A lecture for fifth stage dentistry college (oral and maxillofacial surgery department )

1. Non odontogenic tumors
Dr .mohammed Rhael ali
Tikrit dentistry college

2. Classification according to its origin
 A. gaint cell lesion
 Gaint cell reparative granuloma
 Brown tumor of hyperparathyroidism
 Cherubism
 B. Vascular
 Vascular tumor
 Vascular malformation
 C. Hematopoietic-reticuloendothelial
 eosinophilic granuloma
 hand-schuller –christian disease
 letterer –siwe disease
 D.Neurogenic
 neurofibroma
 shwannoma

3. giant cell lesions

4. • Giant cells are very large, multinucleate,
modified macrophages which may be formed
by coalescence of mononuclear cells or by
nuclear division without cytoplasmic division
of monocytes, particularly in response to the
presence of a foreign body.

5. Giant cell lesions include :
• aneurysmal bone cyst
• chondroblastoma
• simple (traumatic) bone cyst
• osteoid osteoma
• osteoblastoma
• osteosarcoma
• giant-cell reparative granuloma
• brown tumor of hyperparathyroidism
• cherubism

6. central gaint cell granuloma
• Mandible more than maxilla
• Female more than male
• Young more than old
• Mostly in anterior region of lower jaw.
• Mainly Asymptomatic ,may cause expansion perforation of cortex
• Present almost exclusively in jaws

7. central gaint cell granuloma
Classified on the basis of biologic behavior as :
 Non-aggressive :
 Asymptomatic, slow
 expansion of the affected Bone
 Aggressive type:
 Painful, rapid growth, root resorption
 perforation of cortical bone
 paraesthesia
Etiology :
 Reactive lesion
 Trauma

10.  Treatment conservatively by local curettage
• Recurrence may occure Recurrence , Varies from 10 – 50 %
• Use of liquid nitrogen after curretage decrease the reccurance rate
 Intralesional steroids:
• • Triamcinolone – Suppresses inflammatory component of lesion
 Calcitonin – s.c. inj.:
• Antagonizes bone resorption by inhibiting Giant cells.
 α-Interferon
 bisphosphonates such as Zoledronate
• Recurrent and aggressive type treated by surgical resection
 Management of associated teeth :
• Preserve teeth in area of lesion : when have adequate bone support , Treat
endodontically before surgery .
• Extract teeth in area of lesion : When have poor prognosis (poor bone
support or Compromising access to the lesion
Treatment

12. PERIPHERAL GIANT CELL GRANULOMA
• Common tumor like growth in the oral
cavity
• Does not represent a true neoplasm but
a reactive lesion
• Arising from periosteum or PDL
membrane. Often called as peripheral
giant cell reparative granuloma.

13. C/F:
Age: 5th 0r 6th decade of life.
Common in females.
Mandible is affected more often.
Occurs exclusively on gingiva
Reddish or bluish nodule, most lesions smaller than 2cm
in diameter.
May be ulcerated due to trauma.
Treatment: Local surgical excision down to the
underlying bone
Differential diagnosis ; CGCG • Pyogenic granuloma

14. Parathormone (PTH) is normally produced by
parathyroid glands, which regulates the Ca+
metabolism.
Hyperthyroidism may be :
Primary : due to over production of parathyroid
hormones
Secondary : due to decrease calcium level in the
blood (as in chronic renal disease)
Brown tumor of hyperparathyroidism

16. BROWN TUMOR OF HYPERPARATHYROIDISM
C/F
 Predilection for females.
 Jaw - not as frequent as in long bones and skull.
 Vague aches, severe bone pain, tenderness following fractures.
 Mobility of teeth
R/F:
• Generalized loss of lamina dura. • Ground glass appearance. • Cortical
plate may be thinned or lost. • There is a cystic type of radiolucency.
Treatment:
• Primary: – Surgical excision of parathyroid adenoma .. Bone lesions
resolve spontaneously.
• Secondary: – Management of kidney disorders.

