Pathology of the oral cavity and oropharynx Flashcards
What is an aphthous ulcer?
About a third of the population has these reoccurring, very painful ulcers of unknown etiology. Other features include:
Last for 5-10 days, and then spontaneously resolve
Triggers are very diverse for different people, and they can recur during flares of autoimmune disease
Tend to be located on ‘soft’ mucosa (such as the buccal mucosa, floor of the mouth, inside of lips) rather than on or near hard surfaces (hard palate, gingiva near teeth)
a shallow aphthous ulcer with a hyperemic rim and thin layer of exudate.
Aphthous ulcers are not specific to the oral mucosa, and can be seen in/on other body parts…
Where else can aphthous ulcers be seen?
Aphthous ulcers can be seen on (predominately non-keratinizing) mucosae in many parts of the body (oral cavity, GI tract, anogenital mucosae, etc.) for unknown reasons
Explain herpes virus infection in both children and adults?
These infections are usually due to HSV-1, start in childhood as a primary infection, remain latent for a period of time, and then can undergo periodic or solitary reactivation for poorly understood reasons.
Most children are asymptomatic, but a minority will present with numerous herpetic oral vesicles, fever, lymphadenopathy (acute herpetic gingivostomatitis). Image: Multiple vesicles have burst and become shallow ulcers, involving the tongue, lips and buccal mucosa. Microscopically, virus particles will appear as classic intranuclear inclusions or fusion of multiple infected cells will produce a viral, multinucleated giant cell.
In adults, at or near the location of the primary infection and due to virus living within the local ganglion cells, recurrent herpetic stomatitis can recur. These lesions will typically resolve in 5-10 days on their own. Again, these usually start as small vesicles that burst and produce ulcers on ‘wet’ mucosa, or may remain as crusty blisters on ‘dry’ surfaces (such as typical with herpes labialis on the external surface of the lips).
Most head and neck neoplasia is? lesion appearance?
The vast majority of the neoplasia that arises in the head and neck is of squamous cell origin (with a 5%, small minority being salivary gland neoplasia; see later content). While precursor dysplastic lesions are often flat or plaquelike, fully invasive SCC usually has ulcer either wholly or partially obvious in the macroscopic mass.
Risk factors for invasive squamos cell carcinoma are?
Risk factors include alcohol and tobacco use
Betel leaf/betel quid/paan consumption – leaf of betel vine is often mixed with other nuts, lime, and/or tobacco, and may contain carcinogens
Radiation (such as sunlight) is a risk factor for lip SCC
HPV (typically high risk types, such as HPV-16) is implicated in approximately 70% of SCC in the oropharynx (tonsils, base of tongue, soft palate), but is only uncommonly present in SCC of the oral cavity
Explain HPV’s oncogenic potential?
HPV’s oncogenic potential can largely be demonstrated by the activities of the two viral genes encoding E6 and E7 proteins, which generally have more activity/affinity in action with the high-risk HPV types.
E6 binds to and mediates the degradation of p53, and some polymorphisms in p53 can potentiate this action (see schema below) o p53 loss means less p53-induced cell cycle arrest, less p53-induced senescence, and less p53 routing into apoptosis o Stimulates the expression of TERT, which is the catalytic subunit of telomerase, facilitating immortalization
E7 has several cell cycle properties that promote growth o Binds to RB protein, and promotes progression through cell cycle o Inactivates the CDK inhibitors p21 and p27B o E7 protein from HR HPV’s can bind and presumably activate cyclins E and A
Wegener’s Granulomatosis can lead to what with the nose?
Granulomatosis with polyangiitis (Wegener granulomatosis): necrotizing vasculitis with granulomas, often with lungs or upper airway involvement, glomerulonephritis, and PR3-ANCA +.
Image: ‘saddle-nose’ deformity as granulomatous inflammation and necrosis involves the nasal cavity, destroys the nasal septum, and causes collapse of the nasal bridge.
Mucormycosis infection?
Mucormycosis (AKA: ‘mucor,’ zygomycosis): Members of subphylum Mucoromycotina are ubiquitous in nature and cause opportunistic infections in the lungs, GI tract, and sinonasal region. These organisms are angioinvasive, can cause tissue necrosis, and then invade locally, such as into periorbital tissues and the cranial vault from a sinus location.
rhinocerebral mucor involving a meningeal vessel. Broad, non-septated hyphae with right angle branching (arrow) are characteristic.
Explain candidiasis?
As C. albicans is a component of the normal oral flora, overgrowth can sometimes occur. Often, this will evident as a superficial pseudomembrane, composed of a mat of organisms and inflammatory cells. This is the entity known as thrush, and the membrane can be easily scraped off the mucosal surface. Other less common forms of candidiasis will appear erythematous and/or hyperplastic.
In immunocompetent - oral candidiasis remains superficial/on the mucosal surface
In immunocompromised - oral candidiasis can become deeper in the tissue or disseminate
Explain hairy leukoplakia?
Like oral candidiasis, this process is more severe and evident in immunocompromised patients (such as in HIV patients). This lesion is caused by EBV, and causes hyperkeratotic thickening of the epidermis. This gives the process a slightly vertical, 3D quality, which some describe with adjectives such as corrugated, shaggy, or ‘hairy’ in appearance (image).
