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COPY BDS3 University of Adelaide Dentistry > Oral Pathology > Flashcards

Oral Pathology Flashcards

1
Q

When does Secondary Syphilis occur?

A

A mucous patch developing 6-8 weeks after the primary stage

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2
Q

Congenital Syphilis results in what dental abnormalities?

A

Hypoplastic 1st Molars (Mulberry Molars)

Notched Permanent Incisors (Hutchinson’s Incisors)

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3
Q

What type of bacteria is Syphilis?

A

Treponema Pallidum (Spirochete)

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4
Q

What sort of necrosis is Gumma (Tertiary Syphilis)?

A

Coagulation Necrosis

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5
Q

How is Syphilis treated?

A

Antibiotic treatment with Penicillin

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6
Q

Candidosis is caused by what fungus?

A

Candida Albicans

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7
Q

What are risk factors that can cause Cancrum Oris (Noma)

A

Malnutrition, contaminated drinking water, proximity to cattle, lowered immunity (AIDS, Measles)

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8
Q

What are 3 local causes of Oral Candidosis?

A

Poor Denture Hygiene
Reduced Vertical Dimension
Xerostomia

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9
Q

What are 8 systemic causes of Oral Candidosis?

A 
Extremes of Age
Endocrine Disturbances
Malnutrition
Blood Dycrasias
Antibiotic Therapy
Advanced Malignancies
Postoperative Stress
Immunosuppression - Drug induced, HIV, Transplant
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10
Q

Mucocutaneous Oral Candidosis is caused by what?

A

Usually T-Cell Deficiency

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11
Q

What are the 3 classifications of Oral Candidosis?

A

Acute, Chronic and Mucocutaneous

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12
Q

Acute Hypertrophic Candidiasis is also known as what?

A

Thrush

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13
Q

With Acute Hypertrophic Candidiasis, the patient has a white/yellow plaque that can be removed off the mucosa. What is the significance of this plaque?

A

Plaque is inflammatory exudate - dead cells and fungal colonies

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14
Q

How is a simple thrush case treated?

A

Use a topical anti-fungal agent and advise patient on good oral hygiene

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15
Q

A Chancre occurs in what stage of Syphilis?

A

Primary Disease after exposure of T. Pallidum

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16
Q

T/F: Hyperplastic Candidosis is typically associated with red lesions?

A

False: White patches

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17
Q

What might be one very severe manifestation of Tertiary Syphilis?

A

Gumma lesion leading to coagulative necrosis and perforation of the palate

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18
Q

T/F: Chancre is the characteristic lesion of Tertiary Syphilis?

A

False, it is the characteristic painless, ulcerated and localised lesion found in Primary Syphilis

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19
Q

Histologically, what can be seen in a Tertiary Syphilis gumma?

A

Coagulative necrosis and high numbers of macrophages. It has a similar histologically appearance to TB

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20
Q

How would you test for arrested TB?

A

Positive skin test

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21
Q

When treating a patient with TB, what would be transmission precautions you would need to take?

A
  • Reappoint where possible
  • Negative Pressure Surgery
  • Special Ventilation
  • Treat patient last in the day
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22
Q

In western countries what demographic are most likely to contract TB?

A

Immunocompromised - elderly, HIV, patients using Immunosuppressants

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23
Q

How would Gonorrhoea manifest symptoms in the head and neck?

A

Symptoms non-specific
Infection of pharyngeal mucosa
Pharyngitis, oral ulceration, mucosal erythema
Swollen cervical lymph nodes

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24
Q

What is the radiographic appearance of Chronic Osteomyelitis?

A

Moth Eaten radiolucency
More commonly affecting the mandible
Areas of Focal Sclerosis

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25
Q

What is the main cause of Acute Atrophic Candidiasis

A

Poor oral and denture hygiene

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26
Q

What are some possible clinical presentations of Chronic Atrophic Candidiasis?

A 
Non-specific red areas in the mouth
Chronic Denture Stomatitis - very clearly follows the location of the denture
Median Rhomboid Glossitis
Papillary Hyperplasia of the palate
Angular Cheilitis
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27
Q

A patient has a form of candidiasis that presents with a mild burning sensation and a non-specific red patch in the mouth. What could this be?

A

Chronic Atrophic Candidiasis

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28
Q

A patient has a form of candidiasis that presents with a fixed white patch in multiple area. What could this be?

A

Chronic Hyperplastic Candidiasis

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29
Q

What microorganisms are responsible for ANUG?

A

Gram Negative Bacteria

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30
Q

What are other risk factors for ANUG?

A 
Stress
Smoking
Fatigue
Poor OH
Decreased Host Immune Response
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31
Q

A firm swelling on the submandible region with numerous small yellow granules that suppurate is probably a sign of what infection?

A

Actinomyces

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32
Q

What bacteria is primarily responsible for acute osteomyelitis?

A

Staph Aureus

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33
Q

What sort of infection is mot likely to occur in the mouth in Australia: bacterial, fungal or viral?

A

Fungal

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34
Q

What is the main high risk group for Syphilis in Australia?

A

Indigenous communities

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35
Q

What are 3 triggers for recurrent herpes simplex

A

Sunlight
Stress
Immunosuppression

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36
Q

T/F: Shingles can cross the midline based if Herpes Zoster is reactivated from the Trigeminal Ganglion?

A

False: Herpes Zoster resides within the neural ganglion of CN V so activation will not cross the midline

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37
Q

What are the main risk factors for Shingles?

A

Being elderly

Immunocompromised

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38
Q

Give 3 examples of localised microdontia

A

Peg Lateral Incisors
Maxillary 3rd Molars
Supernumerary Teeth

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39
Q

What type of disorder is Ectodermal Dysplasia?

A

X-Linked Recessive

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40
Q

What are the symptoms of Ectodermal Dysplasia?

A
  • Hypodontia
  • Atypical cone-shaped teeth
  • Lack of alveolar bone development
  • Hypotrichosis: Malformed hair + cutaneous appendages (Nails)
  • Anhidrosis (No Sweat Glands)
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41
Q

When might a patient have pseudonodontia?

A

If they have had teeth extracted

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42
Q

How many teeth need to be missing to qualify as Oligodontia?

A

6 or more teeth missing from development

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43
Q

What is a Compound Odontome?

A

A mass of tooth tissue, lots of little teeth inside

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44
Q

What is a Complex Odontome?

A

A tooth with a complex mixture of enamel, dentine and pulp

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45
Q

How would the tooth count change if a patient was affected by a single instance of dental fusion

A

1 less tooth - Fusion is the union between dentine/enamel between 2 or more teeth

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46
Q

What is Gemination?

A

Partial development of two teeth from a single tooth bud following incomplete division. Clinically you would see 2 Crowns sharing same root.

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47
Q

What is the likely cause of concrescence?

