-

What is this? What is the main cause and what is it treated with?
- ANUG
- Fusiform bacillus & Borrelia vincentii
- Treated well with Metronizadole (Flagyl)
- * Lymphadenopathy and fever seen
-

What is this? What causes it and how it is treated. Possible complications?
- Streptococcal tonsillitis and pharyngitis
- Caused by group A, Beta hemolytic strepcocc
- Person to person transmission, can be confused with viral
- Chairside test to confirm bacteria, Usually self-limiting within 4days but complications can occur
- Scarlet fever: skin rash, bacteria in blood (strawberry tongue)
- Rheumatic fever: can progress to rheumatic heart disease after strep throat, endocarditis
- Post strep Glomerulonephritis: destroys basement membrane and cant filter
-

What is this and what causes it?
- NOMA (cancrum oris)
- Fusobacterium and Prevotella
- Usually affects children un underdeveloped countries with HIV and severe immunocompromise
- Treatment: debridement of necrotic tissue, antibiotics and resconstruction
-

What is this? What causes it?
- Actinomycosis, caused by Actinomyces israelli
- Usually enters thru tissue of prior trauma
- *Swelling indurated "woody" area of fibrosis, draining sulfur granules
- Antibiotic treatment (high dose)
-
Bartonella henselae enters the skin thru a bite or scratch of an animal and papule/pustule develops with lymph enlargement 3 weeks later.
- Cat scratch disease
- Usually in an immunocompromised person
-
Traponema pallidum causes this disease and what are the stages?
- Symphilis (can be from sexual contact, or mother-fetus)
- Primary: infectious, chancre (ulcer with raised red border, genital or oral), lymphadenopathy
- Secondary: infectious, rash, skin hands, oral lesions, patches
- Tertiary: non-infectious, gumma (granulomatous inflammation) , CNS involvement
-
Oral manifestations of syphilis..
- Seen in congenital syphilis, Treponeme crosses the placenta. Can be cured with AB
- Hutchinson Triad: deafness, keratitis (pain and blurry eye), tooth defects (mulberry molar, hutch incisor)
-
Oral manifestations of tuberculosis?
- Chronic non-healing, progressively enlarging indurated ulcers
- Nodular granulomatous proliferations, painless
- Granulomas (collection of giant cells, macrophages and giant cells) are necrotizing
-
Osteomyelitis can present in 2 ways
- Acute: extension of abscess, bacteremia and not seen in xrays
- Chronic: long-standing inflammation (pagets, irradiation) xray shows diffuse and irregular RL with focal R.O. (sequestrate of dead bone). Requires biopsy
- **You know bone is dead because there are no osteocytes in the Lacunae, cells around are neutrophils

-
Treatment for osteomyelitis
- Drainage
- Debridement
- Antibiotics
- Hyperbaric oxygen (because of anaerobic bacteria)
-
In HSV there are two types of infections, what are they and where do they manifest?
- Primary infection: Herpetic gingivostomatitis
- Secondary: Herpes labialis & intra-oral herpes
- *Not every patient will manifest these,, infections in other places too, whitlow, eye.
- ({14-49 age} HSV1 53.9%, HSV2 15.7%)
- In HSV1 or 2 the genital lesions are indistinguishable
- HSV1 more whites, 2 more blacks
-

