Connective Tissue Lesions of the Oral Region Flashcards
1
Q
Define Tumor
A
Swellings
2
Q
Benign vs. Malignant
A
Benign ends in -oma and can’t metastasize or kill the host.
3
Q
Hypertrophy vs. Hyperplasia
A
-trophy is an increase in cell size while -plasia is an increase in cell number.
4
Q
What is the difference between a hyperplasia and a neoplasm?
A
A hyperplasia will get to a stage where it will stop growing. A neoplasm never stops growth.
5
Q
Other names for Irritation Fibroma.
A
Traumatic Fibroma, Focal Fibrous Hyperplasia.
6
Q
Irritation Fibroma
A
Most common hyperplastic growth of the oral cavity. Results from long-standing irritation. Akin to a scar. Ex: you bite your tongue.
7
Q
Irritation Fibroma Clinical Appearance
A
Firm, pale, elevated nodular mass. Tongue and buccal mucosa are the most common locations. Lesion may be ulcerated (most likely through biting) and become painful. Low grade chronic inflammation is the cause.
8
Q
Irritation Fibroma Histopathology
A
Covered with normal epithelium, it is the CT that is hyperplastic. The bulk of the lesion is composed of hyperplastic collagen. May be proliferation of endothelial cells, fibroblasts and vascular channels.
Stellate giant cells may predominate and is called a giant cell fibroma. This has no meaning clinically.
9
Q
Irritation Fibroma Treatment and Prognosis
A
Surgical excision is curative and recurrence is uncommon.
10
Q
Peripheral Ossifying Fibroma General Features.
A
A form of reactive hyperplasia exclusive to the gingiva. Associated with long-term irritation and often contains bone. Arises from the PDL or periosteum. Origin may explain more aggressive behavior. Appears as a gingival nodule. Bump on the gum. Occurs most often in women.
11
Q
Peripheral Ossifying Fibroma Clinical Features.
A
Bump on the gum. Can be hemorrhagic and vascular or very dense, it depends on what stage it is in.
12
Q
Peripheral Ossifying Fibroma Histopathology.
A
Covered with epithelium that may be ulcerated. Lesion is composed of fibrous CT. Reactive bone fragments are present in 70% of cases. Fibroblasts have switched to producing bone. Epithelial Odontogenic rests may be present.
13
Q
Peripheral Ossifying Fibroma Treatment and Prognossis
A
Surgical excision. Must include the PDL base. If it has extended into the PDL and has destroyed alveolar bone it is very important to get the entire lesion out or it will keep growing. Recurrence is often in the 15% range. No malignant potential but can be destructive locally.
14
Q
Peripheral Giant Cell Granuloma General features.
A
Occurs exclusively on the gingiva at any age. Most common in the mandible. May arise from the PDL. Periapical radiograph may show a saucerized radiolucency.
15
Q
Peripheral Giant Cell Granuloma Clinical Features
A
Appears as a bump on the gum, or gingival nodule that is dome shaped. May resemble the common pyogenic granuloma.
16
Q
Peripheral Giant Cell Granuloma Histopathology
A
Vascular CT stroma. Filled with foreign body type giant cells. Hemosiderin may be prominent. The histology is not specific. Looks similar to brown tumor or hyperparathyroidism, cherubism or Central Giant Cell Granuloma.
17
Q
Peripheral Giant Cell Granuloma Treatment and Prognosis
A
Surgical excision. Steroid injections may reduce size of large lesions. PDL involvement explains recurrence rates of 12-20%. The recurrent lesions may require extraction of associated teeth.
18
Q
What is another name for Inflammatory Fibrous Hyperplasia?
A
Epulis Fissuratum.
19
Q
Inflammatory Fibrous Hyperplasia General Fetures
A
Proliferation of fibrous CT associated with long-standing Irritation. Most commonly comes from an ill-fitting denture flange in either MX or MN dentures.
20
Q
Inflammatory Fibrous Hyperplasia Clinical Features
A
Appear as hyperplastic folds around denture flange. Folds appear as flabby, soft, freely moveable tissues.
