Pathology Of Oral Cavity

Question 1

Caries Cause

Answer 1

destruction of tooth structure by acid end products of sugar or fermentation by
bacteria

Question 2

Gingivitis

Answer 2

reversible inflammation of the mucosa surrounding the teeth

Question 3

Gingivitis associated with buildup of

Answer 3

dental plaque and calculus

Question 4

Periodontitis

Answer 4

chronic inflammatory condition that can lead to the destruction of the supporting
structures of the teeth with eventual loss of dentition

Question 5

Periodontitis associated with

Answer 5

poor oral hygiene and altered oral microbiota.

Question 6

Aphthous ulcers

Aka

Answer 6

Canker sores

Question 7

Aphthous ulcers (Canker sores)

Answer 7

superficial mucosal ulcerations painful and often recur

Question 8

Aphthous ulcers (Canker sores)
Cause

Answer 8

unknown cause but tend to be familial

Question 9

Aphthous ulcers (Canker sores) association wit

Answer 9

celiac disease,

inflammatory bowel disease, and Behçet disease

Question 10

Aphthous ulcers (Canker sores)

common sites:

Answer 10

inside of lips, tongue, soft palate, gum-lip crease

Question 11

Aphthous ulcers (Canker sores)
Morphology

Answer 11

shallow white/gray sores with a red edge (rimmed by narrow zone of erythema), solitary
or multiple

Question 12

Normal Tonsils

Answer 12

small and not visible/ prominent

Question 13

Acute Tonsillitis

Answer 13

Symmetrically enlarged and reddened tonsils

Question 14

Chronic Tonsillitis

Answer 14

tonsils can be shrunk

Question 15

asymmetric tonsils can suspect

Answer 15

pharyngeal cancer

Question 16

Viral

Tonsillitis

Answer 16

adenovirus, 
rhinovirus, 
influenza, 
coronavirus, and 
respiratory syncytial virus

Question 17

Bacterial

Tonisilitis

Answer 17

Group A β-hemolytic streptococcus

Question 18

Diff btw viral and bacterial

Answer 18

viral: swelling, redness
Bacterial: exudate

Question 19

Infectious mononucleosis

Cause

Answer 19

EPV

Question 20

Infectious mononucleosis

Sypmtoms

Answer 20

Classic triad:
fever,
pharyngitis,
lymphadenopathy

Question 21

Infectious mononucleosis

Gross

Answer 21

gray-white exudative membrane

Question 22

Monospot test?

Answer 22

detects heterophil antibodies caused by EBV

Question 23

Diphtheria caused by

Answer 23

Corynebacterium diphtheria (C diphtheria) → bacilli

Question 24

Diphtheria forms

Answer 24

Pseudomembrane in any portion of the respiratory tract

Question 25

Diphtheria

Answer 25

respiratory failure

Question 26

Scarlet fever | Caused by ?

Answer 26

Group A β-hemolytic streptococci

Question 27

Scarlet fever sypmtoms

Answer 27

fever, Pharyngitis, rash, strawberry tongue

Question 28

Herpes simplex infections (oral) | HSV1 can cause:

Answer 28

oral herpes/ cold sores/ fever blisters( swelling that contains watery fluid)

Question 29

HSV-1 is usually transmitted by

Answer 29

saliva in childhood

Question 30

Herpes simplex infections is Self-limited but can becoome latent in

Answer 30

sensory nerve ganglion cells → recurrence if | Triggered by ……

Question 31

HSV-2 usually causes———, but oral HSV-2 is increasing due to

Answer 31

genital herpes changing sexual practices

Question 32

Primary infection of HSV in children is usually asymptomatic but can manifist as

Answer 32

acute herpetic gingivostomatitis with | abrupt onset of vesicles and ulcerations

Question 33

Most adults harbor latent HSV-1, and the virus can be reactivated, resulting in

Answer 33

cold sore” or recurrent herpetic stomatitis.

Question 34

Recurrent lesions appear as

Answer 34

groups of small vesicles, (The lips (herpes labialis), nasal orifices, buccal mucosa, gingiva, and hard palate are the most common locations)

Question 35

The infected cells become? intranuclear inclusions. Adjacent cells commonly?

