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COPY BDS3 University of Adelaide Dentistry > Oral Pathology Part 2 > Flashcards

Oral Pathology Part 2 Flashcards

1
Q

What are mucocutaneous diseases?

A

A pathology that manifest on both mucosa and skin. There is a high level of variation between oral mucosal versus presentation on other mucosa or skin.

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2
Q

What are the most likely groups to have Lichen Planus?

A

65% Female Mostly over 40 years of age

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3
Q

Where are the likely sites of Lichen Planus?

A

Bilateral symmetrical presentation on 1. Buccal Mucosa (most common) 2. Dorsal Surface of Tongue 3. Gingiva (appears as desquamative gingivitis) 4. Cutaneous Lesions on the skin

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4
Q

What is the classic presentation of Lichen Planus?

A

Bilateral white striae on buccal mucosa with atrophic margins

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5
Q

What are the 4 patterns of presentation for Lichen Planus?

A

Striae / Reticular Atrophic Erosive Plaque

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6
Q

What is the aetiology of Lichen Planus

A

Immune mediated: so either an Autoimmune or Hypersensitivity Reaction However, the target antigen has not yet been identifed

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7
Q

What immune marker is associated with Lichen Planus?

A

Increased T-Lymphocyte Infiltration (CD4/CD8 Cells) Also increased mobility of APC cells: Macrophages, Langerhan’s Cells + Mast Cells (However they do not have an phagocytosis role as there is no infection)

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8
Q

What are the steps for progression of Lichen Planus?

A
  1. Unknown Initiator 2. Focal Release of Regulatory Cytokines from APCs 3. Up-regulation of Vascular Adhesion Molecules 4. Recruitments and Retention of T-Lymphocytes 5. T-Cells trigger cytotoxicity of Basal Keratinocytes 6. Apoptosis into Civatte Bodies
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9
Q

What is the histology of Lichen Planus?

A
  1. Hyperkeratosis 2. Hyperparakeratosis 3. Saw-tooth appearance of rete pegs 4. Basal Cell Layer Degeneration: Formation of Civatte Bodies 5. Band-like Lymphocytic Infiltrate in the lamina propria
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10
Q

What are Civette Bodies?

A

Histologically dark pink dots: They are apoptotic (programmed cell death) of Basal cells. Found in Lichen Planus and Erythema Multiforme

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11
Q

How do cutaneous Lichen Planus lesions present?

A
  • Purple Papules, Scaly Lesions - Wrists most common site - Superficial Fine Wickham’s Striae
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12
Q

How would you differentiate between Lichenoid Reactions and Lichen Planus?

A
  1. Lichenoid Reactions are more diffused than lichen planus 2. Deeper cluster closer to highly vascularised areas 3. Medical History + Medication (example Gout, Hypertension, Tetracycline meds)
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13
Q

What medications are implicated in Lichenoid Reactions?

A

Allopurinol (Gout) Angiotensin-Converting Enzyme II Inhibitors (High BP) Enalapril (ACE Inhibitors) Furosemide (Hypertension) Gold Salts: Rheumatoid Arthritis Hydroxychloroquine: Malaria prevention/treatment Mercury (Possible from Amalgam fillings) Methyldopa: hypertension, down regulates dopamine > adrenaline/noradrenaline as a competitive inhibitor NSAIDS Phenothiazine: Antipsychotic Propranolol: tremors, angina (chest pain), hypertension, heart rhythm disorders Quinidine: Class I antiarrhythmic agent. Aids in increased action potential duration Tetracyclines: protein synthesis inhibitor antibiotics Thiazides: family of diuretics for hypertension

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14
Q

What are treatment options for Lichen Planus?

A
  1. Chlorhexidine Gel: palliative effect 2. Corticosteroids: Modulate inflammation and immune response 3. Topical / Local Steroids 4. Antifungal Therapy (for secondary infections) 5. Topical Retinoids (Vit A) + Vitamin E (possible efficacy)
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15
Q

T/F: Pemphigus results in slow growing, largely asymptomatic blisters

A

False, it is typically rapid development with widespread oral ulceration

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16
Q

What are the primary clinical signs of Pemphigus

A

Rapidly developing skin bullae (>5mm), filled with clear fluid that can become haemorrhagic

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17
Q

What is the risk of untreated Pemphigus?

A
  1. Dehydration from inability to self-care from blister sites 2. High risk of secondary and systemic infections that has a 6% of mortality from septicemia
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18
Q

What is a vesicle?

A

A blister less than 5mm in diameter

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19
Q

What is a bullae?

A

A blister more than 5mm in diameter

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20
Q

What groups are more predisposed to Pemphigus Vulgaris?

A

Increased susceptibility in Mediterranean, South Asian population

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21
Q

What is the cause of Pemphigus Vulgaris?

A

An autoimmune condition with a strong genetic link. Patients with Pemphigus have high levels of circulating IgG antibodies that attack the desmoglein protein. This group of proteins are involved in desmosome connection between epithelial cells. Autoimmune reactions cause breakage of desmosome links creating clefts of intraepithelial vesicles and rupture of the epithelium to form ulcers

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22
Q

What is the histology of Pemphigus Vulgaris?

A
  1. Acantholysis: Splitting of epithelial histological layers 2. High titre of circulating IgG to desmoglein 3 proteins 3. Epithelial Cleft Formation superior to basal cells 4. Tzanck Cells: free floating epithelial cells
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23
Q

What are the 2 types of Pemphigus affecting the oral cavity?

A
  1. Pemphigus Vulgaris 2. Paraneoplastic Pemphigus
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24
Q

How would you differentiate between Pemphigus Vulgaris + Paraneoplastic Pemphigus?

A

Paraneoplastic Pemphigus has more persistant, severe and multiple outbreaks. It can also have further distribution to the oropharynx/nasopharynx/oesophagus and cutaneous lesions

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25
Q

What neoplastic diseases is Paraneoplastic Pemphigus associated with?

A

Lymphoproliferative Diseases such as: Lymphoma Chronic Lymphocytic Leukaemia Castleman’s Disease

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26
Q

What treatment options are available for Pemphigus Vulgaris?

A
  1. Early Diagnosis - Pathology Biopsy 2. Systemic Immunosuppressive Treatment - Prednisolone (steroid) + Azathioprine (Immunosuppressant)
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27
Q

T/F: Pemphigoid is a non-fatal indolent mucocutaneous disease

A

True

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28
Q

What groups are most likely to have Pemphigoid?

A

Affects Females and the Elderly

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29
Q

What site in the body is usually the first site of involvement for Pemphigoid?

A

Oral Mucosa as erosion of non-keratinsed mucosa

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30
Q

What is the major long term risk of untreated Pemphigoid?

A

Involvement of the mucosa around the eye causing blindness

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31
Q

How does IgG immunoglobulin autoimmunity differ between Pemphigoid and Pemphigus Vulgaris?

A

Pemphigus Vulgaris: affects epithelium to epithelium attachment via desmosomes Pemphigoid: affects attachment of epithelium to basement membrane by attacking basal lamina hemidesmosomes

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32
Q

T/F: Both Pemphigoid and Pemphigus Vulgaris involve IgG autoimmunity

A

True but to different target proteins: Pemphigus Vulgaris: desmosomes Pemphigoid: hemidesmosomes

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33
Q

What would you expect to see histologically in Pemphigoid?

A

Full clefting of the epithelium from the dermis. A void exists between the basal layer and the dermis There wouldn’t be the existence of free floating epithelial islands

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34
Q

Which bullae would be more susceptible to rupture: Pemphigoid or Pemphigus Vulgaris?

A

Pemphigus Vulgaris as the separation occurs within the epithelium. Pemphigoid the whole epithelium comes off as a layer, so is more resistant to rupture

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35
Q

What is the main clinical feature of Benign Mucous membrane pemphigoid that doesn’t occur in Bullous Pemphigoid?

A

Scarring of the mucosa - scar tissue is left by the formation of new connective tissue over the healing bullae

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36
Q

Which pemphigoid has mostly oral involvement?

A

Benign Mucous membrane pemphigoid

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37
Q

Benign Mucous membrane pemphigoid affects which type of epithelium?

A

Stratified squamous mucous membranes

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38
Q

What treatment options are available for pemphigoid?

A

Corticosteroids to control progression and symptoms. Topical application appears to be the most responsive method

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39
Q

T/F: Erythema Multiforme is a Self-limiting hypersensitivity inflammatory condition

A

True

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40
Q

What are the 5 clinical symptoms of Erythema Multiforme?

A

1) Systemic fever 2) Swollen, split, crusted lips that bleed 3) Widespread erosive lesions in the mouth 4) Conjunctivitis 5) “Target” lesions on the skin

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41
Q

T/F: Erythema Multiforme can have both infectious and drug induced aetiologies?

A

True 1) Infectious: Erythema Multiforme Minor + Major 2) Drug Induced: Stevens Johnsons Syndrome + Toxic Epidermal Necrolysis

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42
Q

What are the high risk groups for Erythema Multiforme?

A

1) Previous viral (herpes, EBV, VZV, Hepatitis), bacterial infections 2) Medications 3) Young adolescent/adult male

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43
Q

What is the histology of Erythema Multiforme?

A

1) Variable Histological Appearance 2) Epithelial Hyperplasia and Oedema 3) Apoptosis of Basal Keratinocytes (Civatte Body) 4) Intraepithelial Vesicle Formation (also subepithelial) 5) Lymphocyte and Macrophage perivascular infiltrate in connective tissue

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44
Q

What are the forms of Erythema Multiforme from most mild to severe?

A

Erythema Multiforme Minor Erythema Multiforme Major Stevens Johnsons Syndrome Toxic Epidermal Necrolysis

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45
Q

How would you differentiate Erythema Multiforme Minor from Major?

A

In Erythema Multiforme Major there are both skin lesions and 2 sites of mucosal infection. Symptoms are more severe and widespread In Erythema Multiforme Minor there are skin lesions, but mucosal involvement is unlikely and limited to 1 site.

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46
Q

How much skin surface would you expect to be affected by Erythema Multiforme Minor from Major?

A

10% of total body surface area = 40 X 50cm patch in total

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47
Q

What are some clinical features of Stevens Johnsons Syndrome?

A

A more severe form of Erythema Multiforme: 1) Drug induced 2) Less than 10% of body surface area, but more severe than EM Major 3) Primarily atypical flat target lesions and macules, rather than classic target lesions 4) More widespread: multiple mucosal sites involved 5) Scarring of mucosa 6) Systemic Effects: prodromal flu-like symptoms

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48
Q

What are some clinical features of Toxic Epidermal Necrolysis?