21
Q
Inflammatory Fibrous Hyperplasia Histopathology
A
The hyperplastic growth will be covered with epithelium that may be ulcerated. Epithelium may be acanthotic (thickened). Inflamed fibrous CT is common.
22
Q
Inflammatory Fibrous Hyperplasia Treatment and Prognosis
A
Large lesions may need to be excised. Small ones may respond to denture rebasing, but the most successful treatment is excision.
23
Q
Inflammatory Papillary Hyperplasia General Features
A
Most often (but not all the time) associated with ill-fitting maxillary dentures. Occurs on the palate 90% of the time. Needs to be differentiated from verrucous carcinoma, an epithelial malignancy.
24
Q
Inflammatory Papillary Hyperplasia Clinical Features
A
Appears as many small, usually red, papillary nodules of the hard palate, giving it a “cobblestone” appearance. Also described as a cauliflower appearance.
25
Inflammatory Papillary Hyperplasia Histopathology
Papillary nodules covered with epithelium and cores consist for fibrous CT often with chronic inflammation.
26
Inflammatory Papillary Hyperplasia treatment and Prognosis
Surgical excision, electrocautery and laser surgery. Lesion has no malignant potential....unless you have misdiagnosed and it is actually verrucous carcinoma....
27
What is another name for Hyperplastic Gingivitis?
Generalized Fibrous Hyperplasia.
28
Hyperplastic Ginvitis General and Clinical Features
A form of gingivitis in which the gingival tissue becomes overgrown and redundant. It is diffuse. Can be associated with puberty or pregnancy. Gingiva appears inflamed and enlarged. Often confused with routine periodontal disease.
29
Hyperplastic Gingivitis Histopathology
The hyperplastic tissue will be covered with keratinized stratified squamous epithelium (masticatory mucosa) with underlying inflamed fibrous CT.
30
Hyperplastic Gingivitis Treatment and Prognosis
Usually resolves after a scaling. May persist through out puberty or pregnancy. Some gingival contouring may be necessary.
31
Hereditary Gingival Fibromatosis General Features
A rare generalized gingival hyperplasia that can be idiopathic or familial. Autosomal dominant or autosomal recessive inheritance may be evident.
Slowly progressive gingival enlargement restricted to fibroblasts.
May be associated with hypertelorism, epilepsy, mental retardation, hypertrichosis when it is familial.
32
Hereditary Gingival Fibromatosis Clinical Features.
Can be firmer and less hemorrhagic than Hyperplastic Gingivitis. Enlarged gingiva may cover the teeth. Starts at puberty and can interfere with tooth eruption. Key to diagnosis is a good history, you can't tell this apart from other gingival disorders.
33
Hereditary Gingival Fibromatosis Histopathology
Covered with stratified squamous keratinizing mucosa. Supported by dense collagen. Proliferating fibroblasts and inflammation are common.
34
Hereditary Gingival Fibromatosis Treatment and Prognosis
Scaling and root planning or gingivectomy. Recurs about 40% of the time. Oral hygiene is usually not a recurrence factor.
35
Drug-Induced Gingival Hyperplasia General and Features
Fibrous gingival hyperplasia in response to medications. Once called Dilantin Hyperplasia, but other medicines such as cyclosporine (immunosuppressant), nifedipine (a calcium channel blocker), Carbamazepine, anticonvulsants, oral contraceptives, erythromycin.
36
Drug-Induced Gingival Hyperplasia Clinical features.
May cause pseudopockets around teeth. Interdental papilla enlargement.
37
Drug-Induced Gingival Hyperplasia Histopathology
Overlying epithelium may show elongated rete ridges. Dense collagen with widely-spaced fibroblasts will characterize the CT. Some inflammation may be present.
38
Drug-Induced Gingival Hyperplasia treatment and prognosis
Gingivectomy and gingivoplasty are the usual treatment. Recurrence common with continuance of medication. Plaque and calculus may exacerbate hyperplasia. Good hygiene may retard recurrences.
39
Indeterminate Fibrous CT proliferations
Desmoplastic Fibroma, Nodular Fasciitis, Benign Fibrous Histiocytoma.
The lesions are all thought to be intermediate between reactive and malignant growths. They can be proliferative destructive fibrous growths.
