2. TYPES OF BENIGN TUMORS
1. ODONTOGENIC:
These are derived from tooth forming elements.
The more primitive the dental tissue found, the
more aggressive the tumor and vice versa
Only found in the jaws
Locally aggressive and rarely malignant
2. NON ODONTOGENIC :
They are not derived from dental tissues
They can be found in other regions of the body.
5. AMELOBLASTOMA
Benign but locally aggressive tumor of the jaw
The name of the tumor derives from the fact the
diagnostic cells resemble ameloblast
Histologically these cells are columnar , basally
staining arranged in palisaded along the basement
membrane.
They are believe to express amelogenin, a
precursor of enamel
They are divided into three distinct types:
1. Solid
2. Cystic
3. peripheral
6.
7. PATHOGENESIS OF AMELOBLASTOMA
1. Over expression of antiapoptotic gene Bcl2
2. TNF alpha
3. MMPs and transforming growth factors
4. Low proliferation rate ki67
5. No p53 mutation
8. SOLID AMELOBLASTOMA
Various histological patterns including follicular,
plexiform, and granular cell variants….does not have
affect treatment or prognosis
SITE: most common in mandible esp angle ,ramus
area. Rare in maxilla, but infiltration is much faster as
marrow spaces and cavities offer less resistance
OCCURRENCE: third to fifth decade of life. Male
to female ratio is approx equal
CLINICAL APPEARANCE:
1. slow growing, expansile lesion.
2. locally aggressive with buccal and lingual
cortical expansion,root resorption is seen
9.
10. INVESTIGATIONS:
1. Radiographic evaluation, OPG shows multilocular
radiolucency with root resorption and
displacement of teeth
2. CT scan in case of larger lesions and esp maxillary
ameloblastoma
3. Aspiration of the swelling will reveal nothing in
case of solid ameloblastoma
4. Incisional biospy, shows typical pallisaded
columnar cells resembling ameloblasts.
11.
12. TREATMENT:
1. For solid lesions, enucleation has a high recurrence rate 60-
80%. Cells are present beyond the radiographical margin.
2. Surgical resection should be with a 1 cm safe radiological
margin and soft tissue clearance if supraperiosteal.
3. IAN is sacrificed
4. Maxillary resections often end in maxillectomy with wide
margin clearance from the sinus, nasal and infratemporal
regions
5. After surgical resections or curettage , liquid nitrogen
cryotherapy plays a good role
13. RECONSTRUCTION:
1. For the mandible, segmental defects of 5 cm can
be reconstructed with bone grafts most commonly
iliac crest.
2. For more larger defects free osseofasiocutaneous
flaps may be used.. DCIA and free fibular flap.
3. Reconstruction plates are used as adjuncts to
grafts or as an interim treatment modality
4. For maxilla, depending upon the defect, local,
regional flaps can be used but prosthetic options
serve the best purpose
14.
15.
16. CYSTIC AMELOBLASTOMA
Unicystic ameloblastoma, less aggressive variant.
Most common in younger population.
Mostly located in posterior mandible and anterior
maxilla
All other features are the same
Enucleation alone may be insufficient, the cavity
should be treated with peripheral ostectomy, or
liquid nitrogen or both.
17. PERIPHERAL AMELOBLASTOMA
Occurs in gingiva with no bony involvement
Painless, sessile growth, firm and exophytic
Complete excision solves the problem
18. CALCIFYING EPITHELIAL ODONTOGENIC
TUMOR
Also called Pindborg tumor after he described it in
1955. derived from stratum intermedium
Wide age range from 13- 80 yrs, no gender
predeliction.
SITE: mandibular premolar area.
CLINICAL BEHAVIOUR: most are asymptomatic,
slow growing in nature. In maxilla may cause, nasal
obstruction, proptosis or epistaxis
INVESTIGATIONS:
1. On radiographs, they appear as mixed radiolucent
radiopaque, unilocular or mutilocular lesions
2. Biopsy will reveal sheets of epithelial cells in a stroma
filled with hyaline like homogenous material and
concentric calcification rings called liesegang rings
19.
20. TREATMENT:
Less aggressive than ameloblastoma, however
malignant variant (odontogenic carcinoma) has
been identified.
Wide excision with 5- 10 mm margin, which in
mandible may result in marginal or segmental
resection followed by reconstruction.
Recurrence rate is 14-20%
21. ADENOMATOID ODONTOGENIC
TUMOR
Occurs only in jaws. Resemblance to structures
present in enamel formation
OCCURRENCE: most common in females; age of
occurrence is 5 -30 yrs.
SITE: anterior maxilla, impacted teeth
RADIOGRAPHIC APPEARANCE: pear shaped
radiolucency with speckled opaque foci indicating
calcification. Divergence of roots is seen
TREATMENT: simple enucleation seems all that
is necessary.
22. SQUAMOUS ODONTOGENIC TUMOR
Rare tumor originates from the rest of malassez
in the periodontium.
