Odontogenic tumours/oral surgery courses by indian dental academy

GITAM DENTAL COLLEGE & HOSPITAL
DEPARTMENT OF
ORAL & MAXILLOFACIAL SURGERY
SEMINAR ON
Odontogenic tumours-
current concepts and its
treatment modalities.
Presented By:
Dr. Sambhav K Vora
III MDS

CONTENTS
INTRODUCTION.
CLASSIFICATION.
ODONTOGENESIS.
GENERAL PRINCIPLES OF MANAGEMENT.
PRINCIPLES OF SURGICAL MANAGEMENT OF JAW TUMOURS.
AMELOBLASTOMA.
CALCIFYING EPITHELIAL ODONTOGENIC TUMOUR.
ADENOMATOID ODONTOGENIC TUMOUR.
SQUAMOUS ODONTOGENIC TUMOUR.
ODONTOGENIC FIBROMA.
GRANULAR CELL ODONTOGENIC TUMOUR.
MYXOMA.
AMELOBLASTIC FIBROMA.
AMELOBLASTIC FIBRO-ODONTOMA.
AMELOBLASTIC FIBRO-DENTINOMA.
ODONTOAMELOBLASTOMA.
CALCIFYING ODONTOGENIC CYST.
BENIGN CEMENTOBLASTOMA.
ODONTOGENIC MALIGNANCIES.
CONCLUSION.
REFERENCES.

INTRODUCTION: -
The embryologic events that initiate control and guide the formation
of human odontogenic structures take place through a complex and finely
regulated series of inductive interactions between epithelium and
mesenchyme, which begin during 5th
and 6th
weeks of intrauterine life and
are completed about 16th
year after birth. During this extended period, there
is ample opportunity for developmental and growth mechanisms to fail in
whole or in part, resulting in the formation of malformations, hamartomas
and neoplasms.
Odontogenic tumors are an imprecise term that encompasses a
wide spectrum of lesions and variants that are derived from the specialized
dental tissues. These tumors do not always meet the criteria for neoplasia
and some appear to represent abortive attempts at odontogenesis. The
distinctions among the above mentioned 3 forms of abnormalities might in
part depend upon the embryologic stage of initiation and histologic and
gross appearance of the lesion at the age of clinical discovery.
Odontogenic tumors are primarily intraosseous lesions, although
extraosseous variants have been described occasionally. These tumors
have a varied clinical and radiographic appearance and can consist of
entirely soft tissue, a mixture of soft and calcified tissues or entirely

calcified tissues. A unique feature of these tumors is the wide range of
biologic behavior that they express. Because of this wide range of
behavior, various methods of treatment have been described for each
tumor ranging from conservative to aggressive therapy. Often the proper
therapy is selected only after careful consideration has been given to
correlate the specific lesion with its clinical behavior pattern. Here let us
discuss the various treatment modalities used to treat the odontogenic
tumors and the present day concepts regarding the management of the
same.
CLASSIFICATION: -
I. GORLIN, CHAUDHRY AND
PINDBORG’S CLASSIFICATION-
A. Epithelial odontogenic tumors:
1. Minimal inductive change in the connective tissue-
(i) Ameloblastoma.
(ii) AOT
(iii) CEOT.
2. Marked inductive change in the connective tissue-
(i) Ameloblastic fibroma.
(ii) Ameloblastic fibrosarcoma.
(iii) Odontoma: -
• Ameloblastic odontoma.
• Ameloblastic dentinosarcoma.
• Complex odontoma.

• Compound odontoma.
B. Mesodermal odontogenic tumors:
1. Myxoma.
2. Odontogenic fibroma.
3. Cementoma-
(i) Periapical cemental dysplasia
(ii) Benign Cementoblastoma.
(iii) Cementifying fibroma.
(iv) Gigantiform cementomas.
II. REICHART AND RIES
CLASSIFICATION-
Ameloblastic Ectomesenchy
mal
Mesenchym
al
Neuroectoderm
al
Ameloblastic Ameloblasto
ma.
AOT.
CEOT.
SOT.
Ectomesenchy
mal
AF.
AFO.
Complex
odontoma.
Compound
odontoma.
Cementoblasto
ma.
Odontogenic
Myxoma.
Odontogenic
fibroma.
Dentinoma.
Mesenchymal “Adamantino Periapical Fibroma.

”
hemangioma.
cemental
dysplasia.
Gigantiform
cementoma.
Cementifying
fibroma.
Lipoma.
Hemangiom
a.
Neuroectoder
mal
Ameloblasto
ma with
neurinoma.
Central
pacinian
neurofibroma.
Neurofibro
ma.
Melanotic and
Neuroectoderm
al tumor of
infancy.
I. WHO CLASSIFICATION (1992)-
I. Neoplasms and other tumors related to the odontogenic
apparatus-
A. Benign odontogenic tumors:
1) Odontogenic epithelium without odontogenic
ectomesenchyme: -
(i) Ameloblastoma.
(ii) SOT.
(iii) CEOT.
(iv) Clear cell odontogenic tumor.
2) Odontogenic epithelium with odontogenic
ectomesenchyme, with or without dental
hard tissue formation: -
(i) Ameloblastic fibroma.
(ii) AFO and AFD.

(iii) Odontoameloblastoma.
(iv) AOT.
(v) Gorlin lesion.
(vi) Complex odontoma.
(vii) Compound odontoma.
3) Odontogenic Ectomesenchymal with or
without included odontogenic epithelium: -
(i) Odontogenic fibroma.
(ii) Myxoma.
(iii) Benign Cementoblastoma.
B. Malignant odontogenic tumors:
1) Odontogenic carcinomas: -
(i) Malignant Ameloblastoma.
(ii) Primary intraosseous carcinoma.
(iii) Malignant variants of other
odontogenic epithelial tumors.
(iv) Malignant changes in odontogenic
cysts.
2) Odontogenic sarcomas: -
(i) Ameloblastic fibrosarcoma.
(ii) Ameloblastic fibro-dentinosarcoma
and Ameloblastic fibro-
odontosarcoma.
(iii) Odontogenic carcinosarcoma.
II. Neoplasms and other lesions related to bone-
A. Osteogenic neoplasms: -
1) Cementifying fibroma
(OF, Cementifying fibroma).
B. Non-neoplastic bone lesions: -

1) Fibrous dysplasia of the jaws.
2) Cemento-osseous dysplasias-
(i) Florid cemento-osseous dysplasia.
(Gigantiform cementoma, familial
multiple cementomas).
(ii) Other cemento-osseous dysplasias.
3) Cherubism.
4) Central giant cell granuloma (CGCG).
5) Aneurysmal bone cyst.
6) Solitary bone cyst.
C. Other tumors: -
1) Melanotic neuroectodermal tumors of
infancy.
III. REVISED VERSION OF WHO
CLASSIFICATION (2002)-
I. Neoplasms and tumor-like lesions arising from the
odontogenic apparatus-
A] Benign: -
1) Odontogenic epithelium with mature, fibrous
stroma; odontogenic ectomesenchyme not
present:
(i) Ameloblastomas.
 Intraosseous (central,
infiltrative).
 Extraosseous (peripheral).
 Desmoplastic.

 Unicystic.
(ii) SOT.
(iii) CEOT.
(iv) AOT.
2) Odontogenic epithelium with odontogenic
ectomesenchyme, with or without dental
hard tissue formation:
(i) AF and AFD (neoplastic).
(ii) AFD (non-neoplastic).
 AFO.
 Complex odontoma.
(iii) Compound odontoma.
(iv) Odontoameloblastoma.
(v) Calcifying ghost cell odontogenic
tumor.
3) Mesenchyme and /or odontogenic
ectomesenchyme with or without included
odontogenic epithelium:
(i) Odontogenic fibroma (simple).
(ii) Odontogenic fibroma (WHO-type).
(iii) Odontogenic Myxoma.
(iv) Benign Cementoblastoma.
B] Malignant (odontogenic carcinomas): -
1) Malignant (metastasizing) Ameloblastoma.
2) Ameloblastic carcinoma-
(i) Primary.
(ii) Carcinoma in intraosseous

Ameloblastoma (dedifferentiated).
(iii) Carcinoma in peripheral
Ameloblastoma (peripheral).
3) Primary intraosseous squamous cell
carcinoma
(i) Solid.
(ii) Cystogenic
 Non-keratinizing cyst.
 OKC.
4) Clear cell odontogenic carcinoma.
5) Calcifying ghost cell odontogenic
carcinoma.
(Malignant epithelial odontogenic ghost cell
tumor).
C] Malignant (odontogenic sarcomas): -
1) Ameloblastic fibrosarcoma
2) Ameloblastic fibro-dentino and fibro-
odontosarcoma.
3) Odontogenic carcinosarcoma.
II. Neoplasms and other lesions occurring in the jaw
bones-
A) Osteogenic neoplasms: -
1) Cemento-ossifying fibroma.
B) Non-neoplastic lesions: -
1) Fibrous dysplasia of the jaws.
2) Cemento-osseous dysplasia
(i) Focal cemento-osseous dysplasia.
(ii) Florid cemento-osseous dysplasia.
3) Other cemento-osseous dysplasia
(i) Cherubism.
(ii) Central giant cell granuloma (CGCG).

4) Pseudocysts of the jaws
(i) Aneurysmal bone cavity.
(ii) Simple bone cavity.
(iii) Lingual and buccal mandibular bone
depressions.
(iv) Focal marrow containing jaw cavity.
C] Other tumors: -
1) Melanotic neuroectodermal tumor of
infancy.
GENERAL PRINCIPLES OF
MANAGEMENT: -
IMAGING-
I. Plain radiography.
II. CT scan and 3-D CT scan.
III. MRI.
IV. Angiography.
BIOPSY-
I. Exfoliative cytology.
II. Aspiration biopsy.
III. FNAC.
IV. Excisional biopsy.
V. Incisional biopsy.

PRINCIPLES OF SURGICAL
MANAGEMENT OF JAW
TUMOURS-
Goals of treatment-
a. Complete eradication of a lesion
b. Preservation of normal tissue as permissible
c. Excision with least morbidity
d. Restoration of tissue loss, form and function
e. Long-term follow-up for recurrence.
Factors to be evaluated before
surgery-
(i) Nature of the lesion-
Before choosing the most appropriate surgical method, it is a
must to identify the lesion histologically with biopsy, whether
benign/malignant.
(ii) Anatomical location of the lesion-
a. The location of the lesion within the jaws may severely
complicate the surgical excision and therefore jeopardize the
prognosis. A benign tumour in an inaccessible area presents
an obvious problem surgically and from the standpoint of the

function rehabilitation of the patient. A more aggressive
tumour in an easily reachable and resectable area, as in the
anterior mandible, offers a better prognosis
b. Maxillary tumours exhibit much more aggressive behaviour
than their mandibular counterpart. Proximity to maxillary
sinus, nasal cavity, orbital cavity, cranial fossa, and
nasopharynx allows these tumours to grow asymptomatically
and more extensively to attain a large size with late symptoms.
c. Proximity of the benign tumours to adjacent vital structures
like neurovascular bundles and teeth is an important
consideration because preservation of these structures should
be attempted. If the tumour is aggressive, then both these
important structures have to be sacrificed.
d. The amount of involvement with in a particular site, mandible,
has bearing on the type of surgical procedure necessary to
obtain a cure with the more aggressive lesions. If the inferior
border is not involved in the lesion, marginal resection can be
carried out without continuity defect. When the tumour
extends through the entire thickness of the involved jaw, a
partial resection then becomes mandatory.
e. If the tumour is confined to the inferior of the jaw, without
perforating cortices, offers a better prognosis than those that
have invaded surrounding soft tissues. In the latter case, one

has to carry out wider resection sacrificing the more amount
of normal soft tissue along with the resection of the bone.
(iii) Aggressiveness of the lesion-
Surgical therapy of the odontogenic tumours ranges from
enucleation / curettage to composite resection. Histological
diagnosis positively identifies and therefore directs the treatment
of the lesion. Locally invasive tumours are treated with wider
resection in order to prevent recurrence.
(iv) Duration of the lesion-
Many odontogenic tumours exhibit slow growth and may
become static in size. The slower growing lesions seen to follow
a more benign course and treatment should be individually
tailored to each case.
(v) Functional rehabilitation of the patient-
After achieving the primary goal of eradicating odontogenic
tumours, next most important consideration is the residual
defects resulting from the extirpative surgery. Reconstruction is
much easier in mandible than in maxilla. When reconstructing
defects in the mandible, treatment goals should be established.
 Restoration of mandibular continuity-using reconstruction
plates.

