Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
52 Cards in this Set
- Front
- Back
|
Fibroma (Irritation fibroma)
|
Clinical: Most common oral “growth”; probably related to chronic trauma. Adults. Buccal mucosa (occlusal line), tongue, labial mucosa, gingiva. Dome-shaped, smooth-surfaced, pale nodule.
Histology: mass of dense fibrous connective tissue +/- chronic inflammation. (giant cell fibroma = large, stellate and multinucleate fibroblasts) Treatment/Prognosis: conservative excision. Little, if any, tendency to recur. |
|
|
Peripheral Ossifying Fibroma
|
Clinical: gingiva associated with the teeth; teens/young adults, females (2:1). Dense, firm, smooth-surfaced nodule, however, often ulcerated. premolar region or anterior segments of the jaws.
Histology: cellular proliferation of plump, spindle-shaped fibroblastic cells; Mineralized component may resemble bone, cementum or dystrophic calcifications (or all three). Treatment/Prognosis: complete surgical excision, remove local irritants. Recurrence rate - 15%. |
|
|
Peripheral Giant Cell Granuloma
|
Clinical: alveolar process +/- adjacent tooth. Adult females, 5th-6th decades,. Smooth-surfaced, dome-shaped nodule, ulcerated mucosa 50%; dusky red to violaceous (liver). Cupping out or "saucerization" of bone by radiograph.
Histology: granulation-like tissue, numerous multinucleated giant cells, extravasated erythrocytes and hemosiderin. Treatment/Prognosis: Complete surgical excision. If tooth-associated, remove local irritants. Recurrence rate - 15%. |
|
|
Pyogenic Granuloma
|
Clinical: Gingiva (75%), tongue, lips and buccal mucosa. Children/young adults. Slightly more common in females, more frequent during pregnancy (pregnancy tumor). Smooth-surfaced, often ulcerated, may be lobular. Bright red to reddish-purple. Painless, can grow rapidly, simulating malignancy, histologic examination is mandatory. May also be seen on skin of the head and neck, hands, trunk.
Histology: granulation tissue; variable amounts of acute and chronic inflammatory cells and edema.Treatment/Prognosis: Excisional biopsy; remove local factors (dental calculus, etc.) for gingival lesions. For pregnancy-related lesions; delay excision after delivery if possible. Recurrence rate 10-15%. |
|
|
Parulis
|
Clinical: Sinus tract opening, associated with non-vital tooth and PA abscess. Painless erythematous papule/nodule on the gingiva/alveolar mucosa. Intermittent foul or salty taste may be reported. pulp-test teeth.
Treatment: Endo or extraction of the non-vital tooth. |
|
|
Chronic hyperplastic pulpitis
|
Clinical: Painless, reddish-purple mass (granulation tissue) emanating from pulp chamber of grossly carious tooth. Children/young adults.
Treatment: Endo or extraction of the tooth. |
|
|
Inflammatory Fibrous Hyperplasia
|
(Denture epulis; Epulis fissuratum;
Denture-induced fibrous hyperplasia) (pp. 510-2) Clinical: Chronic trauma secondary to ill-fitting denture or partial. Buccal vestibule of edentulous areas. Smooth-surfaced, reddish to normal color. Histology: Dense fibrous connective tissue, chronic inflammation. Treatment/Prognosis: Excision. Remake/reline denture. Epulis = exophytic gingival mass, clinical term only, denotes alveolar site |
|
|
Inflammatory Papillary Hyperplasia
|
Clinical: Palatal mucosa under poorly fitting denture. Associated with lax hygiene and constant denture use. Asymptomatic red papules, typically involves center of hard palate.
Histology: Papillary epithelial and fibrous hyperplasia, chronic inflammation. Treatment/Prognosis: Benign process, may not require treatment but advanced cases will not resolve completely. Some prosthodontists will insist on removal prior to new denture construction. |
|
|
Dilantin-Induced Gingival Hyperplasia
|
Clinical: Affects roughly 50% of patients who take Dilantin (phenytoin); correlated with oral hygiene. Diffuse fibrotic gingival enlargement.
