1. SWELLINGS OF THE JAW
ARJUN SHENOY
Postgraduate student
Dept of Maxillofacial Surgery

2. CONTENTS
 CLASSIFICATION
 ELABORATION OF TYPES
 CLINICAL FEATURES
 TREATMENT
 HEMIMANDIBULECTOMY

3. CLASSIFICATION
FROM
TOOTH GERM
FROM
MUCOPERIOSTEUM
OSSEOUS
INFLAMMATORY
MALIGNANT
BENIGN

4. ARISING FROM MUCOPERIOSTEUM
• EPULIS
• FIBROUS
• GRANULOMATOUS
• MYELOID
• SARCOMATOUS
• CARCINOMATOUS

5. ARISING FROM TOOTH GERM
1. EPITHELIAL ODONTOMES
2. CONNECTIVE TISSUE ODONTOMES
3. COMPOSITE ODONTOMES

6. OSSEOUS TUMORS
1. BENIGN
a. Fibrous dysplasia
b. Ivory osteoma
c. Pagets disease
1. MALIGNANT
a. Maxilla
b. mandible
CA OF
MAXILLARY
ANTRUM
SCC ,
BURKITTS
EXTENSION
FROM ORAL
CAVITY AND
TOUNGE

7. INFLAMMATORY
• ALVEOLAR ABSCESS
• OSTEOMYELITIS

8. EPULIS
• Generic term applied for tumor of gingiva or
alveolar mucosa
• Tumor like hyperplasia of the fibrous connective
tissue
• Classification
• FIBROUS
• GRANULOMATOUS
• MYELOID
• SARCOMATOUS
• CARCINOMATOUS

9. CLINICAL FEATURES
• Seen in middle and old age
• Female prediliction 2/3rd to 3/4th
• Typically appears as single or multiple folds of
hyperplastic tissue facial aspect of alveolar
ridge and lingual to mandibular ridge
• Redundant tissue is firm and fibrous
• Size – 1 cm to whole of vestibule
• May appear ulcerated or erythematous

10. • Anterior portion of jaw affected more than
posterior portion
• Associated with history of ill fitting dentures

11. TREATMENT
• Surgical removal with microscopic examination
of the excised tissue
• Partial thickness or full thickness
surgical blade excision
• Curettage
• Electrosurgery/cryosurgery

12. ODONTOGENIC TUMORS
• Comprise of complex group of lesions of diverse
histopathological types and clinical behaviour
• tumor of odntogenic epithelium- Odontogenic
epithelium
• Mixed odontogenic – odontogenic epithelium +
ectomesenchyme
• Tumor of odontogenic ectomesenchyme-predominantly
ectomesenchyme

13. ODONTOME
COMLEX
ODONTOME
COMPOUND
ODONTOME

14. 19Y/ F
COMPOUND
ODONTOME

20. TUMOR OF ODONTOGENIC EPITHELIUM

21. • INTRODUCTION.
• PATHOGENESIS.
• CLINICAL FEATURES.
• HISTOLOGICAL TYPES.
• RADIOLOGICAL FEATURES.
• MANAGEMENT.
• PROGNOSIS.

22. INTRODUCTION
• Ameloblastoma {amel – enamel, blastos -
germ} is rare benign tumour of odontogenic
epithelium. (ameloblasts).
• Also called “ADMANTINOMA”.[1885 by
French Physician Louis-Charles Malassez]
• Term “AMELOBLASTOMA”- By Ivey &
Churchill(1930).

23. • “AMELOBLASTOMA” has been defined by
ROBINSON as usually unicentric, non
functional, intermittent in growth,
anatomically benign & clinically persistent
tumour.

24. CLINICAL FEATURES
• AGE 20 – 40 years, no sex predeliction.
• SITE Mandible 80% and maxilla 20% 75 %
in molar and ramal region.
• SIGNS AND SYMPTOMS asymptomatic in
earlier stages until the lesional growth
produces intraoral and for extra oral jaw
swelling, tooth eruption and dental occlusal
disturbances or incidental findings in the
radiograph.

25. • Later stage with nerve involvement, there will be
sensory changes of the lower lip. Pain of
secondary infection.
• Large persistent lesion may exhibit fluctuation
 “eggshell crackling”.

