion with scalloped margins. It
also shows impacted molars and resorption of tooth roots. The commoner multilocular
ameloblastoma appears as the classic ‘‘soap bubble’’ appearance on an X-ray. For
ameloblastoma arising from the maxilla, an MRI is more useful than CT, as it better
characterizes any extension to the skull base, orbit, or paranasal sinuses. MRI is also
the imaging modality of choice for desmoplastic ameloblastoma since it has ill-defined

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soft tissue borders that can be misdiagnosed as a fibro-osseous lesion. The unicystic
ameloblastoma is usually diagnosed only after a histopathologic examination because
it appears like an odontogenic cyst both clinically and radiologically. On imaging
modalities such as CT or MRI, the unicystic ameloblastoma has the appearance of a
thinly corticated unilocular radiolucency usually in association with an un-erupted
tooth and often leading to jaw expansion. In the case of metastasizing ameloblastoma,
a positron emission tomography (PET) scan is generally preferred to detect distant
metastasis.7–9

A B

Figure 8. (A) unilocular ameloblastoma in the anterior mandible with signs of

root resorption. (B)Multilocular appearance of an ameloblastoma in the anterior
and posterior regions of the mandible.(C) multilocular, soap-bubble appearance
of an ameloblastoma in the right mandible. (D)Multilocular lesion with a spider-
like appearance of an ameloblastoma in the mandible.

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Since none of the radiological features are pathognomonic, the definite diagnosis of
ameloblastoma is only established by biopsy. Histopathology helps in differentiating
ameloblastoma from ossifying fibroma, osteomyelitis, giant cell tumor, cystic fibrous
dysplasia, myeloma, and sarcoma. Preoperative staging in cases of malignant
ameloblastoma is also established by biopsy. Trucut needle biopsy can be obtained
under CT guidance via a dental socket or a window of cortical erosion. For an incisional
biopsy, disruption of the mucosa is required, which will ultimately need to be removed
at surgery. Peripheral ameloblastoma can be easily biopsied since it is not covered by
bone.8,9

Based on clinicopathological features, Yang et al. staged ameloblastomas into

three stages: stage I, the maximum tumor diameter ≤6 cm; stage II, the maximum
diameter of tumor >6 cm or tumor invasion into the maxillary sinus or orbital floor;
and stage III, tumor invasion of the skull base or metastasis into regional lymph nodes.
There is a significant relationship between time to recurrence and tumor stage, with the
earliest recurrence in stage III tumors.10

2.2.5 Differential Diagnosis

It is difficult to differentiate benign ameloblastoma from malignant
ameloblastoma on histology alone as it can look benign on histology but be clinically
invasive or even metastasize. Benign ameloblastoma is histologically identical to
malignant ameloblastoma but has no metastases. However, malignant variations are
extremely rare, with only approximately 30 cases of malignant ameloblastoma in the
literature, and about several hundred cases of ameloblastic carcinoma.1

Ameloblastic fibroma may share the same features histologically, such as small
cords and islands of ameloblastic epithelium that's just two cells thick containing dense
collagenous stroma which is often immature. It can also occasionally contain
cementum or dentin production as well as stellate reticulum. The main feature of
ameloblastic fibroma is that the stroma is more primitive and it should not metastasize.

16
Primary squamous cell carcinoma of the lung and metastatic disease in the lung that
has spread will have histologic features of malignancy but no other features of
ameloblastoma (no polarization, no peripheral palisading, no stellate cells, etc.). 1

2.2.6 Treatment
The treatment modality of choice for ameloblastoma is surgery. Other modalities
like chemotherapy or radiotherapy have a limited role and only in select situations.

₋ Surgery
The goal of surgical treatment of ameloblastomas is to minimize
recurrences and restore good function and aesthetics with minimum morbidity
in the donor area. The currently recommended surgery for classic
ameloblastoma (solid/multicystic type) is complete en bloc resection (radical
surgery) with an adequate margin of safety, which is classified as segmental or
marginal osteotomy for the mandible and partial or total maxillectomy for the
maxilla. Due to the high recurrence rate after conservative surgery, particularly
for solid/multicystic ameloblastomas, a wide resection with a 1 to 1.5 cm bony
margin is recommended. However, a recent meta-analysis could not prove the
superiority of radical surgery over conservative surgery. Recurrence is
attributed to the infiltration of tumor cells into the cancellous bone beyond the
periphery of radiographic margins. Immediate or delayed bone reconstruction
and dental rehabilitation have to be ensured to help with speech and swallowing
and improve patient outcomes.
However, radical surgery leads to aesthetic deformities, functional
impairments, and psychological distress. To avoid these complications,
conservative surgery has also been tried, which includes marsupialization,
enucleation, curettage, enucleation combined with Carnoy’s solution,
enucleation combined with curettage, and curettage combined with
cryotherapy. However, these conservative approaches lead to a high recurrence
rate, which has been reported to be 40% in a recent meta-analysis. For treatment

