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ORAL CAVITY and SALIVARY GLANDS PATHOLOGY - Coggle Diagram
ORAL CAVITY and SALIVARY GLANDS PATHOLOGY
normal aspect of oral mucosa
pink, smooth, shiny, thin, transparent
from a histological POV:
stratified squamous epithelium
(superficial non-keratinized epithelium and stratum spinosum)
stratum basale (where cells proliferate)
stroma (rich in blood vessels, connective tissue and fibroblasts)
lesions may occur as a consequence
of epithelial thickening
there is the formation of stratified squamous keratinized tissue, which leads to the formation of white plaques
clinical evaluation
surface lesions
white
epithelial thickening
LICHEN PLANUS
chronic inflammatory AID
white and purple lesions with a cyclic pattern affecting skin and mucosae
association with HCV infection
specific features
lesions are bilateral and symmetrical
reticular pattern
sometimes, other types of lesions (erosive, plaque or atrophy)
all these lesions have the same origin
activation of T cells moving from the stroma of the connective tissue towards the epithelium
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sometimes, "pseudolichen" is described
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diagnosis
histopathological criteria
presence of T cells
basal layer liquefaction
parakeratosis
clinical criteria
symmetrical and bilateral lesions
EPITHELIAL DYSPLASIA
LEUKOPLAKIA
clinical term used to describe white plaques of questionable risk after having excluded other known diseases (e.g. lichen)
these lesions must be monitored to avoid the evolution in carcinioma
more common in middle-aged and elderly males, prevalence increases with age
etiology
tobacco use
alcohol
traumas
lack of hygiene
betel mastication
idiopathic
site
mouth floor
tongue
soft palate
palatine pillars
at inspection and palpation
thin, flat, uniform in colour, sometimes heterogeneous in thickness
surface can be granular, fissured, nodular or verrucous
differential diagnosis
lichen planus, aphtous ulcer and candidiasis
macroscopically: leukoplakia and aphtous ulcer are not removable, while candidiasis is removable; ulcers are very painful, leukoplakia is usually painless
histologically, leukoplakia presents "true" keratinization on the superficial layer, the underlying layer is characterized by dysplastic cellular alterations
ERYTHROPLAKIA
red patch that cannot be characterized clinically or pathologically as another definable lesion, less common than leukoplakia
if white and red plaques are in the same lesions (non-homogeneous pattern), the risk of malignancy is lower than erythroplakia with only red plaques
treatment must be prompt
redness is due to thinning of the epithelium and increase in the number of vessels (dilated due to inflammation)
at inspection
thin, slightly depressed, red patch
HPV infection
it may induce dysplasia in the mouth; the persistent of the lesions can lead to precancerous lesions and then carcinoma
morphological changes
changes in colour (white), size, shape of the cells (fried eggs) and thicker basal layer; a peculiar cell type is called "koilocyte" (large white cytoplasm, large/bi-nuclei)
increasing the dysplasia, the number of layers increases as well with a thickening of the basal layer
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HPV penetrates into the epithelium until it reaches and activates those genes involved in the transport of dysplastic cells
the main protein involved is p16, that inhibits cyclin D1
p16 must be detected to perform a diagnosis!!!
