rank 1 sem 1 Flashcards

1
Q
  1. Chronic hyperplastic gingivitis
A

= hyperplasia due to fibrous connective tissue deposition, not inflammation
a. Tx: 1) Improve OH 2)gingivectomy in extreme case

DDx: drug induced gingival hyperplasia

https://www.msdmanuals.com/en-nz/professional/dental-disorders/periodontal-disorders/gingival-hyperplasia

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2
Q
  1. Drug related gingival hyperplasia
A

= self explanatory
a. Tx: 1) Stop drug 2) improve OH 3) gingivectomy in extreme case

DDX: chronic hyperplastic gingivitis

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3
Q
  1. Pyogenic granuloma
A

= soft, deep red swelling of granulation tissue caused by poor OH or local irritation/trauma
a. Tx: 1) remove irritant/trauma becomes fibrous excise

DDx: Pyogenic granuloma, pregnancy epulis, peripheral giant cell granuloma

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4
Q
  1. Peripheral giant cell granuloma
A

= identical presentation and cause as pyogenic granuloma, but CONTAIN OSTEOCLAST LIKE GIANT CELLS HISTOLOGICALLY – hence cause SLIGHT BONE RESORPT
a. Tx: same as pyogenic granuloma, but excision to TO PERIOSTEUM (this is why you must properly diagnose, or else bone resorption will continue if giant cells aren’t excised)

DDx: pyogenic granuloma

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5
Q
  1. Pregnancy epulis
A

= hormonally induce pyogenic granulomas during pregnancy

a. Tx: what till hormones wanebecome fibrousexcise

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6
Q
  1. Fibroepithelial polyp
A

= healed pyogenic granuloma not located on gingiva
a. Tx: excision

Looks identical to, but you wouldn’t DDx with fibrous epulis, b/c the latter only exists on gingiva

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7
Q
  1. Fibrous epulis
A

= same a a fibroepithelial polyp, but on gingiva

a. Tx: excision

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8
Q
  1. Denture-induced hyperplasia
A

= ill-fitting denture flange
a. Tx: 1) excise 2) fix denture

https://escholarship.org/content/qt99z2d3tc/1.jpg

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9
Q
  1. Inflammatory papillary hyperplasia
A

= ill-fitting denture base

a. Tx: 1) cant really excise all those tiny papules?

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10
Q
  1. Amalgam tattoo
A

= amalgam particles that have penetrated lamina propria and bind connective tissue
a. Tx: 1) can leave no risk 2) if aesthetics concern…. incise

Note: has to have amalgam filling nearby and history of soft tissue trauma during surgery. Otherwise not an amalgam tattoo and DDx include the below, and so you’d have to excise to exclude diagnosis of melanoma

DDX: Acquired melanocytic nevus, amalgam tattoo, Congenital melanocytic nevus, melanocytic macule, melanoma, blue nevus, physiological pigmentation

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11
Q
  1. Acquired melanocytic nevus
A

= benign melanocyte neoplasm very common on skin, but does rarely manifest on hard palate or gingiva
a. Tx: nothing 1/1million chance of malignant transformation

DDx: Acquired melanocytic nevus, amalgam tattoo, Congenital melanocytic nevus

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12
Q
  1. Congenital melanocytic nevus
A

= mole present at birth; benign melanocyte tumor
a. Tx: small – 1%, large 15% chance of malignant transformation  excise large

DDx: Acquired melanocytic nevus, amalgam tattoo, Congenital melanocytic nevus

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13
Q
  1. Blue nevus
A

= blue mole; due to melanocyte dendrites extending deep into lamina propria
a. Tx: Excision – typically appears suddenly and grows fast, so needs to be excised to rule out melanoma

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14
Q
  1. Oral melanotic macule
A

= up-regulation of melanin by normal melanocytes post-trauma (is a macule - i.e. just change in color without elevation or depression
a. Tx: excise to rule out melanoma

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15
Q
  1. Melanoma
A

= melanocytes malignancy (when reading all the types, recall that melanocytes are located in the basal layer of mucosal epithelium, so that’s where the melanoma would always start); Tx for all is Excision with 3mm margin

5 types

a. Lentigo maligna = proliferate, but spread radially along basal layer of mucosal epithelim
i. Lentigo maligna melanoma = lentigo maligna that develops ability to vertical spread into lamina propria
b. Superficial spreading melanoma = melanoma that first vertically invades superficial epithelial layer, and once that’s complete, then starts vertical invasion of structures deep to basal membrane
c. Nodular melanoma = only vertical (HAS THE WORST PROGNOSIS OF THE BUNCH)
d. Acral lentiginous melanoma - ??? FUCK THIS ONE

