Pathology Of Oral Cavity Flashcards
Caries Cause
destruction of tooth structure by acid end products of sugar or fermentation by
bacteria
Gingivitis
reversible inflammation of the mucosa surrounding the teeth
Gingivitis associated with buildup of
dental plaque and calculus
Periodontitis
chronic inflammatory condition that can lead to the destruction of the supporting
structures of the teeth with eventual loss of dentition
Periodontitis associated with
poor oral hygiene and altered oral microbiota.
Aphthous ulcers
Aka
Canker sores
Aphthous ulcers (Canker sores)
superficial mucosal ulcerations painful and often recur
Aphthous ulcers (Canker sores) Cause
unknown cause but tend to be familial
Aphthous ulcers (Canker sores) association wit
celiac disease,
inflammatory bowel disease, and Behçet disease
Aphthous ulcers (Canker sores)
common sites:
inside of lips, tongue, soft palate, gum-lip crease
Aphthous ulcers (Canker sores) Morphology
shallow white/gray sores with a red edge (rimmed by narrow zone of erythema), solitary
or multiple
Normal Tonsils
small and not visible/ prominent
Acute Tonsillitis
Symmetrically enlarged and reddened tonsils
Chronic Tonsillitis
tonsils can be shrunk
asymmetric tonsils can suspect
pharyngeal cancer
Viral
Tonsillitis
adenovirus, rhinovirus, influenza, coronavirus, and respiratory syncytial virus
Bacterial
Tonisilitis
Group A β-hemolytic streptococcus
Diff btw viral and bacterial
viral: swelling, redness
Bacterial: exudate
Infectious mononucleosis
Cause
EPV
Infectious mononucleosis
Sypmtoms
Classic triad:
fever,
pharyngitis,
lymphadenopathy
Infectious mononucleosis
Gross
gray-white exudative membrane
Monospot test?
detects heterophil antibodies caused by EBV
Diphtheria caused by
Corynebacterium diphtheria (C diphtheria) → bacilli
Diphtheria forms
Pseudomembrane in any portion of the respiratory tract
Diphtheria
respiratory failure
Scarlet fever
Caused by ?
Group A β-hemolytic streptococci
Scarlet fever sypmtoms
fever, Pharyngitis, rash, strawberry tongue
Herpes simplex infections (oral)
HSV1 can cause:
oral herpes/ cold sores/ fever blisters( swelling that contains watery fluid)
HSV-1 is usually transmitted by
saliva in childhood
Herpes simplex infections is Self-limited but can becoome latent in
sensory nerve ganglion cells → recurrence if
Triggered by ……
HSV-2 usually causes———, but oral HSV-2 is increasing due to
genital herpes
changing sexual
practices
Primary infection of HSV in children is usually asymptomatic but can manifist as
acute herpetic gingivostomatitis with
abrupt onset of vesicles and ulcerations
Most adults harbor latent HSV-1, and the virus can be reactivated, resulting in
cold sore” or recurrent herpetic stomatitis.
Recurrent lesions appear as
groups of small vesicles,
(The lips (herpes labialis), nasal orifices, buccal mucosa, gingiva, and
hard palate are the most common locations)
The infected cells become?
intranuclear inclusions.
Adjacent cells commonly?
- ballooned and have large eosinophilic
- fuse to form large multinucleated polykaryons.
Herpes simplex infections Microscopy:
molding (blending/fusing nuclei), multinucleated giant cells, inclusion
bodies (cowdry A), ground glass (cowdry B)
Oral candidiasis is known as
thrush
Oral candidiasis
Predisposing factors:
immunosuppression, broad-spectrum antibiotics (alter microbiota
and promote candidiasis)
Clinical forms of oral candidiasis:
pseudomembranous, erythematous, hyperplastic
Pseudomembranous (thrush)
superficial gray to white
inflammatory membrane composed of matted organisms enmeshed in an exudate that
can be scraped off (white spots or patches that can be scraped off)
Oral candidiasis (thrush) Microsco
pseudohyphae / budding
Fibromas
submucosal nodular fibrous tissue masses
Fibromas formed when
chronic irritation results in reactive connective tissue hyperplasia
Fibromas most often on the
buccal mucosa along the bite line
Pyogenic granuloma
inflammatory lesion in gingiva of children, young adults, and pregnant women
(pregnancy tumor),
proliferation of immature vessels
Lesions in Pyogenic granuloma characterized by ?
richly vascular and ulcerated, which gives them a red to purple color
Pyogenic granuloma
may regress, mature into
dense fibrous masses,
peripheral ossifying
fibroma
Premalignant lesions of oral mucosa
Leukoplakia
Erythroplakia
Leukoplakia
white patch in the oral cavity or plaque that cannot be scraped off
Leukoplakia Can be dysplastic and increase risk of
SCC (squamous cell carcinoma)
Leukoplakia Histology
mostly no dysplasia, thick keratin layer
Erythroplakia
red, velvety, eroded lesion that is flat or slightly depressed
Erythroplakia
- risk for malignant
- age/gender
- cause
- histology
- more risk than leukoplakia
- 40-70, male
- multifacgorial (tobacco)
- dysplasia with nuclear and cellular pleomorphism
Squamous cell carcinoma (SCC) Common locations:
tongue, floor of mouth, lower lip, soft palate, gingiva
SCC arise from two distinct pathogenic pathways:
- exposure to carcinogens (chronic alcohol, tobacco (smoked or chewed), betel
quid/paan): cause mutations in TP53 and RAS - infection with high-risk human papilloma virus (HPV-16)
(tumors often overexpress p16, a cyclin-dependent kinase inhibitor )
(HPV-16)
tend to occur
tonsillar crypts or the base of the tongue
Squamous cell carcinoma (SCC)
Microscopy:
hyperkeratinized pearls
SCC morphology
Early cancers: appear as raised, firm, pearly plaques or roughened, verrucous mucosal
thickenings
As lesions enlarge, they form ulcerated protruding masses that have irregular borders
SCC Infiltrates locally then metastasizes to
Sites of distant metastasis:
cervical lymph nodes
lungs, liver
ameloblastoma arise from
odontogenic epithelium.
Autoimmune diseases:
o SLE →
oral ulcers
o Scleroderma →
pursed lips and mask-like facies
o Sjogren syndrome →
fissured tongue
Hematologic
o Iron deficiency anemia →
atrophy and pallor of the mucosa and atrophic glossitis
o Pernicious anemia →
erythema of the tongue (magenta tongue)
o Hematopoietic neoplasms and coagulopathies→
hemorrhages and gingival bleeding
• Systemic infections:
HIV related oral manifestations:
