Week 1-2 Flashcards
1
Q
What is this lesion?
A
Oral Squamous Cell Carcinoma (SCC)
Oral squamous cell carcinoma is a type of cancer that originates from the flat, squamous cells lining the inside of the mouth, making it the most common form of oral cancer; it can develop on the lips, tongue, floor of the mouth, and gums, and is often linked to risk factors like tobacco use, heavy alcohol consumption, and poor oral hygiene.
Early Stage OSCC:
Small, subtle lesion.
May appear as white or red patch, non-healing ulcer, or thickened area.
Often asymptomatic.
Middle Stage OSCC:
Larger and more distinct lesion.
Irregular shape, raised edges, induration.
Ulceration is common.
May cause pain, bleeding, numbness, or difficulty swallowing.
Late Stage OSCC:
Significantly larger tumor invading surrounding tissues.
Very irregular shape, may be fixed to underlying structures.
Ulceration and necrosis are common.
Causes severe pain, difficulty eating and speaking, facial disfigurement.
May spread to lymph nodes.
2
Q
What is the clinical appearance of a traumatic ulcer?
A
Redness, swelling, yellow-white center
3
Q
How would you differentiate between minor and major aphthous ulcers based on size?
A
Minor aphthous ulcers are typically <10mm, while major ones are >10mm.
4
Q
What is the key characteristic of geographic tongue in terms of its appearance?
A
It has a map-like appearance with red patches and white borders that change over time.
5
Q
What is the usual cause of frictional keratosis?
A
Rubbing or irritation
6
Q
What type of infection causes oral candidiasis?
A
Fungal infection
7
Q
What are the two main clinical presentations of oral lichen planus?
A
- White lacy lines (reticular)
- Red ulcers (erosive)
8
Q
What is the link between oral submucous fibrosis (OSMF) and betel nut chewing?
A
OSMF is a pre-cancerous condition linked to betel nut chewing.
9
Q
Why is biopsy essential in the case of leukoplakia?
A
To rule out cancer, as leukoplakia can be pre-cancerous or cancerous.
10
Q
What is the level of cancer risk associated with erythroplakia?
A
High risk
11
Q
What are the common sites for oral lesions?
A
- Buccal mucosa
- Tongue
- Floor of mouth
- Lips
12
Q
What are the key factors to consider when describing the appearance of an oral lesion?
A
- Color
- Texture
- Shape
- Size
- Number of lesions
- Presence/absence of ulcers or raised areas
13
Q
What aspects of an oral lesion should be noted when considering its consistency?
A
Palpation findings (firm, indurated, soft, fluctuant)
14
Q
What are some associated symptoms that might accompany an oral lesion?
A
- Pain
- Bleeding
- Numbness/paresthesia
- Burning
- Itching
- Difficulty swallowing
- Limited mouth opening
15
Q
What does ICDAS 4 indicate in the context of dental caries?
A
Dark shadow from dentin, with or without enamel breakdown
16
Q
What is the color and consistency of an active carious lesion?
A
Yellowish-brownish in color, soft and leathery
17
Q
What are the characteristics of an arrested lesion?
A
Darker in color, absence of plaque, hard upon probing
18
Q
What are the criteria for ICDAS score 2?
A
Distinct visual changes in enamel
19
Q
What does ICDAS score 5 represent?
A
Distinct cavity with visible dentin
20
Q
Which heart conditions generally require antibiotic prophylaxis before dental procedures?
A
- Prosthetic cardiac valves
- Previous infective endocarditis
- Congenital heart disease (CHD) with specific criteria
- Cardiac transplant with valvulopathy
- Rheumatic heart disease
Tetralogy of Fallot has four heart problems, including a hole between the bottom chambers (VSD), causing blue-ish blood to go to the body. Transposition of the Great Arteries means the main arteries are switched, often needing a hole (VSD or ASD) to survive. Tricuspid Atresia, a missing valve blocking lung blood flow, often needs a hole (VSD or ASD) to get some blood to the lungs. Truncus Arteriosus is one big mixed-blood vessel, usually with a VSD. Total Anomalous Pulmonary Venous Connection means lung blood vessels connect wrongly, mixing clean and used blood, and may involve an ASD.