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16
Q
  1. Physiological pigmentation
A

= self explanatory

a. Tx: n/a

17
Q
  1. Fordyce granules
A

= ectopic sebaceous glands on buccal mucosa or adjacent to vermillion border; TINY YELLOW PAPILLAE (80% of people have it)
a. Tx: n/a

18
Q
  1. Leukoedema
A

= white lesion due to oedemic acanthosis – can tell from leukoplakia b/c stretching the mucosa makes the whiteness disappear

both leukoedema and leukoplakia are diagnoses of exclusion, leukoplakia has worse prognosis i.e. more likely to become malignant, whereas leukoedema has virtually zero likelihood of becoming malignant.

a. Tx: no treatment, very common

19
Q
  1. Candidiasis [1)causes 2)types and presentation of each 3) treatment]
A

– all can occur during 1)AB therapy 2) immunocomp 3) xerostomia (saliva has immune/sterilizing components) – BECAUSE OPPORTUNISTIC INFECITON – but some can occur idiopathically

a. Pseudomembranous candidiasis (aka thrush) = scrapable white slough, dead epithelia
b. Hyperplastic candidiasis aka candida leukoplakia = non-scrapable white plaque
c. Erythematous candidiasis – red macules + burning sensation (specific subtypes below)
1. Acute atrophic - idiopathic (red patch over whole dorsal tongue)
2. Median rhomboid glossitis - idiopathic (red macule at center of dorsal tongue)
3. Angular cheilitis - idiopathic (red patch at angles of mouth)
4. Denture stomatitis – poor OH + maxillary denture (red patch on palate)
d. Tx: Nystatin lozenges, triazoles if nystatin doesn’t resolve

20
Q
  1. Frictional hyperkeratosis
A

= most commonly due to chronic biting or denture rubbing against lateral tongue or buccal mucosa.

a. Linea abla = specifically friction hyperkeratosis of the buccal mucosa, due to biting of mucosa
b. Tx: remove cause of “friction” – i.e. the biting or rubbing

21
Q
  1. White hairy tongue
A

= “hairy” due to lengthening of filiform papillae, and “white” due to hyperkeratosis of filiform papillae; can be caused by anything (antibiotics, candida, OH, mouth rinse i.e. chemical); only on dorsal tongue
a. Tx: remove/treat cause

22
Q
  1. Oral hairy leukoplakia
A

= Opportunistic EBV (HHV4) infection in immunocompromised. “hairy” due to ballooning degeneration and “leukoplakia” due to hyperkeratosis; only lateral tongue whereas white hairy tongue is only dorsal tongue
a. Tx: rest and fluids… it’ll self resolve. If not, antiherpesviral drug

23
Q
  1. Pemphigus vulgaris
A

caused by autoimmune type II hypersensitivity destroying desmosomes causing “shallow blisters” i.e. intraepithelial bulla – since desmosomes connect epithelial cells together, so cavity is created upon destruction

note: rare to just have oral presentation and not the systemic
a. Tx: topical steroids if pemphigus vulgaris/systemic corticosteroids for general pemphigus …. 50-90% chance of becoming fatal IF NOT TREATED WITH STEROIDS!!!

24
Q
  1. Mucus membrane Pemphigoid
A

= caused by autoimmune type II hypersensitivity destroying hemidesmosomes causing “deep blisters” i.e. subepithelial bulla – since hemidesmosomes connect epithelial cells to basement membrane
a. Tx: topical steroids for mucus membrane pemphigoid/systemic corticosteroids for general pemphigoid… general can clear sponanteously 1-2 years, oral wont unless treated… rarely fatal if untreated

25
Q
  1. Erythema multiforme
A

= type III hypersensitivity mediated vasculitis; results in widespread ulcers PRECIPITATED BY INFECTIONS, MOST COMMONLY HSV.
a. Prognosis depends on which severity of disease is observed
NOTE: ALWAYS PRESENTS GLOBALLY NOT EVER JUST ORALLY
i. EM minor – good
ii. SJS syndrome <10% of skin (10% fatal)
iii. Toxic epidermal necrolysis >30% of skin involved (30% fatal)
b. Tx:
i. Minor = soft diet + painkillers
ii. SJS = corticosteroids
iii. TEN = manage in burn unit

26
Q
  1. Allergic contact stomatitis
A

= allergic reaction that’s inflammatory and vesicular (i.e. <5mm blister), located adjacent to cause
a. Tx: identify and remove cause