 Restoration of alveolar bone heights, restore the adequate
bulk of the mandible-primary/secondary reconstruction
method-to prevent pathological fracture.
Gold, Upton and Marx in 1991 have presented a standardized surgical
terminology for the excision of lesions in the bone
(i) Enucleation
(ii) Curettage
(iii) Marsupialization
(iv) Recontouring
(v) Resection without continuity defect
(vi) Resection with continuity defect
(vii) Disarticulation.
1. Enucleation with/without curettage-
Enucleation- removal of an entire structure, without rupture, as one
shells kernel of a nut.
Curettage- a scraping, usually of the interior of a cavity/tract, for the
removal of new growths or other abnormal tissues, or to obtain
material for tissue diagnosis using hand instruments.
Eventhough, this is mainly used for the cystic lesions; non-
aggressive small benign tumours can also make use of enucleation
with/without curettage.

Indications-
1) Surgical excision of the tumours, which tend to grow by
expansion, rather than by infiltration of the surrounding
tissues.
2) Lesions occurring in the bone with a distinct separation
between the lesion and the surrounding bone.
3) Often there is a cortical margin of bone that delineates the
tumour or cyst from the bone.
4) Indicated in following tumours:
(i) Odontogenic tumours-
a. Odontoma
b. AF.
c. AFO.
d. AOT.
e. Cementoblastoma
(ii) Fibro-osseous lesions and nonodontogenic tumours
• Ossifying fibroma
• Cherubism
• CGCG.
• Osteoblastoma
(iii) Other lesions
i. Hemangioma
ii. Eosinophilic granuloma

iii. Neurofibroma
iv. Neurilemanoma
v. Pigmented neurectodermal tumour.
Marginal resection or resection without continuity
Defect / peripheral osteotomy / en block
resection:
Enblock resection- this is a procedure that allows complete excision of the
tumour, at the same time, a continuity of jawbone is retained. And thus
deformity, disfigurement, and the need for secondary cosmetic surgery and
prosthetic rehabilitation are avoided.
Peripheral osteotomy- a procedure in which scraping usually of the interior
of a cavity/tract, for the removal of new growths or other abnormal tissues
are done using rotary instruments.
Indications-
1. Benign lesions with a known propensity for recurrence.
2. In those lesions that are incompletely encapsulated or tend to
grow beyond their surgically apparent capsule.
3. Recurrent lesions
4. Indicated in the following tumours-
a. Ameloblastoma
b. CEOT
c. Myxoma

d. Ameloblastic odontoma
e. Squamous odontogenic tumour,
f. Benign chondroblastoma
g. Haemangioma
Intraoral marginal resection (surgical procedure) –
The circumgingival incision is taken and the releasing incisions can
be extended into the buccal mucosa on either side of the lesion leaving at
least one or two adjacent teeth on either side. Using periosteal elevator
reflects the full thickness mucoperiosteal flap. Care is taken not to
perforate the lesion. If the lesion is perforated, then overlying mucosa
should be sacrificed along with the excision of the tumour. The tooth next
to the tumour mass should be extracted on either side. The vertical
osteotomies are performed through the sockets of the extracted teeth on
either side using bur or saw blade.
Both the vertical osteotomy cuts are extended from the buccal to
lingual cortex. These cuts are joined with a horizontal cut, placed well
beyond the tumour mass including margin of the normal bone. Horizontal
cut is also completed through and through the buccal and lingual cortex.
Using osteotome carries out the complete excision of the tumour along
with some amount of normal bone. Teeth involved in the tumour mass are
removed with the block in toto. The remaining bony margins should be
checked for sharp areas and contoured by using round bur or bone file.
The excess mucoperiosteal flap is trimmed off and approximated to suture

the wound. This type of excision can be done under local anaesthesia with
sedation for smaller lesions or it can be planned under general
anaesthesia.
Extraoral peripheral osteotomy-
Since complete resection of large segments involving both the
horizontal and the ascending rami or disarticulation of the segment causes
considerable amount of disability, this method is useful, which will allow
complete removal of the pathology, but is less debilitating than complete
resection. The procedure is based on the observation that the cortical
inferior border of the horizontal body, the posterior border of the ascending
ramus and the condyle are not generally involved in the benign tumour
process. Bone regeneration will start from such areas even though a thin
rim of bone is preserved, especially in young patients result in
considerable restoration of the jaw anatomy.
Indications-
Large lesions involving posterior mandible.
Operative procedure-
In dentulous patients, intraoral crevicular gingival incision is taken
around dentulous area, both buccally as well as lingually. Buccinator and
mylohyoid muscles are separated after reflecting the mucoperiosteal flap.
In edentulous patients there is no need to take intraoral incision.
Extraoral submandibular incision is taken and the inferior border of
the mandible is exposed, if required posterior border of the ramus is also

exposed. The site of peripheral osteotomy is already decided by studying
CT scans or radiographs. The drill holes are made with the electrical dental
drill in the healthy bone around the periphery of the lesion. These holes
are connected until the tumour mass is separated from the thin span of
bone to be retained. The part to be excised is now separated from the
attached soft tissue on the external surface. The masseter and buccinator
muscles are detached with care, so that not to injure the branches of the
facial nerve. Then the mucoperiosteum of the alveolar process is elevated
and the specimen in turned outward to get access to the inner surface to
detach the mylohyoid and the internal pterygoid muscles. The temporalis
muscle is severed above the coronoid, after which the inferior alveolar
nerve and vessels are identified and grasped with a hemostat, ligated and
cut off. The remaining bone is now carefully inspected. Intraoral wound is
closed with watertight suturing. An immediate bone graft can be inserted
through the extraoral wound and fixed with intraosseous wires or bone
plates. The wound is closed in layers with a small rubber drain inserted to
prevent formation of a hematoma. An external pressure bandage is
applied. Careful long-term following up is mandatory.
Segmental resection of the jaw-
It is carried out for more extensive lesions, which include the inferior
border of the mandible.
Partial resection- A procedure wherein resection of a tumour by removing
the full thickness portion of the jaw is carried out. In mandible, this can

vary, depending on the site of the tumour from a small continuity defect to
hemi-mandibulectomy.
Disarticulation- Whenever condylar head is included in the resection of the
part of the mandible, then a procedure is called as hemi-mandibulectomy
with disarticulation.
Whenever the condylar head is retained for rehabilitation procedure
then the procedure is called hemi-mandibulectomy without disarticulation.
Total resection- Excision of a tumour by removal of the involved bone is
carried out. Maxillectomy or mandibulectomy procedures can be carried
out.
Composite resection- Requires much more radical intervention with wider
margins of excision of uninvolved tissues. Surgery may include along with
resection of the jaw, neck dissection. Radiotherapy or chemotherapy alone
or in combination with surgery may be used. This is usually used for
malignancies.
Indications-
1. For treatment of lesions that are infiltrative or
have a tendency to recur.
2. Those lesions, which extend close to the inferior
or posterior border of the mandible, the maxillary
sinus or the nasal cavity.
3. It is also used for malignant lesions with huge
recurrence potential.

4. Recurrent odontogenic tumours with difficulty in
examining and gaining an access surgically.
5. Maxillary ameloblastomas with high recurrence
rate.
6. Lesions close to the borders of the jaw, with the
possibility of postoperative pathologic fracture.
Resection of mandible-
Intraoral approach-
Advantages-
a. Excision of overlying mucosal tissue involved in the lesion is
facilitated.
b. Easy access for application of arch bars, extraction of
involved teeth, ligation of the inferior alveolar neurovascular
bundle, closure of the maxillary sinus and maintaining the
forward stability of the tongue, whenever required.
c. An external scar is avoided.
d. An extraoral tissues are preserved for a later reconstruction
procedure
Disadvantages-
a. Contamination of the surgical wound by the oral flora.
b. Lack of dependent drainage of the dead space.
c. Difficult access to the most posterior portions of the mandible.

d. The risk of damage to the branches of the internal maxillary
artery, deep in the wound.
e. Immediate bone graft reconstruction by oral route has a higher
rate of infection and loss of the bone graft (30%).
Surgical procedure-
For mandibular lesion extending posterior to the mental foramen,
ligation of the inferior alveolar neurovascular bundle prior to resection may
prevent significant intraoperative hemorrhage. The incision is designed to
expose the lesion on both the facial and lingual aspect with or without
inclusion of overlying tissues in the specimen. The same incision is
extended posteriorly through the buccal mucosa approximately 7 mm
lateral and parallel to the anterior border of the ascending ramus and
external oblique ridge. Blunt dissection is carried out along the surface of
the buccinator muscle to expose the periosteum and periosteum is
elevated lingually to expose the retromolar area of the mandible, internal
oblique ridge and medial surface of the ramus, till the lingula. The inferior
alveolar neurovascular bundle is located and a curved aneurysmal needle
can be passed around it with a ligature threaded through its eye. The
neurovascular bundle is ligated at the higher level above the lingula.
After this, the entire lesion is exposed by reflecting the
mucoperiosteal flap on buccal and lingual side till the inferior margin of the
mandible. The anterior and posterior bony cuts are then outlined as
planned and the cuts are finished by using bur or saw blade from buccal to

lingual cortex. In the tooth bearing area, one or two teeth may be removed
prior to sectioning the jaw, bony cut can be carried out through an empty
socket. Separation of the bony cuts can be completed with an osteotome.
The specimen is separated from its bony and soft tissue attachments and
inferior alveolar neurovascular bundle is sectioned below the ligature level.
Whenever the anterior portion of the mandible is removed, it is mandatory
to hold the genioglossus muscles with the hemostat prior to separation
from the specimen and then these muscles should be secured with a
suture in the forward position to the soft tissues of the chin or to the
reconstruction plate to prevent airway obstruction due to tongue fall
postoperatively. Primary closure of the wound is done. Intermaxillary
fixation or reconstruction plate is necessary to preserve the alignment of
the fragments.
Extraoral approach-
1) Segmental resection with disarticulation:
The surgical approach is through a combined postramal (Hinds) and
submandibular (Risdon) incision placed at least 2cm below and
parallel to the inferior and posterior borders of the mandible. After
the incision through the skin, subcutaneous tissue and platysma is
taken, the dissection plane is made deep to the platysma, along the
investing fascia to the inferior border of the mandible. The
pterygomasseteric sling and periosteal layer is divided at the inferior
border of the mandible. Subperiosteal reflection of the masseter

muscle is done along the lateral surface of the mandible to expose
the coronoid process, sigmoid notch and condylar neck. The anterior
portion of the resection is determined and dissected. Care should be
taken to prevent an intraoral communication, using the bur or saw
blade, the osteotomy is completed. By swinging the specimen
laterally, it is freed from its medial attachments subperiosteally. The
temporalis muscle is detached from the coronoid process. The
condylar head is separated from lateral pterygoid muscle
attachments. Care should be taken to prevent damage to the
maxillary artery and its branches. The specimen is completely
removed and the surgical wound is irrigated. The proximal portion of
the segment is smoothened to prevent intraoral perforation.
Reconstruction plate with condylar prosthesis is placed and fixed on
to the proximal stump with screws. The wound is closed in layers
after proper hemostasis.
2) Segmental resection involving the mandibular midline:
An incision of at least 2cm is made below the inferior border of the
mandible. Incision is taken through the skin, subcutaneous tissue. At
the level of platysma muscle the tissues are undermined. Platysma is
cut sharply and dissection is followed to the investing layer of the
deep cervical fascia. Incision through this layer is taken till the
periosteum at the inferior border of the mandible. The dissection is
carried out subperiosteally to detach the left and right digastric as

