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Lesions and patches Flashcards

1
Q

Useful websites

A

https://www.rdhmag.com/pathology/article/14291269/white-lesions-of-the-oral-cavity-and-oral-systemic-health-a-review-for-the-dental-hygienist

https://www.rdhmag.com/pathology/article/14296806/red-ulcerative-lesions-a-literature-review-of-those-nonwhite-lesions

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2
Q

White patches caused by a variation of normal anatomy? (2)

A
  1. Fordyce spots
  2. Leukoedema
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3
Q

What is a hereditary cause of a white patch?

A

White sponge naevus

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4
Q

What are infectious causes of white patches? (3)

A
  1. Fungal: candidosis
  2. Viral: oral hairy leukoplakia
  3. Bacteria: syphilis
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5
Q

What are inflammatory causes of white patches? (2)

A
  1. Oral submucous fibrosis
  2. Erythema Migrans (geographic tongue)
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6
Q

What is an idiopathic causes of white patches?

A

Leukoplakia

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7
Q

What are systemic causes/immunological causes of white patches? (4)

A
  1. Oral lichen planus
  2. Oral lichenoid lesions
  3. Graft vs host disease
  4. Systemic/discoid lupus erythematosus
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8
Q

What are reactive causes of white patches? (6)

A
  1. Frictional keratosis
  2. Occlusal keratosis
  3. Tobacco associated lesions
  4. Chemical burns
  5. Thermal burns
  6. Actinic chelitis
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9
Q

What are 3 infectious causes of red patches?

A
  1. Fungal: candidosis
  2. Viral: oral hairy leukoplakia
  3. Bacterial: syphilis
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10
Q

What are 2 inflammatory causes of red patches?

A
  1. oral submucous fibrosis
  2. erythema migrans (geographic tongue)
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11
Q

What are 2 vascular causes of red patches?

A
  1. Capillary haemangioma
  2. Cavernous haemangioma
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12
Q

What is an idiopathic cause of red patches?

A

Geographic tongue (erythema migrans)

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13
Q

What are 3 neoplastic causes of red patches?

A
  1. Erythroplakia
  2. OSCC - oral squamous cell carcinoma
  3. Kaposi sarcoma
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14
Q

What are 4 systemic/immunological causes of red patches?

A
  1. Oral lichen planus
  2. Oral lichenoid lesions
  3. Graft vs host disease
  4. Systemic/discoid lupus erythematosus
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15
Q

What are 2 causes of endogenous pigmentation? (broad categories)

A
  1. increase number of melanocytes
  2. increase melanin production
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16
Q

What are 5 exogenous factors causing pigmentation?

A
  1. Tattoo on oral mucosa
  2. Foreign bodies - e.g. amalgam fragments embedded in tissue = amalgam tattoos
  3. Heavy metals e.g. mercury can cause pigmentation secondary to heavy metal poisoning
  4. Smoking = smoker’s melanosis
  5. Drugs = minocycline, oral contraceptive, arsenic, heroin drug use.
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17
Q

What are 4 forms of oral endogenous focal pigmentation? (+ 3 added extras)

A
  1. Oral nevi - increase in melanocytes
  2. Melanotic macules - increase in melanin production
  3. Malignant melanoma - malignant increase in melanocytes
  4. Oral melanocanthoma - increase in melanocytes
    –> could also be ecchymosis, bleeding + trauma
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18
Q

What are 7 forms of oral endogenous diffuse pigmentation?

A
  1. Oral melanotic macules (ephelis)
  2. Racial pigmentation
  3. Addison’s disease
  4. ACTH producing tumours
  5. Physiological pigmentation of pregnancy (melasma)
  6. Peutz Jegher’s syndrome
  7. Post inflammatory melanin incontinence
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19
Q

What are 8 types of diffuse swellings in the OC?