21
Q
What is the recommended antibiotic prophylaxis regimen for patients who require it?
A
Amoxicillin 2g orally, 1 hour before the procedure
22
Q
Are patients with isolated ASD or VSD generally required to take antibiotic prophylaxis?
A
No
23
Q
What factors should be considered when deciding whether to place a fissure sealant (FS) or fissure protectant (FP) on a molar?
A
The maturity of the molar and the level of caries risk
24
Q
Why might you choose FP over FS for a newly erupted molar with high caries risk?
A
FP has remineralizing effects, which are beneficial for immature molars.
25
How would you approach placing FS and FP on a hypomineralized tooth?
FP the occlusal surface due to poor bonding and FS with flowable composite on the buccal surface for longevity.
26
What is the typical location of root caries?
Root surfaces, cementoenamel junction (CEJ), or under existing restorations
27
What are some possible causes of root caries?
* Prominent recession
* Periodontitis
* Xerostomia due to medications
28
What is the difference between ICDAS Root Code 1 and Code 2?
Code 1 has clear discoloration but no cavitation, while Code 2 has clear discoloration with cavitation (≥0.5mm).
29
What are some preventive strategies for managing root caries?
* Dietary advice
* Tailored oral hygiene and plaque control
* High fluoride toothpaste
* Saliva substitutes
* Fluoride varnish
30
What is an easy and minimally invasive strategy to arrest root caries in elderly or special needs patients?
Silver fluoride
31
What are the key differences between subgingival caries and calculus in terms of color, texture, and consistency?
* Caries: Often dark, rough/softened, may be softer.
* Calculus: Usually yellow/brown/black, hard/rough, firmly attached.
32
How does the radiographic appearance of subgingival caries differ from calculus?
* Caries: May appear radiolucent.
* Calculus: Appears radiopaque.
33
What does ICDAS Root Code E indicate?
Unable to be visualized directly due to gingival tissues or lack of air-drying.
34
What is the recommended management for ICDAS Root Code 0?
Maintain good oral hygiene and regular check-ups.
35
What type of restoration is recommended for ICDAS 4?
Amalgam restoration
36
What are the different types of pain that a patient might experience in relation to a dental condition?
* Sharp
* Dull
* Throbbing
* Constant
* Intermittent
37
What stimuli can elicit pain in a tooth with pulpal involvement?
* Cold
* Heat
* Biting
* Spontaneous
38
What aspects of pain duration and location should be recorded?
* Duration: Brief, lingering, constant.
* Location: Localized to one tooth, radiating.
39
What are the possible pulpal diagnoses based on cold test response?
* Normal
* Reversible pulpitis
* Irreversible pulpitis
* Necrosis
40
What does 'WNL' stand for in the context of pulpal testing?
Within Normal Limits
41
What are the different levels of severity that can be recorded for percussion and mobility during periapical testing?
* None
* Slight
* Moderate
* Severe
42
What are the possible periapical diagnoses based on the findings of the testing?
* Normal
* Symptomatic apical periodontitis (SAP)
* Cracked tooth
* Periodontal involvement
* Possible abscess
43
What are the clinical signs/symptoms of a traumatic ulcer?
* Pain
* Redness
* Swelling
* Yellow-white fibrinous exudate
44
What is the dental management for a traumatic ulcer?
Address the cause if possible, ensure healing within 2 weeks, referral if persists beyond 2 weeks
45
What are the three subtypes of aphthous ulcers?
* Minor
* Major
* Herpetiform
46
What is the dental management for aphthous ulcers?
Topical corticosteroids, check for nutritional deficiencies (B12, folic acid, iron)
47
What are the clinical signs/symptoms of oral squamous cell carcinoma (SCC)?