well as the mylohyoid muscle from the medial aspect of the
mandible. The genioglossus and geniohyoid muscle attachments are
located and a suture is passed around them. Then the muscles are
detached from the genial tubercles. The subperiosteal dissection is
carried on the buccal surface of the mandible to expose the planned
resection portion. The mental nerves are identified and protected.
The lateral extent of the resection is defined in the dentulous jaw by
extracting the teeth and placing the bony cuts through the sockets. A
mucoperiosteal flap is developed intraorally to free the specimen
from the soft tissue attachments. Prior to the removal of the
specimen, the remaining segments should be stabilized by carrying
out temporary intermaxillary fixation. The reconstruction plate is
contoured prior to excision of the bone and immediately secured it
following the resection by means of screws. This prevents the
collapse of the segments and allows jaw function during healing and
prior to reconstruction and also prevents scar contraction. The oral
mucosa is closed intraorally, using a horizontal mattress suture to
obtain as watertight seal as possible. The genioglossus and
geniohyoid muscles are pulled forward with suture, which is secured
to the reconstruction plate. Extraoral wound is closed in layers.
Maxillectomy-
Access to the maxilla is generally obtained by designing the classic
Weber- Fergusson incision. The eyelids are closed temporarily by taking

tarsorrhaphy sutures. For esthetic good results, it is recommended to
tattoo the vermilion border and other points on both sides of the incision
with methylene blue. These points are then matched during closure. The
typical incision splits the midline of the upper lip. But better cosmetic
results can be obtained by incising the philtral ridges and then offsetting
the incision at vermilion border. The incision is turned laterally at the base
of the columella, then around the alar base and along the side of the nose
to within 2mm of the medial canthus. Intraorally the incision is continued
down through the gingival margin. It is connected with a horizontal incision
at the depth of the labiobuccal vestibule, extending back to the maxillary
tuberosity. From here the incision turns medially across the posterior edge
of the hard palate. It then turns 900
anteriorly, several mm to the proximal
side of the midline, if possible to cross the gingival margin once again.
The incision is carried to the bone, except beneath the lower eyelid,
where the orbicularis oculi muscle is preserved. The cheek flap is then
reflected back to the tuberosity. The central incisor on the involved side is
extracted and the gingival and palatal mucosa is elevated back to the
midline. The incision extending around the nose is then deepened into the
nasal cavity. The palatal bone is then divided near the midline with a saw
blade or bur. The basal bone is then separated from the frontal process of
the maxilla with an osteotome. The orbicularis oculi muscle is retracted
superiorly and the bone cut is extended across the maxilla, just below the
infraorbital rim into the zygoma. If the posterior wall of the maxillary sinus

has not been invaded by the tumour, it is separated from the pterygoid
plates with a pterygoid chisel. The entire specimen is removed by severing
the remaining attachments with a large curved scissors placed behind the
maxilla.
After removal of the specimen, some amount of brisk bleeding is
expected, which is controlled with packing and electrocautery. Branches of
the maxillary artery in the pterygomaxillary fissure area may require
ligation. While packing in place, the specimen should be inspected to make
sure that complete tumour has been excised. All sharp bony projections
should be trimmed. The palatal flap is turned up to cover the medial bony
margin. A split- thickness skin graft is then sutured to the wound margins
to cover the entire defect. Graft is maintained in place by placing softened
impression compound ball in the defect. The surgical obturator, which is
prefabricated, is placed to seal the defect and support the packing. The
obturator is fixed to the remaining teeth by means of interdental wiring. The
main cheek flap is then turned back and closed in layers.
Modifications-
(i) When the tumour extends upto the roof of the maxillary sinus, but
does not invade, then the orbital floor should be included in the
resection.
(ii) When the tumour invades the roof of the maxillary sinus, orbit or
the ethmoid sinuses, orbital exenteration is mandatory.

(iii) The tumours, which are confined to the posterior aspect of the
maxillary sinus, may be managed with amore conservative
resection that spares the premaxilla.
Postoperative management-
1) Patients are kept in ICU for first one or two days for cardiovascular
monitoring and necessary maintenance of fluid and electrolyte balance.
2) Patients are kept on liquid diet.
3) Instruct to maintain the oral hygiene.
4) Prophylactic antibiotics are advocated for 5-7 days.
5) The surgical obturator is removed after 15 days and the wound is
irrigated with warm saline.
6) Excess skin graft and other debris are removed.
7) Long-term follow-up is necessary.
RECONSTRUCTION-
After surgical resection with continuity defect, there is
disfigurement, deviation of the mandible along with resultant altered
mandibular movements with facial asymmetry.
Need for reconstruction:
• For restoration of the movements and equilibrium of the mandible.
• For maintenance of normal occlusion, floor of the mouth and tongue’s
anatomical position.
• For restoration of near normal feeding.

• For acceptable esthetics and function.
• For more favourable social acceptance.
Immediate reconstruction:
Advantages-
1. Single stage surgery.
2. Early return of the function.
3. Minimal compromise of esthetics.
Disadvantages:
1) Recurrence in the grafted bone.
2) Loss of graft from infection.
Three ways of immediate reconstruction:
A] Performing the surgical excision and grafting, both via intraoral
approach.
B] Surgical excision utilizing both intraoral and extraoral approach, first
obtaining the watertight oral closure and grafting is done through extraoral
approach.
C] Earlier extraction of the involved teeth and waiting for 6-8 weeks for oral
healing and then surgery at second stage, with complete procedure via
extraoral approach to avoid communication of the graft.
Delayed reconstruction (second stage):
Here the consideration should be given to maintain the residual
mandibular fragments with their normal anatomic relationship with
intermaxillary fixation or using reconstruction plate. This is to avoid

cicatricial and muscular deformation and displacement of the segments,
which aids in the secondary reconstructive efforts at a later date. Usually
six months waiting period is observed for recurrence.
I. AMELOBLASTOMA.
Synonym:
Adamantinoma
Introduction:
It is a true neoplasm of odontogenic epithelial origin. It is the second most
common odontogenic neoplasm. Its incidence combined with its clinical
behaviour makes Ameloblastoma the most significant odontogenic
neoplasm of concern to oral and maxillofacial surgeons. Opinions differ
regarding its terminology, etiology, histological pattern, classification,
clinical and biological behaviour, diagnosis, treatment aspect and
malignant potential.
History:
1827 – first recognized by Cuzack.
1879 – described by Falksson.
1885 – Malassez coined the term Adamantinoma.
1934 – Ivy and Churchill coined the term Ameloblastoma.
Definition:
Robinson defined Ameloblastoma as usually unicentric, nonfunctional,
intermittent in growth, anatomical benign and clinically persistent.

WHO – “ it is a true neoplasm of enamel organ type tissue which does not
undergo differentiation to a point of enamel formation.”
Types:
I. Clinically-
a. Central or intraosseous.
b. Peripheral or extraosseous.
c. Desmoplastic.
d. Unicystic
II. Histologically-
a. Follicular
b. Plexiform
c. Acanthomatous
d. Granular cell
e. Basal cell
Pathogenesis:
The origin of Ameloblastoma is not known with certainty. According to
Thoma, Williams in 1993, the tumour may be derived from various origins.
 Late developmental sources – cell rests of enamel organ, either
remnants of dental lamina or epithelial cell rests of Malassez or
remnants of Hertwig’s sheath, follicular sacs.
 Early embryonic sources – disturbances of developing enamel
organ, dental lamina, tooth buds.
 Basal cells of the surface epithelium of the oral mucosa.

 Secondary developmental sources – epithelium of odontogenic
cysts, particularly primordial, lateral periodontal cyst, dentigerous
cyst and odontomas.
 Heterotopic epithelium in other parts of body, especially from the
pituitary gland.
 With concepts of neoplasia in general, it is likely the result of
alterations or mutations in the genetic material of cells involved in
odontogenic cysts.
 Environmental factors
 Patient variables – general health status, nutritional status.
Clinical features:
Frequency – it accounts for approximately 1% of all oral tumours.
18% of all odontogenic tumours.
Age – the average age at diagnosis is around 33 – 39years. And most
cases cluster between 1st
decades to 7th
decade.
Sex – men = female.
Race – more common in blacks and some studies identifies Asians as most
commonly affected population.
Site - mandible is most commonly affected area. (5:1). There is a
predilection for posterior maxilla and posterior molar-ramus of the
mandible.
Clinical presentation-
(i) Asymptomatic

(ii) C/o swelling and facial asymmetry.
(iii) Swelling is usually slow-growing, hard, non-tender, and ovoid
which is often large in size.
(iv) Pain – occasional sign, if secondarily infected.
(v) Ulceration of the overlying mucosa.
(vi) Tooth mobility.
(vii) Occlusal alterations
(viii) Failure of eruption of teeth.
(ix) Exfoliation of teeth
(x) Ill fitting dentures
(xi) Nasal obstruction
(xii) Later stage with nerve involvement – sensory changes of the
lower lip.
(xiii) Large persistent lesions may exhibit fluctuation and egg-shell
crackling.
If not treated,
It invades into the neighboring tissues by replacing them. Invasion into the
medullary space is the first feature. When the tumour attains larger size
with bone erosion, there is escape into the periosteum mucosa and
muscles of adjoining region.
Root resorption will occur. Locally aggressive invasion in
maxillofacial region – may compress vital structures, obstruct airway,
impairs swallowing, erode major arteries, or invade middle cranial fossa.

The extensive tumours can cause gross facial deformity.
Size – ranges from 1 cm upto 16 cm.
In maxilla, it may enlarge to involve maxillary sinus, and nasal cavity
leading to nasal obstruction and even proptosis of eye.
Radiographic findings:
(i) It presents as a unilocular / multilocular radiolucent lesions.
(ii) 50 % of ameloblastomas appear as multilocular radiolucent
lesions with sharp borders. 2 % of the Ameloblastomas are
peripheral. 6 % appear as Unicystic lesions.
(iii) The apparent lesional edge may be distinct or indistinct.
(iv) Multilocular cyst like radiolucency with compartmentalized
appearance due to bony septa ( honey comb or soap bubble
appearance ) resembles fibromyxoma, giant cell lesions.
(v) Small or large unilocular or multilocular lesion may contain
unerupted deciduous or permanent teeth and may resemble a
dentigerous cyst.
(vi) Lesions in dentulous area cause root resorption (30 %) and tooth
displacement.
(vii) Buccolilngual cortical expansion (80%), this tendency is stronger
than a cyst.
(viii) The displacement of neurovascular bundle at the inferior border
is often seen.