A

Trauma or Overcrowding

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48
Q

How would dilaceration appear clinically?

A

A traumatised tooth with angulated roots appearing on a radiograph

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49
Q

What is concrescence?

A

Roots of one or more teeth united by cementum after crown formation

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50
Q

Which teeth are often affected by Dens in Dente?

A

Maxillary Lateral Incisors

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51
Q

Would a tooth with Taurodontism be more likely to be affected by furcation involvement?

A

No, due to an elongated crown, the furcation is hence apically displaced

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52
Q

When is pulpitis radiographically viable?

A

When it has progressed to a periapical granuloma or cyst

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53
Q

Which has more severe pain symptoms: Acute or Chronic irreversible pulpitis?

A

Acute Irreversible Pulpitis

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54
Q

What sensitivity test will be positive to reversible pulpitis?

A

Sensitivity to cold

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55
Q

What immune cells are primarily involved with acute irreversible pulpitis?

A

Mostly neutrophils

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56
Q

What is the likely cause chronic pulpitis?

A

Inflammation resulting from long-term/low-grade injury

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57
Q

What immune cells are primarily involved with chronic irreversible pulpitis?

A

Plasma Cells + Lymphocytes. Very few PMNs

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58
Q

Why is pulpal necrosis the likely end point for pulpitis?

A
  1. Limited Capacity for drainage: anatomy
  2. Limited Access for Repair
  3. Limited space for swelling
  4. Concentrated Stimulus
  5. Limitations of Materials to treat
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59
Q

A periapical abscess that drains extra-orally is known as?

A

A Fistula

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60
Q

A periapical abscess that drains intral-orally is known as?

A

Sinus Tract

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61
Q

What can be found in the contents of a periapical granuloma formation

A
  1. Granulation Tissue
  2. Fibrous Tissue
  3. Inflammatory Cells - Macrophages, Lymphocytes, Plasma Cells, PMNs
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62
Q

Where does Herpes Simplex 1 (HSV1) tend to reside?

A

The Trigeminal Ganglia

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63
Q

Where does Herpes Simplex 2 (HSV2) tend to reside?

A

The Sacral Ganglia

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64
Q

Is it possible to have HSV2 manifest symptoms in the mouth?

A

Yes, if HSV-2 is contract through contact with oral sex with an individual with an active outbreak/sore

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65
Q

T/F: You would manage a recurrent bout of

HSV-1 with a topical Acyclovir (Zovirax): antiviral. creme

A

No, topical are for a sores for recurrent infections. A buccal tablet or oral liquid of Acyclovir can be taken for primary HSV-1 infections

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66
Q

What is the most common viral infection in the mouth?

A

Core Sores from Herpes Simplex Virus 1

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67
Q

What are the main clinical signs of a primary HSV-1 infection?

A
  • Difficulty eating/drinking
  • Vesicular lesions on attached epithelium such as hard palate or dorsum of tongue
  • Primary Gingivostomatitis
  • Swollen Lymph Glands in the submandibular region
  • Fever and Pain
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68
Q

What is the management for a primary HSV-1 infection?

A
  • Analgesics for pain control
  • Ensure hydration
  • Soft Diet
  • Metronidazole Antibiotic Coverage
  • Chlorhexidine mouthwash and gel: helps to maintain OH
    Acyclovir (Zovirax): antiviral. Taken orally as buccal tablet or oral liquid
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69
Q

What are the clinical symptoms of a secondary HSV-1 infection

A

Tingling/Buring sensation
Development of blister
Crusting and healing within 10-14 days

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70
Q

How is a secondary HSV-1 lesion treatment

A

Early topical acyclovir (zovirax) applied in prodromal period may reduce severity of pain

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71
Q

Histologically, what can be seen in a HSV-1 infection?

A
  • Virally infected multinucleated giant cells
  • Formation of very shallow intraepithelial vesicles
  • Inflammation at site
  • Acantholysis: loss of desmosomes resulting in loss of layering of the epithelium. This is what makes the vesicles prone to rupture
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72
Q

Why is varicella-zoster less commonly seen?

A

Due to effective immunisation program for chicken pox

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73
Q

How is varicella-zoster transmitted?

A
  1. Inhalation of droplets

2. Direct Contact

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74
Q

What is the incubation period for varicella-zoster virus?

A

2 weeks

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75
Q

Where does the Varicella-Zoster Virus remain dormant?

A

Sensory Ganglion

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76
Q

What are the triggers for Shingles?

A

Reactivation of Varicella-Zoster Virus due to age / lowered immune function

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77
Q

What is Ramsay-Hunt Syndrome?

A

Reactivation of Varicella-Zoster Virus in the facial and auditory nerve - leading to hearing loss or facial paralysis

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78
Q

What are treatments to minimise severity of shingles?

A

Application of topical acyclovir (Zovirax) within 72 hours of the vesciular rash appearing

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79
Q

Presence of a Oral Hairy Leukoplakia from Epstein-Barr virus is a possible indication of what?

A

Progression of HIV to AIDS

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80
Q

Where is Oral Hairy Leukoplakia most likely found?

A

Fixed white lesion on the lateral border of the tongue

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81
Q

Who are the most at risk for Epstein-Barr Virus?

A

HIV

Organ Transplants, Bone Marrow Transplant, Stem Cell Transplant (Immunosuppressed)

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82
Q

How does Kaposi’s sarcoma (Human Herpes 8) present clinically?

A

Very dark, deep red lesion in sulcus areas

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83
Q

What are 3 main groups affected by Kaposi’s sarcoma

A

Mediterranean older men
African origin
Immunosuppressed Patients

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84
Q

What are the typical symptoms of Cytomegalovirus (CMV) in a healthy individual?

A

Flu-like illness that lasts a few days

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85
Q

In which group would you likely see oral manifestations of Cytomegalovirus (CMV)

A

Oral ulceration in HIV and immunosuppressed individuals

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86
Q

Type 2 and 4 Human Papillomavirus are commonly associated with what?

A

Veruca Vulgaris (Common Warts)

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87
Q

A slow growing cauliflower-like lesion on the hard/soft palate is a possible sign of what?

A

Squamous Papilloma (Oral Wart) from Oral HPV infection

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88
Q

Focal Epithelial Hyperplasia is caused by what and where can it be found?

A

Oral HPV Infection: numerous lesions involving buccal/labial mucosa and the tongue

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89
Q

What is the high risk group for Coxsackie Viruses?

A

Young children due to poor hygiene and transmission through saliva and faecal-oral spread

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90
Q

How does Hand-Foot-And-Mouth disease manifest orally?

A

Mild mouth ulceration, difficulty eating and drinking

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91
Q

Where is Herpangina more likely to present orally?

A

Vesicular lesions that are posteriorly towards the Fauces and Soft Palate

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92
Q

Why would metronidazole be given to a a HSV-1 primary infection?