26. CLINICAL CLASSIFICATIONS
• A. the solid / multicystic / intraosseous
type. (conventional).
• B. the unicystic type
• C. peripheral type (extraosseous)
• D. malignant ameloblastoma.
• E. Pituitary ameloblastoma
(craniopharyngeoma / rathkes pouch
tumour)

27. CLINICAL CLASSIFICATIONS
Pituitary
unicystic
malignant
peripheral multicystic

28. • Solid ameloblastoma has a high recurrence
rate if not removed adequately as they tend
to infiltrate between the trabecullae of the
cancellous bone without actually
destroying the trabecullae

29. • In the absence of the treatment:-
• The ameloblastoma keeps on enlarging & causes
thinning of surrounding bone leading to
fiuctuation.
• Since it is not encapsulated tumour,it enlarges &
invades into the neighbouring tissues by
replacing them rather than pushing them as seen
in cysts.

30. • Invasion of the medullary space is first
feature (bone destruction by direct pressure &
distension) when the tumour attains in large size
with bone erosion,then there is escape into
periosteum & mucosa & muscles of adjoining
region.

31. • Root resorption is caused without osteoclastic
activity.
• Locally aggressive invasion in maxillofacial
area, may compress vital structures, obstruct
airway, impair swallowing, erode major arteries
or invade middle cranial fossa.
• The extenisve tumours can cause gross facial
deformity.

32. SIZE:-
• It may range from lesion as small as 1cm in
diameter & upto disfiguring tumour measuring
as large as 16 cm.
• In maxilla, it may enlarge to involve the
maxillary sinus, nasal cavity leading to nasal
obstruction & even proptosis of eye. (The
spread in maxilla is more extensive,
because of cancellous nature of the bone.)

33. SPREAD:-
• Though it is a benign, locally invasive lesion, in
some rare instances or late stages shows
spread to distant sites.

34. The factors contributing to spread :-
• 1) Duration
• 2) Extensive local spread
• 3) Multiple operations/Radio therapy
• 4) Proximity to anatomical passages

35. • Occasional transformation in to malignant
from(2 to 4%)metastasizing to lung & lung
bone.
• Most common sites are lungs & it considered to
be the result of aspiration of tumour cells during
extensive manipulation.

36. • Metastatic lesions prior to any surgical
intervention, give an indication for hematological
spread.
• Other sites where metastasis is seen include
regional lymph nodes, liver, spleen, kidney, lung,
bones, skull, cranium, lumbar vertebrae, ilium etc.

37. Radiographic features
• Conventional/ solid ameloblastoma
•  multilocular appearance where
numerous, well defined cystic spaces of varying
diameter is seen
•  when radiolucencies are small, lesion is
described as “honey comb/ soap bubble”
configuration.

39. Histological Appearance
1. Follicular type
2. Plexiform type
3. Acanthomatous type
4. Basal cell type
5. Granular type
6. Desmoplastic type

40. key points to be known:-
• Amelobalstomas are generally slow growing but
locally invasive tumours and have high
recurrence rate after treatment.
• Tumors normally extend beyond radiographic
margins in cancellous bone but not at the cuticle
margin. So ,it is difficult to define actual
margins of the lesion within the
cancellous bone on radiographic
examination

41. • MANAGEMENT
• 1 curettage (not advocated now)
• 2 En block resection.
• 3 peripheral osteotomy
• 4 segmental resection
•
• 5 cautery

42. 1) Curettage:- (Least desirable form of
therapy).
▫ Removal of tumors by scrapping it from the
surrounding normal tissue.
▫ High recurrence rate after treatment due to fact
that nest of tumor cells extend beyond the clinical
radiographic margins of the lesion making it
impossible to eradicate the lesion completely
by scrapping.
▫ Used for small lesions in the mandible for
unicystic ameloblastoma.

43. 2. En-block resection (without continuity
defect)
• Most frequently used method for treatment.
• “Removal of tumor with a rim of uninvolved
bone but maintaining the continuity of the jaw ”
• Requires osteotomy approximately 1-2 cm from the
margin of tumor .
• Wide resection of soft tissue, if involved.

44. • Advantages:- not violating the tumor margins
during resection , which might provide the
possibility of tumor seeding in the surgical site.