(ix) Maxillary lesions often involve the maxillary sinus and change the
normal radiolucency of the sinus to a more opacified appearance.
(x) The radiographic image of Ameloblastoma is at the most
suggestive and not pathognomonic. CT scan with 3-D reconstruction will
show the exact extent of the lesion.
(xi) One of the variants of the Ameloblastoma – the desmoplastic
Ameloblastoma most often found in the anterior maxilla or mandible
appears as a relatively radiopaque lesion because of its dense connective
tissue content (solid type lesion).
Histopathology:
The Ameloblastoma is composed of nests, strands and cords of
Ameloblastic epithelium, all separated by relatively small amounts of
fibrous connective tissue stroma. The characteristic histological features
of the Ameloblastoma are the orientation of the outer epithelial cell nuclei,
which are positioned (polarized) away from the basement membrane.
Two main patterns are seen:
1. Follicular type (resembles tooth follicle) –
consists of small to large odontogenic epithelial
nests (the follicles) and variously shaped and
sized ameloblastomatous islands (more common
pattern). Cyst formation is commonly seen.
2. Plexiform type – consists of interlacing strands of
narrow or wide odontogenic epithelial trabeculae

resembling the dental lamina. Both these
patterns may be observed in the same tumour.
Both these types have a columnar or cuboidal outer epithelial cell layer
bordering the connective tissue stroma and enclosing the inner epithelial
cells.
Subtypes –
(i) Acanthomatous type – compression of stellate reticulum into a
squamoid mass with squamous metaplasia is seen. Sometimes
keratin formation in the central portion of the tumour islands is
noticed. Occasionally epithelial or keratin pearls may be seen.
Usually seen in follicular type of Ameloblastoma or peripheral
Ameloblastoma.
(ii) Basal cell type – bears resemblance to the basal cell carcinoma of
the skin. The inner follicular and outer follicular cells may
assume a basal cell appearance throughout the lesion.
(iii) Desmoplastic type – variant of solid Ameloblastoma. Abundant
fibrous tissue stroma can be seen in this variety. Some areas of
calcification also can be seen. Marked stromal desmoplasia is
noticed. High recurrence rate.
(iv) Granular cell type – stellate reticulum like cells, get transformed
into cells with coarse granular, eosinophilic cytoplasm. This type
is found to be more aggressive type with high chances of
recurrence and metastasis (malignant transformation)

(v) Mural Ameloblastoma –another name for Unicystic lesion, which
is found in children and young adults. The Ameloblastic
epithelium lines the luminal surface and may proliferate into the
cyst (mural growth). Often ‘budding’ aggregates of basal cells,
follicular cells, or plexiform strands extend from the luminal lining
into the cystic wall. Further growth of the lesion takes place by
creation of microcystic and macrocystic formations in the
budding Ameloblastic elements that extend and enlarge the
primary cystic lumen or the cyst wall by resorption of host bone.
Differential diagnosis-
II.Radiologically-
 Dentigerous cyst,
 Odontogenic keratocyst,
 Cherubism,
 Giant cell granuloma,
 Odontogenic myxoma,
 ABC.
II. CALCIFYING EPITHELIAL ODONTOGENIC TUMOUR.
Synonym: Pindborg’s tumour.
Acronym: CEOT.
Introduction:

CEOT is an uncommon odontogenic tumour that appears to occupy
a position between hamartoma and aggressive neoplasm.
CEOT has been categorized by 1992 WHO classification as a benign,
locally invasive odontogenic neoplasm that is exclusively epithelial in its
tissue origin.
History:
Described by J J Pindborg in 1955.
Thoma and Goldman (1946) and Ivy (1948) have erroneously reported
the case of CEOT as Ameloblastoma.
1976-Franklin and Pindborg have reported that 113 cases of CEOT have
been described in literature since 1955.
2002-Neville, Damn, Allen and Bouguot have reported that around 200
cases of CEOT have been described in the literature.
Types:
I. Based on site of occurrence-
 Intraosseous-within the bone.
 Extraosseous-outside the bone.
II. Based on histopathology-
• Classical type.
• Clear cell variant.
• CEOT associated with AOT, dentigerous cysts and
odontomas.
Pathogenesis: -

A confirmed etiology still remains elusive. The probable
mechanisms are-
i. Reduced enamel epithelium.
ii. Stratum intermedium c ells of enamel organ.
iii. Immunologic response to stratum intermedium cells.
iv. Remnants of the primitive dental lamina.
v. Basal layer of oral epithelium.
Clinical features-
Frequency- uncommon to rare odontogenic neoplasm. Represents less
than 1% of all odontogenic neoplasms.
Extraosseous-5 to 6% of all CEOT’S.
Age – ranges from 8-92 years.
Most commonly reported in patient during 4th
, 5th
and 6th
decades of life.
Average patient age between late 30’s to early 40’s. 37-43 years.
Extraosseous – 12-48years.
Sex – no sex predilection.
Race – occurs more frequently in whites.
Site - mandible is preferred site than maxilla (3:1) may occur in any area of
the jaw, but premolar/molar region appears to be favoured. (65%)
Extraosseous – anterior region. Predilection for incisor/premolar region.
Intraosseous lesion-

2. Usually asymptomatic, discovered through
routine radiographic examinations.
3. Present as a slow-growing, painless, expansile,
hard, bony swelling – cortical bone thinning –
egg-shell crackling – perforation – soft tissue
infiltration.
4. May cause associated tooth tipping, rotation,
migration and/or mobility secondary to root
resorption.
5. In maxilla, the lesion may invade maxillary sinus,
pterygoid space, ethmoid and sphenoid sinuses
by extension.
Extraosseous lesion-
a. Painless mucosal-coloured to red swelling
of about 6-month duration that may
produce saucerization of the underlying
bone.
b. Sometimes may produce pain.
Radiographic features-
Not pathognomonic.
Radiographic features ranges with regard to

i. Lesion size and
ii. Bone pattern.
Routine dental radiographic images show-
65% - mixed radiolucent and radiopaque pattern.
32% - completely radiolucent.
3% - totally radiopaque.
“ Wind - driven snow” appearance – scattered flecks of calcification
throughout radiolucency.
May be unilocular and cystic, often associated with an unerupted teeth but
cyst like hydraulic pattern of cortical expansion is absent.
May be multilocular –
i. Honeycomb pattern – locules appearing small, round and somewhat
corticated.
ii . Soap bubble pattern – large spaces.
Radiographic border between tumour and surrounding bone appears to be
diffuse / well defined and circumscribed.
3 features associated with teeth that assist in the diagnosis of CEOT –
I. Embedded tooth that is rarely impacted e.g. I/II molar.
II. Inferior displacement of mandibular unerupted tooth causing
protuberance in this region because of penetrating apex of the
tooth into the inferior cortex.
III. Apical extension of the occlusal c luster that may obscure the
embedded tooth.

Erupted teeth may be displaced and root resorption may be seen in
adjacent teeth.
CT scan-
Expansion and thinning of buccal and lingual cortical plates by a
well-defined mass containing scattered radiopaque areas of varying size
and signal intensity.
MRI –
Predominantly a hypointense lesion on T1-weighted images.
A mixed hyperintense lesion on T2-weilghted images.
Hilstopathological features: -
Has characteristic histopathologic features-
1. Trabeculae and/or sheets of large, eosionophilic staining,
squamoid shaped epithelial cells frequently with prominent
intercellular bridges.
2. Tumour cells vary from polygonal to round to oval in shape. It
may be irregular, pleomorphic and ominous in morphology.
3. Scattered cells with clear glycogen rich cytoplasmic contents
may be seen.
4. Nuclear morphology and staining is highly variable. Single to
multinucleated cells that has normal to very large nuclei,
abnormal/pleomorphic in shape and have hyperchromaticity with
deep basophilic staining characteristics.

5. Increased number and/or abnormal mitotic figures are
uncommon.
6. Connective tissue stroma is usually inconspicuous between the
islands and sheets of epithelium.
7. Presence of a homogeneous, eosionophilic substance which has
been identified as amyloid-characteristic
8. Ultrastructural studies show 2 forms of amyloid-
i. Immunamyloid-arise from the light chain fragments
of immunoglobulins.
ii. Apudamyloid-arise from the cells of certain
endocrine tumours, which may be derived from the
endocrine polypeptide cells of neural crest origin of
amine precursor uptake and decarboxylation.
9. Immunohistochemical and electron microscopy reveals that the
amyloid is derived from-
a. Degenerative process involving the cytokeratin
intermediate filaments in tumour cells.
Or
b. Degeneration of type IV collagen associated with basement
membrane.
10.Special staining for amyloid-
i. Crystal violet – stains metachromatically.

ii. Congo red – display bright orange to red hue when
exposed to polarized light – apple green
iii. Thioflavin T – fluoresces to a blue colour decreases
an UV light.
11.Prominent or scattered calcifications, in concentric crenate like
shapes – liesegang rings are seen maturing within the amyloid
stroma.
12.Chen et al, reported that CEOT expresses bone sialoprotein.
Liesegang’s rings and epithelial cells near them demonstrated
positive histochemical staining to bone sialoprotein antibodies
evidence of a n in situ hybridization bone sialoprotein mRNA
signal respectively.
II. Clinically-
1. Ameloblastoma
2. Odontogenic Myxoma
3. Fibro Myxoma
4. Fibroma
5. Ameloblastic fibroma
6. Ameloblastic fibro odontoma
7. Large dentigerous cysts
8. OKC.
9. OF.

10.CGCG.
11.Central giant cell lesion.
12.Osteoma.
13.Osteoblastoma.
14.Cementoblastoma.
15.Primary odontogenic carcinoma.
16.Metastatic carcinoma of jaws.
17.Osteosarcoma.
18.Chondrasarcoma.
III. Radiologically-
A. Radiolucent-
1. Dentigerous cyst
2. OKC.
3. Gorlin cyst.
4. AOT
5. Central giant cell lesion
6. Early stage of ossifying fibroma
7. Early stage osteoblastoma
B. Mixed-
1. AOT
2. Gorlin cyst
3. Ameloblastic fibroodontoma
4. Maturing / advanced stage of ossifying fibroma

5. Osteoma
6. Osteoblastoma
C. Completely radiopaque-
1. Odontoma
2. Gorlin cyst associated with odontoma
3. AOT associated with odontoma
IV. Histologically-
1. Squamous cell carcinoma.
2. Metastatic carcinoma of jaws.
3. Unknown primary metastatic adenocarcinoma.
4. Primary intraosseous mucoepidermoid
carcinoma.
5. Osteosarcoma.
Management-
The surgical treatment of CEOT should be case specific and is
dependent on:
(i) Size and location of the neoplasm
(ii) Patient’s overall medical condition or tolerance to withstand the
surgical procedure.
(iii) Clinical activity (perforation of the cortical bone, periosteal/nerve
involvement etc.)
(iv) Recognized behavioural characteristics
(v) Skill / experience level of the operator

Small, intrabony mandibular lesions with well-defined borders – simple
complete but conservative tumour enucleation / curettage followed by
indicious removal of a thin layer of bone adjacent to the tumour.
Small maxillary lesions – surgically excised by either through intrabony
curettage or conservative enblock resection.
Maxillary tumours can be treated more aggressively than a similar sized
lesion in the mandible.
Resection without continuity defect or resection with continuity
defect can also be used.
Resection with continuity defect – segmental resections-significant
bone discontinuity requiring either distraction osteogenesis/graft and
reconstruction procedures.
Treatment of atypical/frankly malignant CEOT-
Early intervention essential.
Radical resection of the affected jaw portion and associated soft tissue
with no less than 1cm in every dissection.
Adjunctive external beam radiotherapy-local spread to cervical
lymph nodes
Adjunctive chemotherapy-controls distant organ metastasis.
Radiotherapy in lieu of surgical resection is contraindicated for CEOT.
Treatment of peripheral CEOT –
According to Houston and Fowler, simple local excision.
Prognosis-

Local recurrence rate 10%-20%
Incidence of malignant transformation to odontogenic calcifying
epithelial pindborg tumour is extremely low.
No reported recurrences in patient treated for peripheral CEOT.
II. ADENOMATOID ODONTOGENIC TUMOUR
Synonyms-
a. Adamantoma
b. Epithelial odontome
c. Tooth germ cyst of the jaw
d. Adenoameloblastoma
e. Glandular Ameloblastoma
f. Adenomatoid Ameloblastoma
g. Ameloblastic adenomatoid tumour
Acronym- AOT
Introduction-
AOT is a benign, nonaggressive odontogenic tumour
characterized by the formation of “duct like structures” by the
epithelial component of the lesion.
AOT is considered as an odontogenic tumour because-
a. Occurs only in the tooth – bearing area of
the jaws.

b. Its histomorphologic resemblance to
components of tooth germ.
AOT is the fourth most frequent odontogenic tumour.
Some investigators consider AOT as an hamartomas because-
i. Limited size of most cases
ii. Lack of recurrence
Others consider AOT to be a non-aggressive, non-invasive benign
neoplasm because –
i. The limited size of the most cases
stems from the fact that most are
detected early and removed before
slow-growing tumour reaches a
clinically noticeable size.
ii. The microscopic features of the
lesional tissues show greater
departure from the arrangement of
the normal odontogenic apparatus,
than should be expected in a
developmental anomaly.
Gardner describes AOT as “benign embryonal neoplasm”
History-
1909-James and Forbes reported case as “epithelial odontome” almost
certainly an AOT (England).