A

To prevent secondary bacterial infection

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93
Q

How would Chicken Pox manifest orally?

A

Oral lesions present as 2-4mm ulcers with erythematous halo (red) with multiple crops developing over 1-2 weeks

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94
Q

Oropharyngeal carcinoma can develop from what viral infection?

A

HPV Types 16/18

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95
Q

What are the high risk groups of Conduloma Accuminaturm?

A

Immunocompromised patients (eg HIV)

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96
Q

What immune cell count reduces with the onset of HIV/AIDs?

A

CD4

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97
Q

What are the 3 main oral manifestations of HIV infections

A
  1. Opportunistic Infections
  2. Atypical presentations of common oral conditions
  3. Side Effects of Combination therapy for HIV
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98
Q

You see a young male patient with angular cheilitis. Is this normal and what could it be?

A

It is atypical, could be a marker for HIV infection or immunosupression

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99
Q

Presence of Oral Hairy Leukoplakia is an indicator of what?

A

Prognostic of viral load for HIV

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100
Q

Where can Oral Hairy Leukoplakia be found?

A
  1. Bilaterally on lateral surface of tongue

2. Ventral surface tongue

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101
Q

What are differential diagnosis for Oral Hairy Leukoplakia

A
  1. Trauma (most common)
  2. Lichen Planus
  3. Neoplasms
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102
Q

What are the atypical presentations of Herpes-Simplex virus in a HIV patient?

A

I/O presentation rather than general E/O cold sores

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103
Q

What are the atypical presentations of Varicella Zoster Virus in a HIV patient?

A

Onset of shingles in a young patient

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104
Q

What are the clinical signs of Necrotising Ulcerative Gingivitis in a HIV patient

A 
Similar to ANUG 
Sudden onset 
Severely inflamed, ulcerated gingiva
Spontaneous bleeding 
Necrosis - particularly around Interdental papillae
Halitosis - is from the necrotic tissue
Plaque - poor OH due to pain
Pain
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105
Q

What is a good immediate treatment for ANUG?

A

Irrigate gums with monojet gun with betadine

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106
Q

Who are contraindicated for Betadine irrigation?

A

People with iodine allergies

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107
Q

What are the high risk groups for Kaposi’s Sarcoma

A

HIV positive homosexual men - thought to be sexually transmitted

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108
Q

What are treatment options for Kaposi’s Sarcoma?

A

Radiotherapy
Chemotherapy
Local, intralesional chemotherapy treatment

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109
Q

What might be seen intraorally with AZT treatment for HIV?

A

Mucosal pigmentation

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110
Q

What group is more pre-disposed to Leukoedema?

A

Dark skinned populations

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111
Q

What sort of inheritance pattern occurs with White Spongy Naevus?

A

Autosomal Dominant with variable expression

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112
Q

What are signs and symptoms of Leukoedema?

A
  1. Lesion is asymptomatic
  2. Bilateral expression
  3. White/Grey translucency
  4. Thickening of mucosa
  5. Poorly defined margins
  6. Lesion disappears when buccal mucosa is stretched
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113
Q

What are signs and symptoms of White Spongy Naevus?

A

Raised and Flappy White thickening of buccal mucosa

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114
Q

Histologically what is happening with Leukoedema?

A
  • Intracellular Oedema of superficial half of the epithelium
  • Large Vacuolated Cells
  • Pyknotic (Condensed Chromatin) Nuclei
  • Epithelial Hyperplasia
  • Broad Elongated Rete Pegs
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115
Q

T/F: Sulcular and Junctional Epithelium normally express rete pegs?

A

False, in the mouth attached gingival exhibits rete pegs (The infolds of Epithelium into the adjacent CT layers)

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116
Q

What is the aetiology of Leukoedema?

A

Normal / Developmental. Heightened by local irritation, particularly for smokers

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117
Q

What is the aetiology of White Sponge Naevus?

A

Genetic inheritance

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118
Q

What is the aetiology of Frictional Keratosis?

A

Physical Trauma

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119
Q

What is the aetiology of Fordyce Granules?

A

Developmental

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120
Q

What is the aetiology of Tobacco-Induced Keratosis?

A

Chemical/Thermal trauma from smoking

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121
Q

What is the aetiology of

Acute Hyperplastic Candidiasis?

A

Candida Infection

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122
Q

What is the aetiology of

Oral Hairy Leukoplakia?

A

EBV Infection

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123
Q

What is the aetiology of

Verruciform Xanthoma?

A

Unknown

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124
Q

What are the common epithelial oral lesions?

A 
Leukoedema
Cheek Biting
Frictional Keratosis
Fordyce Granules
Tobacco-Induced Keratosis
Acute Hyperplastic Candidiasis
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125
Q

What are some uncommon epithelial oral lesions?

A

Chemical Burns
White Sponge Nevus
Oral Hairy Leukoplakia
Verruciform Xanthoma

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126
Q

A patient presents with an asymptomatic enlargement of the gingiva, so much so it covers over the teeth.

There is no bleeding or exudate. What could this be?

A

Gingival Fibromatosis

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127
Q

What are the 2 known types of Gingival Fibromatosis?

A
  1. Hereditary

2. Idiopathic

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128
Q

Histologically, what occurs during Gingival Fibromatosis?

A
  1. Epithelial Rete Pegs
  2. Mild chronic inflammatory cell infiltrate
  3. Growth of avascular dense fibrous CT
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129
Q

What are some differential diagnosis to Gingival Fibromatosis?

A
  1. Drug Induced Gingival Hyperplasia
  2. Neoplastic Disease
  3. Granulomatous Disease (Foreign Body, Sarcoidosis, Crohn’s)
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130
Q

What are some differential diagnosis to Leukoedema?

A

Frictional keratosis, tobacco-related keratosis, white sponge nevus

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131
Q

What syndromes are Haemangioma’s commonly associated with?

A
  1. Sturge-Weber Syndrome

2. Hereditary Hemorrhagic Telangiectasia

132
Q

What is a Haemangioma?

A

A vascular proliferation of endothelial cells that either occurs shortly after birth or later in life (approx 30 years)

133
Q

What is the distribution of Haemangioma when associated with Sturge-Weber Syndrome?

A

Intra-orally with skin lesions corresponding to the distribution of the trigeminal nerve

134
Q

What is a Lymphangioma?

A

A malformation of the lymphatic system with thin-walled cystic lesions

135
Q

What is Cystic Hygroma?

A

A life threatening, rare congenital lesions that involves a large Lymphangioma of the lateral net that can disfigure and cause respiratory distress

136
Q

Which nerve is congenitally extending all the way to the lower lip in Calibre-Persistent Labial Artery?

A

The IAN maintaining it’s size after the mental foramen and becoming superficial to the lower lip.

