This document provides an overview of several non-odontogenic tumors of the oral cavity, including oral submucous fibrosis, basal cell carcinoma, fibroma, giant cell fibroma, and peripheral ossifying fibroma. It describes the definition, etiology, clinical features, histopathology, treatment and prognosis of each tumor type. The document is intended as a reference for professionals to understand and identify these tumor types.

1. Non- odontogenic
tumors of oral cavity-I

2. Index
1. ORAL SUBMUCOUS FIBROSIS
2. BASAL CELL CARCINOMA
3. FIBROMA
4. GIANT CELL FIBROMA
5. PERIPHERAL OSSIFYING FIBROMA
6. CENTRAL OSSIFYING FIBROMA OF BONE
7. NON-HODGKIN’S LYMPHOMA
8. PRIMARY LYMPHOMA OF BONE
9. BURKITT’S LYMPHOMA
10. HODGKIN’S LYMPHOMA

3. ORAL
SUBMUCOUS
FIBROSIS

4. Definition
• Definition- an insidious chronic disease
affecting any part of the oral cavity and
sometimes the pharynx, ocassionally
preceded by a vesicle formation and always
associated with juxtaepithelial inflammatory
reaction followed by a fibroelastic change of
the lamina propria with epithelial atrophy
leading to stiffness of oral mucosa and causing
trismus and inability to eat.

5. Etiology
• Alkaloids- areca nut- arecoline
- quinidine, cinchonine
- histamine, pilocarpine
• Flavanoids- capsesine (green chillies)
• Although the etiology is obscure, the above
factors are responsible for pathogenesis.
• Also vitamin B deficiency is responsible.

6. Causative factors and pathogenesis
• Areca nut, betel quid chewing habits
• Vitamin deficiency
• Genetic: HLA-A10, -B7
• modulate metalloproteinases, lysyl oxidases,
and collagenases, all affecting the metabolism
of collagen increasing fibrosis
• High production of collagen, less degradation.

7. Clinical features
• Lesions
• TRISMUS

8. Clinical features
• Chief complaints- less mouth opening
- burning on eating food
- difficulty in swallowing
- ulcers and excess salivation
• Features- vesicles, ulcerations, recurrent
stomatitis, excessive salivation or xerostomia,
stiffening of oral mucosa, fibrotic bands in
buccal mucosa, soft palate, lips,tongue.

9. Histological features
1. Normal OMM 2.Classical OSMF
3. Advanced OSMF-
subepi changes

10. Grades

11. Treatment and prognosis
• Withdrawal of causative factors
• Alteration in eating habits
• Systemic corticosteroids
• Local hydrocortisone
• Administration of vitamin B12
• Administration of vitamin E and antioxidants
• Physiotherapy
• Surgical removal on regular basis.

12. BASAL CELL
CARCINOMA

13. Basal cell carcinoma
• Basal cell carcinoma doesn’t invade oral cavity
unless it comes there by infiltration from skin
surface.
• Basal cell carcinoma (BCC) is a nonmelanocytic
skin cancer that arises from basal cells.
• BCC occurs mostly on the face, head (scalp
included), neck, and hands.

14. Clinicopathologic types
1. Nodular- cystic, pigmented, most common
type
2. Infiltrative- tumor invades dermis, margins ill
defined.
3. Micronodular- not prone to ulceration, firm
on touch, well defined border.
4. Morpheaform- white/yellow, waxy, sclerotic
plaque, firm, fibrotic.

15. Signs and symptoms
• Waxy papules with central depression
• Pearly appearance
• Erosion or ulceration: Often central and pigmented
• Bleeding: Especially when traumatized
• Oozing or crusted areas: In large BCCs
• Rolled (raised) border
• Translucency
• Telangiectases over the surface
• Slow growing: 0.5 cm in 1-2 years
• Black-blue or brown areas.