A

The most severe form of Erythema Multiforme: 1) Poorly defined erythematous macules and flat targets 2) With Spots: up to 30% body surface. Widespread purpuric macules/flat atypical targets 3) Without Spots: up to 10% body surface. Large epidermal sheets without macule/targets 4) Secondary Infection + Septicemia possible

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49
Q

How would differentiate between Herpes and Erythema Multiforme?

A

Erythema Multiforme: Young adult onset. Large oral/lip ulcers + skin target lesions affecting buccal, tongue, lips, palates and extremities Herpes: Children, small oral/perioral + skin ulcers affecting gingiva, lips and skin

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50
Q

What is the treatment for Erythema Multiforme?

A

Hospitalisation Palliation of Symptoms Infection control - prevention of secondary infection Antibiotic Cover Steroids

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51
Q

What are some clinical features of Systemic Lupus Erythematosus?

A

Oral Ulceration - usually painless Fever, Malaise, Anaemia Arthralgia (Joint Pain) Malar Rash - butterfly rash on the cheeks Alopecia (Spot Baldness) Photosensitivity Joints: Non-erosive Polyarthritis Kidney: Glomerulonephritis Mucous Membranes: Oral Ulceration Nervous System: Polyneuritis, Cerebralis Vascular: Raynaud’s Phenomenon Heart: Pericarditis, Endocarditis, Myocarditis Lungs: Pleuritis Eyes: Anterior Uveitis Blood: Autoimmune Haemolytic Anaemia, Thrombocytopenia

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52
Q

Which groups are most likely affected by Systemic Lupus Erythematosus?

A

Young Women of African / Asian descent

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53
Q

What are some histological features of Systemic Lupus Erythematosus?

A

1) Epithelial Basal Cell Destruction 2) Hyperkeratosis 3) Areas of epithelial atrophy and acanthosis (Discoid has no acanthosis) 4) Subepithelial and Perivascular Lymphocytic Infiltration 5) Vascular Dilation 6) Immunofluorescence Studies - Lupus Band Test: deposits of IgG and IgM at the basement membrane zone

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54
Q

What are some dental implications for Systemic Lupus Erythematosus?

A

1) Increased incidence of Sjogren’s Syndrome 2) Risk of Endocarditis: need prophylactic AB cover prior to surgical dental treatment

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55
Q

What are some treatment options for Systemic Lupus Erythematosus?

A

Systemic Steroids Immunosuppressive Agents Organ Specific Treatment

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56
Q

What are clinical symptoms of Discoid Lupus Erythematosus?

A

1) Skin Lesions, face and scalp, sun exposed areas 2) Rash: not too painful 3) Disc shaped Erythematous Plaques 4) Hair Follicle Involvement: leading to permanent hair loss 5) 25% Patients have oral lesion: a white keratotic striae similar but weaker than Lichen Planus

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57
Q

A patient has a White, Keratotic Striae on the buccal mucosa. What mucocutaneous lesion could this be? How could test for this?

A

1) Lichen Planus (most likely) 2) Discoid Lupus Erythematosus You could order a Antinuclear antibody (ANA) serology test. Only Lupus would return positive

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58
Q

T/F: progression from Progression from Discoid Lupus Erythematosus to Systemic Lupus Erythematosus is rare

A

True

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59
Q

What is the histology of Discoid Lupus Erythematosus?

A

1) Epithelial Basal Cell Destruction 2) Hyperkeratosis - striae 3) Epithelial Atrophy - red/erosive areas 4) Subepithelial and Perivascular Lymphocytic Infiltration 5) Chronic immune mediated process 6) Vascular Dilation - causes redness, accounts for lymphocyte infiltration via cytokine signalling 7) Immunofluorescence Studies - Lupus Band Test: deposits of IgG and IgM at the basement membrane zone

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60
Q

What is the treatment for Discoid Lupus Erythematosus?

A

Topical Steroids

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61
Q

How would serology differentiate between Discoid and Systemic Lupus?

A

Discoid: Autoantibodies not detected Systemic: Positive Antinuclear Antibody (ANA), anti DNA antibodies

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62
Q

What is Sjogren’s Syndrome?

A

A Chronic autoimmune disease affecting the exocrine glands

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63
Q

What are subjective symptoms of Sjogren’s Syndrome?

A

Dry mouth (xerostomia)

Dry eyes (keratoconjunctivitis sicca)

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64
Q

What is the resting flow rate of saliva?

A

Depending on age: 1.5ml/min

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65
Q

Why might there be a false negative when taking salivary resting flow rate from a patient?

A

In the dental chair, patients are likely nervous already, so sympathetic nervous system is activated => reduces flow rate

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66
Q

What is the average stimulated salivary flow rate?

A

4-5ml/min

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67
Q

What are the implications for drugs acting on the sympathetic nervous system on salivary flow?

A

SNS activation = decreased salivary + exocrine output = dry mouth

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68
Q

What is the steps of pathological damage in Sjogren’s Syndrome?

A
  1. Lymphocytic infiltration of glands
  2. Acinar epithelium cell atrophy
  3. Progressive fibrosis
  4. Destruction of gland parenchyma
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69
Q

What is Primary Sjogren’s Syndrome?

A

The subjective symptoms (patient’s perspective) of Dry Eyes and Dry Mouth

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70
Q

What is secondary Sjogren’s Syndrome?

A

The Symptoms of Primary Sjogren’s Disease (Dry Eyes + Dry Mouth)

AND

Presence of other autoimmune diseases:

Rheumatoid arthritis

Systemic lupus erythematosus

Polymyositis

Scleroderma

Primary Biliary Cirrhosis (Bile duct)

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71
Q

What other medical professionals can you work with in order to accurately diagnose Sjogren’s Syndrome?

A

Rheumatologist (for other autoimmune disease)

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72
Q

What are possible aetiological causes of Sjogren’s Syndrome?

A

Exogenous Agents (possibly viral via EBV)

Hormonal (post menupausal fibrosis)

Genetic Predisposition

Microchimerism (transfer of non-self cells to the foetus from the placenta. Autoimmune response)

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73
Q

What is the epidemiology of Sjogren’s Syndrome?

A

80% more females than males

Onset 50 years+

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74
Q

Why are sufferers of Sjogren’s Syndrome more at risk for fungal and bacterial infections?

A

Lack of Salivary Clearance

Low levels of Salivary IgA (host anti-bacterial immunoglobulin)

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75
Q

What infections are common in sufferers of Sjogren’s Syndrome?

A

Candidiasis: pseudomembranous and erythematous candidiasis

Angular cheilitis

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76
Q

What are the possible oral clinical presentation of Sjogren’s Syndrome?

A

Dry Mouth (Xerostomia)

Increased Caries

Burning sensation

Difficulty eating dry food and swallowing

Difficulty controlling dentures

Dry/Fissured Tongue

Taste alteration, malodour

Fungal/Bacterial infections

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77
Q

What are some things to observe during an oral examination for signs of Sjogren’s Syndrome?

A

Lack of salivary pooling

Frothiness of saliva

“sticky” mucosa

Red inflammated Mucosa

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78
Q

What are some clinical feature of Dry Eye as part of Sjogren’s Syndrome?

A

Sensation of grittiness, itching, dryness, blurred vision

Keratoconjunctivitis sicca (redness and crusting in corner of eye)

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79
Q

What are 2 long term complications that can happen with Sjogren’s Disease?

A

Salivary Gland Enlargement - Lymphocyte mediated inflammation

Increased risk of Lymphoma - chronic inflammation of MALT in Salivary Glands

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80
Q

What Objective Findings can be used to diagnose Sjogren’s Syndrome?

A

Ocular Signs

Salivary Gland Involvement

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81
Q

What Subjective findings can be used to diagnose Sjogren’s Syndrome?

A

A. Ocular symptoms

Daily persistent dry eyes for >3 months

Recurrent sensation of sand or grit in the eye

Need to use “tear drops” >3 times daily

B. Oral symptoms

Daily feeling of dry mouth > 3 months

Recurrent or persistently swollen salivary glands

Frequent need to drink fluids to help swallow dry food

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82
Q

What are other findings that can be used to diagnose Sjogren’s Syndrome?

A

Histopathology

Serum Auto-antibodies

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83
Q

What are 2 Salivary Gland tests that can be used to diagnose Sjogren’s Syndrome?

A
  1. Sialography: special imaging to detect diffuse sialectasis (cystic dilatation of the ducts within salivary gland)
  2. Sialometry: clinical salivary flow testing
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84
Q

What Histopathological features can be found with minor salivary gland biopsy?

A

Focal sialadenitis

Inflammation

Fibrosis

Fatty atrophy

Duct dilation

Hyperplasia

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85
Q

What can minor salivary gland biopsy be taken to reduce post op complications?

A

Lower labial mucosa

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86
Q

What is the primary lymphocyte marker in oral pathology biopsy identification for Sjogren’s Syndrome diagnosis?

A

T Helper Lymphocyte Count

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87
Q

What can happen to salivary gland ductal epithelium over time in Sjogren’s Syndrome

A

Squamous metaplasia obliterating duct lumens creating islands of epithelium known as epimyoepithelial islands

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88
Q

Is the presence of SS-A (Ro) and SS-B (La) serum antibodies itself a clear diagnosis for Sjogren’s Syndrome?

A

No, as these serum antibodies can appear in systemic autoimmune diseases. However this could possibly indicate secondary Sjogren’s after the patient reports symptoms of Primary Sjogren’s.

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89
Q

How is Sjogren’s Syndrome treated?

A

Palliation of oral symptoms

  1. Saliva substitutes: Oral 7
  2. Dietary advice
  3. Fluoride programs: Tooth Mouse, Clin Pro
  4. Management of Infections
  5. Good OH
  6. Monitor caries
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90
Q

What is Scleroderma?

A

Connect tissue disease : hardening of skin with excessive collagen manufacture

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91
Q

How is systemic scleroderma potentially life threatening?

A

Fibrosis of Organs

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92
Q

What are the 2 types of Scleroderma?

A
  1. Morphea: Disfiguring localised cutaneous form
  2. Systemic Scleroderma: Potentially life threatening
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93
Q

What is the aetiology of Scleroderma?

A

Unclear, but underlying serological evidence of elevated rheumatoid factor and antinuclear antibodies indicative of some sort of autoimmune response

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94
Q

What groups are more at risk of Scleroderma?

A

Very rare (50 per 1,000,000)

3-14x more Females than Male

Onset 30-50

Familial clustering: high frequency of other autoimmune disease in families

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95
Q

What clinical features of Scleroderma are important for dentists?

A
  1. Facial Changes
  2. Fibrosis of fingers/atrophy of skin - OH is difficult
  3. Limited Mouth opening from rigidity of perioral skin
  4. Salivary Gland fibrosis
  5. Bone Resorption / Periodontal Disease
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96
Q

What are some histopathological signs evidence in Scleroderma?