137
Q

What is an ectopic lesion?

A

Normal tissues that are found in abnormal sites

138
Q

What is a fordyce spot?

A

A sebaceous gland (sweat) located in the oral cavity

139
Q

What does a fordyce spot look like and how does it present clinically?

A
  1. Yellow Nodule
  2. More likely to present in older patients
  3. Affects upper lip and buccal mucosa, retromolar pads and palatoglossal areas
140
Q

T/F: Lingual Thyroid Tissue are a result of hyperplasia of thyroid tissue

A

False, It is actually is the thyroid gland, but has embryologically failed to descend along the thyroglossal duct to the neck

141
Q

Where is Lingual Thyroid Tissue likely to be found?

A
  1. More common in females

2. Base of the tongue in the foramen caecum area

142
Q

What is the aetiology of a lingual tonsil?

A

Lymphoid Hyperplasia or

Lymphoepithelial Cyst Formation

143
Q

What are lingual tonsils?

A

Possible variation to anatomy, they are benign lymphoid aggregates found in:

  1. Posterior Lateral Tongue
  2. Soft Palate
  3. Floor of the mouth
144
Q

What is a hamartoma?

A

A Non-Neoplastic growth that looks like a tumour

145
Q

What is a hematoma?

A

A Blood Blister

146
Q

T/F: Geographic tongue is a loss of fungiform papillae on the tongue?

A

False - filliform papillae

147
Q

What symptom can accompany geographic tongue?

A

Burning mouth syndrome

148
Q

Histologically what can be seen with Benign Migratory Glossitis (Geographic Tongue)

A

Microabscesses on surface of epithelium with inflammation - neutrophils and lymphocytes

149
Q

Benign Migratory Glossitis is also known as what?

A

Geographic tongue

150
Q

What is the aetiology of Geographic Tongue?

151
Q

What are two pigmented lesions that can be found in the mouth

A

Oral Melanotic Macula
Naevi
Amalgam Tattoo

152
Q

What is the aetiology of an Oral Melanotic Macule?

A 
1. Syndromic: Addisons Disease,  McCune-Albright Syndrome, 
Peutz-Jegher’s Syndrome
2. Racial / Physiological Pigmentation
3. Smoker’s Melanosis
4. Lung Carcinoma
5. Medications
153
Q

What are the signs and symptoms of a oral melanotic macule?

A
  1. Well demarcated
  2. Uniform color
  3. Asymptomatic
  4. Same consistency as surrounding mucosa
154
Q

Histologically, what is happening with an oral melanotic macule?

A

Normal Stratified Squamous Epithelium
Increased melanocytes in basal layer => Increased melanin deposition
Melanic Incontinence (pigmentation “leaks” into CT)
Melanin deposition causes chemotaxis gradient
Attracts macrophages deemed “Melanophages”
`

155
Q

What is a Mucosal Melanocytic Naevus?

A

Benign proliferation of naevus cells (similar to meoanocytes), resulting in a painless, small black/brown/blue pigmented lesion that grows at the same rate as neighbouring tissue

156
Q

What is usually the cause of epithelial hyperplasia?

A

Low grade chronic trauma

157
Q

What is usually the cause of cellular hypertrophy

A

Response to a stimulus for increased activity

158
Q

What is a polyp?

A

Any small growth projection in a cavity

159
Q

What are the implications of surgically removing a sessile vs a pedunculated lesion?

A

Pedunculated will have a thinner diameter - therefore will result in a smaller hole and less likely to require a suture

160
Q

What defines a papillary lesion?

A

Any small growth projecting into a cavity

161
Q

What defines a verrucous lesion?

A

A warty surface appearance

162
Q

What defines a epulis?

A

A non-neoplastic lump on the gum

163
Q

What is the cause of linea alba?

A

Lesion from low grade mechanical trauma from cheek biting

164
Q

What is the management of linea alba?

A

Nothing required

165
Q

Histologically what is the cause of linea alba?

A

Hyperkeratosis

Acanthosis: thickening of prickle cell layer

166
Q

How does linea alba differ from cheek biting?

A

Cheek biting is higher grade trauma resulting in an inflammation response

167
Q

Describe the appearance of cheek biting

A
  • Unilateral or bilateral white patch on the buccal mucosa
  • Roughened white mucosa similar to linea alba
  • May be surrounded by red patches of localised inflammation
168
Q

What is the aetiology of smoker’s keratosis?

A
  • Tobacco smoking (heat? Combustion products?)

- Seen more in people who smoke from a pipe and reverse smoking

169
Q

What is the clinical symptoms of smoker’s keratosis

A
  • Diffuse, white, moderately thickened palate
  • Sometimes roughened
  • Involves entire palate
  • Characterised by presence of 1-2 mm diameter red “Dots”
170
Q

Generally white lesions will involve what 2 histological changes?

A

Hyperkeratosis and acanthosis (thickening of prickle cell layer)

171
Q

What are the histological changes involved to smoker’s keratosis?

A

Hyperkeratosis
Thickening of the prickle cell layer (acanthosis)
Subepithelial chronic inflammation
Periodontal inflammation in the minor salivary glands

172
Q

T/F: Smoker’s keratosis is a premalignant change to the oral mucosa

A

False, it’s a non-malignant chronic injury marker, but good education tool to show patients the changes smoking can causes

173
Q

Chronic Hyperplastic Candidiasis is caused by what?

A

Microbial imbalance caused by antibiotic use. Candida fungi infection results in changes in epithelial laer

174
Q

Fibroepithelial Hyperplasia is commonly called what?

A

Denture Hyperplasia

175
Q

What occurs during Fibroepithelial Hyperplasia?

A

Cellular proliferation growth in response to chronic physical trauma and inflammation - usually from ill-fitting dentures

176
Q

What are the clinical signs of papillary hyperplasia of the palta?

A

Nodular overgrowth from ill-fitting dentures that causes on/off suction against the palate

177
Q

T/F: A Fibroepithelial polyp (Fibroma) is neo-plastic in nature

A

False - it is a hyperplastic lesion of the fibrous tissue

178
Q

What is the cause of a Fibroepithelial polyp?

A

Chronic physical trauma and inflammation - look to sites prone to trauma

179
Q

Where can Pyogenic granuloma typically occur in the mouth and why?

A

Occur on the gum margins around where there is subgingival calculus or ill-fitting crowns

180
Q

When are Pyogenic granuloma more likely to be clinically evident?

A

Hormonal factors during pregnancy + puberty in females

181
Q

What are the clinical signs of a Pyogenic granuloma

A

Sudden onset
Rapid growth
Bright red ulcerative surface that bleeds easily
Located on the gum margins - around subgingival calculus or poor crow margins

182
Q

What would you expect to see histologically on a pyogenic granuloma

A

High vascular lesion
Lots of granulation tissue
Thin/Non-existant epithelial layer (as lesion is ulcerated)
Surface area of fibrin
Inflammatory cells
Bacterial colonies
Epithelial hyperplasia in non-ulcerated areas (areas of healing)

183
Q

What is the treatment for a pyogenic granuloma?