Treatment/Prognosis: Gingivectomy, oral hygiene measures. Recurrence likely if oral hygiene is not controlled. |
|
|
Cyclosporine-Induced Gingival Hyperplasia
|
Clinical: similar to Dilantin, affects roughly 25% of patients
Treatment: same as Dilantin. C. Ca-Channel Blocking Agent-Induced Gingival Hyperplasia Clinical: same to Dilantin, 25% affect rate. Treatment: same as Dilantin. (Note: A, B, and C can have synergistic effects in the same patient) |
|
|
Traumatic Ulcerations (including traumatic granuloma)
|
Clinical: Tongue, lips, buccal mucosa, palate. History of trauma is common. Pain usually not severe. Erythematous ulcer with white to yellowish fibrin membrane and a periphery that varies from ragged to smooth. Margins may be rolled and firm due to fibrosis, mimicking oral Ca.
Histology: Non-specific, loss of surface epithelium with fibrin over inflamed granulation tissue (ulcer bed). In traumatic granuloma, inflammation often includes abundant eosinophils, but no true granuloma formation. Treatment/Prognosis: If present a few hours or days: symptomatic tx: Zilactin. Topical corticosteroids are contraindicated. If present for several weeks: biopsy. |
|
|
Traumatic Neuroma
|
Clinical: Tender or painful, dome-shaped papule/nodule; mental foramen area, tongue, lower lip. Adults. Can be intraosseous.
Histology: Tangled mass of small peripheral nerve bundles and fibers within dense fibrous connective tissue. Treatment/Prognosis: Excisional biopsy. Recurrence rare. |
|
|
Mucocele/Ranula
|
Clinical: Most occur in children/young adults. Lower lip (75%), buccal mucosa, ventral tongue. Sudden appearance of a soft, nontender swelling. Hx of swelling followed by rupture, drainage and re-filling may be elicited. Corresponds to spillage of mucus into the submucosal tissue from disrupted salivary gland duct. Ranula = mucocele in the floor of the mouth.
Histology: Extravasated mucin, inflammatory cells and granulation tissue. Treatment/Prognosis: Excision of the mucous deposit as well as the involved minor salivary gland. “unroof” a ranula. May recur. |
|
|
Amalgam Tattoo/Foreign Body Tattoo
|
Clinical: Black, blue or grey macule. Amalgam most common, graphite. Gingiva, alveolar/buccal mucosa favored sites for amalgam implantation. Radiograph may detect metal particles.
Histology: Amalgam preferentially stains reticulin fibers, often with little inflammation. Coarse or finely dispersed dense particles. Treatment/Prognosis: No tx if radiographic evidence of foreign body. Without X-ray confirmation, biopsy to rule out melanocytic lesion. |
|
|
Aspirin Burn
|
Clinical: White, wrinkled appearance to mucosa, often followed by sloughing of epithelium. Often seen adjacent to symptomatic, carious tooth.
Histology: coagulative (retention of architecture) necrosis of the epithelium. Treatment/Prognosis: discontinue application of aspirin to mucosa. |
|
|
Dentifrice-associated slough
|
Relatively common, esp. with tartar-control/whitening formulas
Clinical: mild superficial sloughing/peeling, usually labial/buccal mucosa. Rarely symptomatic, may increase sensitivity to acidic/spicy foods. Tx: If symptomatic, replace offending dentifrice with bland formulation |
|
|
Electrical or Thermal Burns
|
Clinical: Hx of food burn usually reported or elicited. Single or multiple areas of white, sloughing mucosa; varying degrees of peripheral erythema.
Histology: coagulative necrosis of the epithelium. Treatment/Prognosis: Analgesics if needed. |
|
|
Radiation Mucositis
|
Clinical: Occurs after ≥ 25-30 Gy (Sv) during radiation tx for malignancy. Only develops within the field of radiation, usually in 2nd week of fractionated therapy. Extremely painful ulcerations with erythema. May be so severe that treatment has to be interrupted in order to allow some mucosal healing. Similar changes often seen with chemotherapy.