40
Desmoplastic Fibroma of the bone
OCCURS IN THE MANDIBLE OF YOUNG PATIENTS. Average age is 14 years. Benign infiltrative fibrous proliferation. Lesion composed of dense collagen. Quite aggressive. May require mandibular resection. 25% recurrence rate. Can occur in the soft tissue. Caused by mutations in the CTTNB1 gene which encodes for beta-catenin.
41
Nodular Fasciitis
Fibrous CT that just keeps growing. Pseudosarcomatous fasciitis. Affects the oral mucosa as a polypoid growth and resembles a sarcoma microscopically. Spindle cell proliferation and 20% recurrence rate.
42
Benign Fibrous Histiocytoma
Combined fibrous and histiocyte proliferation. May occur in soft tissue or bone. Appear as nodular swellings or radiolucencies.
43
Benign Fibrous Histiocytoma Microscopic findings, treatment and Prognosis
Storiform or cartwheel accumulation of histiocytes. Wide excision is necessary. 20% recurrence rates are common.
44
Fibrosarcoma General Features
Rare collagen associated cancer. Malignant neoplasm of fibroblasts. Affects both soft tissue and bone, with a higher incidence in soft tissue.
45
Fibrosarcoma Clinical Features
Often associated with pain, paresthesia, bleeding. In the bone, root resorption, tooth displacement, cortex expansion and cortical erosion are common.
46
Fibrosarcoma Histopathology
Highly cellular tumor composed of atypical fibroblasts. Show a "herringbone" pattern with marked cytologic atypia.
47
Fibrosarcoma Treatment and Prognosis
Surgery, radiation therapy and chemotherapy. Poor prognosis. Death usually occurs in 5 to 7 years where survival rates range from 40-60%.
48
Neural Tissue Tumors General Features
Oral nerve tumors are relatively common. Some are hyperplasias, others are true neoplasms. Most arise from proliferation of nerve sheath cells.
49
Neural Tissue Tumors Classifications
Hyperplasias
Hamartomas
Benign Neoplasms
Malignant Neoplasms
50
Traumatic Neuroma General Features
Hyperplasia. Not a true neoplasm. Painful. Proliferation of nerve tissue after nerve injury or transection. Nerve displacement may prevent nerve sheaths from reuniting.
51
Traumatic Neuroma Clinical Features
Nerve sheath cells proliferate producing a painful submucosal mass.
Appears as a painful nodular growth.
Mental nerve, the tongue, and the lower lip are the most common sites.
52
Traumatic Neuroma Histopathology
Proliferation of axis cylinders, schwann cells and perineural fibroblasts. Appear as jumbled mixture of these hyperplastic elements. Cause continuous communication.
53
Traumatic Neuroma Treatment and Prognosis
Surgical excision. Only successful 6/10 times. Recurrence is uncommon.
54
Multiple Endocrine Neoplasia Syndrome General Features
Hamartoma. Called MEN Syndrome. An autosomal dominate disorder that affects the parathyroid, pancreas, thyroid, adrenal glands and oral cavity.
55
Define Hamartoma
Over proliferation of a cell type that is native to the site.
56
MEN IIB Syndrome Features
Associated with multiple oral neuromas, often on the tongue. Appear as small nodular excrescences that are true neoplasms. Oral neuromas may be the first sign. Caused by a germline mutation of the RET proto-oncogene. Mucosal neuromas, medullary thyroid carcinoma, adrenal pheochromocytoma.
57
MEN Syndrome Histopathology
Similar to traumatic neuromas and consists of hyperplasia of nerve bundles.
58
MEN Syndrome Treatment and Prognosis
Surgical excision of oral neuromas. May develop malignant neoplasm of endocrine glands: Thyroid carcinoma, pheochromocytoma.
Send them to someone else to manage.
59
Other name for Neurilemoma?
Schwannoma
60
Neurilemoma/Schwannoma General and Clinical Features
Benign neoplasm of schwann cells or neurilemma cells. Appear as well-demarcated soft tissue swellings, but can rarely appear in bone as a radiolucent lesion Usually painless. If it affects the acoustic nerve, it is called an aucoustic neuroma.
61
How do you tell the MEN syndrome apart from a neurilemoma?