Answer 35

- ballooned and have large eosinophilic | - fuse to form large multinucleated polykaryons.

Question 36

Herpes simplex infections Microscopy:

Answer 36

molding (blending/fusing nuclei), multinucleated giant cells, inclusion bodies (cowdry A), ground glass (cowdry B)

Question 37

Oral candidiasis is known as

Answer 37

thrush

Question 38

Oral candidiasis | Predisposing factors:

Answer 38

immunosuppression, broad-spectrum antibiotics (alter microbiota and promote candidiasis)

Question 39

Clinical forms of oral candidiasis:

Answer 39

pseudomembranous, erythematous, hyperplastic

Question 40

Pseudomembranous (thrush)

Answer 40

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)

Question 41

``` Oral candidiasis (thrush) Microsco ```

Answer 41

pseudohyphae / budding

Question 42

Fibromas

Answer 42

submucosal nodular fibrous tissue masses

Question 43

Fibromas formed when

Answer 43

chronic irritation results in reactive connective tissue hyperplasia

Question 44

Fibromas most often on the

Answer 44

buccal mucosa along the bite line

Question 45

Pyogenic granuloma

Answer 45

inflammatory lesion in gingiva of children, young adults, and pregnant women (pregnancy tumor), proliferation of immature vessels

Question 46

Lesions in Pyogenic granuloma characterized by ?

Answer 46

richly vascular and ulcerated, which gives them a red to purple color

Question 47

Pyogenic granuloma may regress, mature into

Answer 47

dense fibrous masses, peripheral ossifying fibroma

Question 48

Premalignant lesions of oral mucosa

Answer 48

Leukoplakia Erythroplakia

Question 49

Leukoplakia

Answer 49

white patch in the oral cavity or plaque that cannot be scraped off

Question 50

Leukoplakia Can be dysplastic and increase risk of

Answer 50

SCC (squamous cell carcinoma)

Question 51

Leukoplakia Histology

Answer 51

mostly no dysplasia, thick keratin layer

Question 52

Erythroplakia

Answer 52

red, velvety, eroded lesion that is flat or slightly depressed

Question 53

Erythroplakia - risk for malignant - age/gender - cause - histology

Answer 53

- more risk than leukoplakia - 40-70, male - multifacgorial (tobacco) - dysplasia with nuclear and cellular pleomorphism

Question 54

Squamous cell carcinoma (SCC) Common locations:

Answer 54

tongue, floor of mouth, lower lip, soft palate, gingiva

Question 55

SCC arise from two distinct pathogenic pathways:

Answer 55

1. exposure to carcinogens (chronic alcohol, tobacco (smoked or chewed), betel quid/paan): cause mutations in TP53 and RAS 2. infection with high-risk human papilloma virus (HPV-16) (tumors often overexpress p16, a cyclin-dependent kinase inhibitor )

Question 56

(HPV-16) tend to occur

Answer 56

tonsillar crypts or the base of the tongue

Question 57

Squamous cell carcinoma (SCC) Microscopy:

Answer 57

hyperkeratinized pearls

Question 58

SCC morphology

Answer 58

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

Question 59

SCC Infiltrates locally then metastasizes to Sites of distant metastasis:

Answer 59

cervical lymph nodes | lungs, liver

Question 60

ameloblastoma arise from

Answer 60

odontogenic epithelium.

Question 61

Autoimmune diseases: | o SLE →

Answer 61

oral ulcers

Question 62

o Scleroderma →

Answer 62

pursed lips and mask-like facies

Question 63

o Sjogren syndrome →

Answer 63

fissured tongue

Question 64

Hematologic o Iron deficiency anemia →

Answer 64

atrophy and pallor of the mucosa and atrophic glossitis

Question 65

o Pernicious anemia →

Answer 65

erythema of the tongue (magenta tongue)

Question 66

o Hematopoietic neoplasms and coagulopathies→

Answer 66

hemorrhages and gingival bleeding

Question 67

• Systemic infections: HIV related oral manifestations: