Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Module 7 Exam > Oral pathology/medicine/periodontology > Flashcards

Oral pathology/medicine/periodontology Flashcards

1
Q

How thin are the sections cut of the tissue embedded in wax?

A

Microtome used to cut sections of 4um thickness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the three most common stain types?

A
  1. Haematoxylin and Eosin (H&E) routinely used
  2. Special histochemical stains e.g. Periodic Acid - Schiff (PAS), Trichromes, Gram
  3. Immunohistochemistry - antibodies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Hyperplasia vs hypertrophy

A

Hyper = increase

Plasia —> number of cells increased
Trophy —> size of cells increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Metaplasia

A

Reversible change in which one adult cell type is replaced by another adult cell type

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Hyperkeratosis

A

Thickening of the stratum corneum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Ulceration

A

Mucosal/skin defect with complete loss of surface epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

White lesions: developmental

A

fordyce granules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

White lesion: normal variation

A

Leukoedema (stretch mucosa and it should disappear)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

White lesions: Hereditary

A

White sponge naevus, Pachyonchia congenita, Dyskeratosis congenita

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q
A

White sponge naevus

no tx required - thickened epithelium with marked hyperparakeratosis (mutation in keratin)
“basket weave” appearance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q
A

Pachyonchia congenita (genetic keratin mutation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q
A

Dyskeratosis congenita (genetic keratin mutation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q
A

Lichen planus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q
A

Lupus erthematosus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q
A

Leukoplakia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q
A

Leukoplakia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What causes Oral Hairy Leukoplakia?

A

Epstein-Barr virus (strongly associated with HIV infection in many cases)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q
A

oral hairy leukoplakia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the key pathological features of oral hairy leukoplakia?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Tx of oral hairy leukoplakia

A

none needed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Histopathology of frictional keratosis

A

hyperkeratosis

prominent scarring fibrosis within submucosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Lichen planus description

A

Common chronic inflammatory disease of skin and mucous membranes —> if effected by skin lesions then 50% chance of having oral lesions too.

Aetiology unknown

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the clinical features of lichen planus?

A

Bilateral and often symmetrical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the pathogenesis of lichen planus?

A

T cell-mediated immunological damage to the basal cells of the epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Histopathology of lichen planus

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What’s important to remember about the histopathology of lichen planus?

A

It is similar to lichenoid reaction to drugs, lupus erythematosus, etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Management of lichen planus

A

manage symptoms - steriods occasionally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

OMPD

A

Oral Potentially Malignant Disorder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are some OPMDs?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Leukoplakia

A

white patch with questionable risk

LOW risk of malignant change

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Proliferative Verrucous Leukoplakia

A

white patch with HIGH risk of progression to SCC

begins as a simple hyperkeratosis that in time becomes exophytic and wart-like

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q
A

Median Rhomboid Glossitis

midline red patch
unknown - often associated w candida

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Histopathology of median rhomboid glossitis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Treatment of median rhomboid glossitis

A

anti fungal medication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q
A

Erythroplakia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q
A

Erythroleukoplakia (speckled leukoplakia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Cause of black hair tongue?

A

Papillary hyperplasia + overgrowth of pigment-producing bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q
A

melanotic macule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Histopathology of melanotic macule

A

NOT an increased number of melanocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q
A

Melanoma - malignancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q
A

Melanotic Neuroectodermal Tumour of Infancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q
A

Left - aphthous ulcer

Right - traumatic ulcer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

How can you differentiate between aphthous ulcer and traumatic ulcer?

A

Clinically - NOT histopathologically

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Histopathology of ulcers

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Histopathology of ulcers

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Blister vs bulla

A

when the blister is greater than 10mm = bulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Vesicles/bullae can be…(2)

A

1.Intrapithelial
2. Subepithelial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What are the two types of intraepithelial vesicles?

A

Non-acantholytic (death and rupture of cells)

Acantholytic (desmosomal breakdown)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Herpes simplex virus in primary herpetic stomatitis and herpes labialis is an example of what type of vesicle?

A

Intraepithelial non-acantholytic (CELL DEATH)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Pemphigus (and Pemphigus vulgaris) are caused by an autoimmune disease resulting in what type of vesicles?

A

Intraepithelial acantholytic (desmosomal breakdown)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Treatment of pemphigus vulgaris

A

steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Histopathology of pemphigus vulgaris

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Histopathological examination of pemphigus vulgaris

A

Direct immunofluorescene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q
A

Mucous membrane pemphigoid (subepithelial vescicles)

Autoimmune disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Histopathology of mucous membrane pemphigoid

A

Direct immunofluorescene investigation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q
A

Epidermolysis Bullosa Acquisita (uncommon, autoimmune blistering dermatitis with subepithelial bullae)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q
A

Epidermolysis Bullosa

(formation of skin bullae which heal with scarring 3 variants; simplex, junctional and dystrophic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q
A

Angina bullosa haemorrhagica

(spontaneous blood-filled bullae, bursts to form ulcers and heal uneventfully - secondary to trauma??)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Oral submucous fibrosis

A

an oral potentially malignant disorder —> HIGH risk of malignant transformation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

WHO 2024 classification of epithelial dysplasia

A

Oral epithelial dysplasia (OED) is a spectrum of
architectural and cytological epithelial changes resulting from accumulation of genetic alterations, usually arising in a range of oral potentially malignant disorders (OPMD) and indicating a risk of malignant transformation to squamous cell carcinoma (SCC).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Histological features of epithelial dysplasia p

A
  1. funky shapes and sizes of cells and nuclei (pleomorphism)
  2. Nucleus getting bigger inside the cell (nuclei-cytoplasmic ratio effected)
  3. Darkened colouring of cells/nuclei (nuclear hyperchromatism)
  4. basal cell hyperplasia with loss of polarity
  5. abnormal keratinisation (dyskeratosis)
  6. drop-shaped retepegs i.e. wider at their deepest part
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

dysplasia; mild, moderate and severe

A

mild = bit disorganised
moderate = reaches suprabasal cells
severe = affects full thickeners of epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

How is epithelial dysplasia different to cancer (SCC)?

A

All the features of dysplasia may be seen in oral
squamous cell carcinoma, however in dysplasia
the atypical cells are confined to the
surface epithelium
In squamous cell carcinoma, the atypical cells
invade into the underlying connective tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What percentage of oral cancers are SSCs?

A

> 90%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

5 year survival rate for oral cancer is

A

55%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Highest risk factor for oral cancer

A

SMOKING.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

TNM classification of malignant tumours

A

T- extent of primary Tumour
N- absence or prescence and extent of regional lymph Node metastasis
M- absence or presence of distant Metastasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

T1N0M0, T4aN2aM1

Which cancer is worse?

A

Each component is given a number, the higher the number the
more extensive the disease, poorer prognosis.

therefore = T4aN2aM1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Definition: Abscess

A

Abscess —> “cess”= puss; collection of pus i.e. infection.

Cyst—> sac of fluid encased partly or wholly by epithelial cells, painless unless grows too big

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Histopathology: Acute periradicular periodontitis

A

Neutrophil, vascular dilation, neutrophils, oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Histopathology: acute periapical abscess

A

Central collection of pus (neutrophils, bacteria, cellular debris)
Adjacent zone of preserved neutrophils
Surrounding membrane of sprouting capillaries and vascular dilation and occasional fibroblasts (granulation
tissue)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

histopathology: chronic periradicular periodontitis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

histopathology: periapical granuloma

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

histopathology: periocoronitis

A

Acute and chronic inflammatory changes including
oedema, inflammatory cells, vascular dilation, fibrotic
connective tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What does a cyst have to be to be classified as an odontogenic cyst?

A

Derived from epithelial residues of tooth-forming organ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What are the two types of odontogenic cysts?

A

inflammatory

developmental

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What are the four layers of the enamel organ

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Development: what forms pulp?

A

ectomesenchymal cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What are the types of inflammatory odontogenic cysts?

A

1 Radicular cyst

2 inflammatory collateral cyst (not necessarily from endodontic cause but by some breach of the oral mucosa which causes inflammation and proliferation of epithelial cells and thus a cyst forming - pericornitis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What is the most common type of jaw cyst?

A

Radicular cyst (55%)

  • mainly in the maxilla
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What does this histopathology show?

A

Radicular cyst

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Marsupialisation

A

Marsupialization is a surgical procedure used to treat large cysts by creating an opening in the cyst wall and suturing the edges to the surrounding tissue. This allows the cyst to drain and shrink gradually over time, preserving surrounding structures and avoiding complete excision, particularly in large or difficult-to-remove cysts.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Enucleation vs marsupialisation of cysts

A

“enucleation” means completely removing the entire cyst lining, while “marsupialization” involves creating a pouch-like opening in the cyst wall, draining its contents, and then suturing the edges to the surrounding tissue, essentially turning the cyst into a “pocket” that gradually shrinks over time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q
A

Odontogenic Keratocyst (OKC)

Developmental cyst
3rd most common jaw cyst
MANDIBLE mainly (80%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Where do OKCs arrise from?

A

Remnants of the dental lamina (Glands of Serres)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Why might OKCs be diagnosed late?

A

Symptomless, anterior-posterior expansion means they don’t show up and a swelling necessarily.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Neoplastic meaning

A

New growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What syndrome may cause a patient to develop multiple odontogenic keratocysts at a young age?

A

Nevoid Basal Cell Carcinoma Syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What is this histopathology characteristic for?

A

Odontogenic Keratocyst

90
Q

What is the recurrence rate of OKC if incompletely removed?

A

25%

91
Q

What is the 2nd most common odontogenic cyst?

A

Dentigerous cyst

92
Q

Where are the dentigerous cysts attached to/derive from?

A

Amelocemental junction/associated with the crown of an unerupted tooth

93
Q

Why might you not be able to diagnose a developmental cyst from it’s histopathological features?

A

These features can be lost if there is secondary infection - it will be indistinguishable from an inflammatory cyst.

94
Q

What are these features of?

A

Dentigerous cyst

95
Q

What is an eruption cyst?

A

A type of dentigerous cyst arising in extra-alveolar location.

Typically the tooth will naturally erupt through the cyst and no treatment is needed.

96
Q
A

Botryoid odontogenic cyst

Botryoid = bunch of grapes (polycystic appearance)

Commonly in the MANDIBLE in premolar/canine region

97
Q
A

Glandular odontogenic cyst
Very rare - anterior mandible

98
Q

Gingival cyst

A
99
Q
A

Calcifying odontogenic cyst

Very rare - GHOST CELLS

100
Q
A

Nasopalatine duct cyst

Most common NON-odontogenic cyst
(epithelial remnants of the nasopalatine duct)
Unknown aetiology

Salty taste in mouth

101
Q

Median palatine cyst, incisive canal cyst, median alveolar
cyst are now considered to represent different presentations
of ______________

A

nasopalatine duct cyst

102
Q
A

Nasopalatine duct cyst

103
Q
A

Surgical ciliated cyst

104
Q
A

Nasolabial cyst

  • can distort nostril
  • derived from remnants of the embryonic nasolacrimal duct or lower anterior portion of the mature duct
105
Q

Dermoid cyst

A
106
Q
A

Lymphoepithelial cyst

  • LYMPHOID tissue in cyst wall
107
Q
A

Thyroglossal duct cyst

108
Q

Why are non-epithelialised primary bone cysts not TRUE cysts?

A

not lined

109
Q
A

Solitary bone cyst - no cyst contents

110
Q
A

Aneurysmal bone cyst

blood-filled spaces separated by cellular fibrous tissue, no lining

111
Q
A

Stafne’s Defect
Stafne’s Idiopathic Bone Cavity
• NOT a true lesion
• Developmental anomaly
• Due to part of submandibular gland indenting lingual
mandible
• Appears cyst-like on radiograph and be mistaken for
a cyst

112
Q

WHO classification 2024: Odontogenic tumours

A

Benign (or malignant)
—»
1. Benign EPITHELIAL
2. Benign mixed EPITHELIAL & MESENCHYMAL
3. Benign MESENCHYMAL

113
Q

Classifciation - Type of tumour: ameloblastoma

A

Benign epithelial odontogenic tumour

114
Q
A

Ameloblastoma

POSTERIOR MANDIBLE commonly
- jaw swelling noted

115
Q
A

Ameloblastoma

116
Q

Tx of ameloblastoma

A

Complete excision with margin of uninvolved tissue, as this WILL recur if not completely excised.

117
Q

What benign epithelial odontogenic tumour may mimic that of a dentigerous cyst as it arrises from an unerupted permanent tooth?

A

Adenomatoid odontogenic tumour

118
Q
A

Adenomatoid odontogenic tumour

119
Q

Classification of Odontoma

A

Benign mixed epithelial and mesenchymal odontogenic tumours

120
Q

Odontoma types

A

“pound” = lots of coins —> lots of little tooth-like structures

“Pl(ex)”—> Plant = cauliflower appearance

Both contain enamel, cementum and dentine.
PAINLESS slow growing lesions.

121
Q

Classification: Cementoblastoma

A

Benign mesenchymal odontogenic tumours

122
Q
A

Cementoblastoma
- Formation of cementum-like tissue in connection with root of tooth.
- painful swelling

123
Q
A

Cementoblastoma
- Formation of cementum-like tissue in connection with root of tooth.
- painful swelling

124
Q

Tx of cementoblastoma

A

COMPLETE removal INCLUDING the tooth

125
Q

Examples of malignant odontogenic tumours

A

Ameloblastic carcinoma

Odontogenic carcinosarcoma

126
Q
A

Central giant cell granuloma (CGCG)
- mandible, female, under 30
- multinucleated giant cells

127
Q

________ is histologically INDISTINGUISHABLE from cherubim’s, brown tumour of hyperparathyroidism, giant-cell tumour, aneurysmal bone cyst.

A

Central Giant Cell Granuloma

128
Q
A

Cherubism (rare inherited disorder)

histologically the same as CGCG etc

129
Q

What is a fibro-osseous lesion?

A

When normal bone (“osseous”) is replaced by cellular fibrous tissue.

  • cannot be diagnosed by histology alone; need clinical/radiographic features
130
Q

What is cemento-osseous dysplasia?

A

Fibro-osseous lesion occurring in tooth-bearing areas of the jaws (teeth can still remain vital)

131
Q
A

Fibrous dysplasia

132
Q

Fibrous dysplasia

A

fibro-osseous lesion of GROWING bones
Painless - rarely malignant change
Aesthetic surgery

133
Q

Types of Ossifying fibroma

A
  1. Cemento(-ossifying fibroma)
  2. Juvenile trabecular (ossifying fibroma)
  3. Psammomatoid (ossifying fibroma)
134
Q

Cemento(-ossifying fibroma)

A

(note this is the only one out of the three types categoried as a benign mesenchymal odontogenic tumour)

DEMARCATED nature is an important feature distinguishing it from fibrous dysplasia.

135
Q

Juvenile trabecular (ossifying fibroma)

A

found in children and adolescents

136
Q

Psammomatoid (ossifying fibroma)

A

“Psammomatoid” comes from the Greek word “psammos” meaning “sand,” and “-oid” meaning “like” or “resembling.” So, psammomatoid refers to something that looks like sand, often used to describe small, sand-like calcifications seen in certain tumors, such as psammomatoid ossifying fibromas.

137
Q

Familial gigantiform cementoma

A

RARE (fibro-osseous lesion of jaws)

138
Q

Segmental odontomaxillary dysplasia

A

RARE

Sporadic

Unilateral

Palatal-buccal expansion

139
Q

Osteoma and Osteochrondroma are types of…?

A

Benign maxillofacial bone and cartilage tumours

140
Q
A

Osteoma
- tumour slow-growing and made of bone.
- mandible

— multiple lesions associated with Gardner syndrome !

141
Q

Two types of osteoma

A
  1. cancellous (inner spongey bone)
  2. compact (outer hard bone)

Depends which part of bone proliferates

142
Q

Osteochondroma

A

• Bony projection with a cap of cartilage
• Continuous with underlying bone
• Rare in maxillofacial bones (occurs at sites of
endochondral ossification)
• Symptoms depend on site of lesion

Treatment
• Complete excision

143
Q

Osteogenesis imperfecta

A

inherited disease (AD)

impaired collagen maturation - thus poorly developed bones.

Bones fracture easily, maybe associated w dentinogenesis imperfecta, malocclusion

144
Q

Osteopetrosis (marble bone disease)

A

Rare genetic disease
Increase and bone density

Osteomyelitis is common (bone infection - V painful)

145
Q

Cleidocranial dysplasia

A

Rare genetic disorder (AD)
No clavicles
Delayed eruption of teeth and many supernumeraries
Narrow high arched palate

146
Q

Achondroplasia

A

Dwarfism
Retrusive maxilla = malocclusion
Abnormal endochondral ossification

147
Q

Osteoporosis

A

NORMAL bone but just LESS bone there.

Seen in diseases that effect endocrine (cushing’ a hyperparathyroidism)
Post menopausal women

148
Q

Rickets and Osteomalacia

A
149
Q

Dry socket (clinical term)

A

Alveolar Osteitis

150
Q

MRONJ definition

A

MRONJ defined as’ exposed bone, or bone that can
be probed through an intraoral or extraoral fistula, in
the maxillofacial region that has persisted for more
than eight weeks in patients with a history of
treatment with anti-resorptive or anti-angiogenic
drugs, and where there has been no history of
radiation therapy to the jaw or no obvious metastatic
disease to the jaws’

151
Q

Pager’s disease of bone

A

Osteitis Deformans

Effects occlusion
May also see hypercemetosis or ankylosis

152
Q
A

Paget’s disease

153
Q

Exostoses

A

Localised bony protuberances e.g. torus

Completely fine to leave alone !

154
Q

Something can only be classified as an epulis if…

A

located on the gingiva

155
Q
A

Fibrous Epulis

156
Q

Even though pyogenic granulomas and pregnancy epulis are technically the same thing; how would you treat them differently?

A

Pyogenic granuloma - local excision
Pregnancy epulis - good OH and should resolve post-partum

157
Q

Giant cell epulis vs pyogenic granuloma

A

While both Giant-Cell Epulis (also known as Peripheral Giant-Cell Granuloma) and pyogenic granuloma are benign oral lesions that appear as soft tissue growths, the key difference lies in their microscopic appearance, with a Giant-Cell Epulis being characterized by a large number of multinucleated giant cells, while a pyogenic granuloma typically has a more vascular structure with fewer giant cells, and often presents with a brighter red color compared to the more bluish-purple hue of a Giant-Cell Epulis; both are usually caused by local irritation or trauma

158
Q
A

Fibroepithelial polyp

—> buccal mucosa, lip, tongue

159
Q
A

Papillary hyperplasia of the palate

160
Q

Fibrosarcoma

A

Malignant (rare)
A fibrous tissue tumour

161
Q

Lipoma or Liposarcoma

A

Adipose tissue tumour

Lipoma - benign
Liposarcoma - malignant

162
Q
A

Lipoma

163
Q
A

Haemangioma

Benign neoplasm

tx - often regress on own

164
Q

Lymphangioma

A

Excise

165
Q
A

Kaposi’s Sarcoma

Locally aggressive tumour of endothelial cells
Associated w HHV-8 infection

tx - antiretroviral therapy/chemotherapy

166
Q
A

Rhabdomyoma

Painless growing mass
Lobules of closely packed mature MUSCLE cells.