They look identical. Tell them apart by the number of swellings.
62
Nurilemoma/Schwannoma histopathology
Two types of cells are seen: Antoni A and Antoni B. Presence of Antoni A tissue is virtually diagnostic.
63
Antoni A cells
Organized as rows of palisading nuclei and fascicles of schwann cells. Dark cells that look like fish.
64
Antoni B cells
Less organized clusters of oval nuclei with vacuolated cytyoplasm and zones of eosinophilia. Acellular.
65
Nurilemoma/Schwannoma Treatment and prognosis
Surgical excision. Recurrence is uncommon. 10%.
66
Neurofibroma Clinical Features
A benign peripheral nerve sheath neoplasm made up of schwann cells and perineural fibroblasts. May be single or multiple. Single lesions: Appear as soft tissue nodules, buccal mucosa and lips are common sites. Children are not commonly affected. No gender predilection. Uncommonly appear in bone as radiolucencies.
67
Neurofibromatosis Type 1
A hereditary disease that occurs in 1 in 3,000 births. Multiple skin/oral neurofibromas. Oral lesions may be pendulous (hanging down loosely). Can have hundreds of neurofibromas. Skin pigmentation (cafe au lait spots) are common.
68
Another name for Neurofibromatosis Type 1
von Recklinghausen's disease.
69
Neurofibroma histopathology
Haphazard accumulation of spindle cells with a lot of collagen in the background.
70
Neurofibroma Treatment and Prognosis
Surgical excision of single lesions. Malignant transformation may be spontaneous in neurofibromatosis and occurs in 5% of cases.
71
Granular Cell Tumor original name?
Granular Cell Myoblastoma. Originally thought it came from muscle cells.
72
Granular Cell Tumor General Features
Soft tissue tumor of nerve sheath origin. Thought to arise from Schwann cells.
73
Granular Cell Tumor Clinical Features
Appears as a painless submucosal mass. Usually occurs in the tongue. Appears to be in the body, not on the surface.
74
Granular Cell Tumor Histopathology
Overlying keratinizing epithelium. Often has pseudoepitheliomatous hyperplasia. Overlying epithelium becomes thicker. Epithelial hyperplasia may be confused with squamous cell carcinoma. Bulk of tumor is composed of large, uniform granular cells of probably nerve sheath origin. Often seen between epithelial rete ridges. Fuzzy looking with lot's of lysosomes in the cytoplasm.
75
Granular Cell Tumor treatment and prognosis
Simple surgical excision. Recurrence is rare and no malignant potential.
76
Congenital Gingival Granular Cell Tumor, additional names.
Congenital Epulis of the newborn. Congenital Gingival Granular Cell Lesion.
77
Congenital Gingival Granular Cell Tumor General and clinical Features
Granulr cell tumor occuring on the gingiva of newborns. AGE IS IMPORTANT. May affect the maxilla or mandible. More common in females. Appears as a pedunculated mass. May become quite large if left untreated.
78
Congenital Gingival Granular Cell Tumor Histopathology
No pseudoepitheliomatous hyperplasia as seen in adult granular cell tumor cells. Bulk of lesion is composed of granular cells that contain different proteins than adult form.
79
Congenital Gingival Granular Cell Tumor Treatment and Prognosis
Complete surgical excision. Recurrences are rare.
80
Melanotic Neuroectodermal Tumor of Infancy General and Clinical Features
Once thought to be of odontogenic origin. Derived from pigmented neural crest cells. Appears as a pigmented maxillary lesion most often. May be brown or black in color. Occurs before 6 months of age and can be seen in other sites including the skull, mandible, testis and brain. Locally destructive.
81
Neuroectodermal Tumor of Infancy Histopathology.
Two cell types: Large granular cells and smaller pigment-containing cells.
Distributed in a CT stroma. Often has melanin in it!
82
Neuroectodermal Tumor of Infancy Treatment and Prognosis
Treated by surgical excision. Recurrences are rare.
83
Name for Malignant neoplasms of nerve origin
Neurogenic sarcomas
84
Malignant Neoplasms of Nerve Origin General Features.