1915- earliest irreputable case reported by HARBITZ, Norway, as
“Adamantoma”.
1916-Ist acceptable American case reported, “Tooth germ
(chorioblastomatous) cyst of the jaw” by Wohl.
1948-Stafne reported first series of AOT as “epithelial tumours associated
with developmental cysts of the maxilla.
1950-BERNIER AND TIECKE, coined the term “adenoameloblastoma”
1951-V annual American Academy of Oral Pathology meeting simple
Ameloblastoma and adenoameloblastoma as separate entities “was
presented for further consideration but was not adopted.
1961-GORLIN et al introduced the term “Ameloblastic adenomatoid tumour.
(AAT)
1963- SHAFER et al adopted the term “AAT’ in his 2nd
edition of Textbook of
Oral Pathology.
1968-ABRAMS et al suggested the term “odontogenic adenomatoid
tumour”
1969-PHLIPSEN AND BIRN, proposed the name “AOT’.
1971-the term AOT was adopted in the initial edition of WHO “Histological
typing of Odontogenic tumours, jaw cysts and allied lesions.”
1992- retained in the 2nd
edition of WHO “Histological Typing of
Odontogenic Tumours, jaw cysts and allied lesions”
Types-
 Based on the location-

1. Intraosseous/central/intragnathic
2. Extraosseous/peripheral/extragnathic
 Radiographically-
1. Pericoronal
2. Extracoronal
Pathogenesis-
A variety of ultrastructural studies attempting to clarify the origin of
AOT have been carried but in vain. The specific stimulus that triggers the
proliferation of the progenitor cells of AOT is unknown. Nearly all
investigations have agreed upon the cytologic resemblance of the
structures of AOT to the dental lamina and components of enamel organ.
Thoma suggested a dual origin for AOT-
(i) Salivary
(ii) Odontogenic
This was ruled out by Smith et al in 1979 who showed the presence of
hemidesmosomes and basal lamina at the luminal pole of the cells that
form the duct like structures.
This was supported by negative reactivity of these cells to lactoferrin and
L1 antichymotrypsin antibodies. (Takahashi et al).
The duct forming cells and non-duct forming cells exhibit secretory
granules and coated vesicles near the luminal pole resembling inner
enamel epithelium cells as they develop through preameloblast stage.

(Smith et al, Schlosnagle and Sameren, Yamamoto et al and Poulson and
Greer).
Spindle cells that are between cell-rich nodules resemble ultrastructurally
the stellate reticulum and those that are immediately adjacent to the
nodules resembles stratum intermedium of enamel organ.
The cell present in the tumour resembles the outer enamel epithelium cells
(Hatakeyama and Sujuki).
The cells present in the tumour have been described to resemble
odontoblasts. (Khan et al).
Philipsen et al, 1992 argued that AOT arises from remnants of the
successional lamina/accessional dental lamina.
Clinical features-
Frequency-3%-7% of all odontogenic tumours.
Intraosseous-97%
Extraosseous-3%
Age – ranges from 3-82 years of age. Its predilection for young patients is
well established.
88% diagnosed in the 2nd
and 3rd
decades of life. (Intraosseous)
Extraosseous 12-14years
Sex – females are commonly affected (2:1) intraosseous extraosseous F;
M= 14:1
Race – more common in b lacks. (Just harvesting phenomenon).

Site – maxilla more commonly affected than mandible (2:1). Marked
predilection for anterior jaw. 85 % of lesions appear anterior to the II
premolar (central and peripheral)
Clinical presentation –
Intraosseous
(i) Usually asymptomatic, but patient may be aware of an area of jaw
enlargement.
(ii) Discovered on routine dental radiographic examination.
(iii) Delayed eruption of permanent tooth or slow-growing bony
expansion – discovery of the central AOT’s
(iv) Mobility of teeth, swelling of the cheek, and asymmetrical facial
swelling has been reported less frequently.
(v) Infection of the tumour or fracture of the mandible – rarely led to
discovery of the lesion.
(vi) Nasal obstruction – rarely encountered.
Extraosseous-
(i) Gingival coloured mass that ranges from 1 – 1.5 mm in diameter.
(ii) Epulis like fibrous swelling that mimics periodontal disease if
bone erosion occurs.
(iii) 10 times more prevalent in maxillary gingival.
(iv) Painless

(v) Peripheral lesions represent central lesions that erupted with
tooth, to complete their development in the gingival.
A. Pericoronal—70 % of AOT’s are associated with the crown of an
unerupted tooth.
6% associated with two or more unerupted teeth.
60% of AOT’s associated with cuspids.
40% with maxillary cuspids.
3% associated with permanent molars.
B. Extracoronal – 30% of AOT’s
The relationship to the roots of adjacent / nearby teeth that
ranges from that lateral / interproximal to Periapical to no relationship at
all.
89% of extracoronal AOT’s occurred adjacent to permanent cuspids.
Radiographic presentation-
1. Not pathognomonic.
2. As well-circumscribed, pear-shaped radiolucency lying between the
diverging roots of the canine and I premolar teeth or
3. As unilocular, radiolucent lesion that is well-circumscribed exhibiting
smooth corticated border.
4. Most lesions are pericoronal or juxta coronal, but the radiolucency may
extend apically beyond the CEJ.

5.Rare multilocular lesions have been reported and a scalloped border is
observed occasionally.
6. Lesion may range from 1.5 – 7 cm and more.
7. May be associated with one or more impacted teeth.
8. Maxilla – slight buccal expansion of cortex.
9. Mandible – significant expansion present.
10. Maxillary lesions may grow into nasal fossa and antrum and may
obliterate the antrum and expand the orbital floor.
11. Evidence of calcification within the lesion (65%) – faint/quite dense
radiopaque foci.
Patterns of calcifications –
 Snowflakes
 Animal prints
 Hand / foot prints
 Doughnuts
 Semicircles
 Groups of dots.
Predominant pattern-even distribution throughout the lesion.
12. Occasionally, intralesional radiopacity may be identified usually
eccentrically positioned within the lesion.
13. Unique feature – presence of capsular space 0.3 –0.8 cm wide – well
defined, radiolucent band, that partly / most often completely surrounds
the periphery of the lesion.

14. Divergence of the roots and displacement of teeth occurs frequently.
15. Root resorption is rare.
16. Gingival lesions rarely are detectable radiographically but those may be
slight erosion of the underlying alveolar bone cortex.
Histologic features-
A. Macroscopic features –
 Soft, roughly spherical mass with a discernible fibrous capsule.
 White to tan solid to crumbly tissue or one/more cystic spaces of
varying size.
 Minimal yellow – brown fluid to semisolid material.
 Fine, hard gritty granular material.
 One to several larger calcified masses.
B. Microscopic features-
Tumour is made up of a cellular multinodular
proliferation of spindle, cuboidal, and columnar cells in
a variety of patterns; usually scattered duct like
structures, eosinophilic material, and calcifications in
several forms; and a fibrous capsule of variable
thickness.
6. Cell-rich epithelial nodules (hyaline droplets /
tumour droplets)
7. Microcysts
8. Internodular epithelial cells

9. Basaloid epithelial cells
10.Calcifying epithelial odontogenic tumour-like foci
11.Cystic space
12.Reduplicated basement membrane
13.Dysplastic dentin/dentinoid
14.Calcified bodies
15.Stroma
16.Fibrous capsule
17.Cytologic atypia
I. Clinically –
 Central odontogenic tumours and cysts
 Benign fibroosseous lesions
 Benign mesenchymal neoplasms
Gingival lesions –
 Gingival fibroma
 Peripheral cemento ossifying fibroma
 Peripheral giant cell lesions
 Other peripheral odontogenic tumours
II. Radiographically –
1. Pericoronal –
1. Dentigerous cyst
2. OKC

2. COC
3. Unicystic Ameloblastoma
5. Early Ameloblastic fibro-odontoma
6. Odontogenic fibroma
7. CEOT.
2. Extracoronal –
a. Aforementioned odontogenic tumours and
cysts
b. Central giant cell lesion
c. Benign fibroosseous lesions (early C-OF).
d. Lateral periodontal cyst
e. Lateral radicular cyst
f. Apical radicular cyst
g. Central benign mesenchymal neoplasms
(neurilemoma).
III. Histologically –
1. Vascular Ameloblastoma
2. Plexiform type of Ameloblastoma
Treatment –
Because of uniformly benign biologic behaviour of AOT and
consistent presence of a well-developed fibrous capsule – conservative

complete surgical excision by means of enucleation and curettage –
treatment of choice.
Impacted teeth incorporated within the lesion should be removed.
Teeth whose radicular bone cover has been resorbed by the lesion –
endodontically treated or removed.
Several reported cases have resolved or failed to progress following
incomplete removal of varying extent – not a preferred treatment –
incisional biopsy above or subtotal excision following confirmatory
incisional biopsy or marsupialization followed by cystectomy.
Prognosis-
1. Growth rate – slow / very slow growing tumour, but no
report of measurements of growth rate over a course
of time could be located
2. Recurrence rate – till date only 5 cases of recurrence
have been reported. Unequivocal case of recurrence
has not been reported.
Association of AOT with other odontogenic cysts and tumours-
 Dentigerous cyst
 Combined epithelial odontogenic tumour
 Odontoma
 Ameloblastoma
 COC
Unusual cases –

(i) Melanotic AOT
(ii) Multilfocal AOT.
Future research-
Modern research methods have facilitated the advancement of our
understanding of the histogenesis of this lesion but unanswered questions
remain. We await the results of in situ hybridization, DNA microassay
analysis, gene rearrangement studies and other developing molecular
biology techniques to solve the remaining mysteries.
IV. SQUAMOUS ODONTOGENIC TUMOUR
Synonyms –
 Benign epithelial odontogenic tumour
 Acanthomatous Ameloblastoma
 Acanthomatous Ameloblastic fibroma
 Hyperplasia and squamous metaplasia of residual odontogenic
epithelium
 Benign odontogenic tumour, unclassified.
Acronym – SOT.
Introduction –
SOT is a relatively rare, benign, but locally infiltrative and
occasionally aggressive odontogenic epithelial lesion that appears to have
hamartomatous and neoplastic characteristics.
History-

1975 – first described by PULLON et al.
Since then a number of papers have amplified details of the clinical
presentations and range of biologic activity of SOT.
Types –
I. Based on the site of occurrence –
 Intraosseous
 Extraosseous
II. Based on histopathology -
 Solid type
 Cystic type
Pathogenesis-
May be multifactorial.
(i) Cell rests of Malassez} intraosseous
(ii) Dental lamina
(iii) Surface stratified squamous epithelium} extraosseous
(iv) Cell rests of Serrae
Clinical features –
Frequency – rare odontogenic epithelium. 1 case of extraosseous lesion
described.
Age – SOT occurs over a wide range of age ranging from 2nd
– 7th
decade
and reported incidence peaks in the third decade of life.