A
  1. Angioedema = severe local swelling of skin
  2. Orofacial granulomatosis = chronic swelling of OF tissue with no GI involvement. Non-caseating granulomatous inflammation on histology slide.
  3. Oral Crohn’s disease = autoinflammatory disease presenting in OC
  4. Melkersson Rosenthal syndrome = orofacial swelling, fissured tongue, facial palsy.
  5. Sarcoidosis = inflammatory disease where granulomas are formed throughout organs
  6. Allergic cheilitis
  7. Irrational cheilitis
  8. SG swellings
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20
Q

Name 4 viruses that present in the OC?

A
  1. Human Herpesvirus (HHV)
  2. Coxsackie virus
  3. Human papilloma virus (HPV)
  4. Human immunodeficiency virus (HIV)
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21
Q

What are 5 types of HHV that present in the OC?

A
  1. HHV1 = Herpes simplex virus 1 (HSV1)
  2. HHV3 = Varicella zoster virus (VZV)
  3. HHV4 = Epstein-Barr virus (EBV)
  4. HHV8 = Human herpes virus 8
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22
Q

Name 8 potentially malignant lesions.

A
  1. Leukoplakia
  2. Proliferative verrucous (warty) leukoplakia
  3. Erythroplakia
  4. Oral lichen planus (OLP)
  5. Oral submucous fibrosis
  6. Discoid lupus erythematosus
  7. Actinic cheilitis
  8. Chronic hyperplastic candidosis
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23
Q

What does HHV1/HSV1 cause? (2)

A

Gingivostomatitis
Sequelae: herpes labialis

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24
Q

What does HHV2/HSV2 cause? (2)

A

Anogenital herpes
Sequelae: oral ulcers

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25
Q

What does HHV3/VZV cause? (2)

A

Chicken pox
Sequelae: shingles

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26
Q

What does HHV4/EBV cause? (3)

A

Glandular fever/infectious mononucleosis
Sequelae: Oral hairy leukoplakia
-> Lymphoma

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27
Q

What does HHV5/CMV (cytomegalovirus) cause? (2)

A

Glandular fever/infectious mononucleosis
Sequelae: ulcers

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28
Q

What does HHV8 cause? (1)

A

Kaposi’s sarcoma

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29
Q

What 2 main lesions does HIV cause?

A
  1. Oral candidiasis
  2. Oral hairy leukoplakia
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30
Q

What are 2 features of dysplasia?

A
  1. Basal cell hyperplasia replaces prickle cell layer
  2. Dropped rete ridges
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31
Q

What are the 6 layers of stratified squamous epithelium?

A
  1. Keratin layer
  2. Granular cell layer
  3. Prickle cell layer
  4. Basel cell layer
  5. Basement membrane
  6. Lamina propria (bound to underlying connective tissue)
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32
Q

What are 12 oral complications of radiotherapy?

A
  1. Mucositis = widespread oral erythema, pain, ulceration + bleeding. Hugely impairs QoL: pain, difficulty eating + drinking
  2. Ulceration
  3. Radiation caries = result from xerostomia if SG affected + disturb flora (shift cariogenic bacteria)
  4. Periodontal disease = periodontal tissues have high turnover rate
  5. Dentine hypersensitivity
  6. Xerostomia = affect parotid and submandibular SG.
  7. Loss of taste
  8. Dysphagia = might be on thickened diets
  9. Opportunistic infection = e.g. candida
  10. Trismus = MOM affected, fibrosed and hard
  11. Osteoradionecrosis
  12. Craniofacial defects (children)
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33
Q

Name 4 general signs of systemic cancer found in mouth.

A
  1. Purpura = thrombocytopenia (below 150x 10^9 per ml)
  2. Excessive bleeding = thrombocytopenia
  3. Infections = neutropenia
  4. Anaemia = atrophic glossitis, aphthous ulcers etc.
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34
Q

What are 3 signs of Type 3 Von Willebrand disease and what 3 treatments may they require?

A
  1. Purpura
  2. Prolonged bleeding post trauma
  3. Gingival bleeding

A. Tranexamic acid
B. Desmopressin
C. Plasma containing vWF

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35
Q

What is the most common type of oral tumour?