Rarely occur in oral cavity. Arise from perineural fibroblasts or schwann cells. Often associated with a nerve trunk. Treat with surgical excitions. Hematogenous metastases at 50%. Prognosis is not good. Most patients die of their disease.
85
Muscle Tumors General Features
Benign or malignant. Smooth or skeletal muscle origen.
86
Name for smooth muscle tumors
Leiomyoma and leiomyosarcoma
87
Name for skeletal muscle tumors
Rhabomyoma and rhabdomyosarcoma
88
In the oral cavity where d o the majority of smooth muscle tumors come from?
Vascular.
89
Leiomyoma
Benign smooth muscle neoplasm. Rarely occurs in the oral cavity. Arises from smooth muscles around blood vessels. Firm, moveable submucosal nodules. Local excision.
90
What do oral leiomyomas look like microscopically? Clinically?
Neurofibroma
| Fibroma
91
Rhabdomyosarcoma
Malignant neoplasm of striated skeletal muscle. All variants have a poor prognosis. Most often seen in children: Most common soft tissue malignancy of childhood. Head and neck region is the most common site. FOX01 chromosomal translocations.
92
What are the 3 histological variants of rhabdomyosarcoma?
Embryonal, alveolar, pleomorphic. All 3 have a poor prognosis.
93
Benign Tumors of Fat.
| Name and most common
Lipoma. Mesenchymal neoplasm in the head and neck region.
94
Lipoma general and clinical features
Appear as soft, yellow submucosal nodules most often in the cheek. Herniated buccal fat pads can be mistaken for lipomas. No gender predilection. Have a characteristic yellow hue.
95
Lipoblastomatosis
Multiple lipomas in the oral cavity. Usually only found in kids and is benign.
96
Lipoma Hisopathologic features
Well-differentiated fat cells. Univacuolated fat cells will be set in a thin fibrous connective tissue stroma. Looks like chickenwire.
97
Lipoma treatment and prognosis
Surgical excision. Recurrences are very rare.
98
Liposarcoma
Malignant. Rare in oral cavity. Multilobular mass. Buccal mucosa and sublingual area. Poorly differentiated fat cells seen microscopically. Radical excision usually attemted as therapy. Poor prognosis.
99
Vascular Tissue Tumors Classification
Hyperplasias
Hamartomas
Neoplasms
100
Pyogenic Granuloma General Features.
"bump" on the gum that occurs on the gingiva and is hemorrhagic. Most vascular of the 3 common ones, very common. DOESN'T HAVE PUS OR MICROORGANISMS. A reactive hyperplastic growth (related to chronic irritation) and is the most common oral vascular tumor. Can be mm to cm. Big sack full of blood vessels. Comes with a chronic inflammatory component. CT holds it together.
101
What is another name for a pyogenic granuloma?
Lobular Capillary Hemangioma.
102
Are hemangiomas and lymphangiomas benign or malignant?
Benign neoplasms of vascular tissue.
103
Are angiosarcomas and kaposi sarcomas benign or malignant?
Malignant neoplasms of vascular tissue. Some angiosarcomas have different/specific names, such as kaposi sarcomas.
104
Pyogenic Granuloma Clinical Features
Fast growing endothelial cell proliferation. Occurs as a gingival nodule 85% of the time. Red in color and often ulcerated. Called pregnancy tumors in pregnancy. And can rise from extraction sites.
105
Epulis Granulomatosum
Pyogenic granuloma arising from an extraction site.
106
Pyogenic Granuloma Histopathology
Granulation tissue is the dominant feature. Dilated vascular channels, endothelial cells and hemorrhage.
107
What can Pyogenic granuloma be confused with histologically?
Kaposi Sarcoma
108
Pyogenic Granuloma Treatment and Prognosis
Complete Excision is curative, but you must remove irritant or recurrence is 15-20%. Doesn't transform to a malignancy.
109
Hemangioma General Features
Benign neoplasm of endothelial cells. Most commonly seen in children. May occur in the bone, most often in the mandible. Tongue is the most common soft tissue site. Severe hemorrhage may be an operative problem with bone tumors.
110
Hemangioma Clinical Features
Tongue is the most common site. Appears as a red/purple lesions. May be bumpy or corrugated. Appear to grow within the body of the tongue as the source is vascular found deeper within the tongue. Cauliflower like.
111
Oral Varix
Dilated vein. Solitary lesion. Biopsy, unless it is an old person. Varicose vein in your mouth.
112
Sturge-Weber Syndrome
Encephalotrigeminal angiomatosis. Unilateral facial "port wine" stain.
Enlarge over time, and then stop growth. Follow nerve and map like a hemorrhagic lesion.
113
Hemangioma Histopathology
Capillary or cavernous. (depends on size of channels, subjective). Endothelial cells and large numbers of RBC.
114
Hemangioma Treatment and Prognosis
Treated with surgery, lasers, sclerosing agents, cryosurgery. Intraosseous and AV malformations require extreme care. Catastrophic hemorrhage is a risk. Angiography may assist in treatment planning. May need to tie-off feeder vessels. Recurrence of hemangiomas is 15-20%
In a kid, watch and wait.
115
Lymphangioma Clinical features
Benign proliferation of lymph vessels. No muscular wall, so more fragile. Present as papillary appearing superficial lesions in the oral cavity. Mostly seen in the neck.
116
What are Lymphangioma lesions found on the neck called? At what age are they normally found?
Cystic Hygroma. Occur before the age of 2. Hard to manage.
117
Lymphangioma Histopathology
Vascular spaces often hug the epithelial CT interface. Spaces will be filled with lymph or proteinaceous coagulum.
118
Lymphangioma Treatment and Prognosis
Watch and wait. It is very easy to not remove the entire lesion and there is a higher recurrence rate. Many lesions will regress after puberty. Surgery, cryotherapy and laser surgery used for persistent tumors.
119
Angiosarcoma
Malignant counterpart of hemangioma. Rapidly growing neoplasm of endothelial cells. Occurs in young patients. Poor prognosis.
120
Kaposi Sarcoma General and Clinical Features
A vascular malignancy that commonly occurs in AIDS patients. Multifocal lesions are common. Appear as flat purple macules or as nodular lesions. Palate and gingiva are the most common sites.
121
What are the three types of Kaposi Sarcoma?
Iatrogenic: Occurs in solid organ transplant patients.
Classic: Late adult life in the extremities.
AID: AIDS patients.
122
Kaposi's Sarcoma Histopathology
Slit-like vascular channels lined with anaplastic endothelial cells: Altered nuclear/cytoplasmic ratios. Cellular atypia. Increase mitotic activity.
123
Kaposi's Sarcoma Treatment and Prognosis
Depends on the type and tumor stage. Sclerosing agents, radiation and chemotherapy. Mean survival for all types is 10-15 years.
124
Soft Tissue Osteoma Clinical Features
Soft tissue submucosal growth. Boney hard nodules. May be part of Gardner's Syndrome.
125
What is Gardner's syndrome characterized by?
Supernumerary impacted teeth. Facial bone osteomas. Cutaneous fibroids. Intestinal precancerous polyps (most important)
126
Soft Tissue Osteoma Histopathology
Compact lamellar bone. Can't tell it from regular bone.
127
Soft Tissue Osteoma Treatment and Prognosis
Typically lesions are left untreated. Surgical excision if function is impaired.
128
Osseus and Cartilaginous Choristoma Clinical Features
Lesions present as firm soft tissue nodules with a calcified central nidus. Choristomas represent a tumor like proliferation of microscopically normal tissue. Similar to a hamartoma. Very rare.
129
Osseous and Cartilaginous Choristoma Histopathology
Benign bone or cartilage. Any stage of osteogenesis can be present. The lesion will be surrounded by fibrous CT.
130
Osseous and Cartilaginous Choristoma treatment
Surgical excision
131
Myositis Ossificans General and Clinical Features
A reactive lesion. Traumatically induced lesion resulting in bone formation. Osseous metaplasia. Occurs within muscle. Masseter and pterygoid muscle are the most commonly affected in boys who play sport.
132
Myositis Ossificans Histopatholgoy
Proliferating fibrous CT with bone spicules and nodules.
133
Myositis Ossificans Treatment and Prognosis
Surgical excision of soft tissue mass. No malignant potential. Often left if not causing problems.