Sex – no sex predilection. But some studies show slight male
preponderance and some others show slight female preponderance.
Race – no racial predilection. But SOT was diagnosed in whites, blacks
and Asians.
Site – maxilla = mandible. Some studies show that mandible is commonly
affected.
Maxilla – lesions centered around the incisor cuspid region
Mandible – lesions had a predilection for the bicuspid molar area.
Lesions may be found singly or multicentrically in all areas of both jaws.
(i) Often asymptomatic. Casually discovered by routine
radiographs.
(ii) Lesions involving dentate areas – alveolar resorption around the
teeth – tooth mobility and pain.
(iii) Tender on percussion – positive
(iv) Occasionally abnormal sensations present.
(v) If cortical bone is penetrated by the lesion, tumour infiltrates
gingival, occasionally unattached alveolar mucosal, palatal soft
tissue and rarely the buccal mucosal.
(vi) Aggressive maxillary tumours may infiltrate the maxillary sinus
and nasal floor and nasal spine.
(vii) Familial SOT’s have been reported.
Radiologic features-

Not pathognomonic of SOT. Presents as a triangular / semicircular
radiolucency within the alveolar bone between the roots of several teeth.
Displacement of one / both the adjacent roots. Destruction of crestal bone.
Presence of smooth sclerotic border at the margin of the lesion. Some
lesions are cystic / are associated with cysts. Thus they may appear
radiographically as dentigerous, periodontal / Periapical in form.
Extraosseous – saucerization of underlying bone.
I. Solid type-
(i) Consists of numerous islands of squamous epithelium dispersed
in a connective tissue stroma.
(ii) Islands are distributed in a uniform fashion and are well
demarcated from the surrounding connective tissue stroma.
(iii) The basal cell layer consists of flat to cuboidal cells and the
internal cells exhibit squamous differentiation.
(iv) The central areas of islands show foci of parakeratin or keratin
calcification or cellular degeneration.
(v) The epithelial cells are uniform and without pleomorphism or
nuclear hyperchromatism or mitotic activity.
II. Cyst type-
 Contains many islands of squamous epithelium in the connective
tissue wall, either completely separated from the odontogenic

epithelium lining the lumen or appearing to arise directly from the
luminal epithelial lining.
 These islands often exhibit vacuolization and microcyst
formation.
 Chronic inflammation may be seen.
I. Clinically –
1. Periodontal disease
II. Radiographically –
1. Dentigerous cyst
2. Apical periodontal cyst
III. Histologically –
 Acanthomatous and Desmoplastic Ameloblastoma
 SCC
Treatment –
Complete excision is required depending on the clinical and
radiographic extent of the lesion.
Intraosseous –
1. Enucleation
2. Curettage
3. Local excision

Clinically aggressive lesions – enbloc excision
Intrabony lesion involving the soft tissue due to the penetration of cortical
bone – soft tissue should be included in the excision.
Teeth within the lesional area – extracted.
Cystic lesion – treated conservatively.
Complete excision by enucleation and / or curettage.
Prognosis-
SOT exhibits a biologic behaviour pattern of aggression that appears
unaccountable in strictly histologic terms.
Recurrences of incompletely excised lesions have been reported.
V. ODONTOGENIC FIBROMA
Introduction-
A benign, relatively rare connective tissue tumour that contains a variable
amount of inactive odontogenic epithelium.
It has a benign behavioural course.
Types-
(i) Based on site of occurrence-
a. Intraosseous / central.
b. Extraosseous /peripheral.
CENTRAL ODONTOGENIC FIBROMA
Introduction-

The odontogenic fibroma is a central tumour of the jaws which is
seen so infrequently that little is known about this neoplasm. There is lack
of unanimity of definition of the lesion. Hence lots of uncertainty regarding
this tumour.
WHO classified COdF under “Odontogenic ectomesenchyme with / without
included odontogenic epithelium”
Slater et al (2001) considers this to be a mixed epithelial Ectomesenchymal
neoplasm.
Philipsen and Reichart (2002) , believes that the fibrous connective tissue
component is of a mature mesenchymal type and not that of an
Ectomesenchymal type.
Definition-
WHO defines COdF as a “fibroblastic neoplasm containing variable
amounts of apparently inactive odontogenic epithelium and in some cases,
calcified material resembling dysplastic dentin or cementum – like
material.”
Types-
1. Simple type – composed of delicate fibrous and myxoid tissue with
scant numbers of inactive appearing islands and strands of
odontogenic epithelium
2. WHO type / complex type – composed of cellular, mature, fibrous
tissue containing numerous strands and islands of odontogenic

epithelium without palisading, reverse polarization or Stellate
reticulum.
Handlers et al (1991) concluded that COdF need not be separated into
simple and WHO types because their histologic patterns did not
correlate with clinical behaviour.
The tumour formerly classified as the simple type was subclassified
as a myxofibroma under Myxoma section in WHO histological typing of
odontogenic tumours.
Basic concepts concerning COdF-
1. It is a lesion around the crown of an unerupted tooth resembling a
small dentigerous cyst.
2. It is a lesion of fibrous connective tissue, with scattered islands of
odontogenic epithelium, bearing some resemblance to the dental
follicle – because of size it may attain appearing to constitute a
neoplasm.
3. It is a lesion as described by WHO, as previously mentioned.
Pathogenesis-
1. Cells in dental follicle – gives origin to COdF associated with
unerupted teeth.
2. Periodontal ligament – gives rise to COdF not associated with
unerupted teeth.
Clinical features-

Frequency – 4% -5% of all odontogenic tumours. Ranges from 0 – 14%.
Age – 5 – 80 years. Mean 37 years.
Sex – female predilection (2.8: 1)
Race – occurs more frequently in whites. (95.5%)
Site – occurs more frequently in mandible (52%). Fonseca found a
predilection for maxilla. 77% of cases were located anterior to the I molar.
1. Asymptomatic
2. Mild tenderness / sensitivity – discomfort.
3. Paresthesia
4. Size 0.3 – 6.0 cm (Avg. 2.2 cm)
5. Duration few weeks to months to years.
6. Slow growing progressive enlargement
7. Unusual finding – presence of a cleft / depression or sinus tract like
defect involving palatal gingival and palatal mucosal. 39% of
maxillary COdF anterior to I molar had an associated palatal cleft.
Mechanism of formation of such palatal clefts is poorly understood -
attributed to the presence of myofibroblasts. COdF extends through
a perforation in the palatal bone adhering to the periosteum and
infiltrating the palatal mucosal. The palatal mucosa clinically seems
to collapse into the bony defect.
1. Expansile, multilocular radiolucency – majority.

2. May have mixed density or completely radiopaque mass.
3. May also be manifested as unilocular lesion
4. May have loculated / scalloped periphery.
5. Most lesions are well defined, with a sclerotic border. But in some
lesions the borders were ill-defined or irregular.
6. May also show – cortical expansion
External resorption of the tooth roots
Displacement of teeth
Tooth mobility
Erosion / perforation of cortical bone
Displacement of the inferior alveolar canal.
7. May be associated with residual odontogenic cyst / roots of erupted
tooth / unerupted tooth.
Histological features-
The microscopic components of COdF are –
1. Fibrous tissue of variable cellularity and density.
2. Variable amounts of inactive – appearing odontogenic epithelium.
3. Variable presence of calcifications resembling dysplastic dentin,
cementum – like tissue or bone
1. Fibrous tissue-
 Mesenchymal component varied from loosely collagenized to
well collagenized, with/without myxoid areas.

 Myxoid areas, when present, were focal to prominent in
distribution.
 Cellularity varied from sparse to moderate to cellular.
 Mitotic activity also was observed.
 Eosinophilic, amorphous globules, which stain weakly for
amyloid but may represent enamel matrix protein – infrequent.
 Pleomorphic plump, stellate shaped and binucleated
fibroblasts – Gunhan et al.
2. Odontogenic epithelium-
a. Inactive.
b. Present as islands / cords ranging from few to numerous.
c. Epithelial cells exhibited cytoplasmic vacuolization.
d. A zone of hyalinization may surround islands of epithelium.
e. Presence of microcystic spaces in epithelial strands – Dunlap.
3. Calcifications-
a. Ranged from focal to florid in distribution.
b. These were interpreted as-
Nonspecific calcifications.
Cementum /cementum – like
Cementum /dentin
Cementum and osteoid
Woven bone
None of the COdF’s were encapsulated.

1. Giant cell granuloma
2. Odontogenic fibromyxoma
3. Desmoplastic fibroma
4. Neurofibroma
6. Follicular sac surrounding the crown of an unerupted tooth.
7. Metastatic carcinoma
8. CEOT
9. Ameloblastoma
10.CEOC
11.CGCG
12.Cementifying fibroma
Treatment-
This tumour is treated by surgical excision. But the excision is
dependent on – clinical extent and anatomic involvement of the individual
lesion. Most lesions can be managed by – enucleation and curettage. The
lesions tended to shell out easily and completely from the surrounding
bone. The lesions associated with palatal defect – dissection of the defect
at their junction with palatal mucosa and periosteum. If the tumour
incorporates the mandibular neurovascular bundle, an attempt should be
made to preserve it. Teeth in the lesional area – extracted. The recurrent
lesions can be treated conservatively. Rare is a resection required.

Prognosis-
Recurrence rate 26%.
Length of follow up ranges from 1 – 10 years. The time interval between
first surgical procedure and the first recurrence ranged from 14 – 48
months. The spectrum of histologic patterns bears no correlation with the
biologic behaviour.
PERIPHERAL ODONTOGENIC FIBROMA
Synonyms-
 Odontogenic gingival epithelial hamartomas
 Peripheral Ameloblastic fibrodentinoma
 Peripheral hamartomas of dental lamina rest
 Calcifying fibrous epulis.
Acronym- POdF
Introduction-
POdF is considered to be the gingival counterpart of the COdF and is
rare in occurrence. POdF can be confused with peripheral ossifying
fibroma, a reactive lesion.
Clinical features-
Frequency – 1.2% of all odontogenic cysts and tumours.
Age – ranges from I to VIII decades.
Sex – M=F
Site – mandible > maxilla. Found anterior to the II premolar.

(i) Measures around 1 – 3 cm in diameter.
(ii) The lesions may be on the attached gingival or alveolar ridge.
(iii) May be pedunculated / sessile.
(iv) May have a normal gingival colour.
(v) Large lesions may displace teeth but do not involve the
underlying bone usually.
Radiographic features –
Radiographs reveals calcification in POdF more often than in the
COdF.
POdF mirrors central lesion in histologic appearance.
Unencapsulated proliferation of cellular fibrous or fibromyxomatous
connective tissue that exhibits variable amounts of odontogenic epithelium
and sometimes foci of calcification in the form of dentinoid, cementicles or
bone.
Differential diagnosis –
1. Peripheral giant cell granuloma
2. Pyogenic granuloma
3. Giant cell fibroma
4. Simple fibroma
5. Peripheral ossifying fibroma
6. Neurofibroma

7. Fibroepithelial polyp
Treatment –
The lesion should be excised to the interface with bone and a
modest perimeter of the uninvolved tissue. Teeth incorporated in the
tumour should be extracted.
Prognosis-
Unknown potential for recurrence. 39% recurrence rate in a 3 – 4
year interval. (Daley et al, 1994 and Gardner, 1982).
VI. GRANULAR CELL ODONTOGENIC TUMOR.
Synonyms-
 Granular cell odontogenic fibroma
 Granular cell Ameloblastic fibroma
 Granular cell tumour of the jaws.
Acronym – GCOT
Introduction-
Rare, benign odontogenic neoplasm that contains variable amounts
of large eosinophilic granular cells and apparently inactive odontogenic
epithelium.
Types-
1. Central GCOT
2. Peripheral GCOT
Pathogenesis –

Uncertain. Microscopic studies and immunohistochemical studies
support a mesenchymal origin for the granular cells.
Clinical features-
Frequency – rare. Only 30 cases have been reported.
Age – ranges from 16 – 77 years. Average – 45.5 years.
Sex – F > M (73.3%)
Site – mandible > maxilla (3:1). Premolar / molar region most common site.
 Asymptomatic.
 Cortical bone expansion – initial examination
 Duration – ranges from months to years
 Displacement of the teeth
 Facial swelling
 Intraoral ulceration
 Cortical perforation
 Maxillary sinus involvement
 Displacement of mandibular canal
(i) May be radiolucent / mixed density / radiopaque.
(ii) Patterns ranged from unilocular to multilocular often with a
sclerotic border.
 Specific.