Treatment/Prognosis: Topical anesthetic (viscous lidocaine) and systemic analgesics. Reassure patient that oral mucosa will heal within 2-4 weeks following cessation of radiotherapy. Note: Supporting bone, esp. mand, may be susceptible to osteoradionecrosis |
|
|
Pemphigus vulgaris
|
Rare, but potentially serious, vesiculoerosive disease of skin and oral mucosa
Etiology: autoantibodies to desmosomal components (desmoglein 3 & 1) Clinical: adults, 30-50s, ave. 50 yrs. Oral: progressive erosions and ulcerations, any intraoral site, “first to show (50%) and last to go” Skin: fragile bullae and erosions. Positive Nikolsky sign - blisters form on normal skin/mucosa following firm lateral pressure. Histology: intraepithelial clefting with acantholysis (breakdown of the spinous cell layer secondary to detachment of desmosomes). Tzanck cells – rounded (“detached”) epithelial cells Immunofluorescence: intercellular IgG/C3 deposits between epithelial cells. Positive by direct and indirect IF. Treatment: systemic corticosteroids, +/- “steroid-sparing” drugs Prognosis: mortality rate of 5-10%, primarily due to the complications of immunosuppressive therapy. |
|
|
Mucous Membrane Pemphigoid (cicatricial pemphigoid)
|
Chronic, blistering disorder affecting primarily mucous membranes (pp. 771-5)
Etiology: autoantibodies directed against basement membrane components Clinical: older females (2:1), ave. 50-60 yrs., ANY mucosal surface (oral, conjunctival and/or vaginal) skin lesions uncommon (< 20%). + Nikolsky Oral: tense vesicles/bullae, ulcers, desquamative gingivitis Ocular: adhesions (symblepharons), fibrosis → blindness. Seen in up to 25% of patients. Histology: clean, subepithelial cleft Immunofluorescence: linear IgG/C3 at BMZ by direct IF, indirect IF negative Treatment: topical steroids for limited oral lesions. Acrylic stints may be helpful with gingival presentations. Tetracycline/niacinamide combination. Systemic steroids +/- steroid-sparing agents like Dapsone for diffuse involvement. Eye lesions: aggressive systemic immunosuppressive therapy. Prognosis: rarely fatal. usually controlled with medications. |
|
|
Bullous pemphigoid
|
elderly population; affects skin (20% with oral lesions). BP is positive with indirect IF as well as direct.
|
|
|
Lichen Planus
|
Chronic, relatively common disease with distinct skin and mucosal courses
Etiology: immunologically mediated, resembles Type IV hypersensitivity reaction, increased cytotoxic (CD8+) T cells, CD4+ T cells, Langerhans cells Clinical: adults, females (3:2) Skin: purple, polygonal, pruritic papules, flexor surfaces of arms, legs. **Lesions typically resolve in 12-18 months. Oral: 2 primary forms - Reticular: white, interlacing papules/lines (Wickham’s striae) bilateral posterior buccal mucosa, tongue and/or gingiva. Most common form, usually asymptomatic. Erosive: epithelial atrophy/ulceration with erythema and peripheral keratotic striae. May present as desquamative gingivitis. Less common, but typically symptomatic. **Oral forms are chronically persistent over years-decades. Other mucosa, particularly genital, may be involved Histology: hyperkeratosis, "saw-toothed" rete ridges, band-like lymphocytic infiltrate hugging epithelium, Civatte (colloid, cytoid) bodies, 25% have superimposed candidias |
|
|
Lupus Erythematosus
|
Chronic, inflammatory disorder that may affect connective tissue, skin (mucosa) or both. 2 major forms are recognized.
|
|
|
Systemic L.E.
|
Serious, multisystem disease – Primarily involving skin, joints, kidney and cardiopulmonary system. American Rheumatism Association has several criteria for SLE, including both clinical and laboratory findings, to help establish the diagnosis in a given patient.
Etiology: unknown, associated with serum anti-nuclear antibodies (ANAs) Clinical: females (8:1 ratio), onset in 3rd-4th decades Widely variable; including fever of undetermined origin (FUO), arthritis, skin lesions (bilateral rash over the malar regions, "butterfly rash"), unexplained weight loss and proteinuria/hematuria. Oral: 5-25% (up to 40% reported) erythematous patches, irregular ulcerations, keratotic areas - palate, buccal mucosa or gingiva. Histology: lichenoid mucositis (band-like, superficial inflammation) or dermatitis with vasculitis (inflammation of vessel walls) Laboratory: ANA’s in over 95%. Autoantibodies against double-stranded DNA (anti-dsDNA Abs, a type of ANA) are considered specific. Anemia. IF: shaggy BMZ IgG, M and C |
|
|
Chronic cutaneous L.E.:
|
Discoid LE) possibly a limited type of SLE, often restricted to the skin of the head and neck.
Clinical: affects females (2:1 ratio), ave. 4th decade, but wider age range than SLE. Skin: well-demarcated, scaly, erythematous patches on face and scalp, often with central scarring. Exacerbated by sunlight exposure. Oral: lesions resemble erosive LP - seen in 10-15%. Histology: lichenoid mucositis or dermatitis with vasculitis (identical to SLE). Laboratory: abnormal findings less common than in SLE. ANA’s in 1/3. Anti-ds DNA Abs almost always absent. Treatment: avoid excessive sunlight. topical corticosteroids or anti-malarials. Prognosis: relatively good. conversion to SLE in about 5%. |
|
|
Erythema Multiforme
|
An acute self-limiting, ulcerative mucocutaneous disorder. About half of all cases are triggered by drug exposure or viral infection (esp. HSV).
Clinical: typically seen in young adult males Sudden onset, variable presentation, mild mucosal involvement (E.M. minor) is most common but severe mucocutaneous disease (toxic epidermal necrolysis) can result. May be recurrent. Oral: hemmorhagic lesions of the lips, labial mucosa, buccal mucosa and tongue. Hemorrhagic crusting of lower labial vermilion is suggestive of E.M.. Oral ulcers are large, widespread with irregular margins. If ocular (conjunctivitis) and genital (urethritis) also present, the condition is termed Stevens-Johnson syndrome (E.M. major). Skin: "target lesions", annular with central purpura. Histology: characteristic (subepithelial vesiculation, necrotic keratinocytes), but not pathognomonic. IF not helpful Treatment: supportive care (topical anesthetics and analgesics) for mild cases. severe cases - systemic corticosteroids or managem |
|
|
Systemic Sclerosis (Scleroderma)
|
Systemic CT disease associated with abnormal deposition of collagen.
Clinical: affects females by a 3:1 ratio, 4th-6th decades Diffuse,progressive induration of the subcutaneous connective tissues; claw-like deformities of the fingers (sclerodactyly), dysphagia if esophagus is involved, pneumonia and dyspnea if lungs are involved, kidney failure and hypertension if kidneys are involved. Oral: “purse-string” perioral skin (microstomia), diffuse symmetrical widening of the PDL, resorption of the distal mandibular ramus, coronoid process or condyle, xerostomia often present. Histology: diffuse deposition of dense collagen in the involved organs, with destruction and displacement of the normal tissues. Laboratory: ANAs esp. anti-Scl 70 Abs, (anti-centromere for CREST) Treatment: nothing works very well. Penicillamine, azathioprine. Extracorporeal photochemotherapy for skin lesions. Prognosis: Generally guarded to poor, except for limited cutaneous cases. |
|
|
CREST syndrome
|
milder form of scleroderma; 1° affects skin and has a better prognosis. Calcinosis cutis, Raynaud's phenomenon, Esophageal dysfunction, Sclerodactyly, and Telangiectasia.
|
|
|
Psoriasis
|
Chronic skin disease characterized by overly rapid epithelial turnover.