Usually occurs on the surfaces of the tongue, particularly the lateral surfaces
Cannot be scraped off (vs. candidiasis)
When seen in immunosuppression, may indicate a more severe disease course or that current anti-viral therapies are waning in effectiveness
White leukoplakia?
When we use the word leukoplakia clinically, the spirit of its first usage is the following: a plaque-like lesion is now being seen and the possibility of neoplasia is now present, but the actual presence of neoplasia will still need to be evaluated. Said another way, dysplasia or invasive SCC is suspected, and will need to be ruled out.
A white patch (2D) or plaque (3D), solitary or multiple, seen anywhere in the oral cavity or oropharynx, and may appear wrinkled, smooth, creased, thickened, etc.
Risk factors are similar to invasive SCC (above), particularly if dysplasia is present
Dysplasia is assumed to be present (only 10-25% of cases), until disproven by biopsy
(Note leukoplakia can be seen elsewhere: esophagus, bladder, anogenital regions)
A minority of cases will evolve into invasive SCC
Erythroplakia?
In contrast to (white) leukoplakia, (red) erythroplakia is a similar process, but is much more likely (90% of cases) to show squamous cell dysplasia, particularly of the high-grade/severe/CIS type. It’s often present as a red patch (2D), as seen in the submitted image.
What is a fibroma?
These are exaggerations of wound healing, whereby a reactive proliferation of fibrous tissue is occurring in a region that is being chronically irritated or traumatized. Histologically, stroma and new collagen will be seen in these lesions.
Usually occur along the gingiva (as in image), or on the buccal mucosa along the bite line
Surgical excision is curative
What are pyogenic granulomas?
These are exaggerations of granulation tissue, and as such, can grow rapidly, can regress, or can organize/mature into a fibrotic nodule (which may appear similar to a fibroma above).
Etiology is not well understood (possibly irritation, trauma, or hormonal)
Children, young adults, and pregnant women (‘tumor of pregnancy’)
Gingival location is most common, but also tongue and nasal cavity (can occur on external keratinized surfaces as well, such as on the digits, scalp, etc)
explain the images?
Left image: a pyogenic granuloma of the tongue, appearing somewhat red and hemorrhagic.
Right image: classic appearing granulation tissue, with many new vessels and abundant inflammatory cells, consisting of neutrophils mostly.
Note: this lesion is neither ‘pyogenic’ (pus-forming) nor a ‘granuloma’ (granulomatous inflammation, which shan’t be confused with granulation tissue). Discuss with friends.
What does the image show?
massive duct expansion with mucoid material; arrow at duct connection with salivary glands; overlying mucosa on very left shows vascular congestion, which likely imparts the bluish color to the clinical mass.
explain the image?
As the name implies, there is papillary growth, present as fingerlike extensions of epithelial proliferation (due to HPV effect on the cell cycle). This image is showing the exophytic growth pattern; the inverted growth pattern would just be the fingerlike, papillomatous growth reversed in direction and growing ‘into’ the underlying stroma.
Explain the image?
Image: squamous cell atypia evident as HPVinduced koilocytic change. Koilocytes are (usually) superficial keratinocytes with shrunken nuclei (so-called ‘raisinoid’ nuclei) and obvious, perinuclear clearing around them. These changes are typical with HPV infection of any squamous mucosa (cervix, vagina, anal canal, larynx, urethra, etc.).
Explain this image? what are other subtypes?
The histology of nasopharyngeal carcinoma can vary, but the more aggressive subtype is seen in this image. It resembles an undifferentiated carcinoma, and consists of vaguely epithelioid, larger tumor cells with pale cytoplasm. Mixed in are abundant smaller lymphocytes, and sometimes the lymphocytes will be so numerous the tumor may resemble a lymphoma. This subtype has been confusingly labeled a lymphoepithelioma in the past. Other subtypes:
Keratizing type: epithelioid tumor cells that produce obvious keratin; scant lymphocytes; poor 5 year survival at about 20%
Non-keratizing type: scant lymphocytes and tumor cells that don’t produce keratin; good 5 year survival at 80-90%
What do the images show?
Right image: a partially solid and partially cystic, hemorrhagic encapsulated mass is arising within the lobulated substance of the parotid gland.
Left image: purposely low power to show the papillary-like proliferation of Warthin tumor. The tumor arranges itself with a distinct bilayer of pink, epithelial tumor cells around the periphery of the papillary projections, with lymphocytes filling the papillary centers. Abundant lymphoid germinal centers can also form (remember the relative lack of lymphocytes in a normal salivary gland). Because of these distinct features, another name for a Warthin tumor is papillary cystadenoma lymphomatosum – features evident to some degree in these images.
Explain the images?
Right image: An encapsulated mass largely replacing the salivary gland of origin. Note the pearly, opaque regions that are present (arrows), which likely represent cartilage differentiation.
Left image: PA’s have diverse histology, and most of the cells centrally are the epithelial component. Notice the loose fibromyxoid connective tissue on the left (right arrow) and the poorly-formed cartilage at the bottom center (down arrow).