16. Pathphysiology
• A well-established relationship exists between
BCC and the pilosebaceous unit, as tumors are
most often discovered on hair-bearing areas.
1. Loss of inhibition of signaling of
hedgehog/patched pathway may lead to nevoid
BCC syndrome(Gorlin’s syndrome)
2. Radiation – by prolongation of cell proliferation,
and by direct DNA damage.
3. DNA mismatch repair proteins- arrests G2
checkpoint, and leads to apoptosis.

17. Etiology
1. Radiation exposure
2. Gene mutations
3. Arsenic exposure through inhalation
4. Xeroderma pigmentosum
5. Epidermodysplastic verruciformis
6. Nevoid basal cell carcinoma syndrome
7. Bazex syndrome
8. Skin type

18. Clinical presentation
Nodular BCC
BCC at
medial
canthus.
Superficial BCC
Pigmented BCC

19. Histology
• Histologically, BCC is divided into the following 2
categories:
• Undifferentiated: When there is little or no
differentiation, the carcinoma is referred to as solid
BCC; this form includes pigmented BCC, superficial
BCC, sclerosing BCC, and infiltrative BCC.
• Differentiated: Differentiated BCC often has slight
differentiation toward hair (keratotic BCC), sebaceous
glands (BCC with sebaceous differentiation), and
tubular glands (adenoid BCC); noduloulcerative
(nodular) BCC is usually differentiated.

20. Management and prognosis
• Surgery [prognosis- excellent, 5%recurrence]
• Radiation therapy [prognosis- favorable]
• Photodynamic therapy[ prognosis-tumor
recurrence with tissue atrophy and scar
formation]
• Pharmacologic therapy- drugs used are topical
flurouracil, imiquimoid, taxarotene.

21. Case
• A 44 year old male patient comes to the
clinician with a complaint of discomfort during
mastication due to lump on the biteline on
buccal mucosa, with a history of cheek biting.
• On examination, a round-to-ovoid,
asymptomatic, smooth-surfaced, and firm
pedunculated mass is seen of diameter
1.5mm, with surface being hyperkeratotic and
ulcerated.

23. And you may think of the following.....
• Buccal surface- fibroma, lipoma,mucocele.
• Lower lip- mucocele, fibroma, hemangioma,
squamous cell carcinoma.
• Upper lip- fibroma, squamous cell carcinoma
• Gingiva- parulis, pyogenic granuloma,
peripheral ossifying fibroma, fibrous
hyperplasia.
• Tongue- fibroma, mucocele(ventral)

24. Fibroma
• Aka-irritation fibroma, traumatic fibroma,
focal fibrous hyperplasia, fibrous nodule.
• Not a true neoplasm.
• Definition- Irritation fibroma, or traumatic
fibroma, is a common submucosal response
to trauma from teeth or dental prostheses.
• Composed of types I and III collagen.
• Found in 1.2% adults.

25. Clinical features
- sessile or
pedunculated,
-Seldom does it exceed
1.5 cm. in size
-asymptomatic,
moderately firm,
immovable mass with a
surface coloration that
is most often normal but
may show pallor from
decreased vascularity,
whiteness from
thickened surface
keratin, or ulceration
from recurring trauma.
Epulis
fissuratum
-irregular, linear,
fibrous hyperplasia
-3 or more waves
of fibrous
redundant tissue

26. Histologic features
• Nodular mass of connective tissue covered
with stratified squamous epithelium.
• Connective tissue is dense and collagenized.
• Encapsulation-absent
• Covering epithelium- absence of rete ridges.
• Surface- hyperkeratosis
• Scattered inflammation may be seen.

27. Differential diagnosis
• Pyogenic granuloma- focal areas of edema is
seen with neurovascularity in middle of mass.
• Neurofibroma- not separated by thin layer of
normal fibrovascular connective tissue.
• Frictional keratosis- dysplastic and melanin in
basal layer.
• SCC- elongated rete peges cut at right angles
may give appearance of epithelial islands deep
in stroma.

28. Syndromes related to fibroma
• Tuberous sclerosis-hamartoma and nevi
• Cowden’s syndrome- hamartoma+ lipoma+
fibroma
• Familial fibromatosis- fibromatous tumors all
over subcutaneous connective tissue.