Occurrence in both mandible(post) and maxilla
(ant)
Presents with pain and tooth mobility
Radiographic appearance is a semilunar
radiolucency associated with erupting teeth.
Treatment is conservative excision
23. MESENCHYMAL ODONTOGENIC
TUMORS
CEMENTOBLASTOMA
Rare tumor , most common in second and third
decade of life, lower molar region.
Intimately associated with the root of tooth.
Tooth remains vital and symptoms of low grade
pain and cortical expansion are present.
RADIOGRAPH: radiopaque lesion attached to and
surrounding the root of a tooth. Must be
distinguished from focal sclerosing osteomyelitis,
odontoma and hypercementosis.
HISTOLOGY: Difficult to distinguish cementum
and bone. It is cemental variant of osteoblastoma
TREATMENT: surgical removal of tooth and lesion.
Peripheral ostectomy is recommended
24.
25. ODONTOGENIC MYXOMA
15-20% of odontogenic tumors. Second most
common tumor
OCCURRENCE: second through fourth decade of
life. More common in females. Two thirds occur in
mandible and one third in maxilla.
CLINICAL APPEARANCE: presents as a swelling
locally aggressive.
RADIOGRAPH: similar to ameloblastoma,
multilocular radiolucency
HISTOLOGY: loose mesenchymal tissue . Derived
from dental pulp or primitive dental papilla. Bland
histological appearance.
26.
27. TREATMENT:
1. Less aggressive than ameloblastoma.
2. Enucleation or radical curettage with peripheral
ostectomy.
3. In larger lesions perforating the cortex,
segmental resection of mandible or
hemimaxillectomy in maxilla may be required.
4. Physiochemical adjuncts can also be employed like
carnoys’s solution or liquid nitrogen.
28. MIXED TUMORS
ODONTOMA
Developmental anomalies. Most common tumor.
Consists of irregularly arranged mature dental
tissues.
May present as a swelling or infected lesion if they
erupt. Often replacing a missing tooth. Most commonly
found in the mandible molar region.
TYPES: complex and compound odontome.
1.COMPLEX: most common in posterior mouth.
Amorphous conglomeration of dental tissues
consisting of enamel,dentin and cementum. Radiograph
shows gives a radiopaque mutilobular appearance.
2.COMPOUND: common in anterior jaw.contains
numerous denticles or tooth like fragments (each
containing enamel with dentin and pulp)
3. Radiographical resembles a bag of teeth
TREATMENT: enucleations cures the problem, no
recurrences
29.
30. AMELOBLASTIC FIBROMA
OCCURRENCE: young people second and third
decade of life. No gender predilection. Most
common site is mandibular bicuspids area.
RADIORAPHIC VIEW: unilocular/ multilocular well
defined radiolucency. Teeth may be displaced but
rarely resorbed.
HISTOLOGY: islands of odontogenic epithel;ium in
myxomatous stroma
TREATMENT: encapsulated lesion so enucleation is
done. Malignant variant is ameloblastic
fibrosarcoma.
31.
32. AMELOBLASTIC FIBRO-ODONTOMA
Combination of ameloblastic fibroma with an
odontoma.(complex or compound).
Radiographically a mixed radiopaque/ radiolucent
lesion
Treatment is enucleation
33. NON ODONTOGENIC TUMORS
FIBRO OSSEOUS LESIONS
1. Fibrous dysplasia
2. Ossifying fibroma
3. Cemento-osseous dysplasia
OSSIFYING FIBROMA:
replacement of normal bone by fibrous tissue and
variable amount of newly formed bone and cementum
like structures
CLINICAL FEATURES:
1. Painless, slowly growing swelling
2. Third and fourth decade of life
3. Females are more commonly affected
4. Mandible(premolar –molar ) most commonly affected
5. Juvenile OF is a variant, occurring in children and
involving the craniofacial complex
34. RADIOLOGICAL FEATURES:
1. Well defined radiolucency with internal
calcifications.
2. The borders may be sclerotic
3. Root displacement and resorption is seen
HISTOLOGY:
Fibrous stroma with bony trabaculae and cementum
like spherules
TREATMENT:
1. Complete surgical excision
2. Stripping of the lesion is easy
3. Root that are resorbed are removed
35.
36. FIBROUS DYSPLASIA
Monostotic
Polyostotic (Mc Cune Albright Syndrome)
Usually in females
In second and third decade of life
Related to hormones
Maxilla more favored site
Ground glass appearance on radiograph
The lesion’s margins are not well demarcated
Similar histological picture as ossifying fibroma
Recontouring after puberty
37. LANGERHANS CELL DISEASE
Formerly known as histiocytosis X and three
clinically distinct diseases
1. Eosinophilic granuloma
2. Hand- Schuller –Christian disease
3. Letterer-Siwe disease
PATHOGENESIS:
characterized by proliferation of Langerhans cells
and eosinophils along with other inflammatory cells.
Langerhan cells are dendritic cells found in
mucosa, epidermis, lymph nodes that process
and present antigens to T lymphocytes.