17. Benign Mesenchymal tumors
(Fibrous dysplasia )

18. Benign Mesenchymal tumors
(Fibrous dysplasia )

19. Benign Mesenchymal tumors
(Fibrous dysplasia )

20. Benign Mesenchymal tumors
(Fibrous dysplasia )
• Replacemnt of bone by immature bone with extensive vascular
fibrous element
• Affect children
• Appear usually as painless enlargment of maxilla of affected side
leading to facial asymmetry
• Ground glass appearance is the typical radiographical feature
treatment
Self limited , usually disappear after completion of skeletal growth
If disfiguaration occure then surgical shaving and recontouring
may done

21. Benign Mesenchymal tumors
(cherubism )

22. Benign Mesenchymal tumors
(cherubism )

23. Benign Mesenchymal tumors
(cherubism )
 It consider as familial inherted type of fibrous dysplasia
 affect mandible more than maxilla
 Clinically Appear as painless slow growing of angle of mandible
bilaterally ,early exfoliation of deciduous teeth
 Multiple missing and impacted permanent teeth
 Radiographically appear as multilocular radiolucency
Treatment :
• shaving and Surgical contouring
• better done after skeletal maturation , but if disfugaration huge
or affect on airway or causing social problem to the patient so
treatment can do early

24. Vascular lesions
• vascular tumors : hemangiomas
which demonstrating endothelial
hyperplasia.
• Vascular Malformations : lesions
with normal endothelial turnover.

25. Hemangiomas
• The word "hemangioma" comes from the Greek
haema-, "blood"; angeio , "vessel"; -oma ,
"tumor".
• A hemangioma is a benign and usually self-
involuting tumor of the endothelial cells that
line blood vessels, and is characterised by
increased number of normal or abnormal vessels
filled with blood.
• Exhibits rapid early growth until 6-8 months of
age, followed by regression by 5-9 years of age.

27. Vascular Malformations
 Vascular malformations are present at birth and unlike hemangiomas, do not go
through a “rapid proliferative phase”
 not “involute”.
 They grow constantly with the patient growth
 Approximately 31% of these malformations are found in the head and neck
region.
 Abnormal development of either arterial or the venous side of vascular network
during this phase of development
 Trauma, infection, and hormonal fluctuation (pregnancy or puberty) may
stimulate increased growth of the vascular malformation.
 The mechanism of growth is not increased endothelial proliferation - which is
within a normal range in these lesions, “but alteration in the flow dynamics
within and around the lesion”.
 This results in recruitment of “collateral vessels” and dilatation of involved
vessels.

29. Classified in to :
1. low flow :
 Cappillary malformation
 Venous malformation
 Lymphatic malformation
2. High flow :
 Arterial malformation , Arteriovenous
Malformations
Vascular Malformations

30. Capillary Malformations ( portwine stain)
• appear as reddish-pink macules over facial
dermatomes may be smooth initially but
become more “ pebble – like” as the patient
grows.

32. Venous Malformations
• Venous malformations are bluish, soft
and easily compressible,
• auscultation reveals no bruits.
The clinical absence of “pulsations or a
thrill” generally indicates a low flow
Venous vascular malformation
 Thrill : Feeling of the mass by finger
 Bruit . Auscalt the mass by stethoscope

33. Lymphatic Malformations
• Low- flow lesions
• Within the oral cavity the LMs are more
commonly found on the anterior 2/3 of
tongue, followed by palate,gingiva, and oral
mucosa.
• Predilection for head and neck and the
axilla, where embryonic lymph sacs are
located

34.  MICROCYSTIC LM (Lymphangioma)
• In the oral cavity appear as multiple translucent non-
compressible cysts or vesicles
 Macrocystic LMs (cystic hygroma)
• usually presents as multiple cysts of >2 cm and are
commonly found in the neck, and in the cervical area just
below the angle of the mandible. They clinically appear as
localized painless non-pulsatile swelling with no bruit or
thrill, having a rubbery compressible consistency, and
covered by normal appearing skin unless hemorrhage or
communication with venous malformations produce a blue
discolouration. Positive to transillumination .
Lymphatic Malformations

35. MICROCYSTIC LM (Lymphangioma)

36. Macrocystic LMs

37. Transillumination of cystic hygroma

38. Arterial / Arteriovenous Malformations
• “High-flow lesions
• create a direct communication between the arterial and venous systems,
• AVM is present at birth, but become clinically apparent only during the 4-5th
decade of life and is often misdiagnosed due to delay in clinical presentation.
• The most common site for AVM is the brain, followed by the head, neck, limbs,
trunk, and viscera.
• They appear as purple-blue raised painful macule, are pulsatile with thrill and
bruit, warm to touch
• do not empty fully on compression, and refill quickly on reliving digital pressure.
• They are associated with embolism, pain, bleeding, ulceration, and congestive
cardiac failure due to increased cardiac load.
• Often a patient presents with severe bleeding as the first sign that a high flow-
lesion is present. They may also complain of recurrent gingival bleeding and loose
or depressible teeth.