A

90% oral squamous cell carcinoma
10% minor salivary gland tumours, lymphomas, malignant melanoma

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36
Q

What are 6 red flags for oral cancers with a lesion?

A
  1. Persistent ulcer (more than 2 weeks).
  2. Difficulty swallowing
  3. Loosening of teeth
  4. Radiographic features e.g. radiolucency as tumour invades bone
  5. Pain/perineural involvement e.g. paraesthesia
  6. Neck mass - indicated metastasis.
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37
Q

What are 6 main non-SSC head and neck cancers?

A
  1. Lymphoma = cancer of lymph nodes
  2. SG malignancy = both major and minor glands
  3. Odontogenic malignancy = ameloblastic carcinoma
  4. Melanoma = cancer of melanocytes
  5. Sarcoma = cancer of mesenchymal origin
  6. Metastasis = secondary tumours having spread elsewhere
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38
Q

What 4 factors affect survival rate from oral cancer?

A
  1. anatomic site
  2. stage (TMN) - size, nodal involvement, metastasis
  3. co-morbidities - heart problems
  4. tumour biology
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39
Q

What are 4 oral manifestations of anaemia?

A
  1. Atrophic glossitis = inflamed tongue
  2. Angular cheilitis = inflamed corners of mouth
  3. Aphthous like ulceration
  4. Dyskinesia = altered sensation e.g. burning
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40
Q

What are 4 differentials for primary herpetic gingivostomatitis?

A

A. Erythema multiforme (recurrent and associated with skin lesions)
B. Herpetiform recurrent aphthous stomatitis
C. Herpangina (caused by coxsackie viruses with similar vesicles but lips not involved)
D. Hand, foot and mouth disease

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41
Q

What are 10 oral manifestations of HIV (decreasing in prevalence)

A
  1. Oral candidosis
  2. Oral hairy leukoplakia
  3. HSV
  4. Kaposi’s sarcoma
  5. Non-specific ulceration
  6. Aphthous ulceration
  7. Perio
  8. SG disease
  9. Oral melanotic hyperpigmentation
  10. Oral warts
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42
Q

What are 8 oral features of orofacial granulomatosis?

A
  1. Cobblestone mucosa
  2. Pyostomatitis vegetans = thin aphthous like ulcers, v painful
  3. Staghorning
  4. Swelling of lips
  5. Fissured lips/tongue
  6. Mucosal tags
  7. Perivermillion erythema (redness around mouth)
  8. Angular cheilitis
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43
Q

What are 6 oral features of IBD (ulcerative colitis/crohn’s disease)?

A
  1. Cobblestone mucosa
  2. Pyostomatitis vegetans (snail-track ulceration)
  3. Staghorning
  4. Fissured swollen lips
  5. Mucosal tags
  6. Severe aphthous ulceration
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44
Q

What are 5 groups of systemic diseases associated with recurrent aphthous ulcers/aphthous like ulceration?

A
  1. GI disease (IBS - crohn’s disease & ulcerative colitis, and coeliac)
  2. Drugs e.g. NSAIDS
  3. Haematological disease (anaemia + haem deficiencies - iron, B12, folic acid deficiency)
  4. Vasculitis (Bechets and SLE)
  5. Immunodeficiency (AIDS)
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45
Q

How does ALU differ from RAU?

A

It is clinically identical however differs by:
- Not starting in childhood
- Does not resolve with age
- Occurs in association with signs+symptoms not seen in RAU
- Occurs in association with systemic disease
- Occurs in association with drugs (NSAIDs)

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46
Q

What is the HPV vaccine and what types does it protect from?

A

Gardasil - vaccinates boys and girls
HPV 6, 11, 16, 18

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47
Q

What is the most common non-oncogenic HPV infections?

A

Squamous papilloma (cauliflower surface) - HPV 6 + 11
Condyloma acuminata (infective warts) - HPV 2, 6 + 11
Verruca vulgaris (mucosal warts) - HPV 2 + 4

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48
Q

How do you confirm a diagnosis of HPV infection and what is the management?