Overwelming allergenic response or viral
etiology
38. CLINICAL PRESENTATION
Affects children and young adults. 3 forms exists
1. Chronic localized or eosinophilic
granuloma….refers to solitary or multiple lesions
bone lesions only
2. Chronic disseminated disease or Hand- Schuller-
Christian disease …clinical triad of lytic bone
lesions, exophthalmos and diabetes inspidus
3. Acute Disseminated Langerhans or Letterer-
Siwe …affects infants, affecting skin, bones and
internal organs esp lungs and liver.
4. Bone lesions involve the skulls, mandible, ribs
and vertebrae. Jaw lesions produce pain,
mobility
39. RADIOGRAPHIC APPEARANCE:
Well defined punched out radiolucency
floating teeth may be seen
Involved teeth are vital
HISTOLOGY:
They are diagnosed with immunohistochemical
studies with S-100 and CD1a antigen.
Langerhan cell contains cytoplasmic structures
called Birbeck granules
TREATMENT:
1. Accessible bone lesions are treated with curettage
and 5mm marginal resection
2. Less accessible lesions are treated with radiotherapy
3. Intralesional steroids are also employed in resolving
the lesions
42. GIANT CELL LESIONS
CENTRAL GIANT CELL GRANULOMA:
Benign proliferation of fibroblasts and
multinucleated giant cells
PATHOGENESIS:
Proliferation of fibroblasts….cytokines release…
of monocytes…transform into multinucleated giant
Cells.. Osteoclasts begin to destroy bone
OCCURENCE:
1. Found in young children and young adults, before
30 yrs
2. Females most commonly affected
3. Lesions occur anterior to 1st
molar and cross the
midline
43. CLINICAL APPEARANCE
Non aggressive , slowly expanding lesion
Aggressive lesion , cortical expansion, root resorption
RADIOGRAPHICAL APPEARANCE:
Unilocular/ multilocular radiolucency
HISTOLOGY:
Few to many giant cells in a background of
Fibroblasts
TREATMENT:
1. Surgical curettage with 15-20 % recurrence
2. Intralesional steroids(weekly injections of
triamcinolone for 6 wks)
3. Subcutaneous injection of calcitonin (giant cell have
calcitonin receptors)…inhibits of osteoclastogenesis
4. Alpha-interferon is also given (will suppress the
angiogenic component of the lesion)
44.
45. HYPERPARATHYROIDISM
Overproduction of parathyroid hormone.
1. Primary hyperparathyroidism…uncontrolled
production due to an adenoma, hyperplasia
2. Secondary hyperparathyroidism..in response to
hypocalcemia due to chronic renal failure
PATHOGENESIS:
Excess PTH.. Stimulates osteoclast mediated bone
resorption…focal bone lesion…brown’s tumor due to
clinical appearance…erythrocyte extravasation
Radiologically and histologically indistinguishable
from GCG
46. HOW TO APPROACH SUCH PATIENTS
Pay attention to clinical signs/ symptoms
Groans, moans, stones and bones
Serum calcium and phosphate, PTH, alkaline
phosphatase are done
Raised PTH, raised serum Ca and raised ALP..
Primary hyperparathyroidism
Raised PTH, Low serum Ca, Normal ALP, Renal
functions abnormal…secondary
hyperparathyroidism
Normal PTH.. Giant cell granuloma
TREATMENT:
Treat the underlying cause.. Regression of lesion
47. CHERUBISM
Autosomal dominant hereditary disorder.
Genetic defect is in chromosome 4p16
CLINICAL APPEARANCE:
Children btw 2 and 5 yrs
Begins as painless bilateral symmetric expansion
of the jaws
Mand angle, ramus, retromolar area, max
tuberosity
Max involvement may raise the orbital floor,
globes may be displaced upwards, resembling
cherubes in renaissance paintings
48.
49. RADIOGRAPHIC APPEARANCE:
Multilocular radiolucency with thin cortices
Premature exfoliation of primary teeth
TREATMENT:
Lesions enlarge uptil puberty, then regress
Later on, residual expansions can be contoured
50.
51. OSTEOID OSTEOMA OSTEOBLASTOMA
Less than 2cm
Femur, tibia and phalanges
Nocturnal pain relieved by
aspirin
Radiographically, mixed
radiolucent-radiopaque
pattern
Histologically irregular
trabeculae of osteoid and
immature bone
Treatment.. Conservative
excision
Greater than 2 cm
Vertebrae and bones
of cranium, mandible
Pain is not nocturnal
and not relieved by
aspirin
Same as osteoid
osteoma
Same
same
52.
53. OSTEOMA
Benign tumors of mature cortical and cancellous
bone
Two types: peripheral osteoma;endosteal osteoma
May arise in paranasal sinuses, skull and facial
bones
Periosteal osteoma may present as slow growing
lesions
Endosteal osteoma are asymptomatic.
Solitary lesions or multiple in no for eg Gardeners
syndrome(multiple osteomas, intestinal polyps,
fibromas skin, odontomes)