What is this, and what presents along with it?
- Primary herpetic gingivostomatitis, usually presents with classic lymphadeopathy and fever. Usually younger patients.
- Pinpoint ulceration on BOTH keratinized and non-keratinized mucosa
- ** Secondary infections ONLY occur non non-keratinized mucosa, sometimes on the tongue (which is specialized mucosa)
-
Reactivation of the HSV in the sensory ganglion of the trigeminal nerve?
- Secondary herpes infection
- Herpes labialis: clusters of vesicles on the lips that rupture within hours then crust
- Intraoral herpes: single or small clusters that occur inside the mouth on keratinized tissue (palate or gingiva) that rupture and painful.
- After the crusting stage the patient is not contagious anymore
- Long term oral antivirals have shown modest evidence of prevention of episodes and systemic antivirals (valacyclovir & famcyclovir) have shown to reduce episode length
-
HPV risk factors...
- Middle aged men
- Multiple sex partners. If more than 20 partners, 1/5 ere infected for 21.5% chance
- Smokers with more than 20 cigs a day had the highest prevalence (unknown)
- High risk HPV are mostly 16 and 18, while Low Risk wart causing are usually 6 and 11
-
What is the pathogenesis of HPV?
- Accesses and infects cells of the epithelial basal layer and breaks through skin or mucosa
- Virus becomes incorporated in the genome of the infected cell, usually occurs in areas of high friction or traffic
-
How are HPV infections transmitted?
- Sexual contact: Men performing cunnilingus on women have higher chance than women doing it on women. Oral sex on a man has less transmission. This is believed to be due to immunity to previous exposure of women with cervical HPV of lower risk types.
- Vertical transmission: Mother to child
- Horizontal transmission: Mother-father
-

What are these?
- Koilocytes: Characteristic cells of HPV infection present as enlarged, squamous epithelial cells with clear halos around a shrunken nucleii.
- The HPV genome encodes a protein that disrupts the cytoplasmic keratin network.
-

What is this?
- Viral Papilloma (usually caused by 6 and 11 types) and the palate is most common site.
- Soft and painless with finger-like projections. M=F, can be sessile or pedunculated
- Irritation fibroma can be differential diag.
-
What is condyloma acuminatum?
Venereal Warts (caused by types 6-11), considered an STD, tends to be larger than papilloma or verruca vulgaris (seen on fingers and anterior part of mouth in kids types 2 and 57)
-
Focal epithelial hyperplasia is caused by what?
- Types 13 and 32 HPV
- Endemic in native american, eskimos and PRicans, usually seen in children

-
HPV infection usually seen in HIV, Down syndrome patients cause by multiple HPV types and has increased prevalence since advent of HAART therapy.
- Florid Papillomatosis: Usually seen as a cluster of bumpy lesions seen in areas of high friction or tension.

-
How are HPV lesions managed?
- Solitary lesions: excision (biopsy if available?)
- Multiple lesions:
- Controversial - Excision/ablation (CO2 laser, electrosurg, scalpel) High power suction is imperative to prevent transmission
- Topical therapy - Podophyllin resin, Imiquimod (extraoral use), Cidofovir and Interferon (also Intralesional therapy).
-
Oral molluscum contagiosum is caused by which virus and where?
- Poxvirus, usually caused pink dome shaped, smooth surface papules on lips, mucosa and palate
- Mostly common in immunocompromised pts
-
Measles is caused by which virus and causes what oral manifestations?
- Paramyxovirus, causes Koplik's spots, blueish white punctate mucosal macules surrounded by erythema, they represent a foci of epithelial necrosis.
- Common on buccal mucosa, where the lesions resembles sprinked salt

-
Coxsackie virus causes which manifestations?
- Hand-foot-mouth disease
- Herpangina
-
Fungal infections are mostly mediated by which cell
- T cell
- TH1 response increases phagocytosis and fungi usually cannot survive this.
- Most oral fungal infections are opportunistic and the deep fungal infections have usually desseminated from elsewhere.
- Deep fungal infections present as non-healing chronic ulcers and SCC is a differential diag (indurated, etc..)
-
Most common deep fungal infection in the US
- Histoplasmosis (Histoplasma capsulatum)
- Dimorphic: (yeast at body temp, mold in soil) Inhaled from Bird and bat droppings
- Can be...
- Acute: Self limiting
- Chronic: lung infection similar to tuberculosis
- Disseminated: Rare, older debilitated and HIV, immunocomporimised pts
- Diagnosis with biopsy (no keratin pearls will mean NOT cancer)
-
Another common deep fungal infection found further to the north from the main one..
- Blastomycosis (Blastomyces dermatitidis), 10x less common than Histoplasmosis
- Lung inhalating, spread of spores, outdoor activities
- Histology: thick cell wall, with a larger cell inside (unlike histoplasmosis)
 - Oral manifestations: less ulcerated, thicker, raised rough exophytic lesions
-
Second most common opportunistic fungal infection found in soil, water or decaying debris?
- Aspergillosis, when seen maxillofacial its from immunocompromised pts, uncontrolled diabetics, max sinus infection can come after tooth ext.
 - Presents as a dark ulcer
 - Histologic appearance is "pretty", hyphae
- Can be a Nosocomial infection
-
Zycomycosis is enhanced by what?
- AKA Mucormycosis
- Its growth is enhanced by iron, immuno-compromised at risk as well as uncontrolled diabetics. Inhaled by spores from decaying vegetation
- Histologically: Forms L shapes, Large