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of primary solid/multicystic ameloblastoma when conservative treatment was
performed, the relative risk of recurrence was three-fold higher in comparison
to radical treatment. Similarly in another meta-analysis that included four
studies on radical versus conservative treatment approach for ameloblastoma, a
higher recurrence rate after a conservative approach compared to the surgical
approach was documented. Thus, the treatment of primary multicystic
ameloblastoma with bone resection is justified.
For mandibular reconstruction, vascularized free bone grafts (from the
fibula, ilium, scapula, or radius) are the standard; the flap of choice is the fibular
free flap, which has the added advantage of reconstructing long segment
mandibular defects.
The iliac crest-internal oblique free flap is particularly well suited for
mandibular reconstruction because of the utility of the internal oblique muscle
in the formation of a soft tissue closure over the bone. For mandibular angle
defects, the iliac crest is favored, eliminating the need for multiple osteotomies
as seen with the fibula. Those patients who are reconstructed with an
osteomyocutaneous free flap may be considered for osteointegrated dental
implants. Pappalardo et al. suggest that osseointegrated implants lead to
significantly better masticatory function, fewer psychological consequences,
and improved quality of life. Distraction osteogenesis is also finding increased
use in mandibular reconstruction following surgical resection of the tumor. The
recent use of virtual 3D surgical planning has further improved outcomes by
making reconstructive surgery much more predictable and precise.
Reconstruction of maxillary defect is done using a skin graft to line the
cavity. An obturator is fitted thus allowing easy access to the resection bed
during surveillance. The cortical bone of the maxilla offers less resistance to
tumor invasion as compared to the mandible and therefore ameloblastoma of
the maxilla has a higher local recurrence rate after a surgical procedure. Hence,

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 free flaps are not used for maxillary defects to avoid covering a potential
recurrence site
For unicystic ameloblastomas, both the radical as well as the
conservative surgical approach, including excision, marsupialization, chemical
electrocautery, curettage, radiation therapy, or combined surgery and radiation,
may be employed.The extraosseous/peripheral ameloblastoma is mostly treated
with wide local excision, and a recurrence rate of 9%-20% following treatment
has been reported.9
₋ Non-surgical treatment
Systemic chemotherapy has no role in the treatment of localized
ameloblastoma, however, in metastatic settings, chemotherapy remains the
only choice of treatment. Numerous agents and combinations have been
employed using cyclophosphamide, methotrexate, 5-fluorouracil, vinblastine,
cisplatin, bleomycin, adriamycin, paclitaxel-carboplatin, doxorubicin, and
gemcitabine. Ameloblastoma may be sensitive to platinum-based anticancer
agents.
Recently, with the elucidation of molecular markers of ameloblastoma,
there have been attempts for the treatment of ameloblastoma with molecular
targeted therapy. These tumors have highly recurrent somatic mutations in the
signaling pathways of mitogen-activated protein kinase (MAPK) and sonic
hedgehog (SHH), which are known to be activated during tooth development.
Within the MAPK pathway, the BRAFV600E mutation is found in 57% of
ameloblastomas, while within the SHH pathway, Smoothened (SMO)
mutations have been identified in 24% of ameloblastomas. Interestingly,
ameloblastomas with BRAFV600E mutations are predominantly (96%) located
in the mandible and ameloblastomas with SMO mutations are predominantly
found in the maxilla (85%). Molecular targeted therapy drugs that have the
potential to be used in ameloblastoma are those which inhibit the functions of
mutated BRAF and MEK. The US Food and Drug Administration (FDA) has

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 approved three molecular targeted therapies for the BRAF V600E mutation:
vemurafenib and dabrafenib for BRAF mutation and trametinib for MEK
mutation. In a recent study, multiple recurrent ameloblastomata in the mandible
with metastatic masses in both lungs responded dramatically to therapy with a
dual BRAF/MEK inhibition by dabrafenib/trametinib . Similarly, another
report showed a notable reduction in tumor volume in a multiply recurrent
ameloblastoma of the mandible in response to single BRAF inhibition therapy
with dabrafenib.
₋ Radiotherapy
Similar to chemotherapy, radiotherapy also has a limited role in the
management of ameloblastoma. It may be utilized in patients with post-surgical
microscopic or gross residual disease, poor surgical candidates, or those with
disease not amenable to re-resection . Dose-fractionation schedules needed for
tumor control are similar to those used for carcinomas and range from 66 Gy in
33 once-daily fractions five fractions per week for microscopic residual disease
to 70 Gy in 35 once-daily fractions for a treatment duration of seven weeks. In
a recent pooled analysis of three studies on radiotherapy for ameloblastoma,
local tumor control was achieved in seven of nine (78%) patients irradiated for
gross disease and three of three (100%) patients treated for microscopic residual
disease after surgery. Newer technologies for radiotherapy such as image-
guided radiotherapy, stereotactic radiotherapy, intensity-modulated
radiotherapy, and proton beam therapy may be beneficial for patients with
extensive maxillary ameloblastomas extending to the skull base to effectively
treat the tumor without significant dose to the CNS and visual apparatus