A

Excision - incomplete excision results in reoccuring lesion

184
Q

Where are you more likely to see a Peripheral giant cell granuloma?

A

Around the gingiva in the anteriors

185
Q

What is the main differentating factor between pygoenic granuloma and peripheral giant cell granuloma?

A

Multinucleated giant cells

186
Q

T/F: A Calcifying Fibroblastic Granuloma will exhibit extensive inflammation

A

False - it is generally painless and lacks inflammation unless ulcerated. It exhibits more like scar tissue.

187
Q

What are the causes of generalised gingival hyperplastic lesions?

A 
Local factors: plaque, calculus
Hormonal imbalance 
Drugs: dilantin, cyclosporine, nifedipine  (Ca channel blocker)
Leukaemia 
Genetic factors
188
Q

What are 2 causes of a traumatic neuroma?

A

1) Injuries to trigeminal nerve during deep oral surgery

2) Most commonly from hard impact of dentures onto the mental nerve

189
Q

What are the signs of Verruciform Xanthoma?

A

Flat, velvety pebbly lesion of the mucosa
Often occurs on the gingiva
Can also be seen on tongue
White / Orange appearance

190
Q

What can be seen histologically in Verruciform Xanthoma?

A
  • Epithelial hyperplasia
  • Parakeratin plugging of rete pegs
  • Large pale foam cells filling CT papillae that are full of Macrophages that produce lots of cholesterol giving foamy appearance
191
Q

What is the cause of Benign Lymphoid hyperplasia?

A

Irritation of existing lymphoid tissue

192
Q

What is the histology of Giant cell fibroma?

A

Large stellate like cells and multinucleated fibroblasts

193
Q

You have a histology slide that shows a thick epithelial layer that is highly mitotic. What is the likely clinical presentation of this oral pathology?

A

White Patch

194
Q

You have a histology slide that shows a thin epithelial layer. What is the likely clinical presentation of this oral pathology?

195
Q

You have a histology slide that shows no epithelium. What is the likely clinical presentation of this oral pathology?

196
Q

What are the 4 main causes of traumatic ulcers?

A

Mechanical
Chemical
Thermal
Radiation

197
Q

What are the clinical presentation of acute traumatic lesion?

A
  • Acute Inflammation
  • Surface has yellow fibrinous exudate
  • Erythematous border or halo
198
Q

What are the clinical presentation of chronic traumatic lesion?

A
  • Minimal Pain
  • Elevated margins, fibroepithelial hyperplasia, epithelial hyperkeratosis
  • Induration (More fibrous tissue)
199
Q

What are the 8 possible causes of Aphthous ulcers?

A
  1. Genetic
  2. Exaggerated response to trauma
  3. Gastrointestinal Disorder
  4. Immunological Abnormality
  5. Infections
  6. Anaemia
  7. Hormonal Disturbances
  8. Stress
200
Q

What are 4 different Haematological Disorders associated with oral lesions

A

Anaemia
Iron Deficiency
Folate Deficiency
B12 Deficiency

201
Q

What are some possible dental implications of haematological disorders?

A

For severe anaemia:

  • Glossitis
  • Bacterial Infection: Angular Cheilitis
  • Aphthous ulceration
202
Q

Behcet’s Disease can manifest in what type of ulcerative lesion?

A

Aphthous ulcer

203
Q

What group are more likely to suffer from aphthous ulcers and behcet’s disease?

A

Mediterranean males below 40

204
Q

What are the clinical signs of Orofacial granulomatosis?

A

Lip or gingival swelling

205
Q

What can Orofacial granulomatosis potentially progress into?

A

Crohn’s disease

Sarcoidosis

206
Q

What is the main histological feature that can be seen in Orofacial granulomatosis?

A

Giant Cells

207
Q

What are some general systemic signs of Crohn’s disease?

A

Inflammatory Bowel Disease
Abdominal Pain
Constipation/Diarrhoea

208
Q

What are some oral mucosal symptoms of Crohn’s disease?

A
  • Diffuse lip swelling
  • “Cobble stone” thickening of mucosa
  • Gingival erythema and swelling
  • Ulcers
  • Hyperplastic Mucosal tags
  • Glossitis
209
Q

What are factors for a patient would potentially increase risk for a potentially malignant lesion?

A
  1. Tobacco Use
  2. Alcohol Intake
  3. UV Light Exposure - particularly for lip
  4. Age
  5. Gender - older males
  6. Location and Presentation of lesion
210
Q

What would be some architecture changes in epithelial atypia?

A 
Drop Shaped Rete Pegs
Irregular Epithelial Stratification
Loss of polarity of basal cells
Increased number of mitotic figures
Superficial Mitoses
Single Cell Keratinisation (Dyskeratosis)
211
Q

What would be some cytological changes in epithelial atypia?

A

Nuclear Pleomorphism: Abnormal variation of either nuclear size/shape
Cellular Pleomorphism: Abnormal variation of either cell size/shape
Increased Nuclear/Cytoplasmic Ratio
Increased Nuclear Size
Atypical Mitotic Figures
Increased number + size of nucleoli
Hyperchromasia

212
Q

What are the 4 forms of dysplasia?

A
  1. Mild Dysplasia
  2. Moderate Dysplasia
  3. Severe Dysplasia / Carcinoma In Situ
213
Q

How would you expect the rete pegs to appear in hard palate tissue?

A

Finger shaped like projections to provide strength against sheer forces

214
Q

What would atypical mitotic figures look like?

A

1 cell trying to divide into 3 or 4 rather than just 2.

215
Q

T/F: Dysplasia can involve cellular changes in the epithelium and connective tissue around it

A

False, Dysplasia is limited to cellular and architectural changes in the epithelium only

216
Q

If Dysplasia involves the full thickness of the epithelium what is this caused?

A

Severe Dysplasia / Carcinoma in Situ

217
Q

What is Leukoplakia?

A

Clinical term to describe a fixed white lesion in the oral mucosa. Once biopsied a more definitive diagnosis can be given

218
Q

What are the 2 types of leukoplakia?

A

Homogenous Leukoplakia

Speckled Leukoplakia

219
Q

Which type of leukoplakia is clinically of more concern?

A

Speckled Leukoplakia - biopsy this straight away

220
Q

What is an easy way to identify lichen planus?

A

Often displays bilateral Symmetrical Lesion on tongue / buccal mucosa

221
Q

If a mass is Pleomorphic what does it look like histologically and what could it represent?

A

Histologically there is a mass of cells with variable cell size, shape or staining. It is indicative of dysplastic or malignant neoplastic cell growth

222
Q

What are architectural changes seen in dysplasia?

