SOFT TISSUE TUMORS COME FROM ANY TISSUE: FAT, NERVE, BV’S, SM. MUSC, SKEL. MUSC CLINICAL: SUMUCOSAL LUMPS, COVERED W/ INTACT SMOOTH EPITHELIUM BENIGN: FREELY MOVEABLE, OR IF BOUND TO BONE-HARD PALATE/GINGIVA MALIGNANT: SARCOMAS LG, BULKY ULCERATING-METAST VIA BLOOD DIFFERENTIATED BY ONE DISTINGUISHING FEATURE
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SOFT TISSUE TUMORS COME FROM ANY TISSUE: FAT, NERVE, BV’S, SM. MUSC, SKEL. MUSC CLINICAL: SUMUCOSAL LUMPS, COVERED W/ INTACT SMOOTH EPITHELIUM BENIGN:
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SOFT TISSUE TUMORS
COME FROM ANY TISSUE: FAT, NERVE, BV’S, SM. MUSC, SKEL. MUSC
– XRAY: TRAM LINE CALCIFICATIONS INVOLVING ½ MENINGES
OSLER-WEBER-RENDU DZHEREDITARY HEMORRHAGIC
TELANGECTASIA(HTT)• AUTO DOMINANT
• MUTATION OF PROTEINS THAT MAINTAIN BV WALL INTEGRITY CAUSING WEAKNESS
• 1-2MM LESION ON SKIN, ORAL, GI MUCOSA
• INCREASING W/ AGE
• BLANCHE W/ PRESSURE - TELANGECTASIA
• CAUSE EPISTAXIS-CLASSIC 1ST SIGN = NOSEBLEEDS
• GI BLEEDS CAUSE ANEMIA-1 BURST SLOW BLEEDING = ANEMIA
• AV MALFORMATIONS IN LUNGS, LIVER, BRAIN
– HI CO FAILURE
– INCREASE RISK FOR BRAIN ABSCESS – FATAL – TRANSIENT BACTEREMIAS CAN GET INTO BRAIN
• ***PREMED FOR DENTAL TX
NASOPHARYNGEAL ANGIOFIBROMA
• BENIGN
• ERECTILE TISSUE – BECOMES NEOPLASTIC CUZ OF BV’S
• PTERYGOPALATINE FOSSA - MAXILLA
• ***ADOLESCENT MALES
• RISK OF FATAL HEMORRHAGE – SPONTANEOUS OR DURING SURGERY IF IT’S NICKED IT BLEEDS LIKE CRAZY
• GROWS LARGE AND FAST IS DESTRUCTIVE AND INVASIVE
• CAUSES NASAL OBSTRUCTION AND EPISTAXIS – NOSEBLEEDS
OF LG DILATED VESSELS AND DENSE FIBROUS TISSUE
• XRAY: ANT BOWING OF POSTERIOR WALL OF MAXILLA-PRESSES ON BONE AND PUSHES IT FORWARD
• RX: SURGICAL REMOVAL W/ HIGH RECURRENCE RATE
LYMPHANGIOMA• HAMARTOMA OF LYMPHATICS CONGENITAL OR W/IN 2YRS EARLY IN LIFE• HEAD AND NECK• INFILTRATE TONGUE CAUSING MACROGLOSSIA W/ PEBBLY SURFACE• ***CYSTIC HYGROMA – GIANT CONGENITAL CAVERNOUS LYMPHANGIOMA OF HEAD AND NECK
INTERFERE W/ BREATHING AND CAN BE FATAL
• LG ONES SEEN W/ INFECTION OR ALLERGY CAUSING ASPHYXIA• RX: DOESN’T DISAPPEAR & CANNOT BE SCLEROSED
• CONGENITAL EPULIS: MAX ANTERIOR RIDGE OF NEWBORN, FEMALES
• NEUROECTODERMAL TUMOR: MAX ANT RIDGE INFANT, PIGMENTED, BONE DESTRUCTION
SALIVARY GLAND NEOPLASMS
• OCCUR IN MAJOR/MINOR SALIVARY GLANDSPAROTID MOST COMMON AND GREATEST VARIETY HISTO. 80% IN SUPERFICIAL LOBEMINOR-PALATE MOST COMMON >50%, UPPER LIP 20%, LOWER LIP LEAST COMMON, TONGUE NOT COMMON-NO SALIVARY GLANDS
FEMALESAFRICAN AMERICANS30-60 YRSPAINLESS, SLOW GROWER, SUBMUCOSA, FIRM LUMPHARD PALATE-OFF MIDLINEPAROTID-IN FRONT OF OR BELOW EAR, PHARYNGEAL MASS, DEEP LOBEMALIGNANT-SLOW GROWER, ENCAPSULATED, WELL DEMARCATED, HISTO-WELL DIFF, NO
HYPERCHROMATISM, PLEOMORPHISM, MITOTIC ACTIVITYBENIGN-INFILTRATE AND PLEOMORPHISM(OPPOSITE TO WHAT WE LEARNED),LARGER THE GLAND THE MORE BENIGN IT IS!
