Oral Pathology II

Most common salivary gland disorder, caused by a severed minor salivary gland duct, escaped saliva accumulates in surrounding c.t, lower lip is most common, on the floor of the mouth it is called a ranula, submandibular/sublingual mucoceles (may produce much trapped secretions in mouth floor, called "plunging mucoceles"), mucoceles in maxillary sinus= antral mucocele, most resemble fluctuant bluish/clear "blisters", may be punctured and recur, accumulation of mucin below normal mucosal epithelium, mucin pool surrounded by granulation tissue, underlying salivary acini may or may not be adversely affected, excision with margin of unaffected tissue cures, marsupialization required for ranulas, "unroofing" of the lesion

involve minor salivary glands, may occur in the parotid gland, may resemble neoplasms or mucoceles, unlike mucoceles, they are epithelial lined, dome shaped fluctuant swelling, cyst lining with central mucous pool, may be compartmentalized, mucin is mucicarmine stain +, simple surgical excision with rare recurrence

salivary duct stones, may occur in major/minor salivary gland ducts, similar to kidney stones, not related to hypercalcemia, mucin may act as a nidus for calcification, most patients are aged 40-50

major glands favored sites, submandibular gland is the most common site, most patients complain of swelling (often on chewing, sialolith may block duct damaging the gland, submandibular= mouth floor swelling), parotid= swelling over the ramus, symptoms may accompany parotid or submaxillary gland swelling, minor gland stones= hard solitary nodules

calcified aggregate, concentric layers with a central nidus, surrounding soft tissue (may be epithelial lined, may be chronic inflammation)

may expel spontaneously, manipulation to remove stone, surgical excision, may be acute inflammation requiring antibiotic therapy

inflammation around acini, ducts remain intact, often accompanies radiation therapy, radiation doses of 50 Gr or 5,000 rad cause damage, glands fibrose and become sclerotic, a lot of people with connective tissue disorders, firm swelling, may resemble neoplasms, xerostomia common with resultant caries

acinar degeneration, surrounded by acute and chronic inflammation, stroma usually fibrotic, fluoride gels to combat caries, meticulous oral hygiene, saliva substitutes, pilocarpine t.i.d. can help, may require removal of damaged gland, patients can get angular chelitis--> candida

caused by salivary gland ischemia, ischemia produces necrosis and duct metaplasia, palate the usual site, M>F, most patients are middle aged, rapid onset, can mimic SSC, palatal 2-3 cm. ulcer, may or may not be painful, generally caused by some dental procedure

ulcerated mucosal epithelium, necrotic salivary gland acini, some acini may show coagulation necrosis, may affect entire lobules, stroma shows scatted inflammatory cells, may mimic mucoepidermoid carcinoma, diagnosis confirmed microscopically, no treatment usually necessary, ulcer usually heals in 1-3 months

viral/bacterial swelling of the parotid glands, common conditions are mumps, cat scratch fever, tubercular sialoadenitis

transmitted by airborne droplets, usually seen in the 1st/2nd decades, usually a painful parotid swelling, sometimes associated with an exudate, complement fixation confirms the diagnosis

can occur after abdominal surgery, probably caused by pyogenic bacterial infection

generally not biopsied, surgical intervention not indicated, bed rest, analgesics, liquid diet usually suffices, antibiotic therapy occasionally needed

infiltration of gland acini by T-lymphocytes, cause lymphocytic and myoepithelial islands in gland, may undergo transformation into malignant lymphoma, production of xerostomia, gland swelling, and rheumatoid arthritis = Sjogren's syndrome, patients at a higher risk for lymphoma

keratoconjunctivitis sicca, uncommon disease (1% of population), predominantly affects females, parotid becomes fibrotic and non functional, bilateral parotid swelling (50%), dry eyes, dry mouth, rheumatoid arthritis, neuritis, pneumonitis, lymphoma, superimposed Candida infestation may cause pain, elevated autoantibodies, similar to patients with radiation therapy

salivary gland fibrosis, acinar destruction by lymphocyte infiltrate, myoepithelial islands are common, occasional lymphoma transformation seen, in between normal salivary gland and scar, ducts are still there, scar as well, no effective treatment, palliation: artificial saliva, Candida control