A
  1. Drop Shaped Rete Pegs -
  2. Irregular Epithelial Stratification
  3. Loss of polarity of basal cells
  4. Increased number of mitotic figures
  5. Superficial Mitoses
  6. Single Cell Keratinisation (Dyskeratosis)
223
Q

What are cytological changes in dysplasia?

A
  1. Nuclear Pleomorphism: Abnormal variation of either nuclear size/shape
  2. Cellular Pleomorphism: Abnormal variation of either cell size/shape
  3. Increased Nuclear/Cytoplasmic Ratio
  4. Increased Nuclear Size
  5. Atypical Mitotic Figures
  6. Increased number + size of nucleoli
  7. Hyperchromasia: very dark staining slide due to lots of nuclear material
224
Q

What are some potentially malignant lesions

A 
Dysplastic Leukoplakia
Erythroplakia
Speckled Leukoplakia
Tertiary Syphilis
Oral Submucous Fibrosis
Chronic Candidiasis
Lichen Planus
Discoid Lupus Erythematosus
225
Q

What are the 3 grades of epithelial dysplasia?

A

Mild
Moderate
Severe / Carcinoma In Situ

226
Q

When is the term leukoplakia used?

A

It is a clinical term used when a fixed white page that can not be characterised clinically as another disease. Once biopsied a more definitive diagnosis can be given

227
Q

What is panleukoplakia?

A

When multiple leukoplakia lesions exist

228
Q

Describe the clinical appearance of Homogenous Leukoplakia

A

Solid white lesion
Usually well delineated
Slightly Raised
Surface variable: smooth, fissured, corrugated, warty

229
Q

Describe the clinical appearance of Speckled (Nodular) Leukoplakia

A

Raised
Rough Nodular appearance
Intermingled Red + White areas
Higher proportion histologically will exhibit dysplasia: biopsy straight away!

230
Q

What elevates the risk of transformation of leukoplakia to SCC?

A

Higher risk based on geographic + tobacco/betel nut use

231
Q

Describe the clinical appearance of Sublingual Keratosis

A

White lesions on floor of mouth + tongue

232
Q

T/F: Erythroplakia has a low risk of malignant transformation

A

False - it has a high risk

233
Q

Describe the clinical appearance of Erythroplakia

A 
Red Patches
Velvety Surface
Variable defined margin
Flat, depressed lesions
Rarely “Plaque-Like”
234
Q

Describe the clinical appearance of Chronic Hyperplastic Candidosis

A

Fixed White Plaque

Locations: Dorsum Tongue, Buccal Mucosa, Commissure

235
Q

What is the aetiology of Oral Submucous Fibrosis

A

Associated with betel quid use

236
Q

What are the signs and symptoms of Oral Submucous Fibrosis?

A

Increased fibrosis of oral mucosa

Increased immobility and contraction

237
Q

What is the disease mechanism of lichen planus?

A
  1. Initiating Factor / Event
  2. Focal release of regulatory cytokines
  3. Upregulation of vascular adhesion molecules
  4. Recruitment + Retention of T-Lymphocytes
  5. Cytotoxicity of basal keratinocytes
238
Q

What are some histological markers of Lichen Planus?

A

1) Predominantly T-Lymphocyte Infiltrate: CD4 / CD8

2) Presence of Macrophages, Langerhans Cells, Mast Cells

239
Q

T/F: Lichen Planus commonly presents with bilaterally symmetrical lesions

240
Q

What is the treatment for Lichen Planus

A

Corticosteroids: Modulate Inflammation + Immune Response
Antifungal Therapy: Treats secondary infection
Topical Retinoids
Topical Vitamin E
Chlorhexidine: controls symptoms

241
Q

What is the aetiology of Lichen Planus?

A

Idiopathic /

Immune Related

242
Q

What are the 3 types of lesions that present in lichen planus

A
  1. Striated
  2. Atrophic
  3. Erosive
243
Q

What is the histology of a striated lichen planus lesion?

A

Hyperkeratosis
Hyperparakeratosis
Saw-tooth appearance of rete pegs
Basal Cell Layer degeneration - formation of civatte bodies
Band-like lymphocytic infiltrate subadjacent to basement membrane

244
Q

What is aetiology of a Traumatic Eosinophilic Ulcer?

A

Typically history of deep mucosa trauma

245
Q

What are the signs/symptoms of a Traumatic Eosinophilic Ulcer?

A

Usually on the tongue
Large cratered ulcer 1-2cms
Edge of ulcer has raised margins and increased mitotic activity to try to cover the ulcer

246
Q

What is the histology of a Traumatic Eosinophilic Ulcer?

A
  • Lack of epithelium
  • Inflammatory infiltrate full of eosinophils
  • Pale plump grey fibroblasts producing collagen (healing)
  • HEVS
  • High mitotic activity at edge of margins (healing)
247
Q

What is the main cause of Mucositis?

A

Side effect of cancer treatment: cells stop dividing in the mucosa, breaking down and ulcerating

248
Q

What are management steps for mucositis?

A
  1. Palliation of side effects of cancer treatment: maintain oral hygiene, control pain, control infections
  2. Palifermin (epithelial keratinocyte growth factor): encourages epithelial growth but has many side effects
249
Q

What is the cause for minor aphthous ulcers?

A

Unknown, but has systemic triggers and more common in patients with history of ulcers

250
Q

What is the cause for major aphthous ulcers?

251
Q

What is the cause for minor herpetiform ulcers?

252
Q

What tissues are involved with aphthous ulcers?

A

Non-keratinised mucosa

253
Q

What does a minor aphthous ulcer look present clinically

A
  • Circular lesion typically affecting non-keratinised mucosa
  • Shallow crater approx 5-7mm across
  • Red margin, yellowish floor (dead fibrin tissue)
  • May see red dots on surface
254
Q

How do minor aphthous ulcers resolve?

A

Typically resolves within 7-10 days without scarring

255
Q

What are treatment steps for minor aphthous ulcers?

A
  • Typically nothing
  • Steroids for persistent ulcers
  • Diffam oral gel (anti-inflammatory)
256
Q

What does Crohn’s disease look like histologically in the gut?

A

Inflammation
Granulomatous tissue
Giant cells

257
Q

Crohn’s disease is associated with what sort of mouth ulcer?

A

Aphthous ulcers

258
Q

What are the 3 biggest risk factors for pre-malignant lesions?

A

Tobacco Use
Alcohol Intake
UV Light Exposure

259
Q

What are the layers of normal epithelium?

A 
Stratum Corneum
Stratum Lucidum
Stratum Granulosum
Stratum Spinosum
Stratum Basale
260
Q

What are the Architectural Changes seen in epithelial dysplasia?