Etiology: cytokine dysregulation Clinical: relatively common; 1-2% of US population. Onset in teens-20s. well-defined erythematous plaques with overlying silvery scale – hairline, scalp, elbows and knees. May follow local trauma (Koebner phenomenon) Oral: Rare, white or red plaques on palatal mucosa. Treatment: Sun exposure (UV light), coal tar derivatives, topical steroids for mild to moderate cases. PUVA (psoralens plus ultraviolet A) or cyclosporine for more severe cases. Prognosis: Condition tends to persist, may be tx problem. Prolonged PUVA therapy associated with increased incidence of actinic-related skin cancers. |
|
|
Behcet's Syndrome
|
Chronic mucocutaneous syndrome affecting eyes, mouth and genital areas, probably immunologically mediated.
Clinical: more common in Japan and Middle East (first described by H. Behcet, a Turkish dermatologist). 20s-30s. males > females (males also have more severe disease). Oral: aphthous ulcerations, often multiple, often soft palate, oropharynx. May be presenting sign. Genital mucosa (75%). Ocular: recurrent uveitis, conjunctivitis, up to 90% of cases Other areas - skin, central nervous system, joints and GI tract. Laboratory: positive pathergy test, skin prick with sterile needle (or sterile saline subQ) that leads to the formation of an inflammatory pustule Treatment: colchicine. corticosteroids +/- other immunosuppressive agents. Prognosis: With only oral and cutaneous manifestations, prognosis is good. With CNS involvement, prognosis is guarded. |
|
|
Keratosis Follicularis (Darier's Disease)
|
Uncommon autosomal dominant genodermatosis with striking skin lesions and subtle oral findings.
Etiology: abnormal intraepithelial (desmosomal) attachments Clinical: onset in childhood or adolescence, multiple erythematous, confluent papules which tend to accumulate keratin on their surface, resulting in foul-smelling crusts. Worse during summer due to sweating. Oral: 15-50% of pts., multiple asymptomatic white flat papules - may impart a cobblestone appearance to the oral mucosa. Histology: central keratin plug overlying acantholytic (intraepithelial clefting similar to pemphigus) epidermis. Grains & corps ronds - dyskeratotic cells. Treatment: Genetic counselling. Keratolytic agents or retinoids for skin. No treatment for oral lesions. Prognosis: Good |
|
|
Epidermolysis Bullosa
|
Group of inherited disorders of the skin and mucosa characterized by the formation of vesicles or bullae following relatively minor trauma.
Etiology: Abnormal production of molecular structures which bind epithelial cells to one another or to the underlying basement membrane and connective tissue, depending on the type of EB. Three broad categories: 1)simplex, 2)junctional and 3)dystrophic. |
|
|
dominant dystrophic
|
autosomal dominant inheritance.
Clinical: blisters on skin exposed to the most trauma (extremities: knuckles, elbows and knees). heal with scarring. loss of the nails. Oral: mild gingival erythema, recession, tenderness. Histology: sub-epithelial clefting. Treatment: localized supportive care Prognosis: good. |
|
|
recessive dystrophic
|
autosomal recessive inheritance.
Clinical: severe, debilitating form; prominent skin blisters with minimal trauma that heal with prominent scarring. mitten deformities. Oral: very fragile mucosa/skin; microstomia Histology: sub-epithelial clefting. Treatment: very soft foods; increased oral hygiene measures as possible. Aggressive management to reduce blistering, scarring and risk of infection. Prognosis: poor |
|
|
Acute Sialadenitis
|
Etiology: penicillinase + Staph, Strept. Sporadically or as complication of reduced salivary flow (dehydration, drugs, disease states). May follow surgery, esp. abdominal (surgical mumps)
Clinical: painful, parotid enlargement (10-25% bilateral); Fever, local erythema, trismus, purulent exudate from parotic papilla (Stensen’s duct). Tx and prognosis: PCNase-resistant penicillin. Culture exudate to adjust antibiotic. Hydrate, moist compresses. May become chronic. Can be life-threatening in debilitated patients. |
|
|
Sialolithiasis and Chronic Sialadenitis
|
SUBMANDIBULAR SAUSAGE APPEARANCE Etiology: Nidus of mucinous/cellular debris, bacteria, etc. may collect in excetory duct and undergo dystrophic calcification, resulting in sialolith (salivary stone). Primarily affects submandibular gland, may also be seen in minor glands. Obstruction a common antecedent to chronic sialadenitis (relatively avirulent bacterial infection may also lead to chronic sialadenitis).
