Can occur in both minor and major salivary glands

• MC site is parotid gland
• 80% occur in superficial lobe
• Variety of histological subtypes
• In the minor glands the MC location is the palate (50%) followed by the upper lip (20%). The lower lip is the least common site (1%)
• F>M
• Blacks > Whites
• MC in 30-60 but can occur at any age
• Generally painless, slow growing, submucosa, firm lump
• If the tumor present on the hard palate the tumor is off midline
• If the tumor is present in the parotid gland it is in front of or below ear or a pharyngeal mass if from the deep lobe.
• Very hard to determine benign vs. malignant clinically and histologically
• Malignant tmors are often slow growing and may appear encapsulated, well-demarcated and histologically well-differentiated with no evidence of hyperchromatism, pleomorphism, or mitotic activity
• Benign tumors may show infiltrativeness and pleomorphism
• If the following are present is suggests malignant tumor:
• Fixed to underlying structures
• Not applicable to hard palate where it is bound to the mucosa does not allow movement of even benign neoplasm
• Ulveration or injection (vascularity) of surface
• Pain or facial paralysis in parotid gland
• Rapid growth

• Parotid Gland: 75-80% are benign
• Treatment of both benign and malignant is superifical lobectomy because of the high recurrence of benign lesions when treated less aggressivel and because most malignant parotid tumors are curable by this means and because of the embedded facial nerve complications second surgeries
• Upper lip: 75-80% are benign
• Submandibular Gland: 40% malignancy
• Sublingual Gland: 80% malignancy
• Palate: 50% malignancy
• Buccal: 50% malignancy
• Lower Lip: 70% Malignancy
• Tongue: 85-90% Malignancy
• Floor of mouth: 85-90% Malignancy
• Retromolar: 85-90% Malignancy
• Submaxillary treatment-removal of the entire gland

Classification of Bengin Salivary Gland Neoplasms

In order of most common

1. Benign mixed tumors (pleomorphic adenoma)
2. Warthin's tumor (Papillary cystademona lymphomatosum)
3. Canicular adenoma
4. Oxiphil adenoma (oncocytoma)

Classification of Malignany Salivary Gland Neoplasms

In order of most common

1. Mucoepidermoid Tumor
2. Adenoid Cystic Carcinoma (cylindroma)
3. Acinic Cell Carcinoma
4. Malignant Mixed Tumor
5. Polymorphous low grade adenocarcinoma (lobular carcinoma)

• Most common neoplasm-70%
• Parotid, palate, upper lip are most common sites
• Origin from intercalated duct + myoepithelial cells
• Variable histology showing ducts, cysts, sheets of basaloid, squamoid or spindle cells, hyaline, mucin, and myxoid areas, chondroidm bone.
• Easy to misdiagnose on frozen section or needle biopsy
• Not truly mixed bc it arises from 1 germ layer.  The chondroid, myxoid, or bone is a myoepithelial or metaplastic stromal product
• Slow growing, benign but presistent and potentially agressive neoplasm
• Tumor buds penetrate capsule, high recurrence if shelled out, less os in minor glands
• 5% undergo malignant transformation

• 6% of benign salivary gland neoplasms
• Develops within the periparotid lymph nodes from entrapped ductal epithelium
• 80% in males- mostly cigarette smokers
• 8% bilateral or multiple unilateral primaries
• Histology: papillary fronds lined by double row of columnar oncocytic cells resting on a non-neoplastic resident lymphoid stroma with germinal centers. The fronds project into a cystic space.
• No recurrence
• No malignant transformation
• Limited growth potential

• Mostly upper lip
• Benign
• Origin from ductal cells
• Forms thin layers and ribbons of columnar ductal lining cells with considerable loose, edematous and vascular intervening stroma
• May show a cribiform pattern and resemble adenoid cystic carcinoma histologically
• Slow growthm freely moveable and encapsulated, low recurrence

• Mostly parotid
• Benign
• MC Elderly females
• Composed of oncocytes (large pink polygonal cells) in sheets, ducts and/or ribbons
•  Never get to large
• Low recurrence or malignant potential

