Path 8: Connective Tissue Lesions

Front 1

Peripheral ossifying fibroma:

1) What is it?
2) Exclusively seen where? Where does it normally arise from? 50% found in what region?
3) What does it look like?
4) Who does it affect? Gender?
5) What do you see microscopically?
6) Tx?
7) Recurrence rate?
8) D/D?

Back 1

1) Common gingival growth that is reactive, not neoplastic
2) On gingiva, from interdental papilla. 50% incisor-cuspid region
3) Nodular mass, pedunculated or sessile, surface frequently ulcerated
4) 2/3rds females, teens and young adults (10-19)
5) Fibrous proliferation associated with mineralized components
6) Local surgical excision - EXCISE DOWN TO PERIOSTEUM
7) High - 8-16%
8) POF, pyogenic granuloma, peripheral giant cell granuloma, gingival fibroma (pre-POF), peripheral ameloblastoma, peripheral COC

Front 2

Peripheral giant cell granuloma:

1) Common "____"
2) T or F: it is a true neoplasm
3) What does it develop in response to?
4) Microscopically, it resembles?
5) Where is it exclusively found?
6) What does it look like?
7) What age does it mostly affect
8) What do you see on the x-ray
9) Tx and prognosis? Recurrence?
10) What other lesion can it look like?
11) If you see bilateral R/L lesion in a long patient, what should you suspect?

Back 2

1) "Tumor"
2) F - it's a reactive lesion
3) Local irritation or trauma
4) CGCG - may be soft tissue counterpart
5) Gingiva or edentulous alveolar ridge
6) Red or reddish-blue nodular mass
7) 50-60 year old
8) "Cupping" resorption of bone in the x-ray
9) Surgical excision down to the bone, 10% recur (must re-excise)
10) Brown tumor of hyperparathyroidism (multinucleated giant cells that can be osteoclastic)
11) Cherubism

Front 3

Drug induced gingival hyperplasia:

1) What can exacerbate the problem?
2) How do the gingival tissues appear?
3) Dilantin hyperplasia starts how?
4) Drugs causing gingival hyperplasia (3)
5) What stimulates overgrowht? What plays a key role?

Back 3

1) Mouth breathing
2) Nodular and not inflamed
3) Overgrowth of interdental papillae
4) Calcium channel blockers (nifedipine - 25%), immunosuppressive drugs (cyclosporine - 25%), phenytoin (50%)
5) Drugs stimulate overgrowth, poor OH plays key role, mouth breathing also critical

Front 4

Lymphangioma:

1) What age does it affect?
2) Does this involute over time?
3) Affects 4% of __ neonates: where? How big? Gender? Involution?
4) Superficially, what does it look like?
5) Deeper, what does it look like?
6) What is the most common site?
7) T or F: cystic hygroma in the neck is life threatening
8) Are the lesions ill-defined or well-defined? Do they recur?
9) Avg of how many surgeries for tongue lesions?
10) "What is the most common cause of congenital macroglossia?"

Back 4

1) First 2 decades of life
2) No
3) AA neonates - bilateral mandibular alveolus, <<1 cm, 2:1 male predilection, spontaneous involution**
4) Nodular (vesicular +/- blood)
5) Cavernous (cystic hygroma)
6) Tongue (macroglossia)
7) T
8) Ill-defined, tend to recur w/ massive swelling
9) 6
10) Lymphangioma

Front 5

Congenital epulis of newborn:

1) Same histology as?
2) Where is it found in the newborn?
3) Gender?
4) Can it regress?
5) Tx?
6) How is it vs. a granular cell tumor?

Back 5

1) Granular cell tumor (but different origin)
2) Anterior gingiva of newborn maxilla > mandible
3) Females
4) Yes
5) Simple excision (curative)
6) Granular cell tumor is recurring, neoplastic condition.

Front 6

Neuofibromatiosis Type 1:

1) AKA?
2) Is it common?
3) How many forms? What is the most recognized type?
4) Inheritance pattern?
5) What mutation?
6) 50% represent?
7) What is type 1 associated with?
8) Clinically, what does it look like?
9) What does the plexiform variant feel like?
10) Variability?
11) What is considered pathognomonic?
12) What else can be seen clinically?

Back 6

1) Von Recklinghausen's Disease of the Skin
2) Yes - relatively common hereditary condition (1/3000)
3) 8, TYpe 1
4) Autosomal dominant
5) NF 1 mutation of 17q11.2 - "neurofibromin' - a tumor suppressor protein
6) New mutations
7) Oral lesions
8) Multiple neurofibromas on th eskin (small papules/large nodules, massive, baggy, pendulous masses (elephantiasis neuromatosa)
9) "Bag of worms" - pathognomonic of NF1
10) Wide variability - few NFs to hundreds and thousands, 2/3rds have relatively mild disease
11) Cafe au lait pigmentation of skin (6+) with smooth boarders (coast of california)
12) 2+ neurofibromas, 1 plexiform neurofibroma, axillary/inguinal freckling (Crowe's sign), lisch nodules (2+ - translucent brown-pigmented spots, iris hamartomas), optic gliomas, osseous lesion, family hx

Front 7

Neurofibromatosis Type 1 continued:

1) Oral manifestations in ___%
2) What are the oral manifestations?
3) X-ray findings?
4) Treatment and prognosis?
5) Possibility of development of?
6) 5 year SR?

Back 7

1) 72-92%
2) 50% fungiform papillae enlargement, 25% intraoral neurofibromas
2) Enlargement of mandibular foramen, enlargement + branching of mandibular canal, > concavity of medial surface of ramus, >dimension of coronoid notch
4) No specific tx, prognosis poor, genetic counseling
5) Neurofibrosarcoma (5%)
6) 15%