Clinical: 30-50 years of age. Asymptomatic to mild-moderate pain, tender swelling localized to affected gland. Waxing/waning course, dramatic swelling may occur at or just before eating. Expressed saliva may have tiny white flecks. Sialolith may be palpable, hard submucosal mass. Radiograph often useful (90% are radiopaque). Sialography/ultrasound/CT to detect radiolucent stones/obstruction. Tx and prognosis: Surgical excision, endoscopy/lithotripsy. If gland is non-functional by sialography, then complete removal of affected gland, also |
|
|
Benign Lymphoepithelial Lesion
|
Etiology: autoimmune process localized to parotid gland(s). Uni- or bilateral. Most represent precursor to Sjogren's syndrome.
Clinical: middle-aged (50’s); females (60-80%). Firm, diffuse, non-tender to mildly symptomatic parotid swelling. Usually unilateral. Histology: diffuse replacement of parotid tissue with lymphocytes. Residual epimyoepithelial islands (epithelial + myoepithelial cells). Tx and prognosis: Systemic corticosteroids, surgery, immunosuppressive drugs and local irradiation have been used to reduce the swelling, but all have significant side effects and/or the potential long-term complications. Increased risk for lymphoma. |
|
|
Sjögren's Syndrome
|
FRUIT ON TREE , MUCUS SECRETION SCHIRMER TEST IN EYES Etiology: Chronic, systemic autoimmune disease, diffuse attack on the exocrine glands, particularly the salivary and lacrimal. Relatively common disease (prevalence ~ 0.5%). HLA-DRw52 associated.
Clinical: Females (90%), mid-late adults. 2 forms (each about 50%): |
|
|
Primary Sjögren's (sicca syndrome
|
Xerostomia (dry mouth) and xerophthalmia (dry eyes, aka: keratoconjunctivitis sicca). Dry oral mucosa, atrophy of the dorsal tongue, angular cheilitis. Diffuse parotid swelling may be present, often bilateral. Caries, candidiasis.
|
|
|
Secondary Sjögren's syndrome
|
sicca syndrome plus another autoimmune disease, particularly RA, SLE, systemic sclerosis, etc.
Labs: Salivary gland bx is helpful. Early finding, focal lymphocytic sialadenitis (focus score used to quantitate lymphocytic component, support dx), full-blown cases essentially like BLEL. Schirmer test - lacrimal gland function. Sialography - punctate sialectasis ("fruit on branchless tree"). Serum- elevated rheumatoid factor, even without RA, autoantibodies (ANAs) - anti-Ro (SS-A) and anti-La (SS-B) are specific for Sjögren's, but not seen in all patients. Tx and prognosis: Primary Sjögren's, symptomatic relief. Sugar-free gum/lozenges, artificial saliva/tears, sialagogues. If natural teeth, topical fluoride therapy, oral hygiene measures. If candidiasis, antifungal meds. Secondary Sjögren's, tx of other autoimmune process, typically immunosuppressive therapy. An important aspect of Sjögren's (especially primary Sjögren’s) is increased incidence of lymphoma - 40 X that of normal population. |
|
|
Necrotizing Sialometaplasia
|
Etiology: ischemic infarction of salivary gland tissue, secondary to trauma?
Clinical: adults, males (2:1). Tender, non-ulcerated swelling of hard/soft palate(75%). After about a week, a portion of the palate may "fall out", leaving a punched-out, painless ulceration. Mimics cancer. Histology: acinar necrosis of minor glands that retains lobular architecture. PEH (pseudoepitheliomatous hyperplasia) may be seen (mimics cancer). Salivary ducts undergo squamous metaplasia – may also be misdiagnosed as cancer by general pathologists not familiar with this lesion Tx and prognosis: No treatment necessary. Healing requires several weeks. |
|
|
Pleomorphic Adenoma (benign mixed tumor)
|
Clinical: Most common salivary gland neoplasm. 30s-50s, mean age = 45. Parotid (80%), submandibular gland and minor glands (each 10%). Palate (post. lateral) most common intraoral site. Non-tender, rubbery-firm, freely movable (except over hard palate) nodule. Slow growth. Ulceration rare.