45. SEGMENTAL RESECTION WITH CONTINUITY
DEFECT
• “Removal of segments of the mandibular maxilla
upto and including hemisection or more,
associated with low reccurence rate” . Includes
hemimandibulectomy & hemimaxillectomy.
• Immediate reconstruction can be carried out if
there is clinical or intra operative frozen section
confirmation of complete excision of the tumor.

46. • If not reconstruction can be delayed until tissue
sections are studied.
• Autogenous free bone graft (iliac/rib graft) is
commonly used.
• An allogenic bone crib with patent marrow may
be used with reconstruction plate.

47. • Reconstruction plate wit or without condylar
prosthesis can be used in very old patients, or where
secondary reconstruction is planned.

50. CAUTERY
• Not commonly used but more effective than
curettage as it has 50% recurrence rate than 90%
of curettage.
• The secondary ischemia and necrosis that
occurs during the rise of cautery for some distance
from the margins of the tumor may destroy
invading tumor cells not reached by direct
instrumentation.

51. JACKSON AND CALLON FORTE (1996)
GUIDELINES DEPENDING ON ANATOMICAL
LANDMARKS
• tumor confined to maxilla without orbital floor
involvement
-- partial maxillectomy
• Involving orbital floor but not the periorbital area –
total maxillectomy.
• Involving orbital contents  total maxilectomy
with orbital exenteration
• Involving skull bone along with skull bone along
with skull bone resection neurosurgical
procedure.

52. PROGNOSIS
• Recurrence Rate:-
• 10 – 20% unicystic ameloblastoma after
enucleating and curettage.
• 15% conventional ameloblastomas after
marginal resection.
• 50% multicystic ameloblastoma during first 5
years post operatively.

53. • FIBROUS DYSPLASIA
Types :
Monostotic
Polyostotic -
Jaffes type
Albright’s syndrome.

54. Jaffe type-
FD involving variable no. of bones &
pigmented lesions of skin( café- au-lait
spots).
Albright’s syndrome –
Polyostotic FD, precocious puberty, café- au-lait
spots + endocrinopathies.

55. • Replacement of normal bone by excessive
proliferation of cellular fibrous connective tissue
intermixed with irregular bony trabaculae
• Painless swelling of the affected area
• Maxilla involved more than mandible
• Mandibular lesions strictly monostotic
• Teeth remain firm but are displaced by the lesion
• Ground glass appearance in radiograph

56. CLINICAL FEATURES
• Involvement of mandible results in not only
expansion of buccal and lingual cortical plate but
also lower border.
• Superior displacement of inferior alveolar
canal is not uncommon
• In maxilla, the lesion displaces the sinus floor
superiorly and commonly obliterates the
sinus
• Associated with asymmetry of craniofacial
skeleton and pathologic fractures

57. • MANAGEMENT
• Smaller lesions- surgical resection in entirety
• Cosmetic deformity with associated psychologic
problems or functional deformity dictate
surgical intervention in younger patients
• Polyostotic disease effectively managed by
bisphosphonate therapy
• Radiation therapy contraindicated due to risk
of post irradiation sarcoma

58. PAGETS DISEASE / OSTEITIS DEFORMANS
It is a condition of abnormal resorption &
apposition of bone. It is initiated by a intense wave
of osteoclastic activity, followed by vigorous
osteoblastic activity.

59. CLINICAL FEATURES
Age : above the age group of 50 yrs.
Sex : M:F 1:1
Site : pelvis, spine, femur, skull& jaw bones.
Clinical features depend on the bone involved
Bone pain
Neurologic pain- due to impingement on foramina,
tinnitus
Bowing of legs, gait difficulties, curvature of spine.

60. Deafness
Need to by bigger hats
Leontiasis ossea.
Oral manifestations :
Maxilla is more commonly involved than
mandible ( 3: 1)
Alveolar ridges become widened & palate is
flattened.

61. Radiographic findings
3 stages
It can cause expansion of cortex & thinning out,
but does not perforate it.
LD could be obliterated
Hypercementosis
Root resorption.

62. • COTTON WOOL APPEARANCE

63. MANAGEMENT
Calcitonin – relieves pain, ↓osteoclastic activity&
↓serum alk phosphatase levels.
Sodium etidronite – covers bone surface &
retards bone resorption & formation.
Diphosphanates – inhibits bone resorption
Mithramycin – is cytotoxic to osteoclasts
Surgery.