"benign mixed tumor", most common salivary gland neoplasm (50-60% parotid, 50% submandibular, 55% sublingual), intraoral sites: palate and lip, more common in females, seen most commonly in 3rd-5th decades, well demarcated, slow going submucosal nodule, usually not ulcerated, in parotid, usually in superficial lobe

encapsulated by fibrous c.t., cords of ductal epithelium, some mucous secreting cells may be present, stroma varies: interlacing fibrous c.t., hyalinized c.t., mucinous c.t. bone and/or cartilage, stroma variation = "pleomorphic," "mixed", large tumor cells with big nuclei

surgical excision with generous margin, in parotid= gland excision or lobectomy, recurrence is common (surgeons don't cut enough out), malignant transformation is rare

benign neoplasm of minor salivary glands, rare in major glands, basal cell adenoma subtype more common in males, usually located in the upper lip, most common site is upper lip, appear as freely moveable soft tissue nodule, may have slight blue tinge, rarely exceeds 2 cm. in diameter

encapsulated, basal cell adenoma = proliferation of basal cells, canalicular adenoma= proliferation of duct-like structures, stroma is sparse, may be multicentric, but benign, surgical excision with margin of normal tissue, recurrences are rare

benign salivary gland neoplasm, arises in major or minor glands, patients are elderly (60-80), appears as nodular mass, most often appears in the parotid

"organoid" arrangement of eosinophilic cells, cells are "oncocytes" with eosinophilic granules (MITOCHONDRIA), no capsule and sparse stroma, surgical excision, lobectomy if in the parotid, wide surgical excision in minor glands, recurrence 5-10%

benign neoplasm, may appear in major or minor salivary glands, more frequent in major salivary glands, also known as "warthin's tumor", 10% of cases are bilateral, self-limiting growth, lesion has a "doughy" texture, no specific intraoral site

accumulation of lymphoid cells and salivary ductal structures (lymphomatosum), columnar epithelial cells arranged in finger-like processes, epithelial structures project into cyst-like spaces (papillary cystadenoma), major glands= superficial lobectomy, intraoral glands= wide surgical excision, 8-10% recurrence rate

malignant salivary gland neoplasm, often appears in 3rd-7th decades, slightly more common in females, most common in parotid or minor palatal glands, in the parotid, facial nerve paralysis may result, most common in soft tissues, central intraosseous cases have been reported, intrabony lesions may result from epithelial entrapment, one of the few that can occur as an intraosseous tumor, superficial 4-5 cm. nodules or ulcerating fungating masses

mixture of mucous secreting and non secreting epithelial cells, three distinct histologic grades: high grade= mostly non secreting cells, low grade = mostly mucous secreting cells, intermediate grade = mixture of both cell types, behavior related to grade (high grade= exceedingly aggressive with lymph node and distant metastasis, low grade= little metastatic potential, but may metastasize 10-20 post-operative years, major glands are more subject to metastasis than minor glands, high grade are aggressive regardless of origin, treatment of high grade include lobectomy (major) and jaw resection (minor), prognosis is good; however 15-30 survival rates drop, adjunctive radiation may be employed

malignant salivary gland neoplasm, tends to invade nerve sheaths causing paresthesia and motor weakness or paralysis, may appear as a small nodule to a fungating mass, may be associated with nerve involvement symptoms

three histologic patterns: cribiform= tumor cells display a "honeycombed" pattern, tubular= tumor cells ramify as basaloid ducts, solid = solid sheets of tumor cells (worst prognosis), nerve sheath invasion is a common observation, aggressive surgical excision is necessary, partial parotidectomy, full parotidectomy, maxillectomy, mandibulectomy, postoperative radiation often used (tumor is radiosensitive), 5 year cure rates are good, 10-30 rates are poor

rare malignant salivary gland neoplasm, parotid gland is the favored site (80%), women and children more commonly affected, appears as an intra-parotid nodule, intra-oral lesions appear as submucosal nodules

proliferation of acinar cells, tumor cells may be mucous or serous secretors, tumor cells are basophilic with prominent nuclei, stroma is scant, wide surgical excision is necessary, radioresistant, 5- year survival rate is 70-80%, drops off in 10-15 years, lung and other metastasis often occurs

recently recognized entity, more common in females, palate most common location, lips and buccal mucosa are other sites, appear as soft tissue nodules, some cases reach 5-7 cm. in diameter, most are smaller than 3 cm.