* Non-healing ulcer
* Indurated/firm
* Irregular margins
* Raised edges
* May cause neurosensory changes
* Tooth mobility
48
What is the dental management for SCC?
Immediate referral for biopsy and staging, multidisciplinary management (surgery, radiotherapy, chemotherapy)
49
What is the typical appearance of geographic tongue?
Red atrophic patches surrounded by white keratotic margins, changing appearance over days, usually asymptomatic
50
What is the dental management for geographic tongue?
Reassurance and explanation
51
What is the typical appearance of frictional keratosis?
White, slightly textured lesion, occurs in areas with chronic low-grade trauma
52
What is the dental management for frictional keratosis?
Identify and address the cause of trauma
53
What are the three forms of oral candidiasis?
* Pseudomembranous
* Erythematous
* Chronic hyperplastic
54
What is the dental management for oral candidiasis?
Topical or systemic antifungal medications, improve oral hygiene
55
What are the clinical signs/symptoms of oral lichen planus?
Chronic, immune-mediated condition, three forms (reticular, erosive, plaque-like), Wickham's striae (white lines), may have ulceration
56
What is the dental management for oral lichen planus?
Referral for symptomatic or erosive forms, topical or systemic immunosuppressive agents
57
What are the clinical signs/symptoms of oral submucous fibrosis (OSMF)?
* Fibroelastic change and epithelial atrophy
* Stiffness of oral mucosa
* Trismus
* Blanching of mucosa
* Depapillation of tongue
58
What is the dental management for OSMF?
Cessation of areca nut chewing, ongoing surveillance for malignant transformation
59
What is the typical appearance of leukoplakia?
White plaques of questionable risk
60
What is the dental management for leukoplakia?
Referral for assessment and biopsy mandatory to establish diagnosis
61
What is the typical appearance of erythroplakia?
Red patch of the oral mucosa
62
What is the dental management for erythroplakia?
Urgent referral for assessment and biopsy
63
64
What's another common name for aphthous ulcers?
Canker sores
65
What is the current thinking about the underlying cause of aphthous ulcers?
An abnormal immune system reaction to a protein in mucosal tissue, triggered by an external factor.
66
What size is a minor aphthous ulcer typically?
Less than 5mm in diameter.
67
Besides a visual examination, what is one type of test that might be done to help diagnose recurrent or severe aphthous ulcers and rule out other conditions?
(Any one of these): Blood test (for deficiencies, coeliac disease), faecal calprotectin test (for Crohn's), swab (for infection).
Yes, Crohn's disease can cause mouth ulcers, also known as aphthous ulcers, which are often painful and can appear during flare-ups of the disease; this is because Crohn's disease can affect the entire digestive tract, including the mouth, meaning oral manifestations like mouth sores are possible.
68
Is there a definitive cure for aphthous ulcers?
No
69
The exact cause of minor aphthous ulcers is unknown, but they are thought to be caused by an abnormal immune response triggered by factors like stress, injury, or nutritional deficiencies. These ulcers appear as small, round, or oval "punched-out" sores inside the mouth, typically on the cheeks, lips, or under the tongue. They have a yellowish center, a red halo, and are less than 5mm in diameter, often causing pain when irritated.
70
Major aphthous ulcers, like their minor counterparts, are believed to stem from a similar abnormal immune response, though the triggers might be more pronounced or the individual's immune system more sensitive. These ulcers are significantly larger, exceeding 10mm in diameter, and appear as deep, crater-like sores with irregular borders, often occurring on the lips, cheeks, tongue, or even the throat. Because of their size and depth, major aphthous ulcers take weeks or months to heal and frequently leave scars.
71
Herpetiform aphthous ulcers, despite their name, are not caused by the herpes virus; their cause, like other aphthous ulcers, is believed to be an abnormal immune reaction. These ulcers are unique in their presentation, appearing as numerous (sometimes dozens) of tiny, pinpoint-sized sores, often clustered together, and most frequently found on the tongue. Although individually small, these clusters can merge, forming larger, irregular ulcers, and they typically heal within a month.
Oral herpes, caused by HSV, presents as fluid-filled blisters that rupture into ulcers, often on the lips, gums, or hard palate, and may be accompanied by fever and swollen glands, whereas, herpetiform aphthous ulcers are not viral. Herpetiform aphthous ulcers are numerous tiny, pinpoint ulcers, usually on the tongue or floor of the mouth, without preceding blisters or systemic symptoms, and are not contagious. Key differences include location (herpes can affect gums/hard palate), initial blister formation (present in herpes), and the presence of viral infection (only in herpes).
72
* Pseudomembranous candidiasis
73
Erythematous candidiasis
To differentiate erythematous candidiasis, look for smooth, red, atrophic patches, especially on the tongue's dorsum or palate (under dentures), and consider predisposing factors like antibiotic/steroid use, dry mouth, or immunocompromise. A key diagnostic step is a cytology smear to identify Candida hyphae/yeasts, differentiating it from conditions like geographic tongue (migrating white borders), lichen planus (white striae), or the precancerous erythroplakia (requires biopsy). Always consider patient history and perform necessary tests to confirm the diagnosis and rule out other possibilities.
74
chronic hyperplastic candidiasis
Differentiating chronic hyperplastic candidiasis (also known as candidal leukoplakia) from other oral lesions is crucial because, unlike other forms of oral candidiasis, it carries a risk of malignant transformation. Here's the breakdown:
1. Clinical Appearance and Location:
Chronic Hyperplastic Candidiasis:
Presents as white plaques or patches that cannot be rubbed off. This is the key distinguishing feature from other forms of oral candidiasis (like pseudomembranous candidiasis, "thrush," which can be wiped off).
The texture can vary from smooth to nodular or speckled.
The lesions are often persistent and don't resolve spontaneously.
Common locations:
Buccal mucosa (inside of the cheeks), often near the corners of the mouth (commissures).
Tongue (lateral borders or dorsum).
Less commonly, the palate or other areas.
May be asymptomatic or cause a burning sensation.
2. Differential Diagnosis (Key Lesions to Rule Out):
Leukoplakia (Idiopathic): This is the most important differential diagnosis. Leukoplakia is a precancerous lesion defined as a white patch that cannot be clinically or pathologically attributed to any other disease. The key similarity is that neither chronic hyperplastic candidiasis nor idiopathic leukoplakia can be wiped off.
Lichen Planus (Hypertrophic): Can present as white plaques, but often has characteristic Wickham's striae (fine, white lines) at the periphery. Biopsy is often needed to differentiate.
Frictional Keratosis: A white patch caused by chronic mechanical irritation (e.g., from a sharp tooth or ill-fitting denture). The history of trauma and the location corresponding to the source of irritation are key. Removing the irritant should lead to resolution.
Hairy Leukoplakia: Usually seen in immunocompromised individuals (especially HIV/AIDS). Appears as white, corrugated or "hairy" patches, typically on the lateral borders of the tongue. Caused by Epstein-Barr virus (EBV).
Chemical Burn: From aspirin or other caustic substances, will usually improve after the causitive agent is removed.
Squamous Cell Carcinoma: Oral cancer can show as persistant white lesion.
White Sponge Nevus: Presents with widespread white patches.
3. Patient History:
Risk Factors for Candidiasis: Similar to erythematous candidiasis (immunosuppression, antibiotic use, steroid use, xerostomia, smoking, poor oral hygiene, denture use), though the association is not as strong as with other forms of candidiasis.
Smoking: A very important risk factor for both chronic hyperplastic candidiasis and leukoplakia.
4. Diagnostic Tests (Crucial):
Biopsy: This is mandatory for chronic hyperplastic candidiasis. The key histological features are:
Hyperkeratosis (thickening of the keratin layer).
Acanthosis (thickening of the spinous layer of the epithelium).
Candida hyphae penetrating the parakeratin layer (this is diagnostic of candidal infection). Crucially, the hyphae are within the epithelium itself, not just on the surface.