A

Dense Deposition of avascular fibrous collagen

Inflammatory + Obstructive Changes in Arterioles/Capillaries

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97
Q

What is treatment for Scleroderma?

A
  1. Oral hygiene maintenance: reduce risk of caries, periodontal disease
  2. Management of concomitant conditions
  3. Stabilisation through systemic medications
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98
Q

What 3 features characterise fibro-osseous lesions?

A
  1. Benign fibrous CT stroma
  2. Trabeculae of immature woven bone
  3. Diagnosis confirmed on clinical features, radiographic features and histopathology
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99
Q

What is an ossifying fibroma?

A

Well demarcated lesion composed of fibrocellular tissue and mineralised material of varying appearances

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100
Q

What are the 3 types of Ossifying Fibroma?

A
  1. Main Type
  2. Juvenile Trabecular Ossifying Fibroma (JTOF)
  3. Juvenile Psammomatoid Ossifying Fibroma (JPOF)
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101
Q

Who is more likely to get ossifying fibroma?

A

More likely females than males

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102
Q

When and where does main type of ossifying fibroma develop?

A

Average Age: 35 years

Location: Posterior Mandible

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103
Q

When and where does Juvenile Trabecular Ossifying Fibroma (JTOF) develop?

A

20 years

Location: Paranasal Sinuses

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104
Q

When and where does Juvenile Psammomatoid Ossifying Fibroma (JPOF) develop?

A

8.5-12 years

Location: Maxilla

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105
Q

What are the radiographic features of Ossifying Fibroma?

A
  1. Bony Expansion: expansive collagen fibres replace bone
  2. Well demarcated lesions
  3. Variable radio-density depending on the maturity of the lesion
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106
Q

T/F: Ossifying Fibroma is a slowly enlarging lesion

A

True

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107
Q

Why is Ossifying Fibroma a lesion where complete surgical excision is recommended?

A

Due to clear, well demarcated borders of the lesion

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108
Q

What is Fibrous Dysplasia?

A

A genetically based sporadic disease that can affect single or multiple bones and replace bone with scar-like fibrous tissue

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109
Q

What are clinical features of Fibrous Dysplasia?

A
  1. Doesn’t cross midline
  2. Noticeable facial asymmetry
  3. Painless swelling
  4. Jaw Involvement: loose / displaced teeth, malocclusion
  5. Cafe Au Lait Skin macules if associated with McCune Albright Syndrome
  6. Impaction of nerves / blood vessels: nasal obstruction, visual impairment, hearing loss, facial pain, headaches, paraesthesia
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110
Q

What are the 2 types of Fibrous Dysplasia?

A
  1. Monostotic Form: Affects Single Bone
  2. Polyostotic Form: Affects Multiple Bones. More likely in women and can be part of McCune Albright Syndrome
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111
Q

Your patient as a painless unilateral bilateral swelling, cafe au lait skin macules on hands and a rapid metabolism. What could this be?

A

Polyostotic Form of Fibrous Dysplasia with McCune Albright Syndrome

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112
Q

What is the radiographic appearance of Fibrous Dysplasia?

A

Ill-defined margins with variable patterns:

  1. Cystic (Radiolucent)
  2. Mixed Radiolucent/Radiopaque
  3. Sclerotic (Radiopaque)
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113
Q

What is the histology of Fibrous Dysplasia?

A

More superficial layer of collagen stroma attempting to wall off lesion

Patchwork of woven + trabecular bone that looks like “chinese characters”

Bone surrounded by Fibroblastic Stroma

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114
Q

What is the treatment for Fibrous Dysplasia?

A

Lesion is typically self-limiting

Orthodontic Treatment for displaced teeth

Conservative Surgical Recontouring

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115
Q

What are Ossifying Dysplasias?

A

Idiopathic dysplastic processes in the periapical region of tooth bearing jaw areas

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116
Q

T/F: The teeth above an ossifying dysplasia lesion are non-vital

A

False - they appear like periapical lesions but are in fact not odontogenic infections. Thus the tooth is likely still vital

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117
Q

What are the clinical features of Ossifying Dysplasia?

A
  1. Replacement of normal bone with fibrous tissue and abnormal metaplastic bone
  2. Teeth are vital
  3. More common in black female patients
  4. Confined to tooth areas of the jaws
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118
Q

What are some radiographic features of Ossifying Dysplasias?

A
  1. Appear like a periapical lesions associated with vital teeth
  2. Varying radiodensity (increases density over time)
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119
Q

What are the 4 types of Ossifying Dysplasias?

A
  1. Periapical Osseous Dysplasia
  2. Focal Osseous Dysplasia (single)
  3. Florid Osseous Dysplasia (contiguous multifocal)
  4. Familial Gigantiform Cementoma
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120
Q

What are some features of Familial Gigantiform Cementoma (a form of Ossifying Dysplasia)?

A

Very rare

Giant mass of cementoid material

Highly disfiguring

Genetic factors

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121
Q

What is the histology of Ossifying Dysplasias?

A

Islands of bony cementoid material surrounded by collagenous stroma

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122
Q

T/F: Periapical Osseous Dysplasia consists of multi-focal lesions

A

False, they contain single, separate lesions under the apex of a tooth

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123
Q

What is the feature of Florid Osseous Dysplasia?

A

Coalescing multifocal lesions of bony cementoid tissue surrounded by collagenous stroma under the apex of multiple contiguous teeth

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124
Q

T/F: Parotid Salivary Gland provides Serous secretion that accounts for 75% of flow

A

True

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125
Q

T/F: Submandibular Salivary Glands account for 18% flow that is both mucous and serous in nature

A

True

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126
Q

T/F: Sublingual Salivary Glands account for 7% flow that is mucous in nature

A

True

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127
Q

T/F: Parotid Salivary Gland secretions are stimulated flow

A

True

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128
Q

Are the minor salivary glands on the circumvallate papilla serous or mucous in nature?

A

Serous

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129
Q

Where can minor salivary glands be found?

A

Oral mucosa (tongue, palate, lips, buccal mucosa)

Pharynx and tonsillar area

Larynx, trachea, major bronchi

Nasopharynx, nasal cavity and paranasal sinuses

Minor salivary glands are predominantly mucous secreting

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130
Q

T/F: minor salivary glands exist on the gingiva and ventral surface of the tongue

A

False

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131
Q

Where are possible locations of ectopic salivary glands?

A
  1. Superficial neck
  2. Within lymph nodes close to or in parotid glands
  3. Lingual deep floor of mouth area
  4. Within the jaw bone (Stafne’s bone cyst)
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132
Q

What sort of salivary gland is this?

A

Serous

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133
Q

What sort of salivary gland is this?

A

Mucous

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134
Q

What are 4 examples of reactive lesions?

A
  1. Mucoceles
  2. Salivary Gland Obstruction
  3. Necrotising Sialometaplasia
  4. Irradiation-Related Sialadenitis
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135
Q

A Mucocoele is a clinical term for what 2 related dental phenomena?

A

Mucus extravasation phenomenon (MEP): more common than MRC

Mucus retention cyst (MRC)

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136
Q

What is a Ranula?

A

It is a Mucocoele located specifically in the floor of the mouth

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137
Q

What is a Ranula that extends through the mylohyoid muscle?

A

Plunging Ranula

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138
Q

What are the potential complications of a plunging ranula?

A

Life threatening airway obstruction

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139
Q

What is the cause of a ranula?

A

Usually due to trauma leading to severance of duct leading to mucus gathering in the tissues

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140
Q

What are the typical clinical presentation in Mucus Extravasation Phenomeon?

A

Site: lower lip is most common, floor of mouth (ranula), retromolar region, soft palate, posterior buccal mucosa (superficial mucocele)

Size – few millimetres to 2cm diameter

Painless, smooth surface swelling

Bluish coloration

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141
Q

What reactive changes eventually occur in a salivary gland affected by Mucus extravasation phenomenon?

A

Ductal dilation

Chronic inflammation

Acinar degeneration/ atrophy

Fibrosis / Scarring

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142
Q

What histological features are evident with in Mucus extravasation phenomenon?

A
  1. Free mucus infiltrates surrounding tissue (mucocoele) - no nucleus present
  2. Mucus elicits inflammation response
  3. CT attempts to remove mucus and repair: but healing is incomplete from continual mucus production
  4. Mucus surrounded by “pseudocystic wall” of inflammatory granulation tissue (fibroblasts, HEVs, endothelial cells)
  5. Can be infiltrated by macrophages
  6. Reactive changes occur to salivary gland
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143
Q

Q: What is the main difference between Mucus Retention Cyst and Mucus extravasation phenomenon?

A

Mucus extravasation phenomenon = trauma resulting in severance of salivary excretory duct. More likely to happen in young people (higher mucous production)

Mucus Retention Cyst = obstruction of duct. More likely in old people (stagnant salivary flow)

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144
Q

What are some clinical features of Mucus Retention Cyst?

A

Less common than mucus extravasation mucoceles

Occurs in older patients : stagnant saliva flow, becomes prone to blockage

Upper lip, palate, cheek, floor of mouth

Size: 3-20mm in diameter

Overlying mucosa is intact and normal colour

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145
Q

What is the histology of a mucus retention cyst?

A

Cystic cavity lined by compressed ductal epithelium (not granulation tissue)

Cyst lumen contains mucus of occasionally a sialolith (salivary gland stone)

Connective tissue shows minimal inflammation as mucus is contained within the epithelium

Reactive changes in salivary gland

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146
Q

What is the aetiology of a mucus retention cyst?

A
  1. Obstruction of Duct
  2. Retention of mucus
  3. Dilation of duct
  4. Development of an epithelial lined cystic lesion
  5. Reactive changes in associated salivary gland
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147
Q

What is the aetiology of a Mucus extravasation phenomenon?

A
  1. Trauma
  2. Severance of salivary gland excretory duct
  3. Mucus Escape
  4. Inflammation in CT
  5. Reactive changes in associated salivary gland
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148
Q

What are 3 causes of a salivary gland obstruction?

A
  1. Sialoliths (Salivary Stone): obstruction of salivary glands
  2. Periductal scarring: scarring around opening of gland
  3. Impinging tumour: rare cases where tumour blocks the ducts
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149
Q

What are the clinical presentation of a salivary gland obstruction?

A

Effects of obstruction are restriction of salivary flow

Leading to intermittent swelling

Pain of involved gland often at mealtimes

Long term: chronic sialadenitis

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150
Q

What is the cause of Sialoliths (Salivary Stone)?

A

Precipitation of calcium salts over time

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151
Q

What are consequences of Sialoliths (Salivary Stone)?

A

Chronic sialadenitis

Fibrosis of gland

Mucous retention cyst

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152
Q

What is management for Sialoliths (Salivary Stones)?