A

Diagnosis: confirm by histopathology
Management: removal by excision biopsy

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49
Q

What is Heck’s disease/Focal epithelial hyperplasia?

A

Heck’s disease is a rare, benign condition that affects the oral mucosa. Caused by HPV 13 + 32
It’s characterized by:
- Soft, painless papules
- Multiple nodular lesions
- Lesions that are often similar in color to the surrounding mucosa
- Lesions that may appear whitish if found in areas of occlusal trauma

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50
Q

What are 4 oral problems of immunosuppression?

A
  1. Increased risk of opportunistic infections e.g. candidosis (fungal) and HSV (viral)
  2. Increased risk of poor wound healing + wound infections
  3. Increased risk of malignancy - skin + lip cancer - lymphomas.
  4. Need for antibiotic cover (only if neutropenic) WBC < 3x10^9.
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51
Q

What are 10 predisposing factors to oral candidosis?

A
  1. Physiological - e.g. age, pregnancy
  2. Local trauma - e.g. mucosal irritation, denture
  3. Antibiotics - e.g. broad spectrum
  4. Corticosteroids - e.g. inhalers, systemic
  5. Malnutrition - e.g. haematinic deficiency
  6. Endocrine disorders e.g. diabetes
  7. Malignancy e.g. SCC, leukaemia
  8. Immune deficiency e.g. HIV infection
  9. Xerostomia e.g. drug related, Sjogren’s syndrome
  10. Anaemia
52
Q

What are 7 features of osteomyelitis?

A
  1. Mixed lytic sclerotic
  2. Ill defined lucency
  3. Moth eaten
  4. Onion skin periosteal reaction
  5. Sequestra
  6. Known/identifiable source
  7. Sinus tract
53
Q

What are 7 features of osteoradionecrosis?

A
  1. Less sclerosis
  2. Ill defined lucency
  3. Slow progression
  4. No periosteal reaction
  5. Sequestra
  6. Previous radiotherapy
  7. Pathological # risk
54
Q

What are 6 features of MRONJ?

A
  1. Mixed lytic sclerotic
  2. Ill defined lucency
  3. Non healing sockets
  4. Periosteal reaction
  5. Large sequestra
  6. Widened PDL with thickened lamina dura
55
Q

What are 7 features of malignancy?

A
  1. Moth eaten
  2. Ill defined lucency
  3. Fast progression
  4. No periosteal reaction
  5. No sequestration
  6. resorption of adjacent teeth
  7. Numbness
56
Q

Where can an infection of upper central incisor spread?

A

Labial sulcus - thin labial cortical plate.
Nasal cavity if long roots

57
Q

Where can an infection of upper lateral incisors spread?

A

Palate - laterals have steep inclination into palate

58
Q

Where can an infection of upper canine spread?

A

Labial sulcus
Infraorbitally up towards eye
Can spread to cavernous sinus: cavernous sinus thrombosis.

59
Q

What symptom can cavernous sinus thrombosis cause?

A

Effects sight and cyanosis
This is because can restrict blood flow to jugular blood return and cause pressure on optic nerve.

60
Q

Where can an infection of upper posteriors spread?

A

Buccal sulcus: due to thin buccal cortical plate and high attachment of buccinator

61
Q

Where can an infection of lower incisor spread?

A

Labial sulcus: thin labial cortical plate.
Submentalis space: as mentalis attach above apices

62
Q

Where can an infection of lower posteriors spread?

A

Spread lingually. Depends on relationship of apices to attachment of mylohyoid (mylohyoid line).
Above mylohyoid line = sublingual space.
Below mylohyoid line = submandibular space
–> 1st molar is variable.
Spaces in neck = retropharyngeal + lateral pharyngeal -> infection can then spread to mediastinum.

63
Q

What is desquamative gingivitis?

