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Oral medicine > White and red lesions > Flashcards

White and red lesions Flashcards

1
Q

1. What is a white lesion of the oral mucosa?

A

An abnormal area of oral mucosa that appears whiter than the surrounding oral mucosa, usually slightly raised, roughened, and of different texture from adjacent normal tissues.

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2
Q
  1. What is a red lesion of the oral mucosa?
A

An area of oral mucosa that appears red compared to surrounding mucosa, which may be smooth and atrophic or granular and velvety.

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3
Q
  1. What changes can fungi cause in white lesions?
A

Fungi produce whitish pseudomembranes composed of sloughed epithelial cells, fungal mycelium, and neutrophils (e.g., candidiasis).

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4
Q
  1. What is hyperkeratosis?
A

Increased production of keratin.

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5
Q
  1. What is acanthosis?
A

Abnormal but benign thickening of the stratum spinosum (e.g., oral keratosis).

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6
Q
  1. What can increased collagen in the connective tissue indicate?
A

It may indicate oral submucous fibrosis.

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7
Q
  1. What are the main types of changes in white lesions?
A

Changes over the epithelium, within the epithelium, and under the epithelium.

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8
Q
  1. What are the main types of changes in red lesions?
A

Changes within the epithelium and under the epithelium.

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9
Q
  1. What is the etiology of frictional keratosis?
A

Chronic rubbing or friction against oral mucosa stimulates the epithelium to respond with an increased production of keratin.

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10
Q
  1. What is the clinical picture of frictional keratosis?
A

White plaque with a rough surface, commonly seen in areas traumatized by lips, lateral borders of the tongue, buccal mucosa along the occlusal line, and edentulous ridges.

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11
Q
  1. What is the recommended treatment for frictional keratosis?
A

Removal of the cause or habit, with follow-up to ensure clinical improvement. Biopsies should be performed on lesions that do not heal.

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12
Q
  1. What is morsicatio?
A

Habitual chewing, a parafunctional behavior done unconsciously, leading to lesions on the buccal and lip mucosa.

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13
Q
  1. What is the treatment for morsicatio?
A

Instruct the patient to stop the habit, or for those unable to stop, make an occlusal night guard.

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14
Q
  1. What is smokeless tobacco keratosis?
A

A white mucosal lesion in the area of tobacco contact, called smokeless tobacco keratosis or snuff dipper’s keratosis, caused by habitually chewing tobacco or dipping snuff.

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15
Q
  1. What are the histopathologic features of smokeless tobacco keratosis?
A

Hyperkeratinization, acanthosis, and epithelial vacuolizations with varying degrees of subepithelial inflammation.

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16
Q
  1. What is the treatment for smokeless tobacco keratosis?
A

Cessation of tobacco use, leading to normal mucosal appearance within 1-2 weeks. Biopsy for lesions that remain after 1 month or show concerning features.

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17
Q
  1. What is smoker’s palate (nicotine stomatitis)?
A

A white lesion that develops on the hard and soft palate in heavy smokers, characterized by a whitish palatal mucosa with slightly elevated white papules and red dots.

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18
Q
  1. What is the treatment for smoker’s palate?
A

Nicotine stomatitis is reversible once the habit is stopped. Biopsy any white lesion of the palatal mucosa that persists after 1 month of discontinuation of smoking.

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19
Q
  1. What are chemical injuries of the oral mucosa?
A

Non-keratotic white lesions caused by caustic chemicals such as aspirin, silver nitrate, formocresol, sodium hypochlorite, dental cavity varnishes, acid etching material, and hydrogen peroxide.

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20
Q
  1. What is the treatment for chemical burns?
A

Prevention, rinsing with water, topical steroid (0.1% triamcinolone paste), topical lidocaine gel, and carboxymethyl cellulose.

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21
Q
  1. What is oral leukoplakia?
A

A predominantly white lesion of the oral mucosa that cannot be characterized as any other definable lesion, considered precancerous with risk of malignant transformation.