• Malignant
• MC parotid cancer. Palate and retromolar pad common intraoral sites
• Origin within excretory ducts
• Histology: infiltrating nests and lobules containing admixtures of squamous cells, mucous cells, and intermediate (clear) cells
• Low Grade: Predominantly cystic and well differentiated with mucouscells preponderance
• High Grade: Tumors are solid, poorly differentiated and have more intermediate and squamous cells.
• Low Grade tumors are more common and rarely metastasize and when they do they may require up to 20 yrs to manifest symptoms
• Most are slow growing but infiltrative and have a high recurrence rate.
• 5 year survival Rate:
• High Grade: 50%
• Low Grade: 92%
• 15 year survival rate remains high in low grade tumors but is 0-20% in high grade tumors
• May clinically resemble mucocele bc of soft systic composition
• "Beware of mucoceles in unusual sites like retromolar pads"
• MC salivary tumor to arise as a primary within bone, usually within a dentigerous cyst. Produces a multilocular posterior mandibular radiolucency

• Common intraoral salivary malignancy-especially palate.  Infrequent in parotid. MC malignany in submandibular gland
• Called "Wolf in Sheep's Clothing"
• Slow growing
• Histologically benign looking
• Devastatingly infiltratice
• Presistent recurrences
• Blood borne metastases up til 20 yrs
• Rarely involved lymph nodes
• Histology shows a cribidorm or "swiss cheese" pattern of monotonous basaloid cells compartmentalized into ovoid cylinders by hyalinized pink material. Histogenesis from ductal and myoepithelial cells
• Extensive perineural and intraneural invasion. Infilratice tumor nests run along nerves for a great distance from main tumor mass
• Clinically causes early pain and, in parotid, facial nerve paralysis
• Treatment demands wide excision including extension up nerve trunks. Neck dissection unecessary bc tumor does not invovle nodes
• Intraoral and submaxiallry examples have poorer survival than parotid tumors.
• 5 year survival rate of 70% and 15 year survival rate of 20%

• Slow growing, pseudoencapsulated, lobulated tumor
• Most parotid
• Tumor cells resemble packed serous acini
• Looks benign-but is malignant
• May feature clear cells
• Wide excision necessary to prevent recurrences
• Blood borne mets may occur and often take many years to produc symptoms
• Prognosis 70-85% (survival rate?)
• Histologic appearance is not a good indication of which tumors act agressively

• Cytologically benign mixed tumor that metastasizes
• Cytologically malignant tumor producing chondroid, hyaline, myxoid matrix etc. (carcinosarcoma)
• A benign mixed tumor which undergoes a focus of malignant degeneration. The malignant portion may be any type of carcinoma already discussed or squamous cell carcinoma or non-specific adenocarcinoma (carcinoma ex mixed tumor)
• MC
• Occurs in mixed sumors that were previously surgerized, radiated or present 10-15 yr
• Typical history of a slow growing timor for years that takes a sudden growth spurt marked by pain, ulceration and fixation
• 5 year survival rate: 50%
• 15 year survival rate: 20%
• Distant metastasis is usual

Polymorphous Low Grade Adenocarcinoma

Lobular Carcinoma

Termal Duct Carcinoma

• MC palate
• F>M
• Malignant
• Characterized by slow growth mimicking a benign tumor
• Origin from proximal (terminal) portion of interlobular duct
• Non-encapsulated, infiltratice
• Pattern of small, closely packed well-differentiated glandular or ductal cells in center of tumor showing polymorphous growth (nests, cords, solid sheets, cystic spaces, or cribiform pattern) but infiltrative pattern at periphery showing a linear, single file "Indian file" arrangement
• Shows perineural invasion
• Occasional recurrences, low metastatic incidence, few fatalities

1. Parotid hemangioma MC
2. Benign mixed tumor MC epithelail glandular tumor
3. Mucoepidermoid tumor MC malignant tumor

• Tender swelling of palate followed in 2-3 weeks by tissue necrosis resulting in a non-indurated crateriform ulcer which heals in 6 weeks
• Believed to represent a local vascular insult leading to ischemic infarction of salivary gland tissue
• Signidicance and differentail diagnosis resembles squamous cell carcinoma or mucoepidermoid carcinoma histologically but not clinically
• SCC are on palate and usually indurated
• Mucoepidermoid is slow-growing and rarely ulcerates