A

Full thickness gingivitis in where there is thinning of epithelium to the extent that it is ‘peeled’ off with any pressure.
Appearance: red, glazed, friable tissues
–> It gets worse as the inflammation is exasperated in areas where it is painful to brush resulting in plaque accumulation.

64
Q

What are 5 differential diagnoses to PV + MMP for Bullous lesions?

A
  1. Dermatitis herpetiformis - linked to coeliac disease.
  2. Linear IG-A disease - common in children
  3. Epidermolysis bullosa acquisita - v rare.
  4. Erythema multiforme
  5. Viral infections - can cause blisters.
65
Q

How do you describe an ulcer?

A

Base - colour?
Firmness - when palpated is it soft or firm?
Edge - is it well demarcated or inflammed?
Painful response - suggests inflammatory response
Local tissues - any changes, any widespread inflammation?
Regional lymph nodes - are inflamed or enlarged suggesting infection or inflammation

66
Q

What are signs of a malignant ulcer?

A

Lasts longer than 2 weeks
Firm
Rolled up wel defined margins
Can be painful or painless

67
Q

What is in included in a Full Blood Count (FBC)?

A

Hb (haemoglobin level)
MCV (size RBCs)
Lymphocyte count (raised when infections + inflammation)
Neutrophil count
Platelet count

68
Q

What is included in Coagulation blood tests?

A

PT = prothrombin time (9-13s)
–> check for warfarin tx and liver disease (alcoholics)

APTT = activated partial thromboplastin time (22-36s)
–> check for defects in clotting system and heparin treatment

69
Q

What is in biochemical blood tests?

A

Liver function test
Random blood glucose
Haematinic assays
CRP

70
Q

What is in immunological blood tests?

A

Autoantibodies
Immunoglobulin levels
Electrophoresis
Complement levels

71
Q

What microbiological investigations are there?

A
  1. Direct lesional sampling - take a swab of infection
    a. Swab for culture and sensitivity (fungal and bacterial)
    b. Swab for PCR
    C. Tissue - biopsy (histopathology)
  2. Serum based assays - blood based investigations where you test for certain antibodies produced.
72
Q

What 3 antidepressants raise serotonin + NA synaptic levels that can be used in chronic pain?

A

Amitriptyline
Duloxetine
Mirtazapine

73
Q

Name 2 GABA agonists

A

Gabapentin
Pregablin

74
Q

What are 3 forms of immunosuppressive drugs?

A
  1. Glucocorticoids e.g. prednisolone
  2. Non-glucocorticoids drugs e.g. tacrolimus (a calcineurin inhibitor), azathioprine and mycophenolate mofetil (which inhibit purine synthesis)
  3. Antibodies e.g. polyclonal + monoclonal e.g. infliximab
75
Q

What are complications of glucocorticoids?

A

S - seizures
T - thinning skin
E - excessive weight gain
R - rapid heartbeat
O - mood changes
I - infection
D - disturbed vision
S - slow wound healing

> risk opportunistic infection
risk poor wound healing
need of Abx cover?

76
Q

What are 3 topical steroids that are prescribed in the mouth?

A
  1. Dermovate = clobetasol proprionate (apply to lesions in mouth)
  2. Clinel inhaler = beclometasone diproprionate
  3. Betnesol = tablet dissolved in water + used as MW.
77
Q

Name 3 drugs used to treat bacterial infections

A

Metronidazole Abx –> ANUG
Bactroban = mupirocin Abx => staphylococcus angular cheilitis
Chlorhexidine gluconate –> fungal + bacterial oral infections

78
Q

What interactions does warfarin have with aspirin?

A

Aspirin displaces warfarin from plasma proteins, leading the greater levels of active warfarin -> therefore increases bleeding risk.

79
Q

What interactions do azole antifungals have with warfarin?

A

Decreased clearance of warfarin leading to elevate blood concentrations of warfarin which increases INR + bleeding risk.

80
Q

What are the 4 main causes of secondary (acquired immunodeficiencies)?