Histology: Mixture of two cell types: ductal epithelial cell and myoepithelial cell, in any ratio. Myoepithelial cell can differentiate along several different lines. Stroma can vary from myxoid, hyalinized, chondroid or even osseous tissue. Variety of histologic appearances = "pleomorphic" adenoma (older term: benign mixed tumor). Encapsulated, but tumor tissue may protrude beyond capsule occasionally - may be important with regard to recurrence. Tx and prognosis: Complete surgical excision that depends on site of tumor. Parotid - excision of tumor and involved lobe of gland. Submandibular - entire gland plus tumor. Hard palate - overlying mucosa plus the tumor, down to and including periosteum. For labial, bucc |
|
|
Papillary Cystadenoma Lymphomatosum
|
Warthin’s tumor) (pp 482-3)
Clinical: 50s, male predilection (from 5:1 to 9:1 reported but recent data indicates more even sex distribution). Parotid gland almost exclusively, represents about 14% of parotid tumors. 5-14% bilateral, synchronous or metachronous. 8X increased risk in smokers. Slowly growing, non-tender mass, tail of parotid. Freely movable and asymptomatic. Histology: encapsulated lymphoid tissue contains cystic spaces with intraluminal papillary projections of eosinophilic, columnar epithelial cells. Tx and prognosis: simple surgical excision, recurrence (10%?). |
|
|
Monomorphic Adenoma
|
Refers to benign SG tumor composed of one cell type; 2 major forms:
Basal cell adenoma Clinical: 60s, females, uncommon. Parotid (75%), upper lip/BM. Slow growth, asymptomatic, may be multifocal, less than 3 cm. diameter. Histology: encapsulated, proliferation of basaloid ductal epithelial cells. Solid (most common) trabecular and membranous patterns of growth. Tx and prognosis: simple surgical excision; recurrence rare, may be due to multifocal nature. Malignant transformation very rare. Canalicular adenoma Clinical: 60s, female, uncommon. Upper lip (75%), buccal mucosa. Slow growth, asymptomatic nodule, may be mutifocal, usually less than 2 cm. Histology: long “canals” or channels lined by single-layers of epithelial cells, may be cystic, loose stroma with prominent vascularity, encapsulated. Tx and prognosis: simple surgical excision, recurrence rare (multifocal?) |
|
|
Basal cell adenoma
|
Clinical: 60s, females, uncommon. Parotid (75%), upper lip/BM. Slow growth, asymptomatic, may be multifocal, less than 3 cm. diameter.
Histology: encapsulated, proliferation of basaloid ductal epithelial cells. Solid (most common) trabecular and membranous patterns of growth. Tx and prognosis: simple surgical excision; recurrence rare, may be due to multifocal nature. Malignant transformation very rare. |
|
|
Canalicular adenoma
|
Clinical: 60s, female, uncommon. Upper lip (75%), buccal mucosa. Slow growth, asymptomatic nodule, may be mutifocal, usually less than 2 cm.
Histology: long “canals” or channels lined by single-layers of epithelial cells, may be cystic, loose stroma with prominent vascularity, encapsulated. Tx and prognosis: simple surgical excision, recurrence rare (multifocal?) |
|
|
Mucoepidermoid Carcinoma
|
Clinical: Most common malignant salivary gland neoplasm, in both adults and children. adults (mean age, 45), but may be seen at any age. Parotid and palate, occasional intraosseous (central) cases. Begin as asymptomatic mass, may have bluish tinge, similar to mucocele. Sometimes pain, tenderness and/or ulceration.
