Benign Non-Odontogenic Lesions Flashcards
Cemento-Ossifying Fibroma clinical features
3-4th decade 5:1 female predilection Common in mandible
Cemento-Ossifying Fibroma radio appearance
Well-demarcated lesion Radiolucent to mixed appearance
Cemento-Ossifying Fibroma histo appearance
Potato-like mass that usually comes out in one chunk Lots of connective tissue and bone/cementum interspersed. NO inflammation seen
Cemento-Ossifying Fibroma treatment
Enucleation This is a TRUE neoplasm.
Fibrous Dysplasia Types of Lesion
Polyostotic Monostotic
Fibrous Dysplasia clinical features
MAXILLA more common Bones have fracture risk because they are weaker. Can have a hockey stick discrepancy. One leg longer than the other Will see SWELLING over time. Can see expansion.
Fibrous Dysplasia radio appearance
Ground glass appearance with ill-defined borders Narrowing PDL space and the lamina dura hard to make out
Fibrous Dysplasia histo appearance
Irregular shaped woven bone (Chinese characters) Bone has NO OSTEOBLAST around it. Distinctive feature. Bone arises in slide via metaplasia from fibroblasts Woven bone becomes more lamellar over time
Fibrous Dysplasia treatment
Resection, but not in children. Lesion will regress over time maybe to 70% of size. Remove at skeletal maturity. Radiation is CONTRAINDICATED. It may actually cause malignant transformation to osteosarcoma.
Fibrous Dysplasia age
Stage of fetal development determines if polyostotic or monostotic (MOST cases are monostotic) 1-2nd decade (YOUNGER) population
Fibrous Dysplasia types of polyostotic involvement
Jaffe Type
- Cafe au lait spots on the trunk and thigh
- Multiple bone involvements
McCune-Albright Type
- Cafe au lait spots
- Endocrine hyperfunction
- Precocious puberty
Types of cemento-osseous dysplasias
Periapical
Focal
Florid
Clinical features of periapical osseous dysplasias
14:1 Black female predilection
30-50 years old
Clinical features of focal osseous dysplasias
80% in Caucasian females
4-5th decade
Clinical features of florid osseous dysplasias
Black females
Location of periapical osseous dysplasias
Mandibular anterior
Multiple lesions
Location of focal osseous dysplasias
Posterior mandible ONE lesion
Location of florid osseous dysplasias
More than one quadrant
Radiograph of periapical osseous dysplasias
Start as RL then add more osteoid and become RO
Radiograph of focal osseous dysplasias
RL to RO. RL rim remains over time
Radiograph of florid osseous dysplasias
Multiple “cotton-wool” radiopacities
Treatment of periapical osseous dysplasias
NONE needed. No biopsy
Treatment of focal osseous dysplasias
Biopsy to rule out cemento-ossifying fibroma
Treatment of florid osseous dysplasias
MAINTAIN DENTITION. Normal alveolar bone will resorb, but dysplastic bone will not and osteomylitis could occur.
Clinical features of all osseous dysplasias
Occur in tooth-bearing areas. Not outside the jaws Reactive lesions with cause unknown All types have the same histology, but are a spectrum along the process. No expansion seen Asymptomatic NO teeth displacement and teeth remain vital
Histo of all osseous dysplasias
Come out as coffee grounds
Clinical features of osteoblastoma
Pain NOT relieved by aspirin
Clinical features of osteoid osteoma
NOCTURNAL PAIN relieved by aspirin
Radiograph of osteoid osteoma
Well-circumscribed with radiolucent rim and central radiopacity.