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22
Q
  1. What are the clinical features of leukoplakia?
A

Occurs in adults older than 50 years, more frequently in men, painless unless ulcerated, variable in size, and may cause loss of pliability and flexibility of the oral mucosa.

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23
Q
  1. What are the types of leukoplakia?
A

Homogenous leukoplakia, non-homogenous leukoplakia (speckled leukoplakia/erythroleukoplakia), verrucous/villiform leukoplakia, and proliferative verrucous leukoplakia (PVL).

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24
Q
  1. What are the clinical changes suggestive of malignant transformation in leukoplakia?
A

Ulceration, erythroplakia, induration, and lymphadenopathy.

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25
Q
  1. How is leukoplakia diagnosed and managed?
A

Diagnosis based on clinical observation and histologic examination, ruling out other conditions, and surgical excision for definitive treatment. Follow-up is important due to recurrence risk.

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26
Q
  1. What is erythroplakia?
A

A red lesion of the oral mucosa that cannot be characterized as any other definable lesion, often asymptomatic but may cause a burning sensation with food intake.

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27
Q
  1. What is oral submucous fibrosis?
A

A chronic disease affecting the oral mucosa, pharynx, and upper esophagus, commonly associated with areca nut chewing, leading to fibrosis, loss of resilience, and interference with speech and tongue mobility.

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28
Q
  1. What is the treatment for oral submucous fibrosis?
A

Focused on cessation of the chewing habits. Early lesions have a good prognosis as they may regress.

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29
Q
  1. What is oral hairy leukoplakia?
A

A white lesion on the lateral or ventral surfaces of the tongue in patients with severe immunodeficiency, strongly associated with Epstein-Barr virus (EBV) and low CD4+ T lymphocyte levels.

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30
Q
  1. What is the clinical picture of oral hairy leukoplakia?
A

Well-demarcated white lesion on the lateral border of the tongue, often bilateral, varying from a flat plaque-like lesion to one with papillary hair-like projections.

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31
Q
  1. How is oral hairy leukoplakia diagnosed and treated?
A

Diagnosis based on clinical characteristics, histopathologic examination, and detection of EBV. No treatment is indicated; the condition usually disappears with antiviral treatment for HIV.

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32
Q
  1. What is a mucous patch?
A

A superficial grey area of mucosal necrosis seen in secondary syphilis, characterized by multiple painless grayish white plaques on the tongue, gingiva, palate, and buccal mucosa.

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33
Q
  1. What is a parulis (gumboil)?
A

A localized accumulation of pus in the gingiva or alveolar mucosa, originating from periapical or periodontal abscesses.

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34
Q
  1. What is the treatment for a parulis?
A

Treatment of the non-vital tooth or periodontal abscess.

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35
Q
  1. What is oral candidiasis?
A

The most prevalent opportunistic infection affecting the oral mucosa, caused primarily by the yeast Candida albicans.

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36
Q
  1. What are the predisposing factors for oral candidiasis?
A
  • Local factors: denture wearing, smoking, steroids, hyperkeratosis, imbalance of oral microflora.
  • General factors: immunosuppressive diseases, malabsorption, malnutrition, immunosuppressive drugs, chemotherapy, endocrine disorders.
37
Q
  1. What is acute pseudomembranous candidiasis (thrush)?
A

An infection seen in patients medicated with antibiotics, immunosuppressants, or with immunosuppressive diseases, characterized by loosely attached membranes that leave an inflamed area when removed.

38
Q
  1. What are the classifications of oral candidiasis?
A
  • Primary oral candidiasis: acute pseudomembranous, acute erythematous, chronic pseudomembranous, chronic erythematous, chronic plaque-like, chronic nodular, and Candida-associated lesions. Secondary oral candidiasis: various syndromes.
39
Q

What are the common predisposing factors for acute erythematous candidiasis?

A

Predisposing factors include antibiotic use, corticosteroid use, immunosuppression, diabetes, and xerostomia.

40
Q

How does immunosuppression contribute to the development of acute erythematous candidiasis?

A

Immunosuppression weakens the body’s defenses, allowing Candida to overgrow in the oral cavity.