A

Surgical removal of stone with/without gland

In some cases the stone may be massaged out - painful but conservative

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153
Q

What are some clinical features of Sialoliths?

A
  1. History of intermittent swelling and pain often at meal times
  2. Increased ductal pressure
  3. Radiographs may show stone in some cases
  4. Location: anywhere along the ductal system, but commonly associated with submandibular gland – Wharton’s Duct
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154
Q

What is the aetiology of Necrotising Sialometaplasia?

A

Local trauma causing Salivary gland ischemia

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155
Q

What are the clinical features of Necrotising Sialometaplasia?

A
  1. Usually affects palate
  2. Benign condition that mimics malignancy
  3. Painful ulceration, typically on hard palate
  4. Abrupt onset, initially presenting as a tender swelling which may have a fluctuant feeling
  5. Gives impression of abscess formation
  6. 1-3cm in diameter ulcer
  7. Extended healing time
  8. Worries patient and operator!
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156
Q

What differentiates Necrotising Sialometaplasia from SCC?

A
  1. Whilst there is squamous metaplasia of the ducts, there is not the cytological atypia expected of SCC.
  2. Preservation of lobular architecture of gland
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157
Q

What is the histology of Necrotising Sialometaplasia?

A
  1. Salivary Gland Infarction with Ductal Metaplasia
  2. Pseudoepitheliomatous hyperplasia of overlying epithelium
  3. Squamous metaplasia of ducts
  4. No cytological atypia expected of SCC
  5. Extravasation of mucus into tissues (occasionally)
  6. Inflammation

Preservation of lobular architecture of gland

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158
Q

What are differential diagnosis for Necrotising Sialometaplasia?

A

Clinical - SCC, Minor salivary gland tumours, Opportunistic fungal infections

Histological - SCC, Mucoepidermoid carcinoma

159
Q

What is treatment for Necrotising Sialometaplasia?

A

No Surgery

Slow healing by secondary intention (6-10 weeks)

160
Q

What is Acute Radiation Sialadenitis and what are the clinical signs?

A

Side effect of radiotherapy for head/neck cancer

Clinical signs:

Onset 24-37 hours

May last up to a week

Swelling, Pain, Xerostomia

Acute Inflammation of gland stroma and early necrosis of acini

161
Q

What is Chronic Radiation Sialadenitis and what are the clinical signs?

A

More extensive and long lasting damage done from head/neck radiotherapy:

Clinical Signs

Persistent Xerostomia

Usually no pain

Possibly permanent depending on damage to gland

Fibrosis, Acinar atrophy

162
Q

What are treatment options for acute/chronic radiation sialadenitis?

A

Monitor Stomatitis and Caries Status

Salivary Substitutes

163
Q

What are the 2 causes of Infectious Sialadenitis?

A

Mumps (RNA Paramyxovirus)

Bacterial Sialadenitis: Ascending duct infection (Strep Pyogenes, Staph Aureus)

164
Q

What are the clinical signs of mumps causing infectious sialadentitis?

A
  1. 2-3 week incubation
  2. Acute onset: Pain and swelling, Difficulty Swallowing, Fever + Unilateral/Bilateral facial swelling
  3. Symptoms develop over 2-3 days then resolve in 7-10 days
165
Q

What are predisposing factors to acute bacterial sialadentitis?

A
  1. Patients post surgery: compromised immune system, opportunistic infection
  2. Xerostomia: lack of clearance
  3. Sialoliths: stones can accumulate bacterial
166
Q

What are clinical signs of Acute Bacterial Sialadentitis?

A

Usually affects Parotid

Can be uni/bilateral

Pain, Swelling, Trismus, Fever

167
Q

What are management options for Acute Bacterial Sialadenitis?

A

Severe: Drainage

Antibiotics: Metronidazole + Amoxicillin

168
Q

What are the clinical and histological signs for saliva and aging?

A

Clinical Signs

Decreased quality/quantity of saliva

Histology

Acinar Atrophy (leaving ducts)

Fibrosis

Fatty Infiltration

Diffuse Chronic Inflammatory Infiltrate: Lymphocytes, Plasma Cells

169
Q

What is Sialosis?

A

Non-inflammatory, non-neoplastic recurrent bilateral swelling of salivary glands of unknown origin

170
Q

What is the aetiology of Sialosis?

A

Aetiology: Unknown but correlation with:

Hormonal Disturbances

Diabetes

Malnutrition

Liver Cirrhosis

Medications: Phenylbutazone (anti-inflammatory), Iodine Containing Drugs

171
Q

What are the clinical signs and histology of Sialosis?

A

Clinical Signs: Usually Painless

Histology

Serous Cell Hypertrophy with decrease in granularity

Stromal Oedema

Fatty Replacement

172
Q

What is the treatment of Sialosis?

A

Treatment of underlying cause

173
Q

In general, where are neoplastic salivary lesions found?

A

Majority: Major Salivary Gland, especially Parotid. Typically Benign

Minority: Minor Salivary Glands, 50% Malignant

174
Q

T/F: Sublingual Salivary Neoplasms are common and typically benign

A

False, very rare (< 1%) and typically malignant (90%)

175
Q

T/F: Parotid Salivary Neoplasms are common and typically benign

A

True: Constitute 65% of salivary neoplasms and are 25% malignant

176
Q

T/F: Majority of salivary gland tumours are epithelial in origin

177
Q

What are the 2 main categories of benign salivary neoplasms?

A
  1. Monomorphic Adenomas (including Warthin’s tumour (adenolymphoma), Oncocytoma, Basal cell adenoma, Myoepithelioma)
  2. Pleomorphic adenoma (Most Common)
178
Q

What is a basal cell adenoma?

A

Rare benign neoplasm characterised by the basaloid (dark staining) tumour cells and absence of the myxochondroid stromal component present in the pleomorphic adenoma

179
Q

How does a Canalicular Adenoma vary from Basal Cell Adenoma?

A

Canalicular Adenoma is almost exclusively found in the upper lip.

Basal Cell Adenoma occurs mostly in the parotid and then submandibular glands

Both have dark staining basaloid tumour cells

180
Q

What is the epidemiology of Basal Cell Adenoma?

A

Age: wide range, 35-80 years

Sex: male predilection

181
Q

What is the histology of Basal Cell Adenoma?

A

Basaloid (dark staining) tumour cells

Monomorphic collection of cells

Solid

Trabecular-tubular

Absence of myxochondroid stromal component present in the pleomorphic adenoma

182
Q

What is a Pleomorphic Adenoma?

A

Benign tumour of variable capsulation characterised microscopically by architectural rather than cellular pleomorphism

183
Q

What are the clinical features of Pleomorphic Adenoma?

A
  1. Most common salivary gland neoplasm
  2. Non-ulcerated, slow growing, painless swelling, commonly in palate
  3. Site: most commonly occur in parotid (60-70% or parotid tumours) but also in minor glands especially the palate (50% of minor gland tumours)
184
Q

What is the Epidemiology of Pleomorphic Adenoma?

A

Age: any age but (40-60 yrs) ++

Sex: M (slightly) > F

185
Q

What is the histopathology of Pleomorphic Adenoma?

A
  1. Encapsulated tumour characterised by capsule of variable thickness
  2. Variable Epithelium Structure: sheets, islands, strands, cords
  3. Variable Epithelial Types: cuboidal, basaloid, squamous, spindle cell, plasmacytoid and clear cells
  4. Squamous Metaplasia
  5. Keratin deposits
  6. Sebaceous Glands
  7. Myoepithelial cells have a plasmacytoid (clock face) appearance. May form a fine reticular pattern or sheets of spindle-shaped cells
  8. Changes in CT Mesenchymal Tissue: mucoid change, hyalinsation, loss of normal collagen structure, pseudo-cartilage

9.

186
Q

What is the management of Pleomorphic Adenoma?

A

Careful excision - excision around parotid gland can involve the facial nerve

Follow up required - recurrences common from incomplete excision around palatal/gingiva

Low risk of malignant transformation

187
Q

What are the 3 main salivary carcinomas?

A

Mucoepidermoid carcinoma

Adenoid cystic carcinoma

Acinic cell carcinoma

188
Q

What is a Mucoepidermoid Carcinoma?

A

A malignant glandular epithelial neoplasm with mucous, intermediate and epidermoid cells with columnar, clear cells and oncocytoid features

189
Q

What are the clinical features of Mucoepidermoid Carcinoma?

A

1) Most common malignant salivary neoplasm
2) Most common in parotid gland (45%), minor glands (50%), Submandibular (7%)
3) Any age but adults ++, F > M

190
Q

T/F: The histopathology of Mucoepidermoid Carcinomas is highly variable

A

True. Features can include Necrosis, Perineural invasion, Number of mitoses, Anaplasia. A scoring system used to grade the tumour

191
Q

What is the histopathology of Mucoepidermoid Carcinoma?

A

Lesions categorised as low, medium or high grade depending on various histological features

Cellular variability: combinations of epidermoid cells, mucous cells + intermediate cells

Biphasic: Cystic or solid areas

Variable Margins: circumscribed lesions / infiltrative

192
Q

What is the histopathological scoring for Mucoepidermoid Carcinomas?

A

points each given if there is the presence of

  1. Cystic Component < 20% (2 points)
  2. Necrosis (2 points)
  3. Perineural invasion (3 points)
  4. Number of mitoses (4+) (3 points)
  5. Anaplasia (4 points)

Tumour is then scored:

Low (0-4)

Medium (5-6)

High (7+)

193
Q

What is Acinic Cell Carcinoma?

A

Malignant epithelial neoplasm of salivary glands

194
Q

What are some features of Acinic Cell Carcinoma?

A
  1. More prevalent in women
  2. Serous Acinar Cell Differentiation (Parotid / Submandibular)
  3. Cytoplasmic zymogen secretory granules
  4. Solid tumour mass
  5. Large pale Basophilic Granular Cells
195
Q

What is the treatment for Acinic Cell Carcinoma?

A

Surgical treatment with/out other modalities

196
Q

What is Adenoid Cystic Carcinoma?

A

Basaloid tumour consisting of epithelial and myoepithelial cells

197
Q

What are the clinical features of Adenoid Cystic Carcinoma?

A

1) Relentless clinical course and usually fatal outcome
2) 5% of major gland tumours, but 25% of minor salivary gland tumours
3) Slow growing, may ulcerate or be painful
4) Malignant but are slow growing tumours that rarely metastasize
5) Difficulty with excision if perineural involvement present

198
Q

What is the epidemiology of Adenoid Cystic Carcinoma?

A

Adults, more females than males

199
Q

What is the histopathology of Adenoid Cystic Carcinoma?

A

1) Variable morphologic configurations including tubular, cribriform (most common) and solid patterns
2) Cribriform pattern: islands of cells have small pseudocystic spaces
3) Formed by basophilic cells => form solid islands, cords, strands of darkly staining epithelial cells in a delicate fibrous connective tissue stroma (with much variability
4) Notable: Perineural invasion
5) Generally cellular atypia is minimal and mitotic figures are rare

200
Q

What are the 4 type of Giant Cell Lesions?

A

1) Hyperparathyroidism
2) Aneurysmal Bone Cyst - technically not a cyst
3) Central Giant Cell Granuloma (also called Giant Cell Tumour)
4) Cherubism

201
Q

What is the common denominator between all Giant Cell Lesions?

A

Presence of multinucleated giant cells, differentiated via clinical, medical history, radiographic and histopathological analysis

202
Q

The presence of fibrous tissues in all types of Giant Cell Lesions is indicative of what?

A

Fibrous tissue accumulation in these giant cell lesions is indicative of body’s process of repairing the space caused by bone destruction

203
Q

What are the 3 types of Hyperparathyroidism?

A

1) Primary: Hypersecretion of PTH resulting in Stimulated Osteoclastic Activity => Bone Resorption
2) Secondary: Occurs in response to hypocalcaemia secondary to renal failure or malabsorption syndromes (inability to resorb calcium back into bloodstream)
3) Hereditary

204
Q

What are 3 reasons for Hypersecretion of PTH (Parathyroid Hormone)?

A

1) Hyperplastic Parathyroid Glands
2) Parathyroid Adenoma
3) Parathyroid Adenocarcinoma

205
Q

What is the epidemiology of Hyperparathyroidism?

A

Increase incidence with Age

Postmenopausal women

​

206
Q

What is the clinical features of Hyperparathyroidism?

A

1) Fatigue, Anorexia, Nausea, Weakness, Arrhythmias, Polyuria, Thirst, Depression, Constipation
2) Bone Pain and Headache, Severe cases have bone fragility
3) Renal, GIT + Pancreatic Complications
4) Neurological Manifestations when serum calcium becomes elevated

207
Q

What is the radiographic appearance of Hyperparathyroidism?

A

1) Increasing Radiolucent blotches
2) Bone Resorption and Replacement
3) Radiographic changes that look like cystic changes within bone
4) Severe cases in jaw: Loosening of teeth, Pulpal Obliteration

208
Q

What is the histology of Hyperparathyroidism?

A

Elevated numbers of purple multi-nucleated osteoclastic giant cells

209
Q

What is the management of hyperparathyroidism?

A

1) Parathyroidectomy
2) Management with endocrinologist - generally very well managed by medical doctors
3) Calcitonin Medication: Aids bone deposition

210
Q

Why is a Aneurysmal Bone Cyst not a cyst?

A

There is no cystic epithelial - rather fibrous tissue containing cavernous/sinusoidal blood filled spaces

211
Q

What is the aetiology of an Aneurysmal Bone Cyst?

A

Unknown, possibly trauma

212
Q

What are the clinical features of Aneurysmal Bone Cyst?

A

Commonly in molar-ramus region

Painful/Tender in affected region

213
Q

What are the epidemiology of an Aneurysmal Bone Cyst?

A

Rare incidence

Young people < 20 years

M = F

214
Q

What is the management for an Aneurysmal Bone Cyst?

A

Surgical Enucleation. However there is often excessive bleeding due to it’s high vascularity

215
Q

What is the histology of an Aneurysmal Bone Cyst?

A

Not a true cyst - no cystic epithelium

Fibrous tissue containing cavernous/sinusoidal blood filled spaces

Multinucleated giant cells and haemosiderin

Can be confused with central giant cell granuloma

Highly vascular

216
Q

What is the aetiology of a Giant Cell Granuloma?

A

Obscure aetiology, but associated with trauma/chronic irritation

217
Q

What are the 2 types of Giant Cell Granuloma?

A

Central Giant Cell Granuloma (CGCG): originates from within the cortical bone

Peripheral Giant Cell Granuloma: pierces the cortical plate and appears clinically as a gum lump

218
Q

If suspecting a Peripheral Giant Cell Granuloma, what additional clinical diagnostics are needed?

A

OPG for differential diagnosis to exclude the possibility of Central Giant Cell Granuloma

219
Q

Where is a central giant cell granuloma most likely to be seen?

A

Anterior mandible

220
Q

What is the epidemiology of a giant cell granuloma?

A

Females 2x more likely

20-30 years

221
Q

What are the radiographic features of a giant cell granuloma?

A

Uniform Radiolucency

Often Multilocular

May be expansile

222
Q

What are some differential diagnosis for Central Giant Cell Granuloma?

A

1) Giant Cell Tumour: CGCG has bone repair, GCT has bone destruction only
2) “Brown Tumour” of hyperparathyroidism (Histologically identical, but CGCG NAD in serum calcium)
3) Cherubism
4) Aneurysmal Bone Cyst

223
Q

What is the management for Central Giant Cell Granuloma?

A

1) Surgical Enucleation (surgical removal of whole mass without cutting into it)
2) Tendency to recur (15-20%)

224
Q

What is the histology of Central Giant Cell Granuloma?

A

Osteoclastic multinuclear giant cells in immature fibrous tissue

Fibrous tissue indicative of tissue repair

Prominent vascular structures and haemosiderin deposits (by-product of RBC breakdown)

225
Q

What is Cherubism?

A

Autosomal Dominant genetic mutation of resulting in fibrous dysplasia of the jaw.

226
Q

What is the aetiology of Cherubism?

A

A rare autosomal dominant genetic mutation that develops in early childhood/infancy.

227
Q

What are clinical signs of cherubism?

A

1) Lower face prominence with “cherub” fat cheeks
2) Normal bone replaced with fibrous tissue - bone becomes weak and subject to expansion
3) Sites: Bilateral, usually posterior (Ramus-Molar Regions)
4) Facial swelling consequent to bony swelling of maxilla/mandible
5) Maxilla can push on lower border of orbit - eyes tilt up, possibly blindness
6) Intraoral signs of bony swelling
7) Loosening/Exfoliation of Teeth
8) Hypodontia of permanent teeth + tooth displacement

228
Q

What are the histopathological signs of Cherubism?

A

1) Basic pathology is soft tissue replacement of normal bone tissue
2) Oedematous fibrous CT
3) Contains relatively large number of multinucleate giant cells
4) Immature and Woven bone spicules may also be present

229
Q

What is the treatment for Cherubism?

A

Course of Disease: condition worsens during childhood, but regresses naturally during late teenage/early adulthood due to hormonal changes

Cosmetic facial surgery, ophthalmic and dental management in severe cases

230
Q

T/F: Paget’s Disease results in net bone loss

A

Sorta both: the condition involves hyperactive bone turnover, with net bone deposition in the long term. There is possibly net bone loss in the early stages

231
Q

What is Paget’s Disease (Osteitis Deformans)?

A

Chronic progressive bone condition of unknown aetiology (but likely metabolic)

232
Q

What is the aetiology of Paget’s Disease (Osteitis Deformans)?

A

Unknown, Genetic basis suspected

Other suspected causes: inflammatory, vascular disorder, metabolic disorder, hereditary, RNA Virus in osteoclasts

233
Q

What is the epidemiology of Paget’s Disease (Osteitis Deformans)?

A

50 years+

3-4%, increases to 10-15% of elderly

14% have familial history

M : F (3: 2)

234
Q

What are the clinical features of Paget’s Disease (Osteitis Deformans)?

A

1) Hyperactive bone turnover: both systemic and in the jaw (20%).
2) Short term bone loss
3) Long term bone deposition
4) Symptoms: pain or deformity of affected bones
5) Dental: patients complain of sudden change to wear/function of dentures - widening of alveolar ridge / flattening of palatal vault
6) Teeth loosen and increase in spacing

235
Q

What is the radiographic appearance of Paget’s Disease (Osteitis Deformans)?

A

1) Early Stage => Osteoporotic Changes (thus more radiolucent)
2) Middle Stage = > Mixed Radiolucent / Radiopaque “Cotton Wool” Appearance (balanced but mixed appearance)
3) Later Stage => Sclerotic Osseous Changes. Possible hypercementosis, root resorption, lamina dura degradation, PDL space obliteration

236
Q

What is the histology of Paget’s Disease (Osteitis Deformans)

A

Early Stage:

Random overactive bone resorption

Purple Giant Cells: Increased osteoclastic activity

Replacement of bone with hypervascular CT: support active bone deposition/resorption

Magenta “Reversal Lines”: indicative of high bone turnover

Late Stage:

Mosaic Pattern of bone as osteoblastic activity increases

237
Q

What is the management for Paget’s Disease?

A

1) Bisphosphonates (first line): reduces bone turnover
2) Calcitonin: Increases bone deposition and reduces calcium blood serum
3) Anti-Inflammatory for pain management
4) Corrective Surgery for Significant Osseous Deformities

238
Q

What 3 diseases are associated with Langerhans Cell Histiocytosis (Histiocytosis X)?

A

1) Letterer-Siewe Disease (Most Severe)
2) Hand-Schuller-Christian Disease
3) Eosinophilic Granuloma

239
Q

What is Langerhans Cell Histiocytosis?

A

Langerhans cell histiocytosis (LCH) is a rare disease involving clonal proliferation of Langerhans cells (Tissue Macrophages), abnormal cells deriving from bone marrow and capable of migrating from skin to lymph nodes

240
Q

What is Letterer-Siewe Disease?

A

It is the most severe form of Langerhans Cell Histiocytosis (Histiocytosis X).

It is a multisystem syndrome causing an abnormal increase in Langerhans cell. If affects infants and is rapidly fatal

241
Q

What are the clinical signs of Hand-Schuller-Christian Disease?

A

Triad of Symptoms: Bone + Eye + Diabetes Insipidus (excessive urine/thirst due to insufficient ADH)

Affects Infants to Children

Multi-bone + Organ Involvement

Exophthalmos = bulging of the eyes

242
Q

What are the clinical signs of Eosinophilic Granuloma?

A

Usually a solitary bone lesion or lesions involving one bone affecting children/young adults

Has the presence of granulomatous tissue - signalling to maintain inflammation response

243
Q

What are the common oral features of all 3 types of Langerhans Cell Histiocytosis (Histiocytosis X)?

A

1) All involve jawbone
2) Proliferation of Langerhans cells (histiocyte) + eosinophils => resulting central soft tissue lesion
3) Lesion affects Jaw bone frequently in load bearing areas
4) Results in cortex being pierced resulting in soft tissue swelling
5) Tooth Mobility/Exfoliation

244
Q

In Langerhans Cell Histiocytosis, if Langerhan’s Cells are Tissue Macrophages, why does it affect bone?