A
  1. Malnutrition - T cell number + function will fall in proportion to levels of protein in body. Resolves if malnutrition tx.
  2. Drugs - many drugs work by suppressing immune system to manage condition e.g. transplant cover, corticosteroids, chemo, biologics/monoclonal antibodies.
  3. Chronic infections - AIDS from HIV infection (CD4 count <200 per ml)
  4. Malignancies - leukaemia, hodgkins lymphoma.
81
Q

What are 11 oral presentations of immunocompromisation?

A
  1. Seborrheic dermatitis - often associated with HIV
  2. Erythematous candidiasis - antibiotic sore mouth - appears red + tender (opportunistic infection)
  3. Acute pseudomembranous candidiasis - classic thrush with white patches that can be removed to leave erythematous tissues.
  4. Oral hairy leukoplakia - triggered by EBV in immunocompromised patients. Presents with white stripes.
  5. Karposi sarcoma - caused by HHV-8 in anyone with weakened immune system. Present as blue swelling, can be treated with intralesional chemo or radiotherapy.
  6. Oral ulceration - associated with neutropenia
  7. Herpes zoster - shingles, causes a rash in one or two adjacent dermatomes, can reactivate.
  8. Parotid swelling - can be due to number of issues e.g. HIV or sialadenitis (infection), lymphoma.
  9. Lymphomas
  10. ANUG - if pt has good OH + non-smoker + young, consider HIV screen
  11. Lymphadenopathy - these pts are prone to infection so lymph tissues which are key in fighting infections will be more stimulated + raised.
82
Q

What are 6 general complications of cancer?

A

C - cachexia + wasting
A - anaemia + infection
N - nutrient deficiencies
C - cutaneous manifestations (skin lesions)
E - endocrine disorders
R - rare manifestations

83
Q

Common metastases that present in the jaws or oral soft tissues are commonly from…?

A

Breast, lung, prostate primaries

84
Q

What are 4 general oral signs of systemic cancers?

A
  1. Purpura - thrombocytopenia (below 150 x 10^9 per ml)
  2. Excessive bleeding - thrombocytopenia
  3. Infections - neutropenia
  4. Anaemia - atrophic glossitis, aphthous ulcers, angular cheilitis, dyskinesia.
85
Q

What are fordyce spots?

A

Prominent sebaceous glands in cheek or buccal mucosa.
They are a variation of normal anatomy.

86
Q

How do you diagnose fordyce spots?

A

Clinical diagnosis. No special investigations needed.

87
Q

What is a leukoedema?

A

White oedematous lesion of buccal + labial mucosa. Diffuse or patchy. Asymptomatic.
Variation of normal anatomy. More common in smokers.
It is most common in the African American population, with reports of patients having this feature since early childhood.

88
Q

How does leukoedema present?

A

Diffuse, milk-white, opalescent lesion on the bilateral buccal mucosa that disappears when the mucosa is stretched.

89
Q

How do you diagnose leukoedema?

A

Clinical diagnosis. Lesions disappear when mucosa is stretched (helps differentiate).

90
Q

What are differentials of leukoedema?

A

Leukoplakia or white sponge naevus.

91
Q

What is hyperkeratosis?

A

Formation of keratin with a thickened stratum cornea keratin layer.
Also called Linea alba, frictional keratosis.

92
Q

How does hyperkeratosis appear?

A

Distinct, localised, translucent-to-opaque white asymptomatic patch, well demarcated.

93
Q

How do you diagnose hyperkeratosis?

A

Clinical diagnosis?
Will not be wiped off with gauze.
If concern/continued keratosis despite removal of cause of biopsy.

94
Q

How do you treat hyperkeratosis?

A

Remove irritant - smooth tooth surface/restoration.

95
Q

What is proliferative verrucous leukoplakia?

A

It is a variant of leukoplakia with hyperkeratosis and verrucous nature.

96
Q

What is the appearance of proliferative verrucous leukoplakia?