Chronic inflammatory infiltrate in the underlying connective tissue.
Epithelial dysplasia may be present (this indicates a precancerous change). The presence and degree of dysplasia are critical for determining prognosis and management.
Cytology/Smear: Not reliable for diagnosis. While it might show Candida hyphae, it cannot differentiate between colonization and true invasion of the epithelium. Also, the hyperkeratosis often prevents adequate sampling of the deeper layers where the hyphae are located.
Culture: Identifies the presence of candida.
In Summary:
Differentiating chronic hyperplastic candidiasis requires:
Recognizing the non-scrapable white patch.
Considering the location (buccal mucosa, tongue).
Taking a thorough history, including smoking.
Performing a biopsy to confirm the presence of Candida hyphae within the epithelium and to assess for dysplasia. This is the only way to definitively differentiate it from leukoplakia and other white lesions.
The presence of Candida hyphae within the epithelium on biopsy, in the context of a non-scrapable white patch, is what confirms the diagnosis of chronic hyperplastic candidiasis. The biopsy also rules out (or confirms) precancerous or cancerous changes, which is essential for management.
75
oral submucous fibrosis
76
icdas
1. Examples of ICDAS 4 caries lesions included in the study. a Tooth 46, dark shadow from dentin with enamel breakdown and no radiolucent zone. b Tooth 36, dark shadow from dentin with enamel breakdown, radiolucent zone at the outer half of dentin
77
icdas 2
78
79
80
81
4
82
3
83
1/2
84
4
85
3
86
2
87
1
88
5
89
enamel hypoplasia
90
enamel hypoplasia
91
enamel hypoplasia
92
enamel hypoplasia
93
enamel hypoplasia
94
enamel hypoplasia
95
enamel hypoplasia
96
hypomin
97
hypomin
98
hypomin
98
hypomin
98
hypomin
99
99
hypomin
100
AI
100
AI
100
AI
100
AI
100
AI
100
F
100
f
100
AI
100
f: Distinguishing hypomineralization (like MIH) from severe fluorosis hinges on the appearance and distribution of enamel opacities: hypomineralization presents with well-demarcated, distinct spots of discoloration (creamy white, yellow, or brown) primarily affecting specific teeth (molars, incisors), and often results in weakened, porous enamel; conversely, severe fluorosis manifests as diffuse, blended opacities with potentially pitted and brown-stained enamel across multiple teeth, reflecting systemic fluoride exposure during tooth development.
101
f: Distinguishing hypomineralization (like MIH) from severe fluorosis hinges on the appearance and distribution of enamel opacities: hypomineralization presents with well-demarcated, distinct spots of discoloration (creamy white, yellow, or brown) primarily affecting specific teeth (molars, incisors), and often results in weakened, porous enamel; conversely, severe fluorosis manifests as diffuse, blended opacities with potentially pitted and brown-stained enamel across multiple teeth, reflecting systemic fluoride exposure during tooth development.
101
F: Distinguishing hypomineralization (like MIH) from severe fluorosis hinges on the appearance and distribution of enamel opacities: hypomineralization presents with well-demarcated, distinct spots of discoloration (creamy white, yellow, or brown) primarily affecting specific teeth (molars, incisors), and often results in weakened, porous enamel; conversely, severe fluorosis manifests as diffuse, blended opacities with potentially pitted and brown-stained enamel across multiple teeth, reflecting systemic fluoride exposure during tooth development.
102
F: Distinguishing hypomineralization (like MIH) from severe fluorosis hinges on the appearance and distribution of enamel opacities: hypomineralization presents with well-demarcated, distinct spots of discoloration (creamy white, yellow, or brown) primarily affecting specific teeth (molars, incisors), and often results in weakened, porous enamel; conversely, severe fluorosis manifests as diffuse, blended opacities with potentially pitted and brown-stained enamel across multiple teeth, reflecting systemic fluoride exposure during tooth development.