A

Bone is affected due to Langerhans Cells originating from the Bone Marrow

245
Q

What is the management of Langerhans Cell Histiocytosis (Histiocytosis X)?

A

1) Curettage if local (unifocal) lesions

Systemic Management involves:

1) NSAIDS: Indomethacin
2) Bisphosphonates
3) Chemotherapy

246
Q

What is the histology of Langerhans Cell Histiocytosis?

A

Long Light purple Langerhans cells: (Tissue Macrophages in Epithelium)

Presence of bright pink Eosinophils

247
Q

What is the radiographic appearance of Langerhan’s Cell Histiocytosis?

A

Radiolucency due to soft tissue lesion

248
Q

What are some features of Haemorrhagic Bone Cyst?

A

Aetiology: Obscure, trauma/developmental

Epidemiology: In Young Males

Clinical: Usually asymptomatic in the body of the mandible

Radiographic: Radiolucent lesion with scalloped superior outline and intact cortex

Histology: blood filled cavity with no epithelial lining

Treatment: surgical enucleation

249
Q

What are the 3 layers of a Cyst?

A

1) Capsule: Collagenous layer, Inflammatory Cells to wall off infection
2) Thin Epithelial Lining: Differential diagnosis is often derived from type of epithelium
3) Lumen: Inflammatory Exudate, Fluid, Keratin

250
Q

What are examples of Odontogenic Cysts?

A

Gingival Cyst of Infants (Epstein Pearls)

Keratocystic Odontogenic Tumour (Odontogenic Keratocyst)

Dentigerous (Follicular) Cyst

Eruption Cyst

Lateral Periodontal Cyst

Gingival Cyst of Adults

Glandular Odontogenic Cyst

251
Q

What are examples of non-odontogenic Cysts?

A

Nasopalatine Dust (Incisive Canal) Cyst

Nasolabial (Nasoalveolar) Cyst

252
Q

What are Odontogenic Cysts?

A

Jaw cysts are thought to arise from residual remnants of embryonic odontogenic epithelium

253
Q

What are 3 embryonic odontogenic epithelium can cause odontogenic cysts?

A
  1. Reduced Enamel Epithelium (REE): final product at the end of amelogenesis, visible on eruption
  2. Rests of Serres: remnants of dental lamina which is the downgrowth of the ectomesenchyme
  3. Rests of Malassez: remnants of Hertwig’s epithelial root sheath (HERS) from root creation.
254
Q

Is Odontogenic Keratocyst (OKC) currently classed as a cyst or tumour?

A

2017 defiition is Odontogenic Keratocyst (OKC)

2005 it was defined as Keratocystic Odontogenic Tumour (KCOT)

255
Q

Why was Odontogenic Keratocyst (OKC) previously defined as Keratocystic Odontogenic Tumour (KCOT)?

A

KCOT classification in 2005 occurred because it was agressive and recurring - hence tumour classification

It has since been reclassified as a cyst due to it’s epithelial origin

256
Q

What is the epithelial aetiology of odontogenic keratocyst (OKC)?

A

Dental Lamine Remnants (Rest of Serres)

257
Q

What is the radiographic appearance of Odontogenic Keratocyst (OKC)?

A

Single or Multiple Foci 2x more likely to seen in the posterior mandible

258
Q

What is the epidemiology of Odontogenic Keratocyst (OKC)?

A

Can occur in children, peaks at 20-30

A commonly referred lesion to Oral Pathologists

259
Q

What is the histology of Odontogenic Keratocyst (OKC)?

A

Capsule

Thin Fibrous Tissue

No inflammatory cell infiltrate

Epithelium CT interface flattened

Epithelial Budding + Daughter Cyst Formation

Epithelium

Uniform, 8-10 cells thick

Palisaded Basal Layer

Polarised + Intensely Stained Nuclei

Surface layer of epithelial layer is parakeratinsed

Lumen

Keratin + Fluid

260
Q

What is the treatment for Odontogenic Keratocyst (OKC)?

A

Surgical Excision

Recurrence: 10-30%

Patients should be evaluated for naevoid basal cell carcinoma syndrome

261
Q

What is Naevoid Basal Cell Carcinoma Syndrome?

A

A systemic syndrome that results in multiple odontogenic keratocysts (OKCs)

262
Q

What are clinical signs of Naevoid Basal Cell Carcinoma Syndrome?

A
  1. Bone Defects: Bifid Ribs + Vertebral and Metacarpal Abnormalities
  2. Multiple Basal Cell Carcinomas
  3. Custaneous Abnormalities - Palm + Sole Pitting, Multiple Milia (white bump keratin cyst on nose + cheeks)
263
Q

What are the 2 types of gingival cysts?

A
  1. Newborn Gingival Cyst (Bohns Nodules)
  2. Adult Gingival Cyst
264
Q

What is the aetiology of a Newborn Gingival Cyst (Bohn Nodules)?

A

Epithelial Origin: Rest of Serres

265
Q

What is the aetiology of an Adult Gingival Cyst?

A
  1. Implants
  2. Epithelial Rests
266
Q

What is the clinical appearance of a newborn gingival cyst?

A

1-3mm White nodule on the dental alveolus

267
Q

What is the prognosis for a newborn gingival cyst?

A

Good - cysts present at birth, the regress to normal

268
Q

What is the histology of a newborn gingival cyst?

A

Lumen: filled with Parakeratin

Epithelium: Flattened Squamous Epithelium

269
Q

What is the histology of an Adult Gingival Cyst?

A

Epithelium: Non-Keratinized thin squamous epithelium

Lumen: Clear Cells containing Glycogen

270
Q

What is a Lateral Periodontal Cyst?

A

Non-keratinised developmental cyst that occur adjacent or lateral to the root of a tooth

271
Q

What is the multioccular version of a Lateral Periodontal Cyst called? [Hint: it’s got something to do with grapes]

A

Botryoid (Grape like) Odontogenic Cyst

272
Q

What are the clinical features of a Lateral Periodontal Cyst?

A
  1. Located around the border of a vital tooth (Mn Premolar/Canines, Mx Laterals)
  2. Asymptomatic
  3. Usually Unilocular (but Multilocular Botryoid Odontogenic Cyst)
  4. Well defined border radiographically
273
Q

What is the epidemiology of a Lateral Periodontal Cyst?

A
  1. Males 2x Likely
  2. Age Range: Adults
  3. Most common 50-60 years
274
Q

What is the histology of a Lateral Periodontal Cyst?

A
  1. Thin, Non-Keratinised Cuboidal/ Low Columnar Epithelium
  2. Glycogen-rich clear cells often forming “whirls”
  3. Epithelium may be split from CT and there may form island in capsule
  4. Epithelium is thinner than OKC and more uneven thick/thin areas
275
Q

What is the aetiology of a Dentigerous Cyst?

A

Derived from pericoronal follicular tissues: epithelium from reduced enamel epithelium

276
Q

What are the clinical signs of a Dentigerous Cyst?

A

Develops around the crown of an unerupted tooth

Very Common to see

1) Usually relatively slow growing, but can be destructive and cause extensive bone loss
2) Common Teeth: 3rd Molars, Impacted Canines
3) Radiographic: Radiolucency around the crown (pericoronal), Monolocular, Well-defined

277
Q

What is the histology of a dentigerous cyst?

A

Capsule

  • Collagenous Fibrous CT
  • May be inflamed or contain cholesterol

Epithelium

  • Highly variable: very pluripotent - so diagnosis needs to incorporate the fact there is an erupting tooth
  • Thin cuboidal / Non-keratinised Squamous / Mucous Cells / Respiratory Epithelium

Lumen

  • Fluid
279
Q

What is an eruption cyst?

A

A peripheral “dentigerous cyst” which has perforated the alveolar bone or develops as the tooth erupts through the alveolar bone

280
Q

What is the clinical appearance of a eruption cyst?

A

Present as bluish soft tissue swelling of the mucosa

281
Q

What is the treatment for an eruption cyst?

A
  1. Eruption cysts can delay tooth eruption
  2. Treat by “marsupialisation”: cut root of cyst then suture edges (so wound is constantly open to allow for drainage)
282
Q

What are Non-Odontogenic Cysts and what are their characteristics?

A

Arise from cystic proliferation of embryonic non-odontogenic epithelium in sites where epithelial rests persist

  • Generally found in adults
  • Often symptomless
  • Embryonic not Odontogenic origin
283
Q

What is a Nasopalatine Duct Cyst (Incisive Canal Cyst)?

A

Well recognised lesion found in anterior maxilla in region of nasopalatine canal (Around roots of central incisors)

284
Q

What is the radiographic appearance of a Nasopalatine Duct Cyst (Incisive Canal Cyst)?

A

Well-delineated borders

Symmetrical radiolucency

Round, Ovoid/Heart shaped

Can cause divergence of incisor roots

285
Q

What is the histology of a Nasopalatine Duct Cyst?

A

1) Variable Epithelium

  • Non keratinised squamous
  • Pseudostratified Columnar (ciliated/non ciliated)
  • Simple Cuboidal / Columnar epithelium

2) Densely collagenous fibrous CT capsule containing prominent neurovascular bundle (incisive nerve)

286
Q

Why is excision of a nasopalatine duct cyst problematic?

A

Surgery can injure/remove part of the incisive nerve

287
Q

What is a Nasolabial Cyst?

A

Slow growing soft tissue cyst found in nasolabial region (upper lip)

288
Q

What is the epidemiology of a Nasolabial Cyst?

A

F > M

Adults 30-50 years

289
Q

What is the histology of a nasolabial cyst?

A

Epithelium: Nonciliated Pseudostratified columnar + goblet cells

290
Q

What are the differentiating feature between a nasolabial cyst and nasopalatine duct cyst?

A

Nasolabial cyst involves soft tissue

Nasopalatine duct cyst involves bone

291
Q

What are 3 types of Inflammatory Cystic Lesions and what are their causes?

A

Radicular Cyst (Most Common, Endo Infection)

Residual Cyst (Post Extraction)

Inflammatory Collateral Cyst (Periodontal Origin)

292
Q

What is a Radicular Cyst?

A

Occurs in non-vital, multiple rooted teeth around exits of teeth. Most commonly from an endo infection.

293
Q

What are the clinical features of a radiocular cyst?

A

1) Asymptomatic unless acute exacerbation
2) Occur in any age/gender
3) Well-defined radiolucency (Apically / Laterally in accessory/lateral canal)
4) Is possible in multi-rooted teeth that whilst one canal is vital, the other could be necrotic with a radicular cyst
5) Large lesions can displace teeth
6) Can be caused by short endo obturation

294
Q

What is the histology of a radicular cyst?

A

Capsule

  • Eosinophilic Rushton Bodies
  • Rests of Malassez
  • Calcifications
  • Cholesterol Crystals (indicative of chronic inflammation + foreign body giant cells)
  • Inflammatory Cells

Epithelium

  • Stratified Non-Keratinised Epithelium
  • If Capsular Inflammation => Epithelial Proliferation
  • Also mucous cells, focal/general keratinisation, ciliated/respiratory epithelium
295
Q

What is a Residual Cyst?

A

A cyst that develops within the jawbone after extraction of a tooth

296
Q

What are the 2 types of residual cysts?

A
  1. Pocket Cyst (80-90%): Cystic epithelium is contiguous with the apex of the root
  2. True Cyst: Discrete/Separate from the apex of the root.
297
Q

What are the clinical implications of a True Radicular Cyst?

A

Cyst remains as a residual cyst after treatment

1) Less likely to remove the cyst with extraction
2) Less successful instrumentation in endo

298
Q

What is the histology of a residual cyst?

A

Epithelium

  • Non-Keratinised, Stratified Squamous Epithelium
  • If Capsular Inflammation => Epithelial Proliferation
  • Can also find Mucous Cells, Focal/General Keratinisation, Ciliated/Respiratory Epithelium

Capsule

  • Rushton Bodies (highly eosinophilic)
  • Rests of Malassez
  • Calcifications
  • Cholesterol Crystals; Chronic Inflammation and foreign body giant cells trying to apoptosis crystals (indicative of large cell turnover)
  • Inflammatory Cells
299
Q

Eosinophilic Rushton Bodies are found in what two cystic lesions?

A

Radicular Cysts

Residual Cysts

300
Q

What is a Inflammatory Collateral Cyst (Paradental / Mandibular Infected Buccal Cyst)?

A

A cyst found at cervical margin of lateral root surface of a vital tooth because of a Periodontal rather than Periapical lesion

301
Q

What is the radiographic appearance of a Inflammatory Collateral Cyst?

A

Well defined radiolucency on lateral root surface

302
Q

What is the histological appearance of a Inflammatory Collateral Cyst?

A

Similar histopathologic feature to radicular cyst

Capsule: Inflamed fibrous CT capsule

Epithelium: Non-keratinised squamous

Derived from Rest of Malassez (erupted teeth) or REE (in partially erupted molar tooth)

303
Q

What is the most common odontogenic tumour?

A

Ameloblastoma

304
Q

What are the 4 classes of odontogenic tumours?

A
  1. Epithelial with no ectomesenchyme
  2. Mixed epithelial and ectomesenchymal
  3. Mesenchymal (with/out epithelium)
  4. Combined/Hybrid tumours (of two or more of above)
305
Q

Which embryonic part of a tooth is of an ectomesenchymal origin?

A

Dental Papilla

306
Q

Which embryonic part of a tooth is of an epithelial origin?

A
  1. Dental Lamina
  2. Enamel Organ (inner enamel epithelium, outer enamel epithelium, stratum intermedium, and the stellate reticulum)
307
Q

What are some Odontogenic Carcinomas?

A
  1. Metastasizing (Malignant) Ameloblastoma
  2. Ameloblastic Carcinoma (Primary, Secondary types)
  3. Primary Intraosseous Carcinoma (Solid Type, Derived from KCOT, Derived from Odontogenic Cysts)
  4. Clear Cell Odontogenic Carcinoma
  5. Ghost Cell Odontogenic Carcinoma
308
Q

What are some Odontogenic Sarcomas?

A

1) Ameloblastic Fibrosarcoma
2) Ameloblastic Fibro-Odontosarcoma
3) Ameloblastic Fibrodentinosarcoma
4) Ameloblastic Odontosarcoma

309
Q

What are some examples of benign tumours of an odontogenic epithelium origin, with mature, fibrous stroma without odontogenic ectomesenchyme?

A

Ameloblastoma

Squamous Odontogenic Tumour

Calcifying Epithelial Odontogenic Tumour

Adenomatoid Odontogenic Tumour

Keratocystic Odontogenic Tumour (Odontogenic Keratocyst)

310
Q

What are some examples of benign tumours of an odontogenic epithelium origin with odontogenic ectomesenchyme with/out hard tissue formation?

A

Ameloblastic Fibroma

Ameloblastic Fibrodentinoma

Ameloblastic Fibro-Odontoma

Odontoma (Odontome)

Odontoameloblastoma

311
Q

What are some examples of benign tumours of an mesenchymal origin and/or odontogenic ectomesenchyme with/out odontogenic epithelium?

A

Odontogenic Fibroma

Myxoma

Benign Cementoblastoma

312
Q

What are the clinical features of a ameloblastoma?

A

80% in the mandible: ¾ in molar-ramus areas

Slowly destruction of bone - expansion rather than perforation

Seldom painful

Metastases very rare

Impinge on IANB - paresthesia

Jaw fracture

Tooth displacement

Bony expansion

313
Q

What are the epidemiology of a ameloblastoma?

A

30-60 years

M = F

314
Q

What is the radiographic appearance of an ameloblastoma?

A

Wide Variation

Typically well defined multilocular radiolucency on OPG

315
Q

What is the histology of an ameloblastoma?

A

Mitotic Figures Very Unusual

No mineralised dental tissues / matrices

Composed of 2 cellular components

    1. Outer Layer: columnar, hyperchromatic and palisaded cells, which resembles pre-ameloblasts
    1. Central Zone: more loosely organised areas of epithelium with the appearance of stellate reticulum, this can demonstrate cystic degeneration

Treatment approach the same for both

316
Q

What are the 5 histological sub-types of Ameloblastoma?

A

FAGPB

  1. Follicular: Discrete islands of tumour epithelium occasionally with cystic change (more volume, less tumour cells)
  2. Acanthomatous: Similar to follicular, but squamous metaplasia centrally within islands of epithelium, May produce Keratin
  3. Granular Cell Type: Granular cell transformation of stellate reticulum-like areas => Increased Eosinophilia,
  4. Basal Cell Type (Least Common): Like Basal Cell Carcinoma, Cuboidal Cells in sheets
  5. Plexiform (Mesh like): Irregular masses of strands of tumour epithelium often in meshwork arrangement
317
Q

What are the 3 variations to an ameloblastoma?

A
  1. Desmoplastic (anterior jaw)
  2. Unicystic Ameloblastomas (less agressive, 3rd molars)
  3. Peripheral Ameloblastomas (gingival soft tissue)
318
Q

What is the treatment of an multiocular ameloblastoma?

A

Resection of the mandible - then replacements with prosthetics

319
Q

What is a Calcifying Epithelial Odontogenic Tumour (Pindborg Tumor)?

A

Benign locally-invasive epithelial neoplasm characterised by the development of intra-epithelial amyloid-like structures which may become calcified

320
Q

What is the aetiology of a Calcifying Epithelial Odontogenic Tumour (Pindborg Tumor)?

A

Something blocking the tooth from erupting

321
Q

What is the Epidemiology of a calcifying epithelial odontogenic tumour?

A

Middle Aged. M = F

322
Q

What are the clinical features of a Calcifying Epithelial Odontogenic Tumour (Pindborg Tumor)?

A

Asymptomatic

Can produce swelling

Mn > Mx (2:1): usually Mn Premolar / Molar

323
Q

What is the radiographic appearance of a Calcifying Epithelial Odontogenic Tumour (Pindborg Tumor)?

A

Mixed Cotton Wool Radiolucency (due to calcification)

Regular/Irregular Border

324
Q

What is the histology of a Calcifying Epithelial Odontogenic Tumour (Pindborg Tumor)?

A

This lesion may not present all these symptoms

  • Large Polyhedral epithelial cells with eosinophilic nucleus arranged as sheets/strands in fibrous stroma
  • Prominent intercellular bridge and pleomorphic nuclei, but mitosis are rare
  • Characteristic Homogenous eosinophilic substance within epithelial sheets (Amyloid) => these are areas that calcify
    • Note: Amyloid are proteins are typically broken down. Alzheimer’s is where amyloid tissue isn’t broken down in the brain
325
Q

What is an Adenomatoid Odontogenic Tumour?

A

A tumour of odontogenic epithelium forming duct-like structure with benign epithelial glandular, reminiscent to an adenoma

326
Q

What are the clinical features of an Adenomatoid Odontogenic Tumour?

A

Slow Growing Swelling

Usually Painless

18 years, F > M (2:1)

Mx > Mn (2:1)

75% in Anterior Region

75% associated with unerupted tooth, usually maxillary canine - perhaps long development time, closer to nose?

327
Q

What is the radiographic apperance of an Adenomatoid Odontogenic Tumour?

A

Well Defined, Unilocular Radiolucency

May contain radiopacities

Resembles Follicular/Dentigerous Cyst

328
Q

What is the histology of an Adenomatoid Odontogenic Tumour?

A

Encapsulated

Clusters of cells with some ducts

Epithelial cells arranged in duct-like(adenomatoid) fashion in a sparse CT stroma with amorphous eosinophilic areas

Calcification Foci often seen

329
Q

What is the source of a Ameloblastic Fibroma and associated lesions?

A

Tumours that develop from proliferating odontogenic epithelium embedded in a cellular ectomesenchymal tissue that resembles the dental papilla. The tumours show varying degrees of inductive change and dental hard tissue formation

330
Q

What are the clinical features of a ameloblastic fibroma?

A

Very early appearance: in teens

Jaw Bone less dense in teens = Lesion can spread faster

Mandibular Pre-Molar/Molar Region

Slow Expansive Growth

Occasionally Symptomatic

331
Q

What is the radiographic apperance of a Ameloblastic Fibroma?

A

Well Defined, unilocular radiolucency

Often similar to ameloblastoma / cystic lesions

332
Q

What is the histology of an ameloblastic fibroma?

A

Mostly Ectomesenchymal tissue

Epithelium not abundant

Found in islands / strands like dental lamina

Columnar Cells peripherally and may occasionally form central stellate reticulum-like cells

Mesenchymal component very cellular (Compared with ameloblastoma) with little collagen

Resembles Dental Papilla

333
Q

How can you differentiate between an Ameloblastoma and an Ameloblastic Fibroma?

A

Ameloblastic Fibroma: surrounding ectomesenchymal cell is highly cellular

Ameloblastoma: stroma not as cellular

334
Q

What is the difference between a Ameloblastic Fibro-odontoma and an Ameloblastic Fibroma?

A

Ameloblastic Fibro-odontoma contains more dental tissue - tumour developers further along the developmental process?

335
Q

What is the histology of a ameloblastic fibro-odontoma?

A

Similar to Ameloblastic Fibroma

Not fully calcified enamel matrix

Highly Ordered Calcified Material (Enamel / Dentine / Cementum)

Other areas highly cellular ectomesenchymal tissues with strands of odontogenic epithelium

336
Q

What is the radiographic appearance of an ameloblastic fibro-odontoma?