29. Treatment
Conservative surgical excision
Recurrence- rare
Borders of excised tissue should be checked
for remnant fibrous tissue.

30. Giant cell fibroma
The giant cell fibroma is a subtype of irritation
fibroma, i.e. it is a localized inflammatory
fibrous hyperplasia, but it differs significantly
from routine fibromas in that its stroma
contains scattered fibroblasts with very large,
usually angular (stellate), but not
hyperchromatic nuclei.

31. Case
• A 48 year old male patient with history of
smoking, and currently on medication crestor,
presents intraoral pedunculated lesion that is
covered by erythematous mucosa of-12.
patient is asymptomatic. No radiographic
changes in IOPA.

32. Clinical features
• Age- any age.
• Site- gingiva> tongue>palate>buccal mucosa>
lip.
• Size, number- 0.5-1cm, multiple.
• Appearance- two or three lobules, or few
small papules on the surface.
• Color- of surrounding normal mucosa.
• Pedunculated/sessile, nonulcerated.

33. Histopathology
• Histology- diffuse, immature, avascular collagenic
stroma with small bipolar and slightly stellate fibroblasts
scattered in moderate numbers with multiple nuclei.
• Pathognomonic cells, never hyperchromatic, truly
dysplastic fibroblasts, and smudged appearance.
• Numerous in the zone immediately beneath the covering
epithelium- normal but may have elongated and narrow
rete ridges.
• At the inferior margin the lesional fibrosis blends into the
normal underlying fibrovascular tissues, with no capsule or
pseudocapsule. Occasional lymphocytes may be seen
beneath the epithelium or around capillaries.

34. Scattered fibroblasts located just beneath
the epithelium are enlarged and angular
but are not hyperchromatic. Some cells
have multiple nuclei.

35. Treatment and prognosis
Conservative surgical approach.
Recurrence more than fibroma.
May remain asymptomatic except traumatic
ulceration.
Healed excised
area after 3
weeks of
treatment.

36. Peripheral ossifying fibroma
Nodular,
nonhemorrhagic
mass of
mandibular
gingiva has
separated
adjacent teeth.

37. Clinical features
• Painless, hemorrhagic and often lobulated mass of the
gingiva or alveolar mucosa, large areas of surface
ulceration.
• Early lesions -quite irregular and red.
• Older lesions- smooth salmon pink surface,
indistinguishable from fibroma.
• Size-1-2 cm,enlarge to more than 4 cm.
• Age- teenagers and young adults, or in individuals with
poor oral hygiene.
• Radiographs-irregular, scattered radiopacities in the
lesion.

38. Histopathology
• Hallmark- aggregated submucosal proliferation of primitive
oval and bipolar mesenchymal cells, plump fibroblast.
• Lesion-highly cellular or may be somewhat fibrotic, but
scattered throughout are islands and trabeculae of woven
or lamellar bone.
• Metaplastic bone may also be seen
• Admixture of bone and cementum.
• Early lesions may contain only small ovoid areas of
dystrophic calcification
• Lesional nidus is not encapsulated
• Surrounding tissues -edematous, with neovascularity and
variable numbers of chronic and acute inflammatory cells.

39. Histology
• The lesion- cellular or may be somewhat
fibrotic, but scattered throughout are islands
and trabeculae of woven or lamellar bone,
usually with abundant osteoblastic rimming.

40. Differential diagnosis
• While the lesional stroma is similar to that
of peripheral giant cell granuloma, the
erythrocyte extravasation of the latter lesion is
not a feature of peripheral ossifying fibroma and
osteoclast-like cells are quite rare.
• classic pyogenic granuloma, irritation fibroma
• osteoblastic osteosarcoma or juxtacortical
osteosarcoma-dysplastic changes, mitotic
figures.
• Pyogenic granuloma- much vascular than POF

41. Treatment and prognosis
1. Conservative surgical excision
2. Diligent curettage of the wound
3. Root planing of adjacent teeth if recurrence
is to be avoided
4. With simple removal the recurrence rate is
greater than 20%. Malignant transformation
has not been reported for this lesion.