A

Rough, irregular surface which slowly expands.
White plaque of thickened skin that forms rough, wart-like (verrucous) lesions that have a cauliflower appearance.
PVL appears as white patches that can’t be scraped off, and can grow on the tongue, gums, cheeks, and soft tissue between the lips and gums

97
Q

How do you diagnose proliferative verrucous leukoplakia?

A

Clinical diagnosis. Biopsy if concerned. Dysplasia is late feature.
Excisional biopsy with histopathological examination to confirm diagnosis?

98
Q

Why is proliferative verrucous leukoplakia concerning?

A

Potentially malignant with high recurrence rate and a high rate of transformation into oral squamous cell carcinoma.

99
Q

Who is proliferative verrucous leukoplakia most common in?

A

PVL has a gender predilection, with a female to male ratio of approximately 4:1, a mean age of 66 years, and a site preference for the buccal mucosa, palate, tongue, and gingivae.12

Conventional risk factors are unknown; however, PVL is known for its aggressive ability for recurrence at 90%, even after excision.12

100
Q

What is a leukoplakia?

A

A white patch that cannot be identified clinically or pathologically, and is not related to any cause other than an association with tobacco smoking.
1-5% of the population has leukoplakia. 1-2% undergo transformation.

101
Q

How can you subdivide leukoplakia?

A

By appearance.
A. Homogenous - white patch with consistent texture, not raised.
B. Heterogenous - white patch but has surface irregularities (incr risk of malignancy )
C. Erythroleukoplakia - white patch with red regions of erosion. (highest risk of malignancy)

102
Q

What percentage of population has a leukoplakia? What percentage undergo transformation?

A

1-5% pop has leukoplakia
1-2% undergo transformation

103
Q

What are risk factors of leukoplakia being malignant?

A
  1. Leukoplakia in absence of tobacco
  2. Female
  3. High risk oral cancer sites (FOM, ventral + lateral tongue, retromolar pad, soft palate)
  4. Raised
  5. Induration (fixed to underlying tissue)
  6. Ulceration
  7. Severe dysplasia (affecting entire thickness)
104
Q

What are the high risk oral cancer sites? (4)

A

Floor of mouth
Ventral and lateral tongue
Retromolar pad
Soft palate

105
Q

What fraction of leukoplakias transform in the first 2 years?

A

1/3 transform in first 2 years –> long term monitoring necessary.

106
Q

How do you diagnose leukoplakia?

A

Histopathological exam. Oral brush biopsy (remove cells from surface).
- see:
keratosis, hyperplasia (thickened epithelium), dropped rete ridges.

107
Q

How do you treat leukoplakias with severe dysplasia?

A

Surgical excision - if not fully removed, still malignant risk

108
Q

What is important for leukoplakias?

A

Monitoring! - need 2/3x/year using photos.
No effective medical tx yet.

109
Q

What is a white sponge naevus?

A

Bilateral white patches involving extensive areas of cheeks.
Presents in childhood or young adulthood. Hereditary disease.
Atrophic sparse white lesions.

White sponge nevus (WSN) is a rare, autosomal dominant hereditary disorder.

WSN is caused by a mutation in the keratin 4 or keratin 13 genes.

110
Q

How does white sponge naevus appear?

A

The patches are thickened, velvety, and sponge-like, and can be white or gray. They can appear as bilateral plaques or macules, and are most often found on the inside of the cheeks (buccal mucosa). They can also appear on the lip, tongue, and floor of the mouth.

111
Q

How do you diagnose white sponge naevus and what is the treatment?

A

Clinical diagnosis +/- histopathology.
No tx required, just reassurance.

112
Q

What is oral submucous fibrosis? (OSMF)

A

Oral submucous fibrosis (OSF) is characterized by abnormal collagen deposition. It is a precancerous disorder and transforms into a malignant tumor in 1.5–15% of all cases. (4-8% in notes)

Oral submucous fibrosis (OSF) is a chronic disease that produces scars, tissue fibrosis, and precancerous lesions. It frequently occurs in the buccal mucosa.