A

Often associated with impacted teeth

Well Circumscribed radiolucency with varying amounts of radiopacity

Weird dystrophic calcifications

337
Q

What is the epidemiology of Ameloblastic Fibro-odontoma?

A

60% Children < 10 years

338
Q

What is an Odontoma / Odontome?

A

Benign tumour where both odontogenic epithelium + mesenchymal cells completely differentiate resulting in formation of irregular dental hard tissue growth

339
Q

What are the clinical signs of an Odontome?

A

Irregular Tooth Hard Tissue

Self Limiting: Stops growing a certain size

Young People (avg 15 years)

Usually Asymptomatic

Often not diagnosed until later

Mx > Mn (2:1)

340
Q

What are the two types of Odontoma?

A

1) Complex Odontoma: irregular mass of calcified / radiopaque material
2) Compound Odontoma: variable number of small tooth-like structure

341
Q

What is the radiographic appearance of Odontome?

A

Irregular Radiopacities often located between tooth roots and unerupted teeth

342
Q

What is the histology of a Odontome?

A

Contains: Normal Enamel / Enamel Matrix (immature), Dentine, Pulp + Cementum

Normal Tooth Follicle

Complex Type: defined well organised dentine with tubules

Compound Type: haphazard and less differentiated dentine

343
Q

What is a Calcifying Cystic Odontogenic Tumour?

A

A benign cystic neoplasm of mixed mesenchymal/epithelial origin, characterised by an ameloblastoma-like epithelium with ghost cells that can calcify

344
Q

What are the clinical features of a calcifying cystic odontogenic tumour?

A

Wide age range

F = M

Mx = Mn

Most occur centrally but can occur peripherally

  • Central: derived from bone
  • Peripheral: derived from soft tissue
345
Q

What is the radiographic appearance of a Calcifying Cystic Odontogenic Tumour?

A

Well defined radiolucency

Contains variable amount of radiopaque calcified material

346
Q

What is the histology of a Calcifying Cystic Odontogenic Tumour?

A

Present as cystic lesions lined by thin ameloblastomatous epithelium (basophilic, palisaded basal layer + oedematous supra-basal epithelium)

347
Q

What is a dentinogenic ghost cell tumours?

A

A Calcifying Cystic Odontogenic Tumour where “ghost cells” have lost their nuclei, and undergo calcification. The body can react to theise calcifications and contain giant cell reaction that

348
Q

What is a Odontogenic Myxoma?

A

A benign locally-invasive neoplasm consisting of rounded and angular cells lying in an abundant mucoid (myxoid) stroma

349
Q

What are the clinical features of a Odontogenic Myxoma?

A

< 30 years

F > M (slightly more)

Mn > Mx (slightly more)

Mostly slow growing, but can expand rapidly

Expands cortical bone

350
Q

What is the radiographic appearance of an Odontogenic Myxoma?

A

Multilocular Radiolucency (“Soap bubble” appearance)

May be well/poorly defined borders

351
Q

What is the treatment for an Odontogenic Myxoma?

A

Aggressive mandible resection (whole structure + tumour extracted)

352
Q
A

Stellate (Star-Shaped) Cells

Not highly cellular

Mucoid Stromal Tissue: lightly staining acellular, afibrillar (not much collagen), lots of ground substance.

Occasional Collagen strands and islands of odontogenic epithelium

353
Q

What is a cementoblastoma?

A

A benign, mesenchymal developmental neoplasm composed of masses/sheets of cementum like tissue forming on the tooth root

354
Q

What is the radiographic appearance of a Cementoblastoma?

A

Well Defined radiopaque mass close to tooth root

Surrounded by Radiolucent Halo

355
Q

How is a Cementoblastoma different from Hypercementatosis?

A

Hypercementatosis = reactive lesion

Cementoblastoma = neoplastic - bigger and more abnormal presentation

356
Q

What is the histology of a cementoblastoma?

A
  1. Lesion attached to vital tooth root, sometimes shortened by resorption
  2. Calcified tissue (like cellular cementum) with prominent reversal lines
  3. Reversal Lines: caused by continual resorption + redeposited.
  4. “Cementoid” (Immature, non-calcified cementum) at periphery
  5. As histologically it is often hard to differentiate mature cementum from bone tissue
357
Q

What are some issues with identification of tumours of cartilage and bone?

A

Difficulty making histological distinction between:

1) Hamartomas (ectopic normal tissue - eg fordyce spots) and Neoplasms
2) Benign vs Malingnant Tumours

358
Q

What are differences between Chondromas vs Chondrosarcomas?

A

Benign vs Malignant

Tubular Bones (Phalanges/Metacarpels) vs Long Bones (Limbs)

Resembles normal hyaline cartilage vs Abnormal Cartilage Formation (but not always true malignant characteristics)

Surgical removal vs Surgical resection

359
Q

If there are multiple chondromas or chondrosarcomas, what is this indicative of?

A

Patient has a Syndromic condition:

Ollier’s Syndrome: Multiple Chondromas

Maffucci’s Syndrome: Multiple Enchondromatosis multiple haemangiomas

360
Q

What are the clinical features of Chondromas and Chondrosarcomas

A

Posterior Mn (Body, Ramus, Condyle, Coronoid Process), Anterior Mx

Usually asymptomatic mass

Slow / Rapid Growth (less vascularised, dense cartilage stroma)

361
Q

What is the radiographic appearance of Chondromas and Chondrosarcomas?

A

Irregular Radiolucency and/or patchy Radiopacities

May cause tooth resorption

362
Q

What is the epidemiology of Chondromas and Chondrosarcomas?

A

F > M, 40-50 years

363
Q

What is the histology of a Chondroma?

A

Chondrocyte lacunas appear normal - a macro view is requires to see displacement of normal tissues

364
Q

What is the histology of a Chondrosarcoma?

A

More chondrocytes

Chondrocytes asre more hyperchromatic (dark)

Cellular atypia

Higher mitotic figures

367
Q

What is the treatment for a Chondroma?

A

Surgical Removal

Recurrence Common

368
Q

What is treatment for a Chondrosarcoma?

A

Surgical Resection

Low grade malignancy but growth on jaw has rapid growth

Not Radiosensitive

Possible metastasis to lung

369
Q

What are the two forms of an Osteoma?

A

Central

Peripheral (Subperiosteal: protruding out of the outer aspect of bone)

370
Q

What are the clinical features of an Osteoma?

A

Most common neoplasm of nose/paranasal sinuses

Mn > Mx

Symptomless bony expansion producing facial asymmetry

Solitary Lesion

Multiple Lesions with Gardner Syndrome

371
Q

What is the radiographic appearance of an Osteoma?

A

Dense Radiopacity

372
Q

What is the histology of an Osteoma?

A

Well circumscribed lesion

Composed of mature lamellar bone with compact and/or cancellous bone architecture

373
Q

Why are Osteomas hard to diagnose?

A

Hard to differentiate true tumour from hyperplasia or other sclerotic condition

374
Q

What are possible differential diagnosis for an Osteoma?

A

Enostosis

Fibrous Dysplasia

Chronic Sclerosing

Osteomyelitis

375
Q

What is an Osteoma?

A

Benign new bone usually growing on another piece of bone

376
Q

What is an Osteoid Osteoma?

A

Excessive proliferation of osteoblasts with osteoid (bone matrix)

377
Q

What are the clinical features of an Osteio Osteoma?

A

Benign - common in femur and tibia

Rare in jaws

Often Painful

378
Q

What is the radiographic appearance of an Osteoid Osteoma?

A

Central radiolucent areas

Not as dense as osteoma (bony matrix is less mineralised)

379
Q

What is the histology of an Osteoid Osteoma?

A

Centrally placed osteoid tissue with prominent osteoblasts and osteoclasts

Reactive sclerotic bone in periphery

380
Q

What are the clinical features of an Osteoblastoma?

A

Similar to Osteoid Osteoma

Slow growing, benign lesion

Usually Painless

381
Q

What is the histology of an Osteoblastoma?

A

Composed of osteoid tissue + osteoblasts but no surrounding zone of reactive bone formation

382
Q

How would you differentiate between an Osteoblastoma and Osteoid Osteoma

A

More common have osteoblastoma than osteoma

Large lesion (> 1.5cm): usually osteoblastoma

Small lesion (< 1.5cm): usually osteoid osteoma

383
Q

What are clinical and radiographic signs of an Osteoclastoma

A

Relatively Uncommon

Presence of Multinucleated Giant Cells (aggregated Osteoclasts)

Note: True giant cell tumours are found in long bones, very rare in jaw (vs giant cell granuloma)

Nonsclerotic and well Defined Border

Radiographic “Soap-bubble” appearance

Locally Aggressive

Possibly malignant - may be a form of malignant angioblastoma or sarcoma

Also referred to as “ameloblastoma” of the long bones

384
Q

What is the most common tumour of the bone?

A

Osteosarcoma

385
Q

What is the aetiology of an Osteosarcoma?

A

May arise subsequent to radiation + trauma (induction of abnormal growth)

386
Q

When are osteosarcomas more likely to be found in the long bones and jaw?

A

Children (in long bones)

Adults (in jaw)

387
Q

What are the clinical features of Osteosarcoma?

A

Occurs in long bones, very rare in jaw

Mn > Mx

Rapid growth (faster than osteoblastoma)

Symptoms depend on location (Resorption + Displacement of teeth, IAN parasthesia, pain in lip/chin)

Ulceration in skin/mucosa in late stages

Can manifest as a peripheral Gum Lump

388
Q

How would you differentiate a peripheral manifestation of Osteosarcoma from other gum lumps?

A

Hard to palpation

Low levels of inflammation compared to other gum lumps

389
Q

What are the two radiographic types of manifestations of Osteosarcoma?

A
  1. Sclerosing Type (Radiopaque): “Sun ray” pattern due to laminae formation from radial bone deposition
  2. Osteolytic Type (Radiolucent): Degrees of bone resorption
391
Q

What are the radiographic features of Osteosarcoma?

A
  1. Either Radiopaque or Radiolucent

Lamina Dura often widened

Furry Border due to infiltrated spread of neoplasm

392
Q

What is the treatment for osteosarcoma?

A

Aggressive treatment: Surgical Resection + Radiotherapy + Chemotherapy

393
Q

What is the histological apperance of Osteosarcoma?

A

Variable, with numerous subtypes or a mix of all of them

  • Fibroblastic: CT
  • Osteoblastic: masses of osteoid + ossesous tissue with irregular osteoblasts
  • Chondroblastic: cartilage

COPY BDS3 University of Adelaide Dentistry (28 decks)

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