A 
Drop shaped rete pegs
Irregular Epithelial Stratification
Loss of polarity of basal cells
Increased mitotic figures
Superficial Mitosis
Single Cell Keratinisation (Dyskeratosis)
261
Q

What are the cytological changes seen in epithelial dysplasia?

A

Nuclear Pleomorphism: Abnormal variation of either nuclear size/shape
Cellular Pleomorphism: Abnormal variation of either cell size/shape
Increased Nuclear/Cytoplasmic Ratio
Increased Nuclear Size
Atypical Mitotic Figures
Increased number + size of nucleoli
Hyperchromasia: very dark staining slide due to lots of nuclear material

262
Q

What is Carcinoma-in-situ?

A

When there is epithelial dysplasia that involves the full thickness of the epithelium without crossing the basement membrane

263
Q

What are the 3 grades of dysplasia?

A

Mild Dysplasia
Moderate Dysplasia
Severe Dysplasia / Carcinoma-in-situ

264
Q

Which dysplastic lesions have a high risk of becoming cancerous?

A

Erythroplakia
Tertiary Syphilis
Oral Submucous Fibrosis

265
Q

What is leukoplakia?

A

A fixed oral white patch that cannot be characterised clinically or pathologically by any other disease. Once biopsied a more definitive diagnosis can be given

266
Q

What are the different presentations of Leukoplakia?

A

Homogenous Leukoplakia: solid white lesion

Speckled (Nodular) Leukoplakia: rough nodular appearance

Sublingual Keratosis: Leukoplakia on the floor of the mouth

267
Q

What are risk factors for Leukoplakia?

A

Trauma, alcohol, infection, smoking, betel nuts, chewing tobacco

268
Q

Sublingual Keratosis is a manifestation of what other oral lesion?

A

It is Leukoplakia on the floor of mouth + tongue

269
Q

Oral Submucous Fibrosis is associated with what sort of habit?

A

Betel Quid / Tobacco chewing

270
Q

What is the difference between Lichen Planus and Lichenoid Reactions?

A

They both share clinical and histopathological similarities,

Difference is from aetiologic cause:

Lichen Planus: unknown but liked to T-cell autoimmunity reaction

Lichenoid Reactions: contact sensitivity, drug interaction, systemic causes

271
Q

What are 3 types of Lichenoid Reactions?

A

Contact Lesions
Lichenoid Drug Reactions
Graft vs Host Disease

272
Q

What is the aetiology of Lichen Planus?

A

Unknown but proposed that it is a T Cell Autoimmune reaction against the basal keratinocytes in the epithelium

273
Q

What are the 6 different types of lichen planus lesions?

A 
Atrophic
Erosive
Plaque (appear similar to leukoplakia)
Striated (spider's web Wickham's Striae)
Bullous
Papular
274
Q

Where are lichen planus lesions typically found?

A 
Buccal Mucosa (Most likely)
Dorsal Surface of Tongue
Gingiva - striated lesions on the interdental regions

Expression is typically bi-laterally

275
Q

What is the management for lichen planus?

A

Corticosteroids - modulates immune response
Antifungal Therapy - Treats secondary infection
Topical Vitamin A + E - promotes mucosal repair
Chlorhexidine - Control of symptoms

276
Q

Is Lichen Planus a risk of Malignant Transformation?

A

No - it is actually low risk (0.5%), however many other white lesions are misdiagnosed as Lichen Planus (eg Dysplastic Epithelium, Subepithelial Lichenoid Infiltration).

Treatment needs to address reducing risk factors for SCC and long term monitoring

277
Q

What are the 3 main categories of malignancies in the oral cavity?

A

Epithelial
Mesenchymal
Hematolymphoid

278
Q

Who are at most risk for Oral Squamous Cell Carcinoma?

A

Males in 50-60 years who have combined smoking and alcohol use

279
Q

What are risk factors for Oral Squamous Cell Carcinoma?

A

Smoking
Alcohol
HPV Infection

280
Q

Where are Oral Squamous Cell Carcinomas most commonly found?

A

Most common site: Lower Lip (UV exposure)

Other SItes: Floor of Mouth, Lateral Border of Tongue, Retromolar area.

Areas of habit - tobacco/betel quid usage

281
Q

Where is the clinical presentation of Oral Squamous Cell Carcinomas?

A

Variable presentation: Red, speckled or white patches

Raised nodule, nonhealing ulcer, “rolled” borders

282
Q

What are the routes of metastasis for SCC?

A

Direct extension into adjacent tissue
Perineural infiltration
Vascular invasion
Lymphatics

283
Q

Why might there be an inflammatory reaction in SCC?

A
  1. Ulceration

2. Very fast tumour growth causes necrosis (insufficient vascularisation)

284
Q

What are the treatment modalities for SCC?

A
  1. Surgery Alone (Gold Standard)
  2. Surgery + Postop Radiotherapy
  3. Radiotherapy Alone
  4. Chemotherapy
285
Q

What is the dentist’s role in the management of malignancies?

A
  1. Accurate diagnosis - be suspicious, biopsy and refer
  2. Follow up
  3. Maintenance before and after therapy
  4. Role in treatment planning with head/neck cancer team
286
Q

What are some side effects of radiotherapy for SCC?

A

Skin Inflammation
Mucositis: ulceration caused by cells that stop dividing
Xerostomia: candida infections, caries
Osteoradionecrosis

287
Q

How can radiation caries be prevented?

A
  1. Pre Operative: extraction of teeth with poor prognosis
  2. Oral Compliance
  3. Post Operative: fluoride, saliva substitutes, regular exams
288
Q

What are implications of surgical removal of SCC?

A

Aesthetics: loss of teeth, soft tissue

Loss of Function: speech, swallowing, mastication

289
Q

What are some side effects of chemotherapy for SCC?

A

Mucositis: ulceration caused by cells that stop dividing
Xerostomia: affect salivary glands
Impact Taste
Opportunistic infections: Candidiasis, Herpes Simplex, Rare Opportunistic Bacterial Infections (Klebsiella, Pseudomonas)

290
Q

What dental care should be taken for patients under pallative treatment with terminal cancer?

A
  1. Focus on quality of life
  2. Minimum treatment
  3. Pain control (non morphine based analgesics)
  4. Antibacterial mouthwashes and gels
291
Q

HPV 16 and 18 are implicated in what sort of oral malignancy?

A

Heighten risk of oropharyngeal cancers

292
Q

What are the 5 histological gradings for tumours?