80% of population contact virus → 1° infection is asymptomatic (60% of population never get herpetic lesion, 40% get 2° herpes)

↓

1% get acute gingivostomatitis as 1° infection

↓

50% of infected peopel get periodic outbreaks of 2° herpes

↓

99% with herpes labialis OR 1% wtih 2° intraoral herpes

20% of people never contact herpes

• Acute, Febrile disease with malaise and cervical adenopathy
• Generalized vesicles and ulcers in mouth that are 3-7 mm
• Acute hemorrhagic gingivitis
• Resolves in 2 weeks
• Does not return
• Occurs mostly in children and young adults  

• AKA cold sores, fever blisters
• 2° HSV-1 infection
• Latent virus in trigeminal ganglion is reactived by
• Colds
• Fevers
• Sun
• Trauma
• Stress
• Menstral Periods
• Cause localized tingling and swelling followed by a crop of vesicles on lip  
• Infection is contained because of prior antibodies
• No fever
• No adenopathy
• Vesicles break, ulcers crust and heal in 2 weeks
• All ages are affected

• Periodic crops of vesicles/ulcers on gingiva/hard palate induvced by:
• Fevers
• Colds
• Stress
• Trauma
• Dental Work 

• Coxsackie Virus
• MC in children and young adults
• Acute outbreak of vesicles and ulcers throughout mouth accompanied by viral constitutional symptoms and cervical adenopathy 
• Concomitant lesions on hands, feet, and buttocks
• Resolved and does not recur
• Resembles 1° herpes but:
• Lacks gingivitis
• Has digital lesions  

• Coxsackie Virus
• Acute, febrile disease with small vesicles and ulcers
• Vesicles and ulcers are limited to the soft palate and pharynx 

ANUG

Anaerobic, acute fusospirochetal gingivitis of young adults

• Unhygienic mouth (plaque and calculus) predisposes and stress or debilitation triggers the disease
• Anterior gingiva are painful and swillen with punched out necrotic ulcers of gingival papillae
• Foul odor
• Sialorrhea
• Fever
• Malaise
• Lymphadenopathy
• Differentiated from primary herpes:
• Necrosis of papillae
• Absence of other oral vesicles or ulcers
• Not Expected to be seen in children
• Treatment: Antibiotics and dental prophylaxis 

• Erythema multiforme affecting the mouth, eyes, skin, and genital mucosa
• Cytotoxic T cell mediated, type IV delayed hypersensitivity reaction to:
• Recent herpes outbreak
• URI
• Medications
• Lymphoma 
• MC in young adult males
• Seasonal recurrences in spring and fall
• Acute onset of debilitating, confluent oral ulcers producing bloody, crusted lips
• Typically spares the gingica
• Skin lesions are red macules, papules, blisters, and target lesions of palms and soles
• Resolves in 1 month
• Differentiation from primary herpes:
•  Spares gingiva
• Confluent slough
• Skin and other mucosal lesions
• Treatment: steroids

• Stomach ulcers
• Canker Sores
• Disease of unknown etology-hypersensitivity is suspected
• Affects 20% of population
• Small, round to oval, painful ulcers on mucosa not bound to bone
• Spares external lips, gingiva, and hard palate
• Recur in response to trauma, illness, GI problem, stress, and mestrual periods
• Heal in 7-10 days
• Dos not affect smokers
• Similarity to secondary herpes:
• Small
• Painful
• Recurrent ulcers that heal in 7-10 days
• Differentiation from secondary herpes
• Different location
• Never forms vesicles
• Treatment-steroids

• Mucocutaneous immune-mediated disease in which there is a T cell response to basal cells
• Sometimes induced by medications (lichenoid drug reaction)
• Skin and oral lesions are seldom present together
• Occurs in 2% of women > 40 yrs
• Chronic lesion that wax and wane, may burn
• Lacy white striae of buccal mucosa sometimes with atrophic red background
• Diffuse, red, shiny, atrophic, burning gingiva
• Large, soft, well-demarcated serpiginous yellow ulcers on red/white background
• Atrophic, bald plaque like white dorsal tongue
• Skin lesions when present are pruitic plaques on wrists and ankles
• Histology:
• Hyperkeratosis
• Band like lymphocytes infiltrate that hugs the basal layer
• Liquefaction of basal cells
• Saw-toothing of rete ridges
• Exocytosis
• Treatment: Topical or systemic steroids for symptomatic lesions

• Autoimmune disease in which autoantibodies are directed against the basement membrane
• Subepithelial vesicles
• Less ommon than lichen planus and seen in women> 40yrs
• Chronic lesions that wax and wane, cause a raw bruning sensation
• Mucosal blisters/bulla that slough
• Peeling, raw, atrophic, shiny, burning gingiva-mimicks gingival lichen planus
• Other mucosal lesions may be present (conjunctival and genital), can heal with scarring
• Treatment: Topical or systemic steroids  

Geographic Tongue

Benign Migratory Glossitis

• Unknown etiology
• Periodically appears on tongue and remits spontaneously
• 2% of pop at any given time
• Appears as red, depapillated blotches surrounded by an elevated, yellow-white C-shaped border.  
• Asymptomatic or causes burning
• Migrates over a period of a few weeks then remits
• May be stress related

• Opportunistic infection secondary to antibiotics, steroids, diabetes, HIV, antineoplastic therapy, and other immunocompromised states, and local conditions such as xerostomia or irritating dentures
• White plaques which when scraped off leave raw, red, mucosa
• Diagnosis- cytologic smear stained with PAS, KOH prep
• Treatment- antifungal and determine cause  

• White fissured lesion in area where smokless tobacco is held
• NOT histologically premalignant but can slowly evolve into malignancy after 20-30 yrs of tobacco application
• Reversible with quitting early 

• Diffuse white lesion across hard palate studded with raised bumps having red centers
• Due to HEAT of pipe smoke
• NOT premalignant 

Dysplasia

Carcinoma in situ

• Seen in long term tobacco users especially those that abuse ethanol
• Chronic sun exposure for lower lip dysplasia (actinic cheilitis
• MC on lower vermillion, lateral tongue, ventral tongue, floor of mouth, soft palate
• Less common on buccal mucosa and gingiva
• Rarely on hard palate, dorsal tongue, lip mucosa, upper vermillion
• Appears as a non-descript white, speckled red-white, or red patch.  Any size or color intensity
• Potentially reversible
• Many of these PREMALIGNANT lesions evolve into indurated, fixed SCC over a period of months to years
• Rule of thumb:
• If a non-descript white, red, or speckled mucosal patch is present fcor 2 + weeks without ovbious cause or attribution to some specific disease AND is in a high risk location for oral cancer get a biopsy!

• 21,000 new cases a year with 6,000 annual deaths
• Etiology: tobacco, alcohol, chronic oral atrophy
• MC in Males > 40 yrs
• Location same as dysplasia/CIS
• Most cases develop in long-standing dysplastic lesions
• Changes from mucosal patch to an elevated, ulcerated red/white mass with indurated,raised borders and fixation to underlying tissue.
• Spreads to cervical nodes
• Kills by extension and neck mets rather than distant mets
• Painless until advanced
• Treatment: Surgery, often debilitating, radiotherapy, adjunctive chemotherapy
• Prognosis: Stage is most important
• Histologic grade less so
• Location: The more anterior the better the prognosis
• Stage I cancer: 85% curable
• Stage IV cancer: 9% 5 year survival rate
• Lip Cancer is more curable than Foor of mouth which is more curable than base of tongue cancer

• Candida-widespread, severe
• Offer clues to undiagnosed HIV infection
• Large ulcers-HSV, CMV, aphthous ulcers
• HIV-P-ANUG with rapid bone destruction
• Hairy leukoplakia-hairy, white, keratinized extensions from lateral tongue, bilaterally (EBV)
• Offers clues to undiagnosed HIV infection
• Kaposi sarcoma- red purple macules, plaques and tumors of gingiva and palate