BENIGN VS. MALIGNANT• THE FOLLOWING SUGGEST MALIGNANCY:
– FIXED TO UNDERLYING STRUCTURES, EXCEPT IN HARD PALATE
– ULCERATION OR INJECTION (VASCULARITY) OF SURFACE – SPONTANEOUS
– PAIN OR FACIAL PARALYSIS – PAROTID
– RAPID GROWTH
– TELANGIECTASIA OVER SURFACE
TX FOR SALIVARY GLAND TUMORS
• PAROTID LUMPS – SUPERFICIAL LOBECTOMY – DUE TO HI RECURRENCE OF BENIGN LESIONS WHEN NOT TREATED AGGRESSIVELY, EMBEDDED FACIAL NERVE COMPLICATES 2ND SURGERIES
• SUBMAXILLARY – REMOVE GLAND
BMT PLEIOMORPHIC ADENOMA
• ***MOST COMMON NEOPLASM – 70%
• PAROTID, PALATE, UPPER LIP
• ORIGIN: INTERCALATED DUCTS AND MYOEPITHELIAL CELLS
• HISTO: DUCTS, CYSTS, SHEETS OF BASALOID, SQUAMOID OR SPINDLE CELLS, HYALINE, MUCIN AND MYXOID AREAS, CHONDROID AND BONE – EASY TO MISDX ON FROZEN SECTION OR NEEDLE BIOPSY
• ONE GERM LAYER – NOT TRULY MIXED, CHONDROID, MYXOID, BONE IS MYOEPITHELIAL OR METAPLASTIC STROMAL PRODUCT
• SLOW GROWER, PERSISTENT, BENIGN
• TUMOR BUDS PENETRATE CAPSULE, HI RECURRENCE IF SHELLED OUT, LESS IN MINOR GLANDS
• KIDS MOST COMMON 11%• MOST COMMON PAROTID CANCER• ORAL SITES – RMP, PALATE – IF YOU SEE ONE AT RMP – THIS IS PROLLY IT• ORIGINATE W/IN EXCRETORY DUCTS• HISTO: INFILTRATING NESTS, LOCULES CONTAINING ADMIXTURES OF SQUAMOUS, MUCOUS
AND INTERMEDIATE CELLS• LOW GRADE = CYSTIC AND WELL DIFFERENTIATED MORE COMMON, RARE METAST• HI GRADE = SOLID, POORLY DIFFERENTIATED, MORE INTERMED/SQUAMOUS CELLS• SLOW GROWER, INFILTRATIVE = HI RECURRENCE RATE• CLINICALLY RESEMBLES MUCOCELE – BEWARE OF SOFT CYSTIC IN RMP – UNUSUAL• MOST COMMON TO ARISE AS A PRIMARY W/IN BONE W/ DENTIGEROUS CYST• XRAY: MULTIOCULAR POSTERIR MAND RADIOLUCENCY
ADENOID CYSTIC CARCINOMA, CYLINDROMA
• COMMON INTRAORAL
• PALATE - MINOR
• INFREQUENT IN PAROTID - MAJOR
• MOST COMMON MALIG IN SUBMANDIBULAR GLAND 15%, PAROTID 2%
• HALLMARK-NEUROTROPISM-TARGET AROUND NERVE - PERI &INTRANEUROINVASION, TUMOR NUGGETS FOUND ALONG NERVE = RECURRENCE
• S/S: EARLY PAIN, PAROTID, FACIAL N. PARALYSIS
• PX: 70-85%, INTRAORAL/SUBMANWORSE THAN PAROTID, 5YR SURVIVAL-70%, 15YR 20%
• IF METEST TO LUNGS – PALLIATIVE TX ONLY
• “WOLF IN SHEEP’S CLOTHING” – SLOW GROWER, HISTO LOOKS BENIGN, BUT INFILTRATIVE, BLOOD BORNE METAST(LYMPH NODE DISECTION NOT NECESSARY)
• HISTO: CRIBIFORM – SWISS CHZ MONTONOUS BASALOID CELLS COMPARTMENTALIZED INTO OVOID CYLINDERS BY HYALINIZED PINK MATERIAL. VIA MYOEPITHELIAL AND DUCTAL CELLS
• LOVES BONE, LIVER, LUNGS, EATS RIGHT THRU BONE
MALIGNANT MIXED TUMOR
• FAST GROWER
• CYTOLOGICALLY IS A BMT THAT METASTASIZES - METAST MIXED TUMOR