more common serotypes associated with cancer are: HPV 16/18
females: cervix
males: oropharynx
CARCINOMA IN SITU
SQUAMOUS CELL CARCINOMA
HPV-related
men
white
<60y
healthy individuals with no or little tobacco exposure
high socioeconomic status
association with orogenital contact
potential benefit of HPV vaccination
prognosis is favorable:
good response to RT+/-CT
pts with p16- SCC have a higher risk of recurrence if compared to pts with p16+ SCC
HPV-independent
morphology is very similar to SCC HPV-related (p16 staining is performed to confirm the etiology)
the carcinoma invades below the epithelium towards the stroma
etiology
tobacco
alcohol use
site
mouth floor
tongue (lateral/ventral)
posterior buccal mucosa
gingiva/areolar mucosa
histology
squamous cells with a roundish shape, forming a sort of pearl
if this structure is present, the staging is G1 (well-differentiated keratinized)
the absence of this structure shifts the staging from G1 to G3 (poorly-differentiated non-keratinized): atypical cells, mitosis, more aggressive carcinoma
invasive SCC
carcinoma that invades lymphatic vessels, reaching the submandibular lymph nodes, located on the floor of the mouth
if the carcinoma is at the level of the tonsils, the latero-cervical lymph nodes would be affected
prognosis depends on the location of the cancer
for the lip survival is 90% after 5 years
verrucous carcinoma
well-differentiated
non-metastasizing, but contiuous growth
warty keratinized surface
specific architecture
no substantial cytologic features of malignancy
slow lateral spread and push
macroscopy
large cauliflower mass, papillary features, grow slowly, possible overinfection
surface debris
CANDIDOSIS
BURN
subepithelial
CONGENITAL KERATOTIC CYSTS
SCAR
FORDYCLE GRANULES
pigmented
localized
intravascular
HEMANGIOMA
small lesion
continuous growth
two types: capillary (small vessels full of blood) and cavernous (large vessels)
light bluish soft nodule
Blanching effct (anemization under compression)
no need for therapy (sometimes, spontaneous regression)
VARIX
irregular, blue/purple lesions
usually multiple
bilateral linear distribution from the posterior part to the apex of the tongue
adults >60y
possible evolution in fibrotic nodules post-thrombolysis
compressible, Blanching effect + (unless there is a thrombus)
KAPOSI'S SARCOMA
more common in immunodeficient pts
uniformly associated with HHV8 infection
proliferation of irregular vessels
sometimes, multifocal
PYOGENIC GRANULOMA
pregnancy tumor
located between two teeth
reactive lesion
regression after pregnancy
etiology: arterial infections, trauma, hormonal imbalances
histology: expansile granulation tissue mass, well-vasculariazed, chronic inflammation reaction
extravasated blood
HEMATOMA
ECCHYMOSIS
PETECHIAE
melanocytic
ORAL MELANOTIC MACULAE
brown pigmented lesions due to increased levels of melanin within the basal layer and incontinent melanin within the lamina propria
NEVUS
MELANOMA
no Bleaching effect
more frequent than nevi
EPHELIS
tattoo
generalized
HEREDITARY
ADDISON'S DISEASE
due to insufficient corticosteroid levels
inadequate production of cortisol and aldosterone
the pituitary gland responds with an increase in ACTH production, leading to higher amounts of melanin
HEAVY METAL INGETSION
PEUTZ-JEGHER SYNDROME
small lesions of lips and oral cavity
mutation of STK11
associated with: brown small spots on the otal side, hamartomatous intestinal polyps, increased likelihood for the development of malignancies in multiple sites (GIT, breast, thyroid, ovaries, testicles and pancreas)
PREGNANCY
SMOKER'S MELANOSIS
small lesions of lips or oral cavity
result of noxious chemicals in cigarette smoke or heat stimulating melanocytes to protectively produce melanin
DRUG-RELATED DISCOLORATION
frequently associated with hydroxychloroquine use (SLE)
lesions with a bluish staining
symmetric gray/black pigmentation of the posterior hard palate
vesicular, ulcerated, erythematous
HEREDITARY
VIRAL
AUTOIMMUNE
IDIOPATHIC
MYCOTIC
deep lesions
reactive
PARULIS/SINUS TRACK
PERIODONTAL ABSCESS
MUCOCELE
FIBROUS HYPERPLASIA
INFLAMMATORY PAPILLARY HYPERPLASIA
NECROTIZING SIALOMETAPLASIA
tumor/neoplasm
benign
EPITHELIAL
PAPILLOMA
VERRUCA VULGARIS
CONDYLOMA ACUMINATUM
benign form of HPV infection
MESENCHYMAL
FIBROMA
nodular lesion
smooth-walled, covered by normal mucosa
aka irritation fibroma
most of all fibromas represent reactive focal fibrous hyperplasia due to trauma or local irritation
surgical excision
histology: dense collagn tissue little cellular coated with normal mucosa
GRANULAR CELL TUMOR
specific white nodule with a preference for the tongue
also found in young patients
formed by cells with granular cytoplasm
benign tumor, until it does not develop mtastases
cells have a neural origin (S100+)
SALIVARY GLAND
benign lesions
CYSTIC LESIONS
traumatic lesions, transparent, containing fluids
mucocele (retention cyst, minor salivary glands of the lip) or ranula (sublingual glands)
histology: salibary pseudocysts
SIALOLITHIASIS
stones within the main duct of the gland
pstients have salivary colics every time there is mouth watering
saliva cannot exit
dilation of the duct with acute
SIALOADENITIS
the acute form can be due to bacterial or viral etiology
the chronic form can be due to sarcoidosis or Sjogren syndrome
Sjogren syndrome is an AID affecting the epithelium, due to accumulation of lymphocytes into the salivary glands
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tumors
benign
epithelial
PLEOMORPHIC ADENOMA
quite frequent
main sign: big mass in the face
symptoms: dependent on which salivary gland is affected (parotid, minor salivary, palate, etc.)