-
Most common systemic fungal infection in HIV/AIDS patients?
- Cryptococcal meningitis (cryptococcosis)
- - Inhalation of organisms from bird droppings
- Histologic: Thick capsule

-
What is the management of deep fungal infections?
- Diagnosis: through Biospy and granulomas, GMS staining (green background, black stain)
- Identify: risk factors (immunosuppresion), uncontrolled diabetes
- Debriding of necrotic tissue.
- Systemic antifungal treatment
- - Ketoconazole
- - Itraconazole
- - Amphotericin B is good but has adverse effects on cardiac failure and kidney damage, skin reactions
-
The most Common opportunistic fungal pathogen?
- Candida (mostly albicans) has the ability to overcome host defenses (dimorphism, phenotypic switching, enzymes)
- - Immunosuppresion
- - impaired barrier functions (dry mouth)
- - disruption of flora (broad spectrum AB)
- These favor growth because more than 50% of humans carry candida
- Can cause candademia, candidal sepsis and endocardidits
-
What factors predispose humans to oral candidiasis?
- Local: Reduced salivary flow, epithelial changes, changes is commensal flora, high carb diet
- Systemic: Altered hormone state, diabetes, hypothyroidism, hyperparathyroidism, adrenal suppresion
- Iron or folate deficiency
- Immunosuppresion drugs
-
What are the clinical types of Oral candidiasis?
- Pseudomembranous candidiasis: wiped off curd-like plaques, sometimes burns, not always a red inflammatory underlying surface because their immune system is weak
- Angular chelitis: Angles of the mouth, associated with lower VDO, may be mixed fungal/bacterial. use Antifungal cream 3x a day
- Erythematous candidiasis: red patches, associated with burning sensation and densure stom..
- Denture stomatitis: erythema found on maxilla of denture patients, limited to tissues covered by the denture. Rarely sympotmatic
- Median rhomboid glossitis: Midline dorsal tongue usually associated with "kissing" lesion on palate.
- Hyperplastic candidiasis: Associated with severe immunosuppression, superimposed on existing leukoplakic lesion vs lesions from candida
-
Diagnosis of oral candidiasis is made...
- Usually made with clinical appearance (wipeable, location etc..)
- If unsure then cytological stains can be done:
- - Periodic Acid Schiff stain (PAS stain)
- - KOH Float (for dermatologic lesions)
- Culture sensitivity: to determine the type of fungii
- Biospy: for hyperplastic candidiasis
-
Management of candidiasis?
- Mild: Clotrimazole troches 10mg (5x a day) or miconazole mucoadhesive buccal 50mg tablet applied over canine fossa once a day
- 7-14 days is recommended
- Alternatives for Mild can be Nystatin suspension 4-6mL 4x a day (swish around)
- Moderate-severe: oral fluconazole (diflucan) 100-200mg daily for 7-14 days
- ...or Itraconazole solution 200mg once daily
- *** Long term use can cause hepititis. Fluconazole may be contraindicated when taken with other medications due to interactions and toxicity
-
The most common mucosal disorder
- Recurrent aphthous ulcer (very painful), usually found on non-keratinized mucosa
- 40% of RAS have 1st degree relatives with RAS
- Can be classified as minor (under 1cm), major (more than 10mm, deep) or herpetiform (crops of ulcers under 5mm that may fuse, resemble herpes)
- Etiology not completely known, but multifactoral including trauma and autoimmune (celiac, chrons, etc). All of this triggers a cytotoxic cascade where T helper cells predominate and affect th1 response, changes in local blood vessels. Cytotoxic T cells mediate keratinolysis which forms the ulcer.
-
Condition that causes recurrent aphthous ulcers (genital/skin/eye) and other lesions onset at 3rd and 4th decade affecting middle eastern men and asian females.
Behcets disease
-
Managing RAS patients
- History of RAS, Medical and Social history
- Weight loss, Recurrence rate, dysphagia
- Healing time, extra-oral lesions, pain
- Associated signs and symptoms, prodrome
- Medications & oral hygiene products
- Diet (vegetarians, b12 deficiency?)
- Treatments: Kenalog in orabase and Prednisone for about 2 weeks (not longer)
-
Diagnosis of Lichen planus?
- Differential:
- Oral Lichen planus: No racial predilection, 1-2% prevalence
- Oral Lichenoid Reactions
- - Oral lichenoid Lesions of Graft vs Host disease
- - Lichenoid drug reactions (gum, mint)
- - Lichenoid contact lesions (amalgams, etc.)
- Hep C infection
- Systemic or discoid lupus
-

What is this?
- Oral Lichen Planus: (bilaeral mostly) classic radiating lines reticular appearance (Wickhams striae), can be seen on the tongue (other places)
- White changes may be the only feature and patients are asymptomatic, associated with erythema, ulceration, some burning and sensitivity to spicy/acid foods
-
Why would lichen planus show FVL (loss of fluorescence)?
- Because of the inflammation present
- Incisional biospy (on white changes of non kerat. areas) is mandated to confirm diagnosis of OLP and differentiate between other lichenoid reactions and rule out dysplasia or carcinoma.
- OLP is a T cell mediated response, with potential for malignant transformation 1% of OLP patients/year avg age 61
-
Treatment of Oral lichen planus?
- Corticosteroids - (prednisone (knocks down Tcels), clobetazol ointment, dexamethasone elixir rinse)
- Oral hygiene
- Calcineurin inhibitors - (Protopic prevents Tcell activation)
- Retinoids"There is insufficient evidence to support superior effectiveness of any specific treatment"
-
What is pemphigus and pemphigoid?
- Mucocutaneous autoimmune bullous diseases characterized by multiple, chronic blisters (bullae) which rupture to form large, non healing ulcers
- Usually in 5th and 6th decades, but can affect all.
- Affects less than 50k, lack of awareness, attention, knowledge (ULTRA ORPHAN ILLNESS, hard to get medications on market)
-
4 questions to narrow down diagnosis of ANY lesion?
- How many? Multiple or single
- How long? Acute or chronic
- Had it before? Primary or Recurrent
- Anywhere else? Local or General
-
Multiple chronic mucocutaneous ulcers autoimmune characterized by intra-epithelial blisters (bullae) which ruptures to form large, non-healing ulcerations, usually seen in the 50s and 60s.
- Pemphigus vulgaris
- Pemphigus and pemphigoid are autoimmune disorders that destroy the proteins important to holding the skin and mucus membranes together
-
Multiple forms of pemphigus?
- Pemphigus vulgaris: most common form on mucosa or skin
- Pemphigus foliaceous: superficial skin only
- Paraneoplastic pemphigus: associated with cancer
- Drug-induced
- Circulated IgG, C3 directed against desmogelin on keratinocyte surface
- Loss of desmosomal attachments
- Dsg-1 and Dsg3 IgG can predict where a person would get lesions (3mucosal, 1 skin)
-
Chronic multiple oral ulcerations, which 3 conditions will it be most of the time? Which are the three stages of treatment?
- Oral lichen planus
- pemphigus
- pemphigoid
- 1. Control: getting existing lesions to heal and new ones to stop forming
- 2. Consolidation: getting the immune (reduce antiody) and inflammatory response under control
- 3. Maintenance: remission
- ** The biopsy technique should include normal epithelium and the sample should be divided in 2 for an H&E and an immunoflouresence DIF (michels solution)
-
What are the main medications for pemphigus and pemphigoid?
- Prednisone 0.5-1.5mg (for inflammatory suppression) can be combined with an immunosuppresant like Cellcept.
- Monoclonal Ab Retuximab can also be given
- Topical steroids can be given to manage local lesions
- Weak: Hydrocortisone and Kenalog
- Strong: Clobetesol and Halbetesol
-
A Mucocutaneous autoimmune disease characterized by sub-epithelial blisters (bullae) which rupture to form large non-healing ulcerations. Usually in people over 45
- Mucous Membrane Pemphigoid
- * Tissue igG directed against BPA2 in basement membrane zone, Separation of epithelium at junction
- Always check for Ocular pemphigoid and esophageal pemphigoid, very morbid
- HYGIENE IMPROVES DISEASE
-
Difference between pemphigus and pemphigoid?
- Pemphigoid is named this way because both conditions present very similarly
- Difference is that pemphigus has Antibodies directed at the connections between epidermal cells
- in Pemphigoid the Antibodies are directed at hemidesmosomes (where epithelial cells attach to the basement membrane), this means that the bullae is actually subdermal this is why the lesions here look more intact (they are below). Pemphigus has more ruptured bullae
-
Special drug that can be used for pemphigoid?
What are the 3 major risks of cortisol?
- Dapsone: but have to check patients G6PD for evaluation of hemolysis risk.
- Prednisone is also used (like in pemphigus)
- 1mg of Prednisone = 5 mg of cortisol
- 1. Hyperglycemia
- 2. Osteoporosis
- 3. Hypertension
-
One of the most common soft tissue lesions of the mouth characterized by fibrotic tissue usually smaller than a cm.
- Irritation fibroma: Firm exophytic lesion presents as pinker than its surrounding tissues, can be sessile or pedunculated and usually caused by a constant source of trauma.
- Dense scar-like connective fibrous tissue
-
A reactive connective tissue hyperplastic lesion of exuberant granulation tissue. (most common of the 3 Ps)
- Pyogenic granuloma (misnomer because its not pyogenic nor true granuloma): Occurs a lot of pregnant women and is a response to injury from calculus.
- Often ulcerated, soft exophytic sessile or pedunculated, deep red color, bleeds easily
- Gingiva is the most common location, but can occure other places.
-
A proliferation of granulation tissue at the opening of a fistula?
- Parulis

-
One of the 3Ps that occurs usually between molars on gingiva but can present with radiographic superficial destruction of alveolar bone.
- Peripheral giant cell granuloma: occurs usually between 40-60yrs old. (not soft, not hard)
 - Present with a Blue-ish hue
 - Presents with GIANT CELLS multinucleated (like the name)
-
Of the 3P lesions, Well demarcated, sessile or pedunculated lesion that appears to originate from the gingival interdental papilla
- Peripheral ossifying fibroma: derived from cells of the PDL, seen in children and young adults, females more than males. recurrence rate of 16%
- Hard lesion that moves teeth around.
- Calcifying bone is seen in histo
-
Treatment of the 3P lesions
Complete excision as well as scaling and root planing of the area to prevent recurrence
-

What is this? How is it treated?
- Epulis fissuratum (denture induced fibrous/inflammatory hyperplasia): usually seen along the denture border of ill-fitting denture, composed of dense fibrous connective tissue.
- Treatment: surgical removal and new denture fabrication
-

What is this?
- Papillary hyperplasia of the palate: form of denture stomatitis caused by candida
- Caused by denture or orthodontic appliance
- Treatment: antifungal (bumps may stay)
-
Gingival enlargement can be caused by many factors such as..
- Drug induced (cyclosporine, dilantin, nifedipine)
- Respose to chronic inflammation
- genetic-inherited
- Hormonal changes
- Leukemia - AML
-
Viral lesions of the oral cavity
- Verruca vulgaris: Common wart, seen on skin commonly (not much mucosa) contagious and self innoculation. (HPV 2,4,6) Tongue and lips seen. Histo has the most Koilocytes.
- Condyloma: Venereal wart, can be seen on labial mucosa and palate.
- Papilloma: (fingerlike projections, caused by 6 and 11 HPV), papillary projections and Koilocyotes are seen in Histo.
-
Benign tumor of mature fat cells, thin underlying epithelium.
- Lipoma: buccal, labial, fat pad usually where more fat exists in the mouth.
- Soft squishy feel
- Floats in water when removed
-
Immunologic diseases can be broken down into 3 categories
- Allergic and hypersensitivity responses
- Graulomatous diseases
- Autoimmune diseases
-
Diffuse edematous swelling of soft tissues with rapid onset, which can occur in solitary or multiple areas where itching is common
- Angioedema: Lpp tongue, eyes, life threatening if throat closes
- IgE mediated, causes mast cells to release huge amounts of histamine
- Type 1 hypersensitivity reaction
- Diagnosis: made clinically and find allergin
- Treatement: antihistamine, epinephrine (for severe cases)
-
An oral mucosal response that occurs at the site of contact with an allergen, can be acute or chronic
- Allergic contact stomatitis
- Many allergens reported, toothpaste, gum
- Treatment: topical steroids, antihistamine
-
A Mucosal reaction to systemic drug therapy in the oral cavity.
- Stomatitis medicamentosa
- Can cause:
- erythema multiforme
- Lichenoid drug reactions
- Pemphigus-like drug reactions
- Aphthous or vesiculoerosive reactions
-
Immunological mediated unknown etiology, can be minor and major depending on site causes skin/mucosal ulcerations when minor and stevens-johnson syndrome when major, Lyell disease when severe
- Erythema multiforme: bleeding crusting lips, ulcerations gingiva, skin lesions
- Immunofloresence doesnt help
- Treatment: steroids, hydration
- Steven-johnson syndrome related to drug reaction, ocular and genital (johnson)
-
Multisystem granulomatous disorder with improper degradation of antigenic material with formation of noncaseating granulomatous inflammation, blacks affected 17x more than whites.
- Sarcoidosis: lungs, skin, lymphnodes and salivary glands are usually the location
- Asteroid body seen in histo that are hard to find, but point to sarcoidosis.
- Pulmonary lesions are essential to diagnose on xray
-
Immune response secondary to a chronic antigenic stimulus, with 2 subtypes, face lips and intraoral sites affected
- Orofacial granulomatosis: edema, ulcers & papules
- Lips are the most common site
- Melkerson-rosenthal syndrome: facial paralysis and fissured tongue
- Chelitis Granulomatosis: only lips
-
Necrotizing granulomatous lesions of the respiratory tract, potentially fatal...
- Wegener granulomatosis: antigen is inhaled
- Strawberry gingivitis is seen
-
Most common type of collagen/vascular connective tissue disease that presents in 3 main types, can resemble lichen planus and aphthous ulcers
- 1. Systemic lupus erythematosus
- 2. Chronic cutaneous lupus erythematosus
- 3. Subacute cutaneous lupus erythematosus
- - Facial butterfly can be seen, Kidneys and heart can be involved
- Treatment: avoid sun, antinflammatory, prednisone (steroid), cyclosporine/methotrexate (immunosuppresive), antimalarials
-
Chronic inflammation due to autoimmunity, damage to small blood vessels, fibrosis in skin and multiple organs.
- Systemic Sclerosis (scleroderma)
- Mouse-like facial appearance, tight fingers, tight skin
- Dense fibrious tissue in biopsies
- PDL space widened due to fibrosis
- Treatment: moisturizer, therapy, immunosuppresants, steroids, surgery
-
What are the 4 neurogenic tumors?
- 1. Neuroma
- 2. Neurofibroma
- 3. Schwannoma (Neurilemoma)
- 4. Granular cell tumor (THE MOST COMMON)
- Most common location for all is the tongue.
- Syndromes associated: MEN syndrome, neurofibromatosis (von Recklinghausen's disease)
-
A reactive proliferation of tissue after injury, usually extraction or surgical procedure, may be painful 1.3rd of the time and usually on mental foramen area or tongue
- Neuroma (aka Traumatic neuroma)
- A person who presents with multiple neuromas may have MEN syndrome:
- Rare autosominal dominant (last types 2B or 3) have oral manifestations, increased risk for thyroid cancer, neuromas on mucosas
- Usually have marfanoid appearance (long Abe linc)
-
A benign tumor arising from Peripheral nerve tissue, slow growing and painless, tongue and buccal mucosa can be seen, can grow in bone.
- Neurofibroma
- Differential sometimes can be fibroma (but those are caused by irritation so location is important)
- Treatment: is excision (like all soft tissue lesions)
- Multiple Neurofibromas is Neurofibromatosis (von recklighausens disease), Cafe-au-lait spots, skin nodules (hundreds-thousands)
- Lisch nodues are Very diagnostic of neurofibromatosis
-
Benign neoplasm of Schwann cell origin, with common presenation on the tongue, common in young and middle aged adults.
- Schwannoma/Neurilemoma: the only lesion that has a capsule, well defined and pops out.
- Usually seen on tongue and lip
-
Most common neural lesion, benign tumor derived from Schwann cells
- Granular cell tumor: Most common site is the dorsal tongue and most common in oral cavity, slow growing and common in middle aged ppl