 Consists of sheets / lobules of round to polygonal cells with
abundant, eosinophilic granular cytoplasm with round to ovoid
nuclei,
 Scattered among the granular cells are cords and nests of
odontogenic epithelium. Epithelial cells often possess clear
cytoplasm.
 Thin septae of fibrous connective tissue separate the lobules
of granular cells.
 The islands of epithelium do not form stellate reticulum.
 Scattered small cementum – like or dystrophic calcifications
seen (50%). Florid distribution of cementum like calcifications
has been reported.
 Ultrastructural studies supported the presence of lysosomes
within the cytoplasm of granular cells.
 Immunohistochemical studies have shown that the granular
cells express –
Vimentin
α1 antiltrypsin
Antichymotrypsin
Lysozyme
CD68
HLA –DR
But stains negative for cytokeratins and S-100 protein.

2. COdF
Treatment-
Treated using conservative approach – enucleation / curettage.
Prognosis-
Does not show an aggressive biologic behaviour but can recur.
VI MYXOMA
Synonyms-
(i) Odontogenic Myxoma
(ii) Myxofibroma
(iii) Odontogenic fibromyxoma
Introduction-
Benign, neoplasm of uncertain histogenesis with a characteristic
histologic appearance, often behaves in a locally aggressive, infiltrating
fashion.
This is grouped under the subheading “Odontogenic
ectomesenchyme with / without included odontogenic epithelium
according to WHO classification.”
Traditionally, myxomas are considered to be neoplasm of
odontogenic origin.
The odontogenic derivation of Myxoma is believed to origi9nate from
the primitive mesenchymal portion of the developing tooth germ as an

inductive effect of nests of odontogenic epithelium on mesenchymal tissue
or as a direct myxomatous change of fibrous tissue in an odontogenic
fibroma.
Definition-
WHO defines myxoma as a locally invasive neoplasm consisting of
rounded and angular cells that lie in an abundant mucoid stroma.
Types-
2 forms of myxomas are recognized in head and neck region.
1. Those derived from the soft tissue.
2. Those derived from facial skeleton – nearly nonexistent.
a. Odontogenic myxomas
b. True Osteogenic myxomas.
Clinical features-
Frequency – 3% - 6% of all odontogenic tumours. Occurs 2 – 4 times less
frequently than Ameloblastoma.
Age – occurs from 11 months to 7th
decade. 75% occurred between 2nd
and
4th
decades. 7% occurred in the I decade.
Sex – slight female preponderance. F: M = 1.5: 1
Site – 66% occurs in mandible. 34 % occurs in maxilla. Mandible: maxilla =
2:1.
Has a definite predilection for molar and premolar regions in both jaws.
May also occur in – sinonasal tract, facial bones, extracranial skeleton.

1. Usually asymptomatic.
2. Painless
3. Slow growing lesion and unilateral, some may cross the midline.
4. Mandible – buccal and lingual swelling.
5. Maxilla – swelling if sinus not involved.
6. Exophthalmos and nasal obstruction.
1. Periapical radiographs and panoramic radiographs – I indicators of
Myxoma of jaws.
2. Not pathognomonic.
3. Ranges from small unilocular lesions to large multilocular lesions.
4. Often displaces the teeth.
5. Rarely resorb the roots of the teeth.
6. The multilocular pattern – honeycomb, soap bubble, tennis racket,
wispy and spider web in appearance.
7. Multilocular myxomas > 4.0 cm. Unilocular – smaller.
8. 5 % of myxomas associated with unerupted teeth.
9. May appear as – radiolucent – common.
Mixed density – 12.5%
Radiopaque – 7.5%
10.1/3rd
exhibited diffuse / poorly defined borders.
11.CT & MRI should be used to clearly define tumour margins and to
define the true extent of the Myxoma before surgery is performed.

12.Imaging help to determine the true extent and involvement of the
neoplasm.
13.Significant cortical expansion and perforation of the cortex with
invasion into the soft tissues.’
14.In maxilla, extension into the antrum – sunburst / hairbrush
appearance.
15.Extension into nasal fossa and zygoma and thinning the orbital floor
and hard palate.
I. Macroscopic features-
1. Well-delineated, unencapsulated, gray-white to tan-yellow mass
that can be rubbery, soft or gelatinous in texture.
2. Margins are ill defined in gelatinous specimens
3. On cut surface, it is glistening, translucent and homogenous.
II. Microscopic features-
Bland in appearance.
1. Composed of loosely arranged, evenly dispersed spindle
shaped, rounded and Stellate cells with long protoplasmic
processes with a lightly eosinophilic cytoplasm in a mucoid –
rich, intercellular matrix.
2. Mild nuclear pleomorphism / hyperchromatism exist. Mitosis /
binucleate cells occasionally be present.

3. Myxoid matrix is rich in hyaluronic acid and chondroitin
sulphate.
4. Myxomas have a fine network of reticulin fibres and some have
low collagen content.
5. Inconspicuous vascularity – supports the diagnosis.
6. Occasional island / rest of inactive – appearing odontogenic
epithelium may be found.
7. Non encapsulated and may pervade surrounding bone by
expansion.
1. Enlarged dental follicle with myxoid change
2. Odontogenic fibroma
3. Dental papilla of a developing tooth
4. Malignant tumours of the jaws
5. Myxoid neurofibroma
6. Myxoid liposarcoma
7. Myxoid chondrosarcoma
8. Desmoplastic fibroma
9. Ameloblastoma
10.Hemangioma
11.CGCG
12.ABC.
13.Hyperparathyroidism

14.Central neurilemmoma
Treatment-
The standard treatment for Myxoma is surgical excision. Radiation
therapy and chemotherapy are ineffective treatments. A number of
surgical methods have been advocated –
1. Excision
2. Enucleation and curettage
3. Curettage with / without electrical or chemical cautery.
4. Enbloc resection
5. Wide resection with and without immediate grafting.
GOLD’S MANAGEMENT PROTOCOL-
1. Biopsy performed in a central area of the lesion and at the
radiographic lesion – host bone interface histologically identifies the
lesion.
2. Excision of the lesion by enucleation and curettage is restricted to
unilocular lesions of no more than 1-2cm in diameter. Chemical
cauterization (e.g. Carnoy’s solution) of the tumour bed may be of
value. Teeth and alveolar process at the edge or within the
radiographic and clinical limits of the lesion should be removed.
3. Extensive lesions should be excised by resection without continuity
defect or resection with continuity defect including a perimeter
margin of tumour – free bone of 1 cm depending upon the anatomic
extent of the lesion.

4. The neurovascular bundle of the mandible should not be sacrificed
routinely, even in lesions that require resection with continuity
defect.
5. The decision for immediate or delayed reconstruction is dependent
upon the
a. Clinical and / or histologic certainity of the complete excision
of the tumour.
b. Tissue requirements for reconstruction.
Prognosis-
Benign but aggressive tumour that has a propensity to infiltrate vital
structures. Recurrence rate ranges from 10% - 33%. Recurrences of
myxomas are related to incomplete removal than to the intrinsic biologic
behaviour of the tumour.
VII. AMELOBLASTIC FIBROMA
Synonyms-
 Soft mixed odontogenic tumour
 Soft mixed odontoma
 Fibroademantoblastoma
Acronym- AF
Introduction-
Relatively rare, true benign mixed tumour in which epithelial and the
Ectomesenchymal elements are neoplastic. It is characterized by the
simultaneous neoplastic proliferation of the mesenchymal and epithelial

components without formation of dental hard tissues, namely dentin and
enamel.
Definition-
WHO defines AF and related lesions as “neoplasms composed of
proliferating odontogenic epithelium embedded in a cellular
Ectomesenchymal tissue that resembles the dental papilla, and with
varying degrees of inductive change and dental hard tissue formation.”
History-
First reported by Kruse in 1891.
Types-
1. Intraosseous
2. Extraosseous
Pathogenesis-
Arises denovo during odontogenesis – result of overproduction of the
basal lamina without odontogenic differentiation.
Clinical features-
Frequency – 1% - 2% of all odontogenic tumours.
Age – predominantly in children and young adults with an age range of 6
months to 42 years (average 14. 6 – 15.5 years).
Sex – no sex predilection (Tradahl). Some authors have reported male
preponderance (Slootweg). Some authors have reported female
dominance.

Site – mandible most commonly affected. Most frequently in the I
permanent molar and II primary molar region. (80%). Rarely in the posterior
maxilla and anterior regions of the jaws.
 Asymptomatic. 20 % of the lesions discovered on routine
radiography.
 Painless, slow-growing and expansile neoplasm.
 Exhibits slower clinical growth than Ameloblastoma and does not
tend to infiltrate bone.
 Enlarges by gradual expansion – periphery of the lesion often
remains smooth.
 Initial presentation – pain, tenderness or mild swelling of the jaw,
discharge, and failure of teeth to erupt.
 Associated with an impacted tooth 75%).
Radiographic features – no pathognomonic radiographic features.
a. Appears as a large, expansile pericoronal radiolucency and is
well defined, unilocular / multilocular with a smooth, well-
defined outline and often with a sclerotic opaque border.
b. Small lesions are typically unilocular, whereas large
mandibular lesions are multilocular. They may range in size
from 1-8cm in diameter.
c. Associated with unerupted teeth / impacted tooth.
d. May be completely with in the bone or perforate the cortex.

e. Root resorption and inferior displacement of the mandibular
canal may be seen.
Appears as a solid, soft tissue mass with a smooth
surface and often exhibits lobulated configuration. A
well-defined capsule may not be present.
II. Microscopic features –
A. Ectodermal portion-
 Proliferating islands, cords and strands of
odontogenic epithelium with a peripheral layer
of cuboidal / columnar cells and central area
resembles the Stellate reticulum of embryonic
enamel organ. (Tumour islands are found
“opening”).
 Mitotic activity uncomm9on.
 Epithelial cells may be rounded / cuboidal.
arranged in slender strands.
 Amount and density of epithelial component
may vary from area to area.
 Cystic degeneration usually not seen.
B. Ectomesenchymal portion-

1. Embryonic, cell-rich mesenchyme that mimics the
dental papilla.
2. The cells are rounded / angular and are fibroblast
like, with little collagen.
3. Degree of cellularity varies.
4. A cell free zone / zone of hyalinization may be
formed around the epithelial – connective tissue
interface ultrastructural examination.
5. Degrees of thickening of lamina densa by
granulofilamentous material.
III. Immunohistochemistry-
 Odontogenic epithelial cells positive for cytokeratins
 Immature dental-papilla-like mesenchymal tissue positive for
tenascin.
 Some areas of dental papilla-like cells and in the basement
membrane positive for vimentin of epithelium.
 Collagen IV predominantly found, collagen I and protocollagen III
were found less.
 Unduliln not detected.
 Proliferating cell nuclear antigen (PCNA). + Rarely encountered –
slow growing nature.
 MIB – 1 expression – recurrent AF and Ameloblastic
fibrosarcoma.

Growth pattern of AF occurs usually by smooth expansion within the jaws
– cortical bone thinning and occasional resorption.
Surgical description – “finger like projections of the tumour extend into the
bone”
Treatment-
AF has been managed by a conservative surgical approach unless the size
of the lesion has dictated the anatomic need for resection procedures.
(i) Most, if not all, recurrences probably result from incomplete
excision. A conservative first approach to management is
acceptable if the lesion is encapsulated.
(ii) Presence / absence of the encapsulation should be established
during the first stages of the surgical procedure. Despite
encapsulation, some lesions may have loculi of the tumour that
escape detection and excision.
(iii) Enucleation and curettage result in successful excision of
unilocular, encapsulated lesions. Careful histologic study of
multiple sections of different areas – detect dysplastic changes.
(iv) Extensive / multilocular lesions are more definitely managed by
resection with continuity defect or resection with continuity
defect from the outset.
(v) Huge lesions require resection without continuity defect or
resection with continuity defect and bone graft. To maintain
anatomic integrity of the jaws.