Less than 2cm in diameter
Radiograph of osteoblastoma
Similar location to OO (outside the jaws)
Greater than 2cm
Can have a RL rim with a mixed center
Histo of osteoid osteoma and OO
Lots of woven bone, NOT lamellar bone in a fibrovascular stroma Both can resemble low-grade osteosarcoma (malignancy) This similarity contributes to their misdiagnosis
TX of osteoid osteoma and OO
Local excision
Curettage
Types of osteoma
Periosteal Endosteal
Clinical features of osteoma
Simply a benign bone lesion Paranasal sinuses are the most common, but can happen in bone
Radiograph of osteoma
Radiopaque
Histo of osteoma
Dense bone combined with cancellous bone
TX of osteoma
Surgical excision or just observation over time
Clinical presentation of Gardner syndrome
Epidermoid cysts GI polyps with 50% becoming malignant by age 30 Desmoid tumors: locally aggressive benign fibrous proliferations at incision site of colectomy Ocular – hypertrophy retinal pigment Oral – impacted supernumerary teeth and odontomas
Key indicator of Gardner syndrome
If you see multiple osteomas think about this lesion
Radiograph of Gardner syndrome
Osteomas
NO radiolucent rim
Supernumerary teeth
Heredity of Gardner syndrome
Autosomal dominant condition
TX of Gardner syndrome
Prophylactic colectomy as GI polyps will become malignant
Age of central giant cell granuloma
2-4th decade with a 2:1 female predilection
Location of central giant cell granuloma
Presents in posterior mandible 70% of time CROSSES MIDLINE
Radiograph of central giant cell granuloma
Radiolucency Start off as unilocular and over time become more multilocular and expansile Displacement of teeth Resorption of teeth possible
Histology of central giant cell granuloma
Granulation tissue Giant cells (frequently around the periphery) Reactive bone around periphery → body is trying to wall off the lesion; bone not made by lesion Extravasated RBC’s
DDX of central giant cell granuloma
ABC
- Typically in children and doesn’t cross the midline Has blood-filled spaces in lesions with GC around the periphery of lesion
Brown tumor
- Need to rule out hyperparathyroidism Have calcium levels checked
Giant cell tumor of bone
- Most common in distal tibia and femur area not jaws
TX of central giant cell granuloma
Curettage Resection if the lesion recurs
Clinical features of Hemangioma of Bone (Vascular Malformation)
Pain and swelling when larger Sulcular bleeding Bruit or pulse if has a artery component. If only venous, no bruit present.
Location of Hemangioma of Bone (Vascular Malformation)
Seen in posterior mandible
Age of Hemangioma of Bone (Vascular Malformation)
2nd and 3rd decades most common
Radiograph of Hemangioma of Bone (Vascular Malformation)
Multilocular Presents as a mixed to radiolucent lesion Occasional sunburst pattern Cortical expansion
Histology of Hemangioma of Bone (Vascular Malformation)
Cavernous and capillary vessels
TX of Hemangioma of Bone (Vascular Malformation)
Make sure to aspirate the lesion before biopsy Pre-surgery embolization with resection, curettage
Types of Langerhans Cell Disease
Acute disseminated (Letterer-Siwe Disease) Chronic disseminated (Hand-Schuller-Christian Disease) Eosinophilic granuloma of bone
Features of Letterer-Siwe Disease
Most severe manifestation of disease Seen in infants and very young children. Usually FATAL. Lesions seen on (SOB) skin, organs, and bone
Features of Hand-schuller-Christian Cell Disease
(SOB) skin, organs, bone also involved, but organ involvement NOT as severe TRIAD: Bone lesions Exophthalmos → histiocytic cells accumulate around the eyeball Diabetes insipidus → histiocytic proliferation involves the posterior pituitary gland
Features of Eosinophilic granuloma of bone
MOST COMMON presentation of this disease
BONE ONLY (solitary or multiple lesions)
No skin or visceral involvement
Location of Langerhans Cell Disease
Skull and mandible in the head/neck area
What is Langerhans Cell Disease
Benign neoplasm consisting of histiocytic cells
What does Langerhans Cell Disease look like on radiograph
Radiolucency Usually well-defined and non-corticated Significant bone destruction Mobile teeth from bone loss
Histology of Langerhans Cell Disease
Large number of mononuclear histiocytic cells Large numbers of eosinophils Diagnosis NOT made only on light microscopy. Need immunohistochemistry with S100 stain. Histiocytes can appear as a coffee bean Look for birbeck cells in histiocytes (Langerhans cells)