2.2.7 Complications
The complications of malignant ameloblastoma are usually due to its local
invasiveness or distant metastatic spread. In terms of local complications, it can lead to

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progressive maxillary and mandibular distortion leading to deformity, pain, and
malocclusion.1

Swelling was present as a pre-operative complication in all 56 cases (100%). Out

of 56 patients, the pain was present in eight cases (10%), numbness or an altered feeling
was present in two cases (2%), breathing obstruction was present in one case (1%), and
swallowing problems were present in two cases (2%). There were no complaints
concerning speech.11

2.2.8 Prognosis
The prognosis for ameloblastoma depends on the age of the patient, location and
size of the tumor, histological type, extent, and stage of disease. Ameloblastoma is a
slow-growing tumor and a meta-analysis calculated the mean specific growth rate of
ameloblastoma to be 87.8% per year. However, if left untreated, ameloblastoma can
grow to a huge size and pose a risk to the airway.7,8

After treatment, ameloblastoma may recur with an overall recurrence rate of

9.8% according to a Chinese study and 19.3% as per a European multicenter study.
Recurrence rates are dictated by the type of surgery used (radical versus conservative),
the adequacy of the surgical margins, and in cases of maxillary ameloblastoma
extension into vital structures such as the orbit, paranasal sinuses, or skull base.
Recurrence following conservative surgery is due to the persistence of residual disease,
which grows slowly within the evacuated cavity while radical surgical resection shows
far lesser recurrence rates. More than 50% of recurrences occur within five years of the
primary surgical intervention. Tumors that are larger than 6 cm in size or involve
adjacent anatomical structures, including soft tissue are associated with a higher
recurrence rate irrespective of the type of surgery. A higher recurrence rate is also
reported in granular and follicular histological subtypes. Generally, maxillary
ameloblastomas are more aggressive and prone to higher recurrence than mandibular,

21
mainly due to the thin maxillary cortical bone that provides a weak barrier for the local
spread of the tumor.9,10,12

Death may occur in patients with untreated maxillary ameloblastoma extending

into the central nervous system or in patients having multiple recurrences.9

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 DAFTAR PUSTAKA

1. Palanisamy, J. C. & Jenzer, A. C. Ameloblastoma. in (2022).

2. Masthan, K. M. K., Anitha, N., Krupaa, J. & Manikkam, S. Ameloblastoma. J.
Pharm. Bioallied Sci. 7, S167-70 (2015).
3. Fuchigami, T., Ono, Y., Kishida, S. & Nakamura, N. Molecular biological
findings of ameloblastoma. Jpn. Dent. Sci. Rev. 57, 27–32 (2021).
4. Drake, R. L., Vogl, W. & Mtichell, A. W. Gray,s Basic Antomy. (Elsevier Inc.,
2023).
5. Speight, P. M. & Takata, T. New tumour entities in the 4th edition of the World
Health Organization Classification of Head and Neck tumours: odontogenic and
maxillofacial bone tumours. Virchows Arch. 472, 331–339 (2018).
6. Cadavid, A. M. H. et al. Ameloblastomas: current aspects of the new WHO
classification in an analysis of 136 cases. Surg. Exp. Pathol. 2, 17 (2019).
7. Ghai, S. Ameloblastoma: An Updated Narrative Review of an Enigmatic Tumor.
Cureus 14, e27734 (2022).
8. McClary, A. C. et al. Ameloblastoma: a clinical review and trends in
management. Eur. Arch. oto-rhino-laryngology Off. J. Eur. Fed. Oto-Rhino-
Laryngological Soc. Affil. with Ger. Soc. Oto-Rhino-Laryngology - Head Neck
Surg. 273, 1649–1661 (2016).
9. Fujita, M. et al. Diagnostic value of MRI for odontogenic tumours.
Dentomaxillofac. Radiol. 42, 20120265 (2013).
10. Yang, R. et al. Recurrence and cancerization of ameloblastoma: multivariate
analysis of 87 recurrent craniofacial ameloblastoma to assess risk factors
associated with early recurrence and secondary ameloblastic carcinoma. Chin. J.
Cancer Res. 29, 189–195 (2017).
11. Ruslin, M. et al. The Epidemiology, treatment, and complication of
ameloblastoma in East-Indonesia: 6 years retrospective study. Med. Oral Patol.
Oral Cir. Bucal 23, e54–e58 (2018).

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12. Boffano, P. et al. The epidemiology and management of ameloblastomas: A
European multicenter study. J. cranio-maxillo-facial Surg. Off. Publ. Eur.
Assoc. Cranio-Maxillo-Facial Surg. 49, 1107–1112 (2021).

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