42. Central ossifying fibroma of bone
• Synonym- central fibro-osteoma.
• True neoplasm
Ossifying fibroma
in a 10 year old
male patient,
otherwise
asymptomatic,
having
hyperparathyroidi
sm.

43. Clinical features
• Age- any age, predilection 9-33 years.
• Sex- female predilected
• Lesion- asymptomatic, noticeable swelling,
mild deformity.
• Early feature- displacement of teeth.
• Slow growth, hence underlying cortical bony
plate may remain intact.

44. Radiographic features
• Extremely variant
• Well circumscribed, demarcated from
surrounding bone.
• Early stage- radiolucent areas, with no
evidence of internal radiopacity.
• Mature stage- flecking by radiopacity, and
then uniform opaque mass.

45. Histologic features
• Lesion- delicate interlacing
collagen fibres, seldom arranged in
discrete bundles, interspersed by
large number of actively
proliferating fibroblasts.. Mitotic
figures, no remarkable cellular
pleomorphism.
• Connective tissue-small foci of
irregular bony trabeculae.
• Matured lesion-coalesced islands
of ossification.

46. Opg of
ossifying
fibroma
patient

47. Differential diagnosis
• Fibrous dysplasia- lesion not well demarcated
from surrounding bone. Chinese character
shaped bony trabeculae.
• Central cementifying fibroma- odontogenic in
origin.

48. Treatment and prognosis
• Excision of lesion conservatively.
• Recurrence rare

49. Lymphomas
1. Non hodgkin’s lymphoma
2. Primary lymphoma of bone
3. Burkitt’s lymphoma

50. The lymphatic system

51. Lymphoma-definition
• It is a neoplastic proliferative process of the
lymphopoetic portion of reticuloendothelial
system that involves cells of either lymphocyte
or histiocyte series.........the character of
involvement is diffuse or nodular and
distribution may be general or
regional..........dependent on occurrence of
bone marrow involvement.

52. Classification

53. Case
• A 44 year old man presented with symmetric
painless swelling in the palatal region that
appeared before 10-12 weeks with no
symptoms of dysphagy.
• Histology- population of small lymphocytes
with slightly irregular intended nuclei and
moderately dispersed chromatin, a follicular
pattern in the glandular tissue of the palate.
• D.D.- lymphoid hyperplasia

54. Non hodgkin’s lymphoma
• Involves both lymph nodes and lymph organs
• Involves extranodal tissues as well as organs
• Extranodal involvement of head and neck is
seen
• A form of cutaneous T cell lymphoma-mycosis
fungoides may manifest in oral cavity and skin.

55. Working formulation

56. Clinical features
• Lymphadenopathy- abdominal and
mediastinal enlargement.
• Fever
• Night sweats
• Unexplained weight loss
• Facial swelling

57. Additional factors
• Hereditary immune deficiency syndromes
1. agammaglobulinemia
2. Wiskott–Aldrich syndrome
3. ataxia teleangiectasia ,
• acquired immune deficiency
1. systemic lupus erythematosus
2. autoimmune thrombocytopenia
3. rheumatoid arthritis

58. Oral manifestations
• Large fungating, necrotic, foul smelling
masses.
• Underlying bone involvement- tooth mobility
• Paresthesia of mental nerve.

59. Histology
• Nodular or diffuse
• Nodular- neoplastic cells aggregate in large
clusters
• Diffuse- monotonous distribution of cells with
no nodularity.
• Cells- lymphocytes, histiocytes, reticulum cells in
various degree of differentiation.

60. Treatment and prognosis
• Radiation and chemotherapy
• Nodular pattern has better prognosis than
diffuse pattern.
• Large cell NHL or histiocytic NHL has poor long
term prognosis.

61. Know patient’s NHL stage.

62. 2. Primary lymphoma
of bone
• Aka- primary reticulum cell sarcoma of bone
• Usually confused with Ewing’s sarcoma,
Hodgkin’s disease, osteogenic sarcoma, and
inflammation.