65. • Definition:
Osteomyelitis may be defined as an
inflammatory condition of bone, that begins as
an infection of medullary cavity and haversian
systems of the cortex and extends to involve the
periosteum of the affected area.

66. I. Based on pathogenesis.
a) Haematogenous osteomyelitis .
b) Osteomyelitis associated with peripheral vascular
diseases.
c) Osteomyelitis secondary to contiguous focus of
infecton.
II. Depending on duration and severity of diseases.
a) Acute osteomyelits.
b) Chronic osteomyelitis.
III.Depending on formation of pus in the infection.
a) Suppurative .
i. Acute suppurative.
ii. Chronic suppurative.
• Primary
• Secondary.
iii. Infantile osteomyelitis.

67. b) Non suppurative.
i. Chronic sclerosing osteomyelits.
• Focal sclerosing.
• Diffuse sclerosing.
ii. Garres sclerosing osteomyelitis.
iii. Actinomycotic osteomyelitis.
iv. Radiation induced osteomyelitis.

68. Acute osteomyelitis Clinical features.
Occurrence.
oIn adults, it is more common in mandible and involves
alveolar process, angle of mandible, posterior part of
ramus and coronoid process.
cases are characterized by
oDeep seated boring, continuous intense pain in the
affected area.
oIntermittent paraesthesia or anaesthesia of the lower lip.
oFacial cellulitis, or indurated swelling of moderate size,
which is more confined to the periosteal envelope and its
contents.
oTrismus.

69. Chronic osteomyelitis.
• .
Clinical features.
• Pain and tenderness.
• Non healing bony and overlying soft tissues wounds
with induration of soft tissues.
• Intra oral and extra oral draining fistula.
• Thickened or wooden character of bone.

70. Management.
 The goal of management is to
 Attenuate and eradicate proliferating pathologial
organisms.
 Promote healing.
 Re-establish vascular permeability.
This include
A. Conservative treatment.
B. Surgical treatment.

71. Extraction of offending teeth.
Debridement.
 Decortication.
 Resection.
 Trephination or fenestration.
 Saucerization.

72. ALVEOLAR ABSCESS

73. MANAGEMENT
• 1 Establishment of drainage
a) extra-oral b) intra-oral
• 2 Removal of source of infection
a) immediate b) delayed
• 3 Antibiotic therapy
a) toxicity b) desirability
c) medical history

74. CARCINOMA OF MAXILLARY SINUS

75. 75
CARCINOMA OF MAXILLARY SINUS
About 80-90% of cancers in sinus area are SCC. It likely originates
from metaplastic epithelium of sinus linning.
Etiology : is not well not well understood, but commonly associated
with wood workers, chemical, shoe & textile workers snuff users.
C/F: Males are commonly affected, with a mean age of 60 years. The
tumour gradually increases in size & fills the sinus cavity before
causing any symptoms.
In early stages symptoms might be similar to chronic sinusitis. As the
malignancy starts eroding the bony walls, the swelling may be
manifested in various locations - intra orally, intra nasally, orbitally &
extra orally.

76. 76
Usually medial wall is erroded first leading to nasal signs &
symptoms- as obstruction, discharge, bleeding & pain.
When floor of the sinus is destroyed – there is intra oral swelling,
expanison of alveolar process, pain, numbness & lossening of teeth.
When roof is destroyed – there could be diplopia, proptosis,
hyperasthesia/ anesthesia & pain over cheek.
When lateral wall is erroded – the swelling becomes evident extra
orally.
Involvement of posterior wall – leads to trismus, obstruction of
eustachian tube causing stuffy ear.

77. 77
Radio: in the initial stages it is difficult to distinguish between maxillary
sinusitis & maxillary ca. maxillary sinus will be filled with soft tissue
shadow. One should carefully evaluate the changes seen in the walls (
medial wall is the one which is eroded first ). Large lesions erode the bone
& cause irregular radiolucency. There might be resorption of roots,
widening of PDL, & displacement of teeth.
CT is ideal to evaluate the extent of the lesion.
Treatment : surgical + radiotherapy.
Prognosis is poor.

78. THANK YOU