41
Q

What are the characteristic clinical features of acute erythematous candidiasis?

A

Clinical features include red, inflamed patches on the oral mucosa, particularly on the palate and tongue.

42
Q

How does acute erythematous candidiasis typically present on the palate and tongue?

A

It presents as red, inflamed, and sometimes painful areas on the palate and tongue.

43
Q

What are the differential diagnoses for acute erythematous candidiasis?

A

Differential diagnoses include erythroplakia, geographic tongue, and mucositis.

44
Q

What is antibiotic sore mouth, and how is it caused?

A

Antibiotic sore mouth, or atrophic candidiasis, is caused by prolonged antibiotic use disrupting normal oral flora, leading to Candida overgrowth.

45
Q

What are the main symptoms of atrophic candidiasis?

A

Symptoms include a sore, red tongue, loss of papillae, and a burning sensation in the mouth.

46
Q

How does chronic plaque-type candidiasis present clinically?

A

Chronic plaque-type candidiasis presents as white, adherent plaques on the buccal mucosa and tongue.

47
Q

What are the distinguishing features of nodular candidiasis compared to other forms of oral candidiasis?

A

Nodular candidiasis presents as white, hyperplastic nodules that are firm and do not scrape off easily.

48
Q

How can chronic plaque-type and nodular candidiasis be differentiated from leukoplakia?

A

Leukoplakia does not usually scrape off and lacks the inflammatory response seen in candidiasis; biopsy may be needed for differentiation.

49
Q

What is denture stomatitis, and what causes it?

A

Denture stomatitis is an inflammation of the oral mucosa under a denture, caused by poor denture hygiene, continuous wear, and Candida overgrowth.

50
Q

How is denture stomatitis classified?

A

It is classified into three types: Type I (localized inflammation), Type II (generalized erythema), and Type III (inflammatory papillary hyperplasia).

51
Q

What are the different types of denture stomatitis according to Newton’s classification?

A

Newton’s classification includes Type I (pinpoint hyperemia), Type II (diffuse erythema), and Type III (granular surface).

52
Q

What are the risk factors for developing denture stomatitis?

A

Risk factors include poor denture hygiene, ill-fitting dentures, continuous wear, and systemic conditions like diabetes.

53
Q

What are the typical clinical signs of denture stomatitis?

A

Clinical signs include redness, swelling, and tenderness of the mucosa beneath the denture.

54
Q

How does denture stomatitis affect the mucosa beneath the denture?

A

It causes inflammation, erythema, and sometimes ulceration of the mucosa.

55
Q

What are the common etiological factors for angular cheilitis?

A

Etiological factors include Candida infection, Staphylococcus infection, nutritional deficiencies, and ill-fitting dentures.

56
Q

How does angular cheilitis present clinically?

A

It presents as red, inflamed, and cracked corners of the mouth, sometimes with crusting or ulceration.

57
Q

What are the common complications associated with untreated angular cheilitis?

A

Complications can include secondary bacterial infection, chronic pain, and scarring.

58
Q

What is the etiology of median rhomboid glossitis?

A

It is believed to be associated with chronic Candida infection and may be linked to smoking and denture use.

59
Q

Describe the clinical appearance of median rhomboid glossitis.

A

It appears as a well-demarcated, red, rhomboid-shaped area on the midline of the dorsum of the tongue.

60
Q

What are the common laboratory methods used to diagnose oral candidiasis?

A

Methods include KOH preparation, culture, histopathological examination, and molecular techniques.

61
Q

How is a potassium hydroxide (KOH) preparation used in the diagnosis of candidiasis?

A

KOH preparation involves scraping the lesion and placing it in KOH solution to visualize Candida hyphae under a microscope.

62
Q

What role does culture play in the diagnosis of oral candidiasis?

A

Culture involves growing Candida species from oral samples to confirm diagnosis and identify specific strains.

63
Q

How can molecular methods aid in the diagnosis of candidiasis?

A

Molecular methods, like PCR, can identify Candida DNA in samples, providing a rapid and specific diagnosis.

64
Q

What are the general treatment principles for oral candidiasis?