63. Clinical features
• Age- wide range- 20-40 years
• Clinical signs and symptoms usually absent
• Localized swelling of involved bone, regional
lymphadenopathy.
• Predilected to mandible
• Predilected to males

64. Case
• A 26-year-old male -persistent pain and swelling
of the left jaw for the past two months following
a left 1st molar tooth extraction.
• associated history-pyrexia+chills and rigors.
• Treated with antibiotics.
• Several weeks later,symptoms progressed.
Physical examination-ill-defined hard swelling
arising from the body of the mandible with an
exuberant soft tissue growth anterior to the left
last molar.
• Increased lymphocytes and platelet counts.

65. OPG of the
patient.
CT scan at level
of mandible-
lytic
destruction of
bone, soft
swelling.

66. Oral manifestations and radiographic
features
• Pain, seldom ulceration of mucosa,
inflammatory appearance, teeth become
exceedingly loose, systemic signs of disease.
• Roentgenogram shows- osteolytic invasive
changes, diffuse radiolucency, destruction of
supporting bone of the teeth.

67. Histology
• Similar to soft tissue tumor
• Classified under diffuse large B-cell
lymphoma(REAL)
• B-cell lymphoma of follicular center cell
origin(FW)
• Accompanying fibrosis, decalcification,large
spindle shaped lymphoma cells.

68. Treatment and prognosis
• Radical surgical excision
• Xray radiation
• Recurrence 5-10 years later is possible

70. Burkitt’s lymphoma
• Aka AFRICAN JAW LYMPHOMA
• Two types- endemic and sporadic
• Endemic to central africa
• Sporadic- related to epstein-barr virus
• Affects B-cells
• May also be seen with immunodeficiency

71. Clinical features
• Early symptom- swelling in the lymph nodes.
• If BL in the chest, throat or jaw- sore throat,
difficulty swallowing or breathlessness.
• May involve maxillary, sphenoid, ethmoidal
sinuses.
• Age- children and young adults
• Titres of EBV are often found.

72. Histology
• Monotonous overgrowth of undifferentiated
monomorphic lymphoreticular cells,usually
showing abundant mitosis.
• Macrophage- clear cytoplasm,scattered uniformly
in the tumor
• Characteristic “STARRY SKY” appearance.
WRIGHT’S STAIN
PREP

73. Treatment and prognosis
• Rapidly and uniformly fatal at one time.
• Cytotoxic drugs may increase survival
duration.

75. Hodgkin’s disease
• Particularly involves cervical lymph nodes
• Reed- Steinberg’s cell is pathognomic
• Classification-Rye’s

76. Clinical symptoms
• Bimodal age incidence peak-young adults, fifty’s
• Predilected to males
• Painless enlargement of one or more lymph nodes
• Persistent lymphadenopathy after URTI.
• Nodes- firm, rubbery consistency, overlying skin is
normal
• Pain- abdomen, back[splenomegaly]
• Generalized weakness,loss of weight, dyspnea,
anorexia, itching, pedal edema, hemoptysis/melena

77. Oral manifestations
• Exceedingly rare
• Usually involves mandible secondarily
• Secondary involvement of alveolar mucosa

78. Histology
• Multi-nucleated Reed-Steinberg cell
• Lymphocytic or monocyte-macrophage origin

79. Histologic types
1. Lymphocyte predominant- abundant
lymphocytes, occasional RSC
2. Mixed cellularity- lymphocytes, plasma cells,
eosinophils, RSC
3. Lymphocyte depletion- sparse lymphocytes,
stromal cells, fibrosis, bizarre RSC
4. Nodular sclerosis- lymphocytes, plasma cells,
eosinophils, RSC(lacunar)

80. Treatment and prognosis
• Radiation therapy
• In combination with chemotherapy
• Type dependent prognosis-
lymphocyte predominant> nodular
sclerosis> mixed cellularity>
lymphocyte depletion
• Stage dependent prognosis- stage
I>stage IV

81. After all we all work for “roti”...