White and Red patches

Question 1

What to do with a white patch?

Answer 1

try to scrape off
- scrapes off = typical debris or thrush
- does not = thickened keratin → severe conditions
ask a thorough history
investigations = biopsy, blood test, immunofloresence

Question 2

What is candida albicans in the oral cavity under normal conditions?

Answer 2

A harmless commensal organism

Question 3

Under what circumstances can candida albicans become pathogenic?

Answer 3

When there is a disturbance of the oral flora or a decrease in immune defenses

Question 4

What local factors should be ruled out first when diagnosing oral candida?

Answer 4

• denture-related issues (friction, not removing at night, denture stomatitis)
• smoking
• xerostomia
• antibiotics use
• topical steroids therapy (e.g. steroid inhalers)

Question 5

What systemic factors can predispose a person to oral candidiasis

Answer 5

• uncontrolled diabetes
• haematinic deficiencies (iron, folate, B12)
• immunosuppression
• certain drugs
• endocrinopathies (e.g. diabetes, thyroid issues)
• HIV

Question 6

What are the clinical variants of oral candidiasis?

Answer 6

• acute pseudomembranous candidiasis - commonly known as thrush
• acute atrophic candidiasis - associated with inahaler use
• chronic atrophic hyperplastic candidiasis: white pathces that cannot be wiped away, often extending to angular cheilitis. Seen in smokers, AIDS patients, and those with immunosuppression. Required fluconazole treatment.
• chronic erythematous candidiasis (median rhomboid glossitis): associated with a kissing lesion, often seen in smokers and inhaler users

Question 7

what is chronic hyperplastic candidiasis, and why is it significant?

Answer 7

It is a form of candidiasis where white patches cannot be wiped away and has an increased potential for malignant transformation. It is often seen in smokers, AIDS patients, and those with immunosuppression

Question 8

what is the treatment of choice for chronic hyperplastic candidiasis?

Answer 8

fluconazole

Question 9

what is chronic mucocutaneous candidiasis associated with?

Answer 9

angular cheilitis, especially in cases with dentures that are too large or in elderly patients with reduced OVD (occlusal vertical dimension)

Question 10

what deficiency is commonly associated with angular cheilitis

Answer 10

vitamin B12 deficiency

Question 11

what are the characteristic features of acute pseudomembranous candidiasis in the oral cavity?

Answer 11

white papules with a milky appearance on the surface of the oral mucosa, which can be wiped off to leave a red, raw base

Question 12

What are the local causes of acute pseudomembranous candidiasis?

Answer 12

• antibiotic use
• steroid use
• xerostomia

Question 13

what are the systemic causes of acute pseudomembranous cadidiasis?

Answer 13

• systemic disease
• malignancy
• immunosuppression

Question 14

what is the first step in treating acute pseudomembranous candidiasis

Answer 14

Remove any contributing factors, such as stopping or reducing use of antibiotics, steroids, or addressing xerostomia

Question 15

what topical antifungals are used to treat acute pseudomembranous candidiasis

Answer 15

• nyastatin oral suspension (4 times a day)
• miconazole gel 2% (can be applied to denture fit surfaces or the corners of the mouth for denture stomatitis)

Question 16

What are the systemic antifungals used for acute pseudomembranous candidiasis?

Answer 16

• fluconazole
• itraconazole
• voriconazole

Question 17

Which antifungals used for treating acute pseudomembranous candidiasis can interact with warfarin and simvastatin, and what are the possible effects?

Answer 17

Miconazole and fluconazole can interact with warfarin and simvastatin, leading to very painful muscle cramps and wasting

Question 18

What are the primary symptoms of acute atrophic candidiasis

Answer 18

a burning sensation in the mouth, which can be painful

Question 19

What are the common causes of acute atrophic candidiasis

Answer 19

• use of asthma inhalers
• broad spectrum antibiotics
• deficiencies in B12, folate and ferritin

Question 20

Where does chronic atrophic candidiasis (denture stomatitis) typically occur?

Answer 20

On the denture-bearing areas of the oral mucosa

Question 21

Is chronic atrophic candidiasis (denture stomatitis) usually symptomatic or asymptomatic

Answer 21

It is typically asymptomatic

Question 22

Which types of dentures are associated with chronic atrophic candidiasis

Answer 22

Both acrylic and Co-Cr dentures, especially chronic denture wearers.

Question 23

What are Newton’s three types of chronic atrophic candidiasis (denture stomatitis)?

Answer 23

Type 1: Pinpoint (localized) erythematous areas
Type 2: Diffuse erythematous areas
Type 3: Erythema associated with granular or multinodular mucosa (indicative of chronic inflammatory papillary hyperplasia)

Question 24

What are the clinical features of chronic hyperplastic candidiasis (candidal leukoplakia) ?