167
Q
A

Pleomorphic adenoma (accounts for approx 60% of all parotid tumours)

benign, painless, rubbery

genetic mutation

168
Q
A

Pleomorphic adenoma

HIGH CHANCE of malignant transformation

169
Q
A

Warthin Tumour

170
Q

Malignant epithelial tumours

A

Mucoepidermoid carcinoma
Adenoid cystic carcinoma
Acinic cell carcinoma

171
Q
A

Adenoid cystic carcinoma —> NEURAL INVASION

172
Q
A

Mucoepidermoid carcinoma

173
Q
A

Acini Cell carcinoma

174
Q

Management of asymptomatic oral lichen planus

A

no treatment required

175
Q

Management of symptomatic oral lichen planus

A

Match treatment to symptom severity
- “STAD”
- Steroids (topical)
- Toothpaste = SLS free
- Analgesic (topical)
- Diet modification

176
Q

Oral lichen planus & recurrent aphthous stomatitis - topical steroids

A

Betamethasone (500mg as a mouthwash)

177
Q

Oral lichen planus & Recurrent aphthous stomatitis - topical analgesic

A

Benzydamine (mouthwash or spray)

178
Q

Potential for malignant transformation of oral lichenoid reaction vs lichen planus

A

Higher for oral lichenoid reaction than lichen planus

179
Q

What is recurrent aphthous stomatitis (RAS)?

A

Recurrent bouts of one or more painful, rounded or ovoid ulcers.
Most aphthous ulcers last for 10-14 days.
It is a common mouth condition affecting up to 20% of the population at any given time.
The severity and frequency of RAS tends to decrease with age.

180
Q

behcet disease

A

Aphthous ulceration and sores also on genitalia etc

181
Q

Pemphigus Vulgaris - screening

A

Autoantibody: Desmoglein 3 —> seen w immunofluorescene

182
Q

Management of pemphigus vulgaris

A

Systemic steroids = Prednisolone (1mg/kg)

+ topical analgesics and steroids

183
Q

Aciclovir

A

Antiviral medication used to treat herpes simplex virus

184
Q

An example of orofacial pain attributed to lesion or disease of the cranial nerves

A

Trigeminal neuralgia

185
Q

Trigeminal Neuralgia

A
  • Recurrent, one-sided, brief (up to 2 mins) SEVERE electric shock-like pains.
  • Specific to one or more divisions of the trigeminal nerve.
186
Q

Classical trigeminal neuralgia

A

Nerve has been compressed by blood vessel (this can be seen surgically or from an MRI)

“ with Concomitant continuous pain
—> pain in the background in that area existing between the main shocks.

187
Q

Secondary trigeminal neuralgia

A

caused by a known underlying disease (multiple sclerosis, lesion etc).

tends to cause bilateral trigeminal neuralgia

188
Q

First line management of Trigeminal Neuralgia

A

Carbamazepine

189
Q

Perio: to proceed to subgingival instrumentation “step 2”

A

you must have an engaged patient

190
Q

Three types of periodontal surgery

A

Resective, reparative and regenerative

191
Q

When is surgical interventions recommended for periodontitis patients?

A

Residual deep sites (>6mm)
Infrabony defects >3mm
Furcation involvement (class II)
OHI NEEDS to be good —> otherwise failure likely!

192
Q

Periodontal surgery: flap design

A

Avoid vertical relieving incisions, consider horizontal extension.

If absolutely necessary, extend just past mucogingival junction and avoid cutting over bulbosity such as canine eminence.

193
Q

Sutures opted for

A

Synthetic mono-filament

194
Q

While sutures present post-op…

A

No brushing in the region
Use chlorohexidine mouthwash to reduce plaque formation

195
Q

Periodontal dressings

A

not really opted for…

196
Q

Probing/instrumentation post perio surgery

A

No probing or instrumentation of site for 3 months (minimum)

197
Q

Effectiveness of periodontal surgery

A

only more effective for deep pockets (>6mm).