no capsule, proliferation of tumor cells in lobular or cribiform patterns, may be confused with adenoid cystic carcinoma, unlike ACC, tumor cells are often arranged in single file patterns (not same predilection for nerves as ACC), wide surgical excision, does not have the aggressive potential of ACC, recurrences occur after incomplete excision, nerve invasion may occur, metastases are uncommon, radiation is contraindicated

very common disease (20% of world's population), commonly known as "canker sores", oral ulcers may represent some underlying disease process, 4 distinct manifestations, minor are more common than major aphthous ulcers, certain foods, stress, URI's, menstruation, trauma can all precipitate an attack

appear as shallow painful ulcers, occur on freely-moveable (lining) mucosa, ulcers have white centers ringed by red margins, ulcers vary from 0.05-1.0 cm in diameter, always occur on non-keratinized mucosa, very painful

non-specific ulcer, necrotic surface debris, granulation tissue at the base, T-4/T-8 lymphocytes prominent at the base, T lymphocytes are causing the epithelium to break down, pain subsides and ulcers heal in 7-10 days, often recurrent (due to stress or diet), topical steroids may help (Decadron, Kenalog, Temovate, Amelexanox), alleviate the pain with topical anesthetics and systemic anesthetics

large, deep, exceedingly painful ulcers, some recur and scar = "periadenitis mucosa necrotica recurrens", last up to 6 weeks, AKA Sutton's Disease, may occur on the labial mucosa, buccal mucosa, soft palate, usually 1-2 lesions; 1.0-4.0 cm in diameter, ulcers are persistent and deep, may be infested with fungi (Candida), will always leave a scar, histologically similar to minor aphthae, prolonged healing, steroid application

rarer than minor/major aphthae, resemble herpetic lesions; however, do not start as vesicles, may require laboratory test to separate the two conditions, appear as clusters of ulcers, can occur on lining and masticatory mucosa, pain can be severe, non-specific ulcer, treat: same as minor/major aphthae, low dose steroids

lesion on tightly bound tissue

lesion on loosely bound tissue

uncommon generalized systemic disorder, oral, genital, ocular ulcers, may show rheumatoid arthritis symptoms, unknown etiology (herpes probably not cause, but have high Herpes simplex titers), may have arthralgia, CNS involvement, aphthous-like painful ulcers, photophobia with ocular lesions, no way to distinguish from aphthous ulcers, lesions are self-limiting, systemic steroids may be necessary

very common, itch like crazy on any "end" of the body, skin and mucous membrane disease, etiology unknown (macs induce T-lymphocytes, T-lymphocytes elaborate and epithelial cytotoxic substance), three classic subdivisions (reticular LP-- most common, erosive LP, plaque-like LP), two other types have been encountered (atrophic LP, bullous LP--starts as blister), usually present as white because of keratin

most common form of oral lichen planus, appears as white striae/lace-like mucosal lesions (Wickham's striae), lesions are elevated, may resemble hyperkeratosis or epithelial dysplasia, generally asymptomatic unless erosive

appear as smooth white dense plaques, resemble hyperkeratosis, OLP plaques are multifocal

mixture of red/white mucosal lesions, ulcerations often occurs ("erosions"), erosions are painful, patients have pain to spicy foods, hot foods, alcohol, etc., can mimic other conditions: candidiasis, benign mucous membrane pemphigoid, pemphigus vulgaris, lupus erythematosus, more common in women, need to biopsy, sometimes only effects gingiva

tend to have thin epithelium and tend to look red, erythematous, translucent lesions

cobbled, raised, red lesions, may be "scratch-like" and "itchy", occur on any skin surface, flexor surfaces, scalp, and nail bed are preferred sites, purple, pruritic, polygonal papules, can get wherever you have constant friction, quite scaly in appearance

many reports of OLP transforming to SCC, transformation rate is 1-3% of cases, transitional phase = "lichenoid dysplasia", changes occur on tongue, females who are infected with HPV are at high risk

seen in patients with bone marrow transplants or transfusions, produces lichenoid reticular mucosal lesions, may be the same cytotoxic pathogenesis as LP, indicates a life-threatening histoincompatibility

epithelial thickening with hyper/parakeratosis, jagged, "saw tooth" rete ridges, lymphocytes/plasma cels in c.t. "hugs" overlying epithelium, "Civatte bodies" may appear in epithelium (eosinophilic globules, dead keratinocytes), erosive form has similar features plus marked liquefaction of the basal cell layer

immunologic histochemical immunofluorescent assay, shows shaggy fibrinogen along the basement membrane, topical steroid therapy (decadron, valisone ointment, methoprednisone, temovate), sometimes systemic steroids are necessary, not life threatening but can be debilitating

lesions mimic OLP, results of ingestion of some medications (antibiotics, antihypertensive drugs, gold compounds, NSAIDs), careful history needed to differentiate, treatment: cessation of meds

more common in women (6:1 ratio), aka cicatricial pemphigoid , 40-60 years old, blistering (vesiculobullous) condition, affects skin, conjunctivae, and oral mucosa, may only affect gingiva = "desquamative gingivitis", not hyperkeratinized and can be rubbed off, difference between LP is scarring, patchy hemorrhagic areas, gingiva particularly affected, gingiva erythematous, non-dimpled, atrophic and thin, rubbing tissue may raise a blister (Nikolski's sign), lesions may affect the eye (cause c.t. bands from lid to sclera, "Sympblepharon"), standard is fire engine red gingiva (80%)

thin, atrophic epithelium; flat rete ridges, epithelium separated from underlying c.t. (sub-basal cleft), diffuse infiltrate of lymphocytes/plasma cells in c.t., immunofluorescence show IgG and C3 along the basement membrane (OLP shows only fibrinogen), systemic or topical steroids, gingiva-only lesions may show dramatic improvement, may be prolonged with pain and loss of life quality, no malignant potential

bullous desquamating disease, affects skin and mucous membranes, mainly affects torso skin; 50% develop oral lesions, most patients are 40-60 years old, Mediterranean or Jewish descent, destruction of desmesomes holding epithelial cells together, loss of epithelial integrity (acantholysis), appear as bullae, then desquamative erosive lesions, gingiva, soft palate, buccal mucosa are favored sites, as bullae collapse, brittle, crusty lesions are formed

differential diagnosis: benign mucous membrane pemphigoid, bullous lichen planus, medication reactions (e.g. penicillamine)

basal cells are intact, acantholysis occurs in the lower stratum spinosum, produces a characteristic cleft (suprabasalar cleft), some detached cells typically occur in the cleft space (Tzanck cells), immunofluorescence shows +IgG binding to sloughed epithelial cells, can see individual cells (acantholytic cells) floating inside space in epithelium, high dose prednisone therapy (150-360 mg/day), life-threatening disease (10%), secondary infections are common, parenchymal destruction of systemic organs can occur

rare disorder, affects skin and oral mucosa, several subtypes, rarely seen in dental patients, more common in kids, may appear as simple oral blisters, may have destructive scarring skin lesions, ulceration and secondary infections can cause loss of digits, everytime hand or foot has friction with something else it will result in scar tissue, mitten hands and sock feet as a result of scarring

common significant hypersensitivity response, can occur in response to: herpes simplex virus, pneumonia, reactions to dilantin, barbiturates, salicylates, G.I. disorders (e.g., Crohn's disease), post herpetic is the most common, allergic reaction resulting in perivascular inflammation, destruction of basement membranes by lytic enzymes, cell attachment destroyed, cell necrosis ensues, appear as ulcers (acute, chronic, major), toxic epidermal necrolysis, ulcers can appear on skin and/or oral mucosa, "target lesions" of skin rather characteristic (have peripheral ring around center), looks like pemphigus

skin and mucosal blisters and bullae, rupture creates crusty ulcers

blisters and ulcers of eyes, genitalia, and esophagus, painful oral lesions, eye lesions may cause blindness, occur commonly around lips

extreme form of erythema multiforme, significant sloughing of skin with chronic inflammation, denuded epithelium resembles burns

necrosis of 2/3 of epithelium, leaves edema, microvesicles, necrosis behind, may be separation at the epithelial-c.t. interface, immunofluorescence shows perivascular IgM and C3, can become subepithelial as well, histopathology is non-specific, holes are dead epithelium/necrotic, looks like a burn, huge vesicles rupture and slough off, most cases are self limiting once cause is identified and corrected, steroid therapy is questionable, lesions may appear chronically for years, toxic epidermal necrolysis form can be fatal

an autoimmune chronic inflammatory condition, affects skin, mucous membranes, and specific systemic organs (e.g. kidney), three clinical forms recognized (systemic lupus erythematosus, subactue lupus erythematosus, discoid lupus erytheatosus), aggressive for with high fatality rates, circulating antibodies to DNA (anti-nuclear antibodies), young female adults most commonly affected, patients may arthritis, arthralgia, heart, lung, kidney involvement, oral lesions seen in about 20%, UV light produces skin vasculitis, UV light produces "butterfly rash" on the nose bridge and cheeks

rare disorder, can be seen in Sjogren patients, subcategory of systemic lupus erythematosus

appears as skin/oral mucosal lesions only, no systemic organ infovlement, 20% have oral lesions (hyperkeratosis, erythematous areas, vesiculobullous lesions, ulcers

features similar to lichen planus and graft vs. host disease, hyperkeratosis, liquefaction of stratum basale, chronic inflammation in the stratum spinosum, parakeratin surface "plugs" and perivascular chronic inflammation are characteristic findings, TREATMENT: steroid therapy, immunosuppressive medications (cyclophosphamide, azathioprine), oral lesions treated by local steroids

generalized condition with c.t. sclerosis and fibrosis, two subtypes are recognized (diffuse, localized), immune complex disease, complexes toxic to capillary endothelial cells, females more commonly affected, skin becomes bound down to bone because loss of collagen, or because collagen becomes avascular, CT becomes dense that the epithelium sticks to it, mobility loss in hands and joints, widening of the pdl space is characteristic, TMJ clicking/popping; trismus, women are commonly affected, scar tissue will just contract, patients get widening of pdl space b/c collagen is affected, ligament becomes avascular and dense, osteosarcoma also causes widening of the PDL space

dense zones of hyalinzed collagen, dense zones replace loose interlacing c.t., hyalinization around blood vessels, steroid therapy, no definite way to halt the disease

several allergic reactions can occur in the oral cavity, most related to contact with some allergen, mediated by IgE (10% of population have IgE sensitized mast cells, re-exposure results in allergic reaction)

common, related to some medicaments (e.g. lipstick, rubber dams), severe reactions can result in anaphylactic shock, red mucosal patches, puffy buccal mucosa, puffy cheeks, swelling of lips, gingiva, burning sensation, distribution may suggest a cause (e.g., denture base acrylic)

no specific histologic findings, some allergens may elicit a "plasma cell gingivitis"

acquired/hereditary disorder mediated by an anti-inflammatory response, most are acquired; mediated by IgE (e.g. penicillin allergy), allergens act act on mast cell membranes releasing IgE? Hereditary form rarer, trauma may initiate the process, swelling of oral tissues, swelling of lips and adjacent structures

swelling of the lower lip, most common in middle age/older males, caused by inflammation of minor salivary glands, unknown etiology, immune mediated?, some patients say it is sunlight-initiated, bacterial infection may play a role in some cases

chronic inflammation around minor salivary glands, fibrosis of stroma, may require surgery, long-standing cases may require lip reconstruction, higher incidence of SCC in some cases

often developed when young, often associated with Melkersson-Rosenthal syndrome (lip swelling, oral-facial swelling, fissured tongue, peripheral nerve paralysis, higher incidence of diabetes mellitus?), one or both lips are swollen, swelling, difficulty in eating

non-caseating granulomas, giant cells, lymphocytes, plasma cells, histiocytes, stroma shows chronic inflammation, remove co-existing infections, surgically reconstruct the site