Answer 24

• Does not wipe off
• mainly occurs in smokers
  often on buccal mucosa near the commisure
• less common on the tongue
• higher risk of developing squamous cell carcinoma (6-8%)

Question 25

What investigations should be performed for chronic hyperplastic candidiasis?

Answer 25

Swab - candida culture FBC, haematinics, blood glucose - histopathology after treating with antifungal agents to assess for dysplasia

Question 26

How is chronic hyperplastic candidiasis treated?

Answer 26

- remove risk factors (eg smoking) - use chlorhexidine 0.2% mouthwash, 100,000 units/ml, 1ml twice daily for 2 weeks - Topical antifungals: = Nystatin oral suspension: 100,000 units/ml, 1ml after food four times daily for 7 days, send 30ml = miconazole oromucosal gel: 20mg/g, pea-sized amount after four times daily, send 80g tube - Systemic antifungals: Fluconazole, Itraconazole, Voriconazole

Question 27

Why is fluconazole first-line treatment for chronic hyperplastic candidiasis?

Answer 27

A non-wipeable white patch indicated invasion into epithelial cells, so topical antifungals alone may not be effective. Fluconazole is first-line alongside smoking cessation and biopsy to assess for dysplasia if the lesion persists

Question 28

What are they key features of white sponge naevus?

Answer 28

- needs to be referred - premalignant - rare autosomal dominant disease - hereditary so must ask family history - soft, white and spongy plaques in the oral muosa - early childhood, adolescence - benign course

Question 29

How is white sponge naevus managed?

Answer 29

Treatment is challenging due to its genetic nature, but options include laser therapy or doxycycline

Question 30

Where is smoker's keratosis commonly found, and is it premalignant?

Answer 30

- Often found on the hard palate - not considered premalignant - associated with smoking or long-term drinking of hot beverages

Question 31

What are the characteristic signs of smoker's keratosis?

Answer 31

Pin-prick-like dots on the palate, caused by heat opening the ducts of minor salivary glands

Question 32

What causes frictional keratosis and where is it commonly found?

Answer 32

- very common - due to regular friction, mostly from teeth or dentures - presents as linea alba in the cheks or buccal mucosa, often bilateral - can be a discrete white patch anywhere in the mouth (esp edentulous ridges) - should resolve if source or irritation removed

Question 33

What is the management for frictional keratosis?

Answer 33

- Remove the frictional cause - symptomatic relief if required - biopsy if there is no improvement or if it is very dense to assess for dysplasia

Question 34

What is leukoplakia and how is it disgnosed?

Answer 34

Leukoplakia is a clinical term for a white patch that cannot be removed and does not fit into other histological or morphologial diagnosis. Clincial descriptor, not a diagnosis Diagnosis is made through histopathology to assess for dysplasia.

Question 35

What are the malignant tranformation risk of leukoplakia?

Answer 35

4-6% risk

Question 36

What are the clinical risk features of leukoplakia?

Answer 36

erythema, density, ulceration, locaation (lateral tongue, floor of mouth), sudden changes, spontaneous pain, hyperplastic margins (exophytic), verrucous keratosis / leukoplakia, pain and speckling

Question 37

What is the management of leukoplakia?

Answer 37

Histopathological assessment for dysplasia, regular monitoring, re-biopsy if clinical changes occur, and avoid risk factors like tobacco and alcohol. - if premalignant needs close monitoring

Question 38

In which condition is hairy leukoplakia most commonly seen?

Answer 38

- most commonly seen in HIV infection - may also be seen in other immunodeficient states like T-cell lymphoma and in patients taking ciclosporin

Question 39

What are the clinical features of hairy leukoplakia?

Answer 39

- classically occurs on the lateral borders of the tongue with a corrugated surface, though it can also be smooth. - Epstein-Barr virus is the likely cause, and it is not considered premalignant.

Question 40

What is the prognostic significance of hairy leukoplakia in HIV patients?

Answer 40

80% of patients with hairy leukoplakia are likely to develop full-blown AIDS within 32 months

Question 41

What viral infections are associated with oral lesions?

Answer 41

Hairy leukoplakia: Epstein-Barr Virus (EBV) Warts and papillomas: Human Papillomavirus (HPV) Koplik spots: Measles

Question 42

Clinical Risk features of oral lesions?

Answer 42

- Speckling or heterogenous - density, - uleration - location (lateral tongue, floor of mouth), - sudden changes - spontaenous pain/pain on palpatation, - hyperplastic margins/exophytic - verrucous keratosis/leukoplakiaappearance

Question 43

What are the differential diagnoses for red patches in the oral cavity?

Answer 43

Atrophic or erosive forms of oral lichen planus Candida infection Vesiculo-bullous lesions Erythroplakia or erythroleukoplakia (often associated with squamous cell carcinoma).