198
Q

Resective surgery

A

Pocket elimination procedures which establish a morphologically normal attachment but with apical displacement of the dento-gingival complex

199
Q

Gingivectomy

A

Type of resective surgery for gingival overgrowth

Overgrowth can be due to inflammation, drugs, systemic conditions.

200
Q

Electrosurgery for gingival

A

Resective surgery
For smaller areas of recontouring

Contraindications: pacemakers

201
Q

Surgical crown lengthening

A

A surgical procedure which apically repositions the soft tissue and alveolar bone to expose more tooth structure, and increase the length of the clinical crown.
MAINTAIN BIOLOGICAL WIDTH WHILST APICALLY REPOSITIONING THE GINGIVAL LEVEL.

202
Q

Open flap debridement

A

Aims of surgery
- Open flat debridement
- Modified Widman flap

203
Q

Open flap debridement vs modified widman flap

A

A modified Widman flap is a specific type of open flap debridement technique, known for its more conservative approach with minimal tissue manipulation, aiming primarily to reattach the existing tissue rather than aggressively removing bone to eliminate deep pockets

204
Q

Open flap debridement advantages

A

Sites >6mm with BoP or suppuration

205
Q

Regenerative surgery

A

Recreation of the complete attachment apparatus of bone/cementum/functionally orientated PDL against previously exposed root surface.

206
Q

What cases warrant regeneration periodontal surgery?

A

Infrabony defect associated with periodontal pocket of >6mm (>3mm vertical defect).
Class II furcation in mandibular molars.
Single class II furcation in maxillary molars.

207
Q

Guided tissue regeneration

A

Use of mechanical barrier (membrane) to selectively enhance the establishment of PDL and peri vascular cells in osseous defectors to initiate periodontal regeneration.

208
Q

Different types of bone grafts: auto, allo, xeno, alloplast

A

auto = donor from SAME person
allo = different person, human
xeno = animal
alloplast = synthetic

209
Q

Emdogain

A

90% amelogenins + propylene glycol alginate (PGA)

= mimics the development of tooth supporting apparatus during tooth formation

210
Q

Management of furcation involved teeth: Grade 1

A

NSPT
Odontoplasty

211
Q

Management of furcation involved teeth: Grade 2

A

Odontoplasty
Open flap debridement
Regenerative procedures

212
Q

Management of furcation involved teeth: Grade 3

A

Tunnelling procedures

213
Q

Odontoplasty

A

Reduces plaque accumulation by reshaping tooth surface with a bur
Can aid in treatment of grade 1 and shallow grade 2 lesions
Surgical procedure involving raising a flap buccal and lingual to the site
Can result in hypersensitivity and caries

214
Q

Regeneration for furcations

A

good for class 2 defects, but limited evidence for class 3 lesions.

215
Q

Root resection

A

“hemisection”
Severe bone loss on 1 or more roots

216
Q

Tunnel preparation

A

Used in mandibular molars with deep Degree 2 and Degree 3 lesions

217
Q

Frenectomy

A

Removal of local muscle insertion to stabilise tissues, improve access for OH, aid recession cases.

218
Q

Pedicle flap vs graft

A

Pedicle = single site surgery, local tissue maintaining own blood supply, limited by local anatomy

Grafts = material from distant donor site, TWO surgeries, larger quantities of connective tissue, more demanding technically

219
Q

Free gingival graft

A

Graft from palate formed of epithelium and small amount of underlying connective
tissue is placed into a region with localised recession
Aims:
To create a band of keratinised mucosa
Remove frenal attachments
Prepare site for second procedure to increase root coverage

220
Q

Connective tissue grafting

A

Surgical procedure where a split thickness flap is raised, released and then replaced
in a more coronal position
Can be combined with a connective tissue graft from the palate, especially when:
Limited attached gingivae apical to recession
Shallow sulcus
Buccally placed root
Interdental CAL

Module 7 Exam (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions