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Contents
Introduction
Aneurysmal bone cyst
Simple bone cyst
Static bone cyst
Mucus extravasation cyst
Antral pseudocyst
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Aneurysmal bone cyst
Long bones
Jaffe & Lichtenstein 1942-
blow out (radiographically)
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Aneurysmal bone cyst
Intraosseous accumulation of variable sized,
blood filled spaces surrounded by cellular
fibrous connective tissue that often isadmixed with trabeculae of reactive woven
bone
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Aneurysmal Bone Cyst
First three decades;
Most common in second decade
Female predilection
Mandible > maxilla (molar region >angle
> ramus)
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Aneurysmal Bone Cyst
Painful swelling
Malocclusion
Rate of enlargement is progressively rapid
Recent displacement of teeth ; which are vital
Perforates the cortex and; covered byperiosteum
Thin shell of boneSpringiness or egg shell crackling, BUT IS
NOT PULSATILE
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Radiographic appearance
Well defined expansileosteolytic unilocular
radiolucency
Changes as it matures
Soap bubble
Honey bomb
Moth-eaten
Radiopaque
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Etiology & Pathogenesis
Traumatic event,
Vascular malformationor
Neoplasmthat disrupts the normalosseous hemodynamics & lead to anenlarging hemorrhage extravasation
Preexisting bone lesion-secondaryphenomenon
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Ewing (1940)
Benign giant cell lesion tumor modified bycommunication with large blood vessels
Jaffe (1950)
Modification of some other lesion which hasbeen destroyed by hemorrhage
Clough & Price (1968)Fibrous dysplasia & chondromyxoid fibroma
Etiology & Pathogenesis
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Solitary bone cysts, giant cell tumors &
osteosarcomas
More commonly with Fibro osseous lesionsWhat changes could have caused the
formation of ABC in these lesions???
Etiology & Pathogenesis
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Formation of microcysts
(Fibrous dysplasia, Central giant cell granuloma)
Enlargement of the microcyst
(stromal break down, giant cells)
Connection with vascular compartment causes
further expansion
Etiology & Pathogenesis
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Pressure on the bony wall
(endosteal resorption)
Thinning of cortex
Etiology & Pathogenesis
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Struthers &Shear
Malignant lesion-breaking the bone
Telangiectatic form of osteosarcomaTo conclude many think that it isNOT a
secondary phenomenonas they did not findany precursor lesion.
However both groups agreed that someareas similar to those of ABC were seen.
Etiology & Pathogenesis
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At operation an intact periosteum and a thin
shell of bone
Profuse bleeding
Cyst contains number of blood filled locules
and friable vascular tissue
No direct communication with any vessels can bedemonstrated at operation
Etiology & Pathogenesis
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Capillaries, blood
filled spaces, linedby flat spindle
shaped cells
Loosely textured
fibrous tissue
HISTOPATHOLOGY
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Large number of
multinucleate
giant cells
Fibroblasts,hemorrhage,
hemosiderin
Looks similar to
giant cell
granuloma
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Differential diagnosis
Giant cell lesions
Osteosarcoma
Rule out any lesion primarily associated
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Treatment
Depend on the nature of the associated
lesion
Curettage
Bone grafting
Can recur-
if recur evaluate the case carefully to see any
associated lesion
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Simple bone cyst(Traumatic bone cyst; hemorrhagic bone cyst,
idiopathic bone cavity; unicameral bone cyst)
Benign , empty or fluid containing cavitywithin bone that is devoid of an epithelial
lining
Common in jaws
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First described by Lucas (1929)
Rushton defined : Avacant or fluid
containing cystic lesion surrounded by a
hard bony wall with no epithelial lining
and no evidence of infection
Simple bone cyst
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Further Donkar and Punnia-Moorthy
subclassified as:
Idiopathic-EmptyFibrous or granulationsolid matter
Extravasation cysts (containing biochemical
profile similar to serum)
Simple bone cyst
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Younger patient; though (7-75 years)
More in males
Mandible mostly
Body and symphysis (ramus also
reported)
Anterior region in maxilla
Trauma prone areas
Simple bone cyst
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Asymptomatic; Diagnosed on Routine
examination
Sometimes may be associated withPain
Swelling
ParaesthesiaHistory of trauma (not always)
Simple bone cyst
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Smooth outlined radiolucentwith thin sclerotic border ,Root
involved - lobulated
Lamina dura may or may not
be lost
Radiographic appearance
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Differential Diagnosis
Periapical cemental dysplasia
OKC
Stafne cyst (Below canal)
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Pathogenesis
Olech, Sicher & Weinmann -
Trauma - hemorrhage theory
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Trauma
intramedullary hemorrhage
Necrosis of bone marrow and endosteum
Osteoclastic resorption of trabeculae
Liquefaction of hematoma(Before viable connective tissue formation)
Some simple cyst contain blood or serosanguineous fluid
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Breakdown products of hematoma
Local rise in osmotic pressure
(Toller study)
Transudation into the cystic fluid
Increase the intraosseous pressure
Osteoclastic activity and swelling
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Transudation progresses
Fluid gets diluted
Drop in the intracystic pressure(Further bleed may cause progression of the lesion)
No more bleeding
Gradual absorption or fluid occurs
Empty cavity
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Histologically Walls lined by athin band of vascular
fibrous connectivetissue or demonstratea thickenedmyxofibromatous
proliferation that
often is intermixedwith trabeculae ofcellular & reactive
bone
Areas of
vascularity, fibrin,erythrocytes &
occasional giant
cells adjacent to
the bone surface
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Diagnosis
Can be confused with Giant cell lesions
Surgical explorationnecessary
EMPTY CAVITY
SMOOTH SHINY WALL
SEROSANGUINEOUS FLUID
Mandibular neurovascular bundle may seen lying
free in the cavity
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Treatment
Induce hemorrhage
Some may resolve by itself
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Stafne cyst(Lingual Mandibular bone defect, static bone cavity,
latent bone cyst)
1942- Stafne described asymptomaticradiolucent lesions located near the angle ofthe mandible
Focal concavity of the cortical bone on thelingual surface of the mandible, remainstable in size , are not congenital
All major salivary gland can cause suchdefect
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Radiographic appearance
Ovoid radiolucency between
inferior alveolar canal and inferior
border of mand inn 2ndor 3rdmolar
Distinguished
bet TBC-
superior to
inferior
alveolar canal
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Pathogenesis
Pressure from the lobe of the gland
Resorption of the bone
Radiolucent defect
1.
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Pathogenesis
Ischemic process in an area adjacent to the
passage of the facial artery + tensile muscle
forces + hemodynamic forces
Pulled the artery from the lingual cortex
Comprising it from nutrition
Atrophy
2.
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Diagnosis
Clinical basis
CT & MRI, Sialography
Biopsy
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HistopathologyMuscle, Fatty Tissue or Normal salivary gland
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Treatment
No treatment required
Mucous extravasation
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Mucous extravasation
cyst
(Mucous escape reaction, mucous escapephenomenon )Two type
Retention (less common) and extravasation
Most commonly found on lower lip, canalso be seen onUpper lip
Floor of mouth and ventral of tonguePalate
Buccal mucosa
Retro molar area
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Mucous extravasation cyst
Painless swelling (specially at meal times-on
and off swelling)Round to oval
Blue and fluctuant/ normal color
Mistaken for lipoma, salivary gland tumor, fibro
epithelial polyp
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Pathogenesis
Trauma to the salivary gland duct or the acini
duct itself (parenchymatous type)
Egress of mucous into the adjacent connective
tissue
Complete ductal obstruction Mucus extravasation cyst
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Histopathology
Usually received with a associated salivarygland and frequently a part of the superficialmucosa
If cut-gelatinous material/ mucinous content
Three distinct pattern (Robinson & Horting-Hansen)
1stand 2ndextravasation
3rdretention
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Histopathology
Mucous acini
CONNECTIVE
TISSUE STROMA
MUCIN FILLED
CAVITY
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Histopathology
Mucin filled cavity
with mucinophages,
neutrophils,histocyte
C.T- B.V,
inflammatory cell
infitrates,
Mucous acini
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Treatment
Surgical excision tends to recur
Removal of the gland is advisable along
with the mucocele
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Antral
Pseudocyst
Antral cysts:
True- secretory
Pseudo-non secretory
Dome shaped lesion of the sinus floor
SINUS
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Antral Pseudocyst
Exudate (serum not mucin)
Accumulated under the maxillary sinus
mucosa causing sessile elevation
SINUS
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Antral Pseudocyst
Odontogenic infection
Sinus infection
Allergies
Winter months
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Kwappis and Whitten(1971)
Severe infection
Alter the integrity of the gland duct in the
sinus lining
Mucus into the connective tissue
Pathogenesis
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Gardner and Gardner and Gullane
Focal accumulation of inflammatory exudate that liftthe antral mucosa
Endodontically treated teeth and periodontitishasalso been implicated
Mechanical stress during coldsharp angle tissuegets rupture
Increased IgG, IgA, and C3presence ofanaerobic infection
Pathogenesis
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Radiographic appearance
Faintly radiopaque
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Histopathology
Calcifications and cholesterol crystals may be seen
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No treatment-regress by itself
If symptoms present
Drain by acnnulationLarge cystremove by caidwell-Luc approach
Treatment