granulomatous disease, more common in black populations in U.S., Caribbean, Africa, most patients are 40-50 year-old females, hormonal alteration?, some have altered histocompatibility antigens (B5, B7, B8), lethargy and breathing difficulty (lung granulomas), granulomas of lips, tongue, buccal mucosa, gingiva, salivary glands, eyes, may mimic salivary gland neoplasms, Heerfordt Syndrome: eye, parotid gland, VII nerve involvement, salivary glands and posterior molars are affected, can see elevated nodule on tip of tongue

non-caseating granulomas, multinucleated giant cells, epithelioid cells, giant cells may contain "asteroid bodies", + serum calcium, altered immunoglobulins, and + angiotensin converting enzymes, Kviem test can assist diagnosis, injection with antigens from sarcoid patients, positive results produce sarcoid-like lesions in 4-6 weeks, manage lung lesions, lesions may regress spontaneously, immunosuppressant drugs have been helpful, lesions may become diffuse producing debilitating arthritis

what shows Civatte bodies histologically?

what has saw tooth rete ridges and lymphocytes and plasma cells in c.t. "hugs"

what has purple, pruritic, polygonal papules?

what is autoimmune generally affecting the skin, kidney, and mucous membranes

what shows circulating antibodies to DNA

salivary gland ischemia (necrosis and duct metaplasia), usually after dental procedures

nerve sheath invader

what has the 3 histologic subtypes: cribiform, tubular, or solid (worst prognosis)

what is sometimes called "Warthin's tumor"

aplomb (m)

lymphoid cells and salivary ductal structures, columnar epithelial cells w/ fingerlike projections, epithelial structures project into cyst like spaces

black population in U.S., Caribbean, Africa

associated with Heerfordt syndrome (eye, parotid, VII nerve, salivary glands and posterior molars)

multinucleated giant cells with asteroid bodies

+ serum Ca++ and +angiotensin converting enzymes

can perform Kviem test to diagnose

acinar degeneration with ducts intact, fibrotic stroma

shows perivascular IgM and C3

destruction of basement membrane by lytic enzymes, necrosis of 2/3 of epithelium

Mediterranean and Jewish, 40-60 year olds

suprabasalar cleft with Tzanck cells

+IgG on sloughed epithelial cells

submandibular gland most common site, 40-50 year olds

most common salivary gland neoplasm (50-60% parotid, 50% submandibular, 55% sublingual)

aka periadentiis mucosa necrotica recurrens or Sutton's

what has the two subtypes basal cell adenoma and canalicular adenoma

flat rete ridges, epithelium separated from c.t. (subbasal cleft), IgG and C3

much more common in women 6:1 ratio, 40-60 year olds

standard= fire engine red gingiva, "desquamative gingivitis"

Nikolski's sign, blister from rubbing

can cause c.t. bands from lid to sclera "sympblepheron"

elevated autoantibodies, salivary gland fibrosis

parotid necrotic, bilateral swelling of parotid= 50%

can be intrabony/intraosseous, sueprficial 4-5 cm nodules

Melkersson-Rosenthal syndrome

immune complexes are toxic to capillary endothelial cells

widening of PDL space

high dose prednisone therapy (150-360 mg/day)

suprabasalar cleft

may mimic mucoepidermoid carcinoma

3rd-7th decades, most common in parotid or minor palatal glands, can cause facial paralysis in parotid

some acini may show coagulation necrosis, may affect entire lobule, stroma shows scatted inflammatory cells

post herpetic most common

"target lesions"

may have high herpes simplex titers even though this is not the cause

caused by antibiotics, antihypertensive agents, Gold compounds, NSAIDs

intact basal cells, acantholysis in lower stratum spinosum, suprabasalar cleft

has 3 forms: minor, chronic, and major (SJS, TEN)

separation at epithelial-ct interface

2 types: SJS, TEN

fatal in 30-35% of patients

liquefaction of stratum basale, chronic inflammation of stratum spinosum

CREST syndrome

lipstick and rubber dam reactions

have histocompatibility antigens (B5, B7, B8)

papilla disappear on tongue

patient at higher risk for lymphoma ~3%

myoepithelial islands are common

if in palate can travel to circle of willis and kill patient