A

Carcinoma In Situ: Pre-invasive dysplasia
Grade 1: Well differentiated
Grade 2: Moderately differentiated
Grade 3: Poorly differentiated
Grade 4: Anaplastic: lack/poor differentiation of tumour cells

293
Q

In TNM scoring, what is the T and give a description of the different scores

A

T: Tumour Size (1-4), the extent of primary tumour

T1: Primary Tumour < 2cm diameter
T2: 2-4cm diameter
T3: > 4cm diameter
T4: > 4cm diameter + invading local structures

294
Q

In TNM scoring, what is the N and give a description of the different scores

A

N: Lymph Nodal Involvement (0-3)
Condition of regional lymph nodes

N0: No nodes clinically
N1: Ipsilateral palpable nodes
N2: Contralateral palpable nodes
N3: Fixed Palpable Nodes

295
Q

In TNM scoring, what is the M and give a description of the different scores

A

M: Metastasis (0,1)
Presence/absence of distant metastases

M0: No metastasis
M1: Evidence of distant metastasis (clinical or radiographic)

296
Q

What defines a stage 4 prognosis using the TNM scale?

A

Tumour with significant lymphatic spread or metastasis to secondary tumour(s)

Tx with N2/N3 OR

Anything with M1 (Metastasis occurred)

297
Q

What defines a stage 3 prognosis using the TNM scale?

A

Large localised tumour or any tumour that has ipsilateral lymph node spread

T3 N0 M0 or

Tx with N1 (Ipsilateral Lymph Node Involvement)

298
Q

What defines a stage 2 prognosis using the TNM scale?

A

Larger localised tumour confined to parent tissue

299
Q

What defines a stage 1 prognosis using the TNM scale?

A

Localised tumour confined to parent tissue

T1 N0 M0

300
Q

What is the nomenclature typically given to malignant tumours of a mesenchymal origin?

301
Q

What is a Mesenchymal tumour?

A

Grouping of all soft connective tissue (non-epithelial) cancers that derive from mesenchymal tissue.

Mesenchymal Tissue typically in Ground Substance of CT.

Tumours are grouped into the tissue they most resemble
Fibrous, Fat, Nervous, Bone, Muscle tissue

302
Q

What is the main diagnostic way to differentiate between non-hodgkin and hodgkin lymphoma?

A

Hodgkin Lymphoma = lymph node histology has the presence of a large malignant B Cell called a Reed-Sternberg Cell

303
Q

Hodgkin Lymphoma typically has the malignant transformation of which cells?

A

B Cells predominantly

T Cells

304
Q

What the clinical signs and of Hodgkin /Non-Hodgkin Lymphoma?

A
  • Painless Lymphadenopathy (swollen Lymph Nodes).
  • Swollen waldeyer tonsillar ring, particularly palatine tonsil
  • Fever, itchy skin, weight loss, night sweats
305
Q

A fixed brown patch appears in the mouth. It is asymmetrical with an irregular border and variable colour. If Nevus and Amalgam Tattoo have been discounted, what could this lesion be?

A

Malignant Melanoma

306
Q

What is the cause of Non-Hodgkin Lymphoma?

A

Currently unknown, but associated with EBV and immunodeficiency

307
Q

Granular Cell (Congenital) Epulis are found in newborns. Where are they found and why might they be an issue?

A

Come out from the alveolar ridge, mostly in the maxilla.

They are vascular, from an odontogenic epithelial source and can interfer with breastfeeding

308
Q

Where can a Granular Cell Tumour be found?

A

Benign painless smooth swelling found on the tongue

309
Q

What is the histology of Peripheral Nerve Sheath Tumour?

A

Spindle Cell Lesion
Increased/Abnormal Mitoses
Atypical Cells: Nuclear Pleomorphism (variability in size/shape)
Immunochemistry: S100

310
Q

What are some malignant tumours found in the mouth?

A
  1. Epithelial
    - Squamous Cell Carcinoma
    - Melanoma
  2. Mesemchymal
    - Peripheral Nerve Sheath Tumour
    - Sarcomas (Fibrosarcoma, Liposarcoma, Angiosarcoma, Leimyosarcoma, Rhabdomyosarcoma)
  3. Hematolymphoid
    - Lymphoma (Hodgkin/Non-Hodgkin)
311
Q

What are some benign mesenchymal lesions found in the mouth?

A 
Fibrous Tissue Neoplasm: Fibroepithelial Polyps, Irritation Fibromas
Solitary Fibrous Tissue
Myoma
Leiomyoma
Peripheral Giant Cell Granuloma
Lipoma
Neuroma
Neurofibroma
Schwannoma
Granular Cell Tumour
Granular Cell Congenital Epulis
312
Q

What histological feature of myxoma is different to other benign tumours

A

Unencapsulated mass - most benign tumours are encapsulated

313
Q

What are the histological signs of myxoma?

A

Unencapsulated lesions - most benign tumours are encapsulated
Infiltrative Growth
“Stellate” and “Spindle Cell” shaped fibroblasts
Myxoma (‘Loose’ pale-to-lightly basophilic, like mucus) stroma appearance

314
Q

Where is Solitary Fibrous Tissue typically found?

A

Lung Plura, but can be found anywhere

315
Q

What is the most common mesenchymal malignancy?

A

Fibrosarcoma

316
Q

What is the aetiology of Fibrosarcoma?

A

Unclear but can progress from pre-existing benign lesions and in previously irradiated tissue

317
Q

What is the clinical presentation of a Fibrosarcoma?

A

Lobulated, Sessile Painless Mass
Variable Growth Rate
May be haemorrhagic

318
Q

What is the histology and immunochemistry of Fibrosarcoma?

A 
Vimentin marker positive
High level of variability
Lots of spindle cells 
Odd anaplastic cells
Big nuclei
Increased mitotic figures
319
Q

How does a lipoma present clinically?

A

Asymptomatic Yellow Mass in Buccal Mucosa, Tongue, Floor of Mouth

Intact Overlying Epithelium

320
Q

Is a Lipasarcoma a fast or slow growing malignancy?

A

Slow growing - well differentiated and pleomorphic

321
Q

What is the histology and immunochemistry of Angiosarcoma?

A

Immunochemistry: Factor VIII Positive
Unencapsulated
Atypical/anaplastic endothelial cells

322
Q

What do leiomyoma, leiomyosarcoma and rhabdomyosarcoma affect?

A
  • Leiomyoma: benign smooth muscle tumour
  • Leiomyosarcoma: malignant smooth muscle tumour
  • Rhabdomyosarcoma: malignant striated muscle
323
Q

Peripheral Nerve Sheath Tumour can progress from what benign growth?

A

Neurofibroma

324
Q

Which lesions test positive to S100 immunochemistry?

A

Schwannoma
Neurofibroma
Peripheral Nerve Sheath Tumour
Melanoma

325
Q

How do neurofibromas present clinically?

A

Cutaneous cafe au lait macules, bone and CNS abnormalities

326
Q

What dental diganostic tool can be used to identify a Peripheral Nerve Sheath Tumour?

A

Mass can appear as a rapidly growing radiolucent mass on an OPG

COPY BDS3 University of Adelaide Dentistry (28 decks)

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