A

General principles include eliminating predisposing factors, maintaining good oral hygiene, and using antifungal medications.

65
Q

How important is the management of predisposing factors in the treatment of oral candidiasis?

A

It is crucial to manage predisposing factors to prevent recurrence and ensure effective treatment.

66
Q

What are the commonly used antifungal medications for oral candidiasis?

A

Common antifungals include nystatin, clotrimazole, fluconazole, and itraconazole.

67
Q

What is the recommended treatment regimen for acute erythematous candidiasis?

A

Treatment usually involves topical antifungals like nystatin or clotrimazole and addressing underlying causes.

68
Q

How should antibiotic sore mouth be managed?

A

Management includes discontinuing or adjusting antibiotics and using topical or systemic antifungal agents.

69
Q

What are the treatment options for chronic plaque-type candidiasis?

A

Treatment options include topical and systemic antifungals and improving oral hygiene.

70
Q

How should nodular candidiasis be treated?

A

Treatment involves antifungal therapy, potentially with systemic agents, and addressing predisposing factors.

71
Q

What are the effective treatment strategies for denture stomatitis?

A

Strategies include antifungal treatment, improving denture hygiene, and ensuring proper denture fit.

72
Q

How can denture hygiene be improved to prevent and treat denture stomatitis?

A

Improving hygiene involves regular cleaning, removing dentures at night, and using antiseptic solutions.

73
Q

What are the key differences between acute and chronic oral candidiasis?

A

Acute candidiasis presents with sudden onset and erythema, while chronic candidiasis involves long-term, persistent lesions.

74
Q

How does denture stomatitis differ from other forms of oral candidiasis?

A

Denture stomatitis specifically affects the mucosa beneath dentures, while other forms can occur on any oral mucosa.

75
Q

What are lichenoid reactions, and what causes them?

A

Lichenoid reactions are inflammatory mucosal lesions caused by immune-mediated responses to various triggers like drugs or dental materials.

76
Q

How can lichenoid reactions be distinguished from oral lichen planus (OLP)?

A

Lichenoid reactions often have a known trigger and can resemble OLP clinically but may resolve upon removing the trigger.

77
Q

What are the proposed etiological factors for oral lichen planus?

A

Etiological factors include genetic predisposition, immune system dysregulation, and potential environmental triggers.

78
Q

How does the immune system contribute to the development of OLP?

A

The immune system attacks the basal cells of the oral mucosa, leading to inflammation and characteristic lesions.

79
Q

What role do genetic factors play in the etiology of OLP?

A

Genetic predisposition may increase susceptibility to OLP, often in conjunction with other factors.

80
Q

What are the potential triggering factors for OLP?

A

Triggers can include stress, trauma, systemic diseases, and certain medications.

81
Q

Describe the typical clinical features of oral lichen planus.

A

Clinical features include white, lacy patches (Wickham’s striae), red, swollen tissues, and ulcerations.

82
Q

What are the common oral manifestations of OLP?

A

Oral manifestations include reticular, erosive, atrophic, and plaque-like lesions, often on the buccal mucosa and tongue.

83
Q

How does OLP typically present on the buccal mucosa?

A

It presents as interlacing white lines (Wickham’s striae) with or without erythematous or erosive areas.

84
Q

What are the characteristic features of OLP on the tongue and gingiva?

A

On the tongue, OLP appears as white patches or erosions; on the gingiva, it often causes desquamative gingivitis.

85
Q

How can OLP be differentiated from other oral white lesions?

A

OLP can be differentiated by its characteristic patterns, chronic nature, and histopathological examination.

86
Q

What are the clinical features of the papular form of OLP?

A

The papular form presents as small, white, raised lesions on the mucosa.

87
Q

How does atrophic OLP present clinically?

A

Atrophic OLP presents as red, erythematous areas, often with a background of reticular striae.

88
Q

Describe the clinical appearance of bullous/erosive OLP.

A

Bullous/erosive OLP presents as painful erosions or ulcers with surrounding erythema and sometimes blister formation.

Oral medicine (7 decks)

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