-
Sessile or pedunculated mass usually found on anterior gingiva/alveolar mucosa, usually on newborn (mostly girls), cells resemble granular cell tumor (NOT Derived from nerves)
- Congenital Epulis
- Surgical excision (no recurrence)
-
Two main types of Hemangiomas (benign proliferation of blood vessels). What is a malignant blood vessel tumor called?
- Capillary: small blood vessels
- Cavernous: bigger vessels, can feel a pulse
- Rapid growth phase then gradual involution
- Angiosarcoma: malignant blood vessel tumor (rare in mouth)
- Venous malformations (not to be confused with hemangiomas which can be more exophytic) are present as birth and dont blanch
-
Vascular proliferation involving tissues of the brain and face, usually unilateral distribution along one or more segments of the trigeminal nerve
- Sturge-Weber Angiomatosis
- Port-wine stain is seen, intracranial calcifications can be seen as well which can cause serious complications
 - Usually follow trigeminal nerves
-
Benign tumor of lymphatic cells and what are the 3 types?
- Lymphangioma
- 1. Capillary
- 2. Cavernous
- 3. Cystic hygroma - on babies neck
- Usually seen on the tongue, tapioca appearance, pebbled
- Treatment is to monitor

-
This lesion is caused by HHV-8 and is aids related and presents in 4 main types.
- Kaposi's Sarcoma
- Classic: late adult life, italian, jewish men on lower extremities
- Endemic: African form
- Iatrogenic immunosuppresive associated: most often occurs in organ transplants
- AIDS-related, uncontrolled CD-4 & viral load
- Treatment: surgical excision or chemo

-

Benign tumor of the smooth walls of blood vessels
- Vascular Leiomyoma: occurs on smooth muscle walls of blood vessels
- Leiomyosarcoma: malignant version of smooth muscle tumor
-
What are the two common tumos of skeletal muscle
- Malignant: Rhabdomyosarcoma - is the most common soft tissue sarcoma in children, most frequent site is head and beck
- Beningn: Rhabdomyoma
-
Malignant tumor of fibroblasts, most common in young children, not painful
- Fibrosarcoma
- Treatment is excision
|
|