Non Neoplastic Flashcards
Fibroma
Hyperplasia of fibrous connective tissue
most common tumor of the oral mucosa
usually sessile, smooth surfaced, normal color, asymptomatic
↑↑ cheek but occurs almost anywhere
Fibroma
Giant Cell Fibroma
Giant cell fibroma (not to be confused with giant cell granuloma)
“papillary” tumor of fibrous connective tissue containing plump,
stellate and often bi or trinucleated fibroblasts
↑ children
↑↑ gingiva, ↑ tongue
often confused clinically with papillomas (see neoplasm)
Fibroma
Peripheral odontogenic (ossifying) fibroma
Reactive fibroblastic lesion of PDL
↑↑ 1-3 decades, occurs only on gingiva, asymptomatic; pedunculated or
sessile mass ± red ± ulceration
Histology: Cellular fibroblastic lesion with bone and/or cementum and/or
dystrophic calcification
Treatment Excision including superficial PDL
recurrence rate 15-20%, highest recurrence of any of the reactive gingival lesions
Inflammatory Fibrous Hyperplasia
(Epulis Fissuratum)
Reactive folds of hyperplastic fibrous connective tissue along border of ill-fitting, over extend denture
Histology: Fibrous hyperplasia ± inflammation
Treatment: Excision and remake/reline denture
Inflammatory Papillary Hyperplasia
Papillomatosis
Hyperplastic response of palatal mucosa to ill-fitting denture
Histology: Papillary hyperplasia + inflammation ± pseudoepitheliomatous
Hyperplasia (PEH)
Treatment: Excise + remake/reline denture
Peripheral Giant Cell Granuloma
Tumor of well vascularized fibrous connective tissue containing numerous multinucleated giant cells
questionable histogenesis but occurs only on gingiva (↑ anterior)
any age, asymptomatic
usually reddish-brown-purple pedunculated or sessile mass
female:male; 2:1
may produce cupping resorption of underlying bone
Treatment: Excision and removal of irritants, may recur
Pyogenic granuloma
Pyo – pus genic – produces (misnomer)
reactive lesion representing hyperplasia of body’s basic reparative tissue –
granulation tissue
reddish, ulcerated pedunculated or sessile mass
↑ 2-4 decades, ↑↑ gingiva but occurs anywhere including skin
Asymptomatic but may bleed easily
↑ females, often in pregnancy “pregnancy tumor”
not uncommon in extraction sockets – epulis granulomatosa
Histology: Hyperplastic granulation tissue, fibroblasts with delicate
collagen, endothelial cells + capillaries and dilated larger vessels
Treatment: Excision and removal of irritants, may recur
Parulis “Gum boil”
Can occur anywhere but on gingiva, it represents draining from a source of odontogenic
infection of either pulpal or periodontal origin
pus (purulence, suppuration) = bacterial infection
Localized juvenile spongiotic gingival hyperplasia
Localized hyperplasia presumably from externalized sulcular epithelium on gingiva
Almost exclusively 1-2 decades, female 2:1,
Almost all anterior gingiva, Max 5:1,
Clinical: red often papillary gingival lesions
Histology: Papillary proliferation of inflamed epithelium with intercellular edema (spongiosis)
Treatment: Excision
Hemangioma
Overgrowth of blood vessels (hamartoma – localized overgrowth of tissues native to the part, often developmental)
rapid proliferation of endothelial cells at birth or shortly thereafter,
characteristically involute
most common tumor of infancy (5-10% incidence)
↑ females 3:1
60% H&N
↑↑↑ 0-5 years, rarely congenital, 90% complete but slow involution by age 10
reddish to purple mass lesions that tend to blanch with pressure
oral ones often later and don’t involute
can occur in bone, often multilocular or soap bubble appearance (why you aspirate before bone biopsy)
Histology: Endothelial cell proliferation with formation of small capillaries
(capillary) or larger dilated vascular spaces (cavernous)
Treatment: Natural history is involution
laser pulse, excision, sclerosing agents, steroids both intralesional and systemic propanolol
Sturge-Weber Angiomatosis
(Encephalotrigeminal angiomatosis)
Nonhereditary developmental, congenital condition characterized by vascular
proliferation of brain and face usually along distribution of ophthalmic branch of the trigeminal nerve
Sturge-Weber and port wine stains are due to somatic activation mutation in GNAQ which
encodes Gαq, a member of the q class of G-protein alpha subunits that mediates
signals between G-protein–coupled receptors and downstream effectors. The difference is when and where the mutation occurs
Large purplish lesions –identical clinically to port-wine stains,
ipsilateral oral mucosal involvement common
leptomingeal angiomas of cerebral cortex
Lymphangiomas
Developmental overgrowth of lymphatic vessels
↑↑ H&N, ↑↑ 0-5 years of age
Orally: ↑↑ tongue (may produce macroglossia)
Superficial ones – pebbly surface covered by translucent vesicles
Deeper ones – more diffuse
Cystic hygroma: variant that infiltrates and becomes very large
(↑ neck)
Histology: Proliferation of thin walled lymphatic vessels capillary sized,
Dilated (cavernous) or cystically dilated (cystic hygroma)
Treatment: Lesions don’t involute
Excision
Deeper ones often recur
Sclerosing agents