This document discusses benign tumors of the orofacial region, classifying them as either odontogenic or non-odontogenic tumors. Odontogenic tumors are derived from tooth forming elements and include ameloblastoma, calcifying epithelial odontogenic tumor, and adenomatoid odontogenic tumor. Non-odontogenic tumors include fibrous dysplasia, ossifying fibroma, and Langerhans cell disease. Ameloblastoma is the most common odontogenic tumor and presents as a slow growing, locally aggressive lesion that is treated with wide surgical resection. Calcifying epithelial odontogenic tumor contains sheets of epithelial cells and concentric calcification rings, while treatment involves wide excision.

1. BENIGN TUMORS OF OROFACIAL
REGION

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.

3. CLASSIFICATION
 BENIGN ODONTOGENIC TUMORS:
1.EPITHELIAL TUMORS:
 Ameloblastoma
 Calcifying epithelial odontogenic tumor
 Adenomatoid odontogenic tumor
 Squamous odontogenic tumor
2.MESENCHYMAL TUMORS:
 Odontogenic fibroma
 Cementoblastoma
 Odontogenic myxoma
 Cementifying fibroma
3.MIXED TUMORS(EPITHELIAL& MESENCHYMAL):
 Odontoma
 Ameloblastic fibroma
 Ameloblastic fibro-odontome

4.  NONODONTOGENIC TUMORS:
1. FIBRO-OSSEOUS TUMORS
 Ossifying fibroma
 Juvenile ossifying fibroma
2. LANGERHANS CELL DISEASE
 Chronic localized
 Chronic disseminated
 Acute disseminated
3. GIANT CELL LESIONS:
 Central giant cell granuloma
 Giant cell tumor
 Hyperparathyroidism
 Cherubism
 Aneurysmal bone cyst
4. NEUROGENIC TUMORS
 Schwannoma
 Neurofibroma
5. OSTEOID OSTEOMA AND
OSTEOBLASTOMA
6. OSTEOMA
CHRONDROMA
7. DESMOPLASTIC FIBROMA

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

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

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.

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

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

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

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.

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

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.

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

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

41. GIANT CELL LESIONS
 CENTRAL GIANT CELL GRANULOMA
 GIANT CELL TUMOR
 HYPERPARATHYROIDISM(BROWN’S TUMOR)
 CHERUBISM
 ANEURYSMAL BONE CYST

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)

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

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

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

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)