Histology: Grading important to prognosis. Low-grade (well-differentiated) looks like parent tissue: mucous-producing cells predominate, cystic spaces, little infiltration. High-grade (poorly differentiated) exhibits a predominance of invasive epidermoid cells (looks and acts like squamous cell Ca), with cellular pleomorphism and only scattered mucous cells. Tx and prognosis: low-grade: complete, conservative surgical excision, (90- 95% 5-yr survival). high-grade: wide surgical excision with radiation therapy (40% 5-yr survival and only 25% 15 year survival, with range of 25-54%). |
|
|
Adenoid Cystic Carcinoma
|
PALATE MOST COMMON, HYPERCHROMATIC NUCLEUS Clinical: 50s, 3rd most common intraoral salivary malignancy. Parotid (25%), submand. (25%), minor glands (50%) (palate). Slowly growing, non-ulcerated (initially), infiltrative mass with constant dull pain. In parotid, facial paralysis may occur. Ulceration commonly develops intraorally.
Histology: Small, dark cells arranged in cribriform ("Swiss cheese") and solid patterns. Perineural invasion common. Tx and prognosis: wide surgical excision, followed by radiation tx. prognosis is poor. 5-yr survival meaningless as tumor grows slowly Patients often die of uncontrollable disease 10, 15 or 20 years after the initial dx/tx. The 15-year survival rate for palatal lesions is 38%, and for parotid lesions, it is 20%. Typically metastasizes to lungs, not regional lymph lymph nodes. |
|
|
Polymorphous Low-Grade Adenocarcinoma
|
Clinical: 50s, females 2:1, 2nd most common intraoral salivary malignancy. Mostly intraoral, hard/soft palate, upper lip. Firm, indolent painless mass.
Histology: Uniform ductal epithelial cells arranged in lobules. Basaloid or spindle-shaped cells, may have many patterns therefore: "polymorphous”. Perineural invasion common. Often confused with pleomorphic adenoma, but peripheral infiltration (often single-file) is seen in PLGA. Also confused with adenoid cystic carcinoma but nuclei typically less hyperchromatic. Tx and prognosis: Wide surgical excision. Prognosis good, only 14% recurrence (9-17% range) , 6% lymph node metastasis, 3% dying of disease. |
|
|
Acinic Cell Carcinoma
|
Clinical: mean in 40s, but any age, Parotid (85%), buccal mucosa, lips. Well-demarcated, slow-growing mass. Asymptomatic to local tenderness.
Histology: "pseudo-capsule", often a well-circumscribed proliferation of cells that closely resemble the acinar cells (granular, basophilic) of normal salivary gland, microcystic/micropapillary patterns also seen. Tx and prognosis: Wide surgical excision. 35% recurrence, 10-15% metastasis to regional lymph nodes. The 5-yr survival rate is not very meaningful, in the range of 80%. At 10 years, however, this drops to 60%, and at 15 years, 45%. Prognosis better for minor glands. |
|
|
Carcinoma-Ex Pleomorphic Adenoma
|
Clinical: Rare, but related to very common pleomorphic adenoma. 50s-70s. Parotid (80%) and palate. Long-standing, asymptomatic salivary gland mass (the pleomorphic adenoma), suddenly becomes tender/painful. May cause facial paralysis or paresthesia (clinical signs of malignant transformation). Ulceration may occur.
Histology: Residual pleomorphic adenoma with areas of malignant transformation to carcinoma or adenocarcinoma Tx and prognosis: Wide surgical excision. Prognosis depends on the extent of invasion - if invasion less than 6mm from the pleomorphic adenoma, all patients survived. if invasion more than 8mm, all patients died of disease. Overall: 50% of patients suffer recurrence or metastasis. |
|
|
Stevens-Johnson syndrome
|
Oral: hemmorhagic lesions of the lips, labial mucosa, buccal mucosa and tongue. Hemorrhagic crusting of lower labial vermilion is suggestive of E.M.. Oral ulcers are large, widespread with irregular margins. If ocular (conjunctivitis) and genital (urethritis) also present, the condition is termed Stevens-Johnson syndrome (E.M. major).
Skin: "target lesions", annular with central purpura. Histology: characteristic (subepithelial vesiculation, necrotic keratinocytes), but not pathognomonic. IF not helpful |