40.  DIAGNOSIS of vascular lesions :
• History
• Clinical examination
• MRI
• Doppler Ultrasound
• CT
• Arteriography

41. Treatment of vascular lesions
Hemangioma :
• Self limited ,usually disappear after 12 y age
• Treatment indicated when the lesion interfer with
development (obstructive vision,recurrent bleeding
,ulcerations,interfere with vocal cords function.
• Treatment options :
• Steroid (systemic or intralesional injection)
• Interferone
• Laser
• Surgical excision

42. Treatment of vascular lesions
Cappillary malformatios:
 Laser
venous malformations
1.Injection of sclerosing agents ( absolute alcohol,sodium
tetradecyle sulphate(std), and bleomycin.
2. Surgical excision
Arterio-venous malformations
 pre-opertative embolization or ligation of feeding artery
followed by surgical resection

43. Treatment of vascular lesions
Lymphatic malformations:
1.Aggressive surgical debulking may be necessary in vary
large lesions.
2. Infections such as upper respiratory infections often cause
dramatic and painful swelling of the lesion and should treated
aggressively by antibiotic and drainge to avoid obstructions of
airway
3. Injection of sclerosing agents or OK423
4. Surgical excision

44. Neurogenic tumors
• NEUROFIBROMAS. -It may occur as solitary
cutaneous lesions (neorfibroma ) , in which case one
finds no café-au-lait spots and no family history of
the disease. -Multiple cutaneous lesions w/café- au-
lait spots, dominantly inherited, referred as
neurofibromatosis that starts to be manifested since
childhood

46. • LANGERHANS CELL HISTIOCYTOSIS
Results from abnormal proliferation of
Langerhans cells or their precursors.
Langerhans cells are specialized cells of the
histiocytic cell line that normally are found in the
skin.
Types :
 Eosinophilic granuloma (Solitary)
 Hand Schuller Christian disease (Chronic
disseminated)
 Letterer Siwe disease (Acute disseminated)
Hematopoietic-reticuloendothelial lesions

47. Esonophilic granuloma
C/F:
• Occurs in older children & young adults.
• Male > female
• May be asymptomatic – incidental finding on radiograph
• Affects skull & mandible, also long bones.
• Local pain, swelling, tenderness.
• General malaise and fever occasionally accompany.
• May cause bony swelling and involve overlying soft
tissue.
• Gingival bleeding, pain & ulceration.
• Loosening of the teeth often occurs after destruction of
alveolar bone.

48. • R/F: • Single or multiple irregular radiolucent
lesions. • Well circumscribed. • Usually
involving superficial alveolar bone. • Cortex
often destroyed. • Tooth ‘floating in air’
appearance. • Pathologic fractures may occur
• Treatment: • Curettage
Esonophilic granuloma

49. hand-schuller –christian disease
C/F:
• Occurs in early life (Age < 5 yrs)
• Widespread skeletal & extra-skeletal lesions.
• Chronic clinical course
• Classic triad of: 1. Multiple ‘punched-out’ lesions of skull.
2. U/L or B/L Exophthalmos. 3. Diabetes insipidus with or
without Dyspituitarism.
• Oral manifestations – earliest signs of diseases.
Stomatitis, Gingivitis, Halitosis
• Loose teeth, premature exfoliation.
• Failure of healing of post-extraction sockets.
• Loss of supporting alveolar bone ,advanced periodontal
disease

50. Treatment:
• Spontaneous regression – approx. half of the patients.
• Curettage / excision
• Radiotherapy – inaccesible lesions
• Chemotherapy
• Prognosis – good

51. letterer – siwe disease
C/F
• Occurs in infants (age < 3 yrs).
• Diffuse involvement of skeletal system.
Ulcerative lesions of oral mucosa. • Gingival
hyperplasia. • Loosening & premature loss of
teeth.

52. Treatment:
• Chemotherapy – only few pt. respond.
• Poor prognosis.
• Rapid course of disease – terminates fatally
in short time.

53. Thank you for listening