113
Q

What are symptoms of oral submucous fibrosis? (OSMF)

A

Symptoms include submucous fibrosis, ulceration, xerostomia, a burning sensation, and restricted mouth opening. All of these greatly interfere with patient quality of life.

OSF patients experience a severe burning sensation in the mouth after ingesting spicy foods. Other symptoms of OSF include dry mouth, pain, taste disorders, restricted tongue mobility, trismus, dysphagia, and altered tone.

114
Q

What are pathological characteristics of oral submucous fibrosis?

A

Pathological characteristics include chronic inflammation, excessive collagen deposition in the connective tissues below the oral mucosal epithelium, local inflammation in the lamina propria or deep connective tissues, and degenerative changes in the muscles.

115
Q

How can oral submucous fibrosis present?

A

Significant keratosis of buccal/palatal mucosa, where pt keeps betel or tobacco, with possible trismus and dysphagia following fibrosis of tissues.

116
Q

What habits predispose pts to OSMF?

A

Betal quid, areca nut, lime, chewing tobacco

117
Q

How can you diagnose oral submucous fibrosis (OSMF)?

A

Incisional biopsy with histopathological examination.
Clinical diagnosis.
Long term follow up

118
Q

Why is OSMF concerning?

A

It is potentially malignant. Can lead to oral squamous cell carcinoma.

119
Q

Can you treat OSMF?

A

No effective tx.
Moderate OSMF reversible with cessation of habit.

120
Q

What is nicotinic stomatitis?

A

Extensive tobacco use results in reactive hyperkeratosis of extensive regions of mucosa. A white palate is caused by hyperkeratosis of palate accompanied by inflammation of minor salivary gland duct openings.
This creates white palate with red interspersed dots.

This is a reactive keratosis due to tobacco smoking. It is benign.

121
Q

How do you diagnose nicotine stomatitis (smokers palate)?

A

Diagnosed from clinical appearance

122
Q

What is actinic cheilitis?

A

Actinic cheilitis is a precancerous lesion that forms most commonly on the lower lip.
It is a premalignant lesion which is due to sun damage/long term sunlight exposure. It increases the risk of malignant melanoma and squamous cell carcinoma.

123
Q

How does actinic cheilitis appear?

A

Very chapped lips with whitening of the lip and loss of vermillion border.
Plaques can form on the lip and the lips can become inflamed.

124
Q

What does UV do to effect cells?

A

UV light damages tumor suppressor gene p53 resulting in uncontrolled replication of defective cells, which is a common gene mutation found with increasing frequency as actinic cheilitis and actinic keratoses undergo malignant transformation to SCC.

125
Q

How do you diagnose actinic cheilitis?

A

Clinical diagnosis but biopsy if cancer is suspected.

Actinic cheilitis is a diagnosis made from clinical and histopathology evaluation. It is essential to distinguish between cheilitis (benign inflammation), premalignant actinic cheilitis, and squamous cell carcinoma. Skin biopsy is the golden standard regarding the evaluation of a persistent suspicious lesion on the lip. Many lesions initially thought to be premalignant actinic cheilitis on exam were found to be SCC upon histological evaluation, which indicates providers are not able to entirely make the diagnosis clinically, and biopsy is helpful when evaluating these lesions.

126
Q

What histopathology would you expect for actinic cheilitis?

A

Biopsy w/ H&E is recommended for persistent suspicious lip lesions to rule out invasive skin cancer. Basic histopathology for actinic cheilitis would be:

Hyperkeratosis: thickening of stratum corneum
Solar elastosis: loss of eosin staining, accumulation of irregular thick elastic fibers and tangled fibrillin
Epithelial dysplasia (mild-moderate): disordered maturation of epidermal cells, loss of rete ridges, variable cytological atypia
Perivascular inflammation: inflammatory cells around the blood vessels
Severe dysplasia: increase in dyskeratosis, keratin pearls, drop-shaped projections, and nuclei related changes such as mitoses and pleomorphism indicate the progression of dysplasia and increased malignant transformation.

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