• ***MOST COMMON - BMT UNDERGOES FOCUS OF MALIGNANT DEGENERATION, CAN BE SCCA, NON-SPECIFIC ADENOCARCINOMA, ANY TYPE OF CARCINOMA – CARCINOMA EX PLEOMORPHIC ADENOMA
• INCIDENCE: CARCINOMA EX MIXED TUMOR IS MORE COMMON AND OCCURS IN MIXED TUMORS THAT WERE PREVIUOULSY SURGERIZED ,RADIATED OR PRESENT 10-15 YRS. HX SHOWS SLOW GROWER THAT TOOK SUDDEN GROWTH SPURT= PAIN ULCERATION AND FIXATION
• Etiology: group A beta hemolytic streptococci• Clinical: edematous, pus, abscess, painful, lymphaenitis. Easily
confused w/viral pharyngitis• Oral lesions: filiform papillae fall off and/or turn white = strawberry
tongue will progress to raspberry tongue • Sequelae: Rheumatic fever, poststrep glomerulonephritis• Diagnosis: instant strep test, culture• Tx: antibiotics for 3-7 days, for recurrent infections = tonsilectomy• Scarlet fever is also caused by group A beta hemolytic strep; toxins
get into blood and cause rash. Easily confused w/measles, EBV, secondary syphilis, coxsackie. Only get Scarlet fever ONCE!
Pulmonary – Primary: Type IV hypersensitivity. Destroys/limits organisms, which causes granulomatous areas in lungs = Ghon focus, if it drains to lymph nodes = Ghon complex (multiple, proliferating, casseous lesions in lungs) harbor for years and can reactivate = Secondary TB (commonly seen in oral cavity as chronic ulcers).
Miliary – systemic spread of TB in immunocompromised. Oral lesions• Diagnosis: AFB- Acid Fast Bacillis; stain used to test for TB;
PPD test- skin test for TB• Tx: Isoniazid- can develop acute chemical Hep
BCG- TB vaccine; will have positive PPD test• Sig to Dentists: TB is aerosol and highly contagious disease if active. DO NOT do
elective tx on active TB pt!! If emergency care needed, do under special ventilation.
• Epidemiology: Black adults in North America• Etiology: unknown, but pine pollen suspected• Pathogenesis: Type IV hypersensitivity• Clinical features:
Skin and lymph nodes, pulmonary involvementCan be found in almost every organ
• Oral features: RareSubmucosal lumps, raised, edematous, cobblestone, can
• Diagnosis: exclusionary, eliminate everything else and then think this. Serum findings (elevated ACE in severe ds) Kviem test, biopsy, special stains
• Tx: immunosuppressants and steroids. 95% controllable w/drugs• Prognosis: 5% fatal; usually just morbid
•Sarcoidosis
Other non-infectious granulomatous disorders
• Chron’s ds- inflammation of small bowel, anus, mouth. Cobblestone, granulomatous raised mucosa and gingiva w/aphthous superficial ulcers in linear pattern- same ulcers found in ileum.
• Pyostomatitis Vegetans- multiple lesions of lips, vestibule, gingiva, abscess looking, purulent ulcers = snail tracks. Painful. Concomitant condt of the skin= pyodermatosis vegetans. Tx: steroids, Abs. This is seen almost exclusively w/IBD (esp Chron’s ds)
• Et: Borrelia (spirochete)• Epidemiology: geographic – wooded areas from deer tick vector• Pathogenesis: Type III hypersens. To spirochetal antigens• Clinical:
Primary stage – annular rash, fever, malaise
Secondary stage – large rash, fever, malaise, migratory arthritis, meningitis, AV block, Bell’s palsy
Tertiary stage – a hypersens rxn rather than infection. Develop long term migratory arthritis
• Tx: Acute primary or secondary – Erythromycin, Tetracycline
Chronic secondary or tertiary - steroids
•Lyme Disease
Who am I?
• Et: Treponema Pallidum – this is the most invasive org. It can penetrate intact skin• Clinical:
Primary: Chancre that lasts 3-4wks and resolves or turns into secondary
Secondary (metastatic): mucocutaneous puritic rash on hands & feet also an oral lesion develops – mucus path
Tertiary: granulomatous, perivascular, bone, neurological condt. Obliterative endarteritis, gumma- a granulomatous necrotic destruction of bone (palate). NOT infectious! A type IV hypersensitivity rxn.
Congenital: uncommon, rare condt. Skull abnormalities, Hutchinson’s triad- nerve deafness, keratin on cornea, hypoplasia of
enamel (perm incisors & all primary teeth). Features of secondary ds, congenital heart ds, eye defects, saddle nose,
saber shin• Diagnosis: dark field exam
– Serology For primary – Non-specific serology: scrape lesion and look for
spirochetes. Use TPI to immobilize treponema. Look for Chancre, no serologic marker
For Secondary & tertiary- Specific tests: +VDRL+ FTA absorption
•Syphilis (lues)
Who am I?
• Et: Nissseria Gonorrhea. Has a urea receptor on it so it clings to mucosa w/urea (urinary tract). Rare in mouth
• Clinical: found in children ages 1-10yo. large, necrotic gingivitis and osteomyelitis. Eats away bone VERY rapidly! Begins as Necrotic infection of ANUG and progresses into deeper tissues. Fetid odor, significant pain, fever, malaise, and regional lymphadenopathy.
• Tx: broad spec antibiotics and correct situation that caused pt to become susceptible. Do NOT aggressively remove damaged area b/c it will aggravate it
•Noma
Who am I?
• Et: Actinomyces isrealii BACTERIA! Even though ds name resembles fungus
• Pathogenesis: anaerobic infection of bone after trauma• Clinical: low grade, mild swelling, sequestrum, fistulas and sinus
tract that drain into skin = lumpy jaw. It can be acute and rapidly progressing or chronic and slowly spreading. The suppurative rxn of the infection may discharge yellowish flecks that represent colonies of the bacteria = sulfur granules. In cervicofacial region it doesn’t spread thru the typical fascial planes and lymph nodes but rather directly thru the soft tissue. Pain is minimal.
• X-ray: ill-defined radiolucency = moth eaten appearance.• Cytologic/Histo: sulfur granule w/in a sea of pus, sunray fungus,
peripheral clubbing, sea of polys• Tx: hi dose antibiotics by IV for 3-6 months. Hyperbaric oxygen
chamber, surgery to remove necrotic tissue.
•Actinomycosis
DITTRICH’S PLUGS
• Need pics, see Tonsillolithiasis on pg. 167
• Hyperplastic tonsils; accumulation of dead cells, bacteria, and inflammatory cells w/in crypts. Turns yellow/white. Is painless and can become large.
• Signs/Symptoms: hallatosis• Tx: can break these off w/q-tip applicator or cotton pliars; pt can do
it at home.• Prog: if they stay there for too long, they can calcify and turn into
• Clinical: erythematous papule forms at site of scratch and then resolves. The assoc lymph node develops acute supperative lymphadenitis, which can resemble salivary gland inflammation. Fever also accompanies.
• Diagnosis: stellate abscess in lymph node; indirect fluorescent antibody assay for detecting antibodies to Bartonella henselae. Or ELISA test or PCR. Before these tests became available dx was made on 4 criteria: contact w/cat, presence of scatch, + cat-scratch ds skin test (Hangar-Rose), negative for other causes of lymphadenopathy, char histopathologic findings
• Tx: self-limiting and usually resolves w/in 4 months. Use of local heat, analgesics, and aspiration of node on suppuration is typical pattern of therapy. Antibiotics reserved for cases that have prolonged course or severe involvement.
• Variant: Bacillary angiomatosis- an unusual subcutaneous vascular proliferation, histopathologically similar to histiocytoid hemangioma that is seen in AIDS pts. The affected areas resemble Kaposi’s sarcoma and can be intraoral.
• Et: Blastomces dermatitidis, found in soil and inhaled after a rainstorm• Pathogenesis: infects immunocompromised pts thru skin and mucous
membranes.• Clinical: Spores reach lungs and grow as yeasts, in most ppl it stops here,
but in ic pts it has hematogenous spread to skin, bone, prostate, meninges, oropharyngeal mucosa and abdominal organs. Pulmonary complaints are the most freq sign/symptom. Acute ds resembles pneumonia.Chronic ds is more common and can mimic TB. Cutaneous lesions are often only sign of ds and begin as erythematous nodules that enlarge and become verrucous or ulcerated. Oral lesions result from extrapulmonary dissemination or local inoculation. They have an irregular, erythematous or white intact surface or may be ulcerations w/irregular rolled borders and varying pain, they resemble SCCa! Clinically.
• Histo: Mix of acute inflamm and granulomatous inflamm surrounding yeast cells. Has pseudoepitheliomatous hyperplasia!!!
• Tx: most pts require no tx, even if symptomatic administration of systemic amphotericin B is indicated only if: seriously ill, not improving clinically, ill for more than 2-3wks. Pts w/chronic ds or extrapulmonary lesions need tx, Itraconazole is usually recommended.
• BLASTOMYCOSIS
• Et: Histoplasma capsulatum; spores found in soil containing bird feces.• The most common systemic fungal infection in the U.S.!!• Clinical: most cases are asymptomatic or symptoms so mild the pt doesn’t
even seek tx. Expression of ds depends on quantity of spore inhaled, the immune status of host, and strain of fungus. Acute ds- self-limited pulmonary infection that develops in 1% of ppl exposed to low # of spores. If exposed to hi # spores 50-100% of ppl will develop symptoms. (fever, headache, myalgia, cough, anorexia) similar to flu symptoms, lasts about 2 weeks.Chronic ds-primarily affects lungs, but much less common than acute ds. Usually found in elderly, emphysematous white men or immunocompromised pts. Similar to TBDisseminated ds- even less common. Progressive spread to extrapulmonary sites. Usually occurs in older, debilitated, ic pts. Can affect oral mucosa (solitary, variably painful ulceration of several wks duration, but some may appear white or erythematous w/irregular surface w/rolled margins and may resemble cancer!
• Tx: usually doesn’t need tx other than analgesics and antipyretics. If chronic ds- amphotericin B (can cause sig kidney damage) use ketoconazole in nonimmunocompromised pts. Disseminated form is 90% fatal if untxed, give amphotericin B.
•Histoplasmosis
Who am I?
• Et: Coccidoides immitis, grows in alkaline, semiarid, deser soil of the SW U.S. and Mexico
• Clinical: most pts are asymptomatic, although approx 40% on infected pts experience flulike illness and pulmonary symptoms w/in 1-3 wks after inhalation. Fatigue, cough, chest pain, myalgias and headache are common. Occasionally, the immune response may trigger a hypersens rxn tht causes the development of Erythema Multiforme or Erythema nodosum. The hypersens rxn in conjunction with coccidiodomycosis = Valley fever and resolves as host immune response limits infection.
Chronic progressive pulmonary cocciddiomycosis- mimics TB and is rare
Disseminated ds - <1% of cases. Areas involved: skin, lymph nodes, bone, joints, meninges. Usually found in immunocompromised pts (hi dose corticosteroids, chemo pts, HIV). Lesions develop in area of central face, nasolabial fold but oral lesions are uncommon.