it may break the nose's bones
it may have satellite nodes (complex surgery)
rare evolution into a malignant form
marco: well-circumscribed, smooth/lobular/irregular borders
cut surface may be brown, chondroid white or gelatinous
cystic changes, hemorrhage, infarction
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WARTHIN TUMOR
(ADENOLYMPHOMA)
aka monomorphic adenoma
soft at palpation (it is cystic), more solid under US
it may have some cystic areas
bilateral
histology: the stroma is completely formed by normal lymphocytes and there are some pink cells (due to granules)
gross appearance: a cystic area with protrusion inside can be seen
tumor removal is easy, with no recurrence
malignant
epithelial
MUCOEPIDERMOID CARCINOMA
it produces mucin and is similar to squamous epithelium of the skin
characterized by a specific translocation: t(11;19)p(q21;p13), expressing CRTC1:MAML2 fusion gene
important for molecular analysis
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ACINAR CELL CARCINOMA
rare, but quite aggressive
3% of pts die after 5y
the histology of acinar and tumor cells is similar (same colours)
inside the cancer, there are granules of saliva (PAS+)
second most common salivary gland malignancy in children
specific translocation: t(4;9)(q13;q31)
macro: greyish, capsulated, solid, microcystic, papillary, follicular
micro: acinic cell like, granular cytoplasm PAS+
ADENOID-CYSTIC CARCINOMA
(CYLINDROMA)
tubuliform tumor
the tumor contains small spaces with PAS+ material and collagen
found in the parotid
most common tumor of the submandibular gland
not capsulated
frequently invading the perineural space
50% survival after 10y (aggressive tumor)
the same tumor may form in the breast
specific translocations: t(6;9) or t(8;9), resulting in MYB::NFIB and MYBL1::NFIB fusions
SECRETORY CARCINOMA
not so frequent
translocation: t(12;15) (p13;q25) resulting in ETV6::NTRK3 fusion (agnostic fusion tumor)
treated with specific anti NTRK drugs (good response)
site: parotid, submandibular
macro: rubbery, tan cut surface, well-circumscribed, not encapsulated, prominent cystic component
micro: lobulated growth pattern separated by fibrous septa, composed of microcystic/solid, tubular, follicular and papillary-cystic structures with distinctive luminal secretions
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cysts
GINGIVAL CYST OF ADULT
LYMPHOEPITHELIAL CYST
EPIDERMOID/DERMOID CYST
THYROGLOSSAL TRACT CYST
malignant
SQUAMOUS CELL CARCINOMA
VERRUCOUS CARCINOMA
LYMPHOMA
METASTATIC CARCINOMA
MELANOMA
SARCOMA
SALIVARY GLAND
ADENOCARCINOMA
NASOPHARYNGEAL TUMOR
(SCHMINCKE)
common in Adrica, because it is associated with EBV; common also in South China among adults; rare in the US
important association with EBV infection
poorly differentiated SCC
good response to RT (1st line therapy)
suspect must arise every time a pt has a single LN growing
--> always perform a FNAB
often, metastases are found in regional LNs
common presentation: unilateral cervical lymphadenopathy
distant metastases may arrive to bones
good prognostic factors: younger age, lower stage, ipsilateral metastases, metastases limited to upper neck, no cranial nerves involvement, orbit or intracranial, non-keratinizing subtype
macroscopy: not identifiable
microscopy: either keratinizing or non-keratinizing (differentiated or undifferentiated)