(vi) Long term clinical and radiological follow up evaluation is
required.
Prognosis-
Recurrence rate 43.5 % (Trodahl’s 1972). 18 % (Zallen et al). Recurrences
are probably regrowth of residual tumour. 45% of Ameloblastic
fibrosarcomas evolve from untreated / incompletely treated AF.
VIII. AMELOBLASTIC FIBRO – ODONTOMA
Acronym- AFO.
Introduction-
Benign, mixed odontogenic tumour that appears to be a combination of AF
and forming complex odontoma. The lesion has expansile growth potential
of AF and inductive ability of complex odontoma. AF represented the least
histologically differentiated lesion that evolves from a moderately
differentiated form of AFO to odontoma. (Cahn and Blum). Some
investigators believe that AF and AFO are variations of the same process.
This represented a hamartomatous lesion.
Definition-
WHO defines AFO as “a lesion similar to AF, but showing inductive
changes that lead to formation of dentin and enamel.”
History-
First delineated by Hooker in 1972 and was clearly separated from
Ameloblastic odontoma.

Pathogenesis-
Similar to AF.
Clinical features-
Frequency – 1% -3% of odontogenic tumours.
Age – found in I and II decades of life. 98% of tumours occur before the
age of 20 years.
Sex – M: F = 3:1
Site – mandible = maxilla. Some studies show mandibular preponderance.
Premolar – molar region. Most commonly in the mandibular posterior
region followed by maxillary posterior region.
Usually asymptomatic.
 Exclusively central / intraosseous lesion.
 Painless, slow growing, expansile lesion.
 Presents with swelling and failure of tooth eruption.
 Most AFO’s associated with unerupted tooth.
(i) The tumour is unilocular / multilocular, with well-defined sclerotic
borders and well-defined pericoronal radiolucency.
(ii) May be seen as mixed radiopaque – radiolucent larger extensive
lesions.

(iii) Associated with unerupted teeth / anodontia / absent teeth.
(iv) Maxillary lesions may involve entire maxillary sinus and displace
the involved tooth proportionately forts size. Cause more tooth
displacement.
(v) These lesions are generally not more than 1 – 2 cm in size.
(i) Composed of strands, cords, islands, fingers, and rosettes of
primitive odontogenic columnar or cuboidal epithelial cells,
resembling dental lamina.
(ii) These epithelial components are distributed in a cell-rich, dental
papilla like Ectomesenchymal stroma with delicate fibrils
interspersed by large primitive fibroblasts.
(iii) Varying amounts of osteodentin / dentin like material and
occasional enamel matrix present.
(iv) Odontogenic epithelium adjacent to the enamel matrix seems to
be preameloblast like.
(v) More calcified lesions exhibits mature dental hard tissues that
resemble rudimentary teeth or a conglomerate of enamel and
dentin.
(vi) May / may not be well encapsulated.
Treatment-

(i) Noninvasive. Expansile characteristics encapsulation / well
circumscribed. – Conservative excision by enucleation.
(ii) Concurrent removal of associated unerupted tooth.
(iii) Bosselated projections / lobular areas of the tumour – carefully
removed.
(iv) Huge lesions – resection (resection without continuity defect /
resection with continuity defect).
a. Site
b. Extent
c. Anatomic involvement.
Prognosis-
Recurrence is probable if residual lesion remains. Ameloblastic
sarcomatous transformation has been reported.
IX. AMELOBLASTIC FIBRO-DENTINOMA.
Synonym – Dentinoma
Acronym – AFD
Introduction-
Extremely rare, benign odontogenic mixed tumour and a variant of AF, in
which odontogenic mesenchyme is induced to form dentin or a dentine-like
product by the odontogenic epithelium. AFD is also considered as an
hamartomas rather than a neoplasm. Some authors consider that AFD is a
variant of AFO.
Clinical features-

Frequency – about 35 cases have been reported 1936 – 1994.
Age – ranges from 4 – 60 years of age. Usual age below 30 years.
Sex – slight male predilection noted. (2:1).
Site – mandible: maxilla (3:1).
Lesions in children are associated with unerupted / missing deciduous
teeth and are usually found in the anterior jaw. Lesions in adults, involving
permanent teeth, show a preference for the posterior region of the jaw.
(i) Asymptomatic
(ii) Painless facial swelling / enlargement of the jaws
(iii) Failure to deciduous / permanent teeth to erupt. – brings the
patient to dentist.
(i) Small / extensive.
(ii) Unilocular / multilocular.
(iii) Often with well-defined borders with a thin rim of sclerotic bone.
(iv) Present as a pericoronal radiolucency with radiopaque flecks
consisting of calcified dentinoid.
(v) Associated with unerupted deciduous / permanent teeth.
(vi) Root resorption of the adjacent teeth.
(i) Can be encapsulated.

(ii) Described as mushroom – like and has white, rubbery
consistency.
II. Microscopic features-
1. Epithelial component-
 Strands and islands of odontogenic epithelium proliferation in a
mesenchymal, cellular, dental papilla – like connective tissue.
 Peripheral epithelial cells induce a dentinoid matrix at interface.
2. Mesenchymal component-
 Mesenchymal tissue may appear hypocellular, eosinophilic, and
hyalinized.
 Various stages of inductio9n of dentine may be demonstrated –
dentinoid, osteodentin and rarely, tubular dentine.
 The dentine may be infrequently and poorly mineralized.
Treatment-
1. Complete excision of AFD.
2. The form of excision is case dependent – enucleation if possible.
Resection without continuity defect / resection with continuity defect – if
surgical circumstance requires.
Prognosis-
Recurrence is not expected. But residual lesion has the capacity to grow.
A long-term follow up is a must.
X. ODONTOAMELOBLASTOMA
Synonyms-

(i) Ameloblastic odontoma
(ii) Adamanto odontoma
(iii) Soft and calcified odontoma
Acronym- OA.
Introduction-
Rare, controversial epithelial odontogenic neoplasm that is composed of
distinct areas of Ameloblastoma and odontoma. (Composite).
Characterized by peculiar proliferation of tissue of the odontogenic
apparatus in an unrestrained pattern, including complete
morphodifferentiation, as well as apposition and even calcification.
Unusuality of this lesion – a relatively undifferentiated neoplastic tissue is
associated with a highly differentiated tissue – both may show recurrence.
Definitions-
1. WHO – a very rare neoplasm, which includes odontogenic
ectomesenchyme, in addition to odontogenic epithelium that
resembles an Ameloblastoma both in structure and in behaviour.
Because of the presence of the odontogenic ectomesenchyme,
inductive changes take place leading to formation of dentine and
enamel in parts of tumour.
2. Gorlin and Torsell and Shafer – tumour in which there is
simultaneous occurrence of Ameloblastoma and a complex or
compound odontoma with in the same tumour.

3. Regezi and Scuiba – rare variant that is essentially an
Ameloblastoma in which there is focal differentiation into an
odontoma.
History –
1944 – Thoma et al reported 1st
case of Odontoameloblastoma.
1953 – Frissell and Shafer reported a case, which showed Ameloblastoma
like areas and dental hard tissue but ghost cells were also present.
1980 – Labnola et al reported a case with definitive Ameloblastoma with a
hard tissue component.
1986 – Gupta and Gupta reported a case with Ameloblastoma like tissue
but hard tissue component.
1991 – Kaugars and Zussman
2002 – Masqueda – Taylor et al reported most recent series of OA.
Pathogenesis –
OA and AFO are one entity (Wachter et al).
Clinical features –
Frequency – very few cases are reported.
Age – common in children I and II decades.
Sex – male predilection.
Site – posterior regions of both the jaws. Mandible > maxilla.
1. Slowly expanding lesion of the bone – facial asymmetry /
deformity.

2. Central lesion – considerable destruction of bone.
3. Mild pain
4. Delayed eruption of teeth.
Radiological features-
1. Small, large / extensive lesion.
2. Well-circumscribed lesion with central radiopaque mass surrounded
by a radiolucent zone or may contain irregular small / large
radiopaque masses interspersed with radiolucent areas and usually
surrounded by a sclerotic border.
3. No radiographic impression of infiltration.
4. Central destruction of bone with expansion of cortical plates is
prominent.
1. Unusual and characteristic
2. Consists of a great variety of cells and tissues in a complex
distribution – columnar, squamous and undifferentiated epithelial
cells as well as ameloblasts, enamel and enamel matrix, dentine,
osteodentin, dentinoid and osteoid material, Stellate reticulum – like
cells, dental papilla, bone and cementum as well as stromal
connective tissue.
3. Many structures resembling normal / atypical tooth germs may be
found, with / without the presence of calcified dental tissues.

4. An outstanding characteristic – presence of sheets of typical
Ameloblastoma, usually basal cell, follicular / plexiform type.
5. Few mitotic figures are present.
1. AFO
2. Ameloblastoma
3. Developing odontoma
4. Dentinogenic ghost cell tumour.
Treatment-
OA initially treated conservatively, including recurrences extensive
maxillary lesion – hemimaxillectomy (LaBriola et al)
Twice recurrent lesion – resection without continuity defect (Frissell and
Shafer)
1. Lesions those are primarily radiopaque and circumscribed by
sclerotic bone – treated enucleation and careful curettage.
2. Lesions that contain significant areas of radiolucency in addition to
calcified odontomatous masses should be biopsied in several areas.
 Histologic assessment determines the presence / absence of a
capsule and the quantity and distribution of Ameloblastic
elements.
 If capsule present – lesion excised by enucleation and curettage.
 If capsule not present – lesion excised by enucleation and careful
curettage / at most resection without continuity defect.

 Histologic analysis of the specimen determines whether a further
surgical procedure is indicated. Rarely resection with continuity
defect is justified.
Management depends on clinical features, radiological features and
anatomic involvement.
Prognosis-
Recurrence rare. Due to growth of residual lesion.
X. ODONTOMA
Introduction-
Most common abnormalities of the jaws. Believed to be a hamartomas.
Odontoma is the end product of the anomalous completion / incompletion
of tooth formation by odontogenic epithelium and odontogenic
ectomesenchyme. WHO classifies odontoma under the category of
tumours containing odontogenic epithelium with odontogenic
ectomesenchyme, with / without dental hard tissue formation.
History –
1866 – Broca first coined the term odontome. Thoma and Goldman
narrowed the term odontoma to include tumours that were composed of
well-differentiated tooth structure.
Definition –
Broca’s – tumour formed by an overgrowth of complete dental tissue.

Shafer and Gorlin – tumour that has developed and differentiated enough
to produce enamel and dentin.
Types –
 Complex odontoma – a malformation in which all of the dental
tissues are represented, and individual tissues mainly are well
formed but occur in a disorderly pattern.
 Compound odontoma – a malformation in which all of the dental
tissues are represented in a more orderly pattern than in the
complex odontoma so that the lesion consists of many tooth –
like structures.
Pathogenesis-
Complex odontoma is formed from other mixed odontogenic tumours.
AF / AFD. I step.
AFO. II step.
Complex odontoma. final step.
Compound odontoma is a malformation, which is more differentiated, and
its pathogenesis more closely is related to the creation of supernumerary
teeth, especially mesiodens. This hypothesis is supported strongly by the
preponderance of compound odontomas in the anterior maxilla.
Origin-
Unknown. Several theories have been proposed.

Odontogenic tumours/oral surgery courses by indian dental academy

Odontogenic tumours/oral surgery courses by indian dental academy

Recomendados

Recomendados

Más contenido relacionado

La actualidad más candente

La actualidad más candente (20)

Destacado

Destacado (8)

Similar a Odontogenic tumours/oral surgery courses by indian dental academy

Similar a Odontogenic tumours/oral surgery courses by indian dental academy (20)

Más de Indian dental academy

Más de Indian dental academy (20)

Último

Último (20)

Odontogenic tumours/oral surgery courses by indian dental academy