• Histo: round spherules that contain endospores
• Tx: Amphotericin B for: ic pts, severe pulmonary ds, disseminated ds, life-threatening situation. For many cases of the ds fluconazole is drug of choice
•Coccidioidomycosis• San Joaquin Valley fever; Cocci
Zygomycosis
• Et: organisms of the class Zygomycetes; grow on decaying organic materials ie. Fruit, bread
• Epidemiology: affects mostly insulin-dependent diabetics who have uncontrolled diabetes and are ketoacidic; also in immunocompromised pts
• Clinical: Rhinocerebral zygomycosis – nasal obstruction, bloody nasal discharge, facial pain, headache, facial swelling, cellulitis, visual disturbances w/concurrent proptosis. Symptoms of cranial nerve involvement (facial paralysis) are often present. If it progresses to cranial vault, blindness, lethargy, seizures may develop followed by death.If max sinus is involved: initial presentation is intraoral swelling or max alveolar process, palate. Palatal ulceration may occur- appears black and necrotic. Radiographically-opacification of sinuses results, difficult to distinguish from max sinus cancer.
• Histo: extensive necrosis w/numerous large branching nonseptate hyphae at periphery which branch out at 90 degree angles
• Tx: radical surgical debridement of infected necrotic tissue and systmeic, high dose amphotericin B. Prog is poor, often fatal.
Aspergillosis
• Fungal ds char by noninvasive and invasive forms. Noninvasive usually affects normal host, invasive form affects immunocompromised host (AIDS, chemo, transplant pts, uncontrolled diabetes mellitus).
• The spores reside in soil, water, decaying organic debris worldwide and inhaled by host resulting in opportunistic fungal infection second in frequency only to candidiasis.
• Clinical: normal host: allergy affecting sinuses or bronchopulmonary tract, asthma, low grade infection of max sinus. Can undergo dystrophic calcification, produces radioopaque body w/in sinus = antrolith.After tooth ext or endo tx: predisposes sinus to infection, results in symptoms of localized pain and tenderness w/nasal discharge. IC pts are particularly susceptible to this. Painful gingival ulcerations and diffuse soft tissue swelling w/gray or violet hue develops. If not txed extensive necrosis may occur.Disseminated ds- occurs in IC pts but symptoms are vague and difficult to diagnosis early
• Histo: varying numbers of branching septate hyphae which branch at acute angles and invade adj small blood vessels. Occlusion of vessels results in char pattern of necrosis
• Tx: IC pts w/noninvasive ds – surgical debridement allergic fungal sinusitis – debridement and corticosteroids invasive ds in normal host – debridement + systemic antibiotics invasive ds in IC pts – aggressive debridement + systemic antibiotics
Who am I?
• Incidence: ALL HIV pts will develop oral form of this disease!
• Pathogenesis: T & B cells usually keep this in check, but in some pts with the above condts, they will be more prone to candida mucositis. Xerostomia - increase risk b/c no Igs = no protect mucosa.
• Acute pseudomembraneous candidiasis– Found in babies shortly after birth b/c they get infected thru the birth canal.– #2 oral manifestation in adults– Causes discomfort, white lesion w/surface coating (made of org) that will scrape
off to reveal red mucosa• Acute atrophic candidiasis
– MOST COMMON oral manifestation in adults– Red lesion, NO pain found on palate, ridge, dorsal tongue– Causes: denture sore mouth, angular cheilitis (perleche), Median Rhomboid
glossitis- midline on posterior 2/3 of tongue has PEH!!• Chronic hyperplastic candidiasis
– Uncommon– A painless white patch, hyperkeratosis w/ PEH!!– Presence of candida in this lesion doesn’t mean it is caused by candida albicans
• Histo/Cyto features– Septate pseudohypae– Can scrape off w/spatula put under microscope w/o any stain and see org– Special stains: PAS (Periodic acid-Schiff)-turns org purple; Methenamine Silver
• Tx– Antifungals (ketoconazole, Nystatin, Clortriamazole, Mycolog) Best is Diflucan 3