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T2 Flashcards

1
Q

What is seen histologically for a pleomorphic adenoma?

A

A fibrous capsule with a bosselated surface, has both epithelial cells and connective tissue.

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2
Q

How is Sjogren’s treated in secondary care? (investigations + treatment)

A

Blood test (SS-A/B), biopsy, schirmers test, sialography/ultrasound, prescribe pilocarpine.

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3
Q

What is Bechets? How does it clinically present?

A

Inflammatory disorder of blood vessels leading to a triad of oral, genital and eye ulceration. A mixture of minor, major and herpetiform ulcers.

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3
Q

What is necrotising sialometaplasia?

A

A benign inflammatory disease of salivary gland leading to a tumour like lesion in the palate, caused by infarction secondary to thrombus or trauma.

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4
Q

What epithelium are most odontogenic cysts lined by?

A

Non-keratinised stratified squamous epithelium.

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5
Q

Name 2 forms of inflammatory odontogenic cysts?

A
  1. Radicular (residual)
  2. Inflammatory collateral cysts
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6
Q

Describe the two forms of inflammatory odontogenic cyst.

A
  1. Radicular cyst is associated with a non-vital tooth from the cell rests of Mallasez.
  2. ICC arise from partially/recently erupted teeth and are as a result of inflammation of pericoronal tissues.
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7
Q

Name 5 features of Gorlin Goltz syndrome.

A

Basal cell carcinomas, frontal bossing, hypertelorism, bifid ribs, multiple keratocysts.

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8
Q

What are 3 radiographic differentials for keratocysts?

A

Dentigerous cyst, ameloblastoma, odontogenic myxoma.

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9
Q

When is carnoys solution used?

A

For enucleation of a keratocyst.

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10
Q

How does a nasopalatine cyst present radiographically?

A

A well-defined radiolucency between roots of central incisors.

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11
Q

What is minor vs major erythema multiforme?

A

Minor is 1 mucous membrane + skin, major is 2 mucous membrane + skin.

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12
Q

What are clinical features of oral chrons?

A

Pyostomatitis vegetens, cobblestone mucosa, lip fissuring, staghorning of sublingual, mucosal tags, angular cheilits. (pain, ulceration, swelling).

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13
Q

What are pyostomatitis vegetans?

A

Erythema and oedema of the mucosa with numerous small, superficial yellow pustules.

Multiple white or yellow pustules on erythematous base may rupture and form folded, fissured appearance resembling a “snail-track”

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14
Q

In what patients can pilocarpine not be prescribed?

A

Patients with asthma or COPD.

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15
Q

How is aphthous like ulceration different to recurrent aphthous ulceration?

A

RAU presents in childhood and gets better as they grow up.
ALU usually has a clear systemic cause or from drugs like NSAIDS.

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16
Q

What systemic diseases is ALU related to?

A

Wegner’s, SLE, Bechet’s, anaemis, immunodeficiency.

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17
Q

What is a ranula?

A

Mucocele that forms on the floor of the mouth.

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18
Q

Differentials for OLP?

A

GVHD, DLE, OLL, candida, leukoplakia, hepatitis C.

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19
Q

What are the clinical features of RAU?
Causes?

A

Small, round, well defined ulcers with an erythematous halo and a grey/yellow base. Caused by trauma, stress, chemical, food (benzoates/cinnamon), smoking cessation.

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20
Q

What is the aetiology of RAU?

A

Immunologically mediated T cell action against mucosa.

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21
Q

Compare minor, herpetiform and major aphthous ulcers.

A
  1. Minor (2-6 episode that last <10 days, no scarring, non-keratinised).
  2. Herpetiform (more than 10 pinpoint ulcers which can join together to form larger, involves keratinised, heals no scarring).
  3. Major (ulcers >1cm that can last over a month and heal with scarring).
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22
Q

What drugs can induce erythema multiforme?

What virus

A

NSAIDs, carbamazepine (anti-epileptics), amoxicillin (ABx - penicillins, erythromycin, tetracyclines, sulfonamides), statins

HSV 1 + 2

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23
Q

What drugs can induce pemphigus vulgaris?

A

Drugs with sulphydryl group (captopril).

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24
Q

What is a stafnes bone cavity - what is seen?

A

Seen as a radiolucency on the lingual angle of the mandible, caused by the submandibular gland on a DPT.

A rare, asymptomatic, unilateral oval shaped radiolucent defect in the posterior region of the mandible below the inferior alveolar canal.

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25
Q

What viruses can lead to salivary gland disorders?

A

Mumps (paromyxovirus) and hepatitis C.

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26
Q

What is sarcoidosis?

A

Inflammatory condition which causes enlargement of lymph nodes and widespread granulomas.

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27
Q

What is primary vs secondary sjogren’s?

A

Primary (just Sjogren’s), secondary (with associated autoimmune condition- e.g. rheumatoid arthritis or lupus).

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28
Q

What is seen histologically for extravasation vs retention cysts?

A

Retention are lined by epithelium whereas extravasation cysts are lined with granulation tissue with mucous centre.

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29
Q

How does sialosis/sialadenosis occur and what does it result in?

A

Occurs from hypertrophy of acinar cells leading to painless bilateral swellings of salivary glands.

Chronic, bilateral, diffuse, non-inflammatory, non-neoplastic swelling of the major salivary glands caused by hypertrophy of the acinar components.

Primarily affects the parotid glands, but occasionally involves the submandibular glands and rarely the minor salivary glands. This can be painless or in some instances tender.

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30
Q

What is Stephen Johnson syndrome?

A

Severe form of erythema multiforme.

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31
Q

What is Warthin’s tumour?

Complications of warthin’s tumour?

A

Warthin tumor is a relatively frequent and benign neoplasm of the major salivary glands. It is histologically characterized by a dense lymphoid stroma and a double layer of oncocytic epithelium with a papillary and cystic architectural pattern. Its etiology remains uncertain.

It can infarct and become infected.

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32
Q

What are 4 clinical features of adenoid cystic tumours?

A

Can cause bone destruction, facial palsy, slow growing and ulcerate.

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33
Q

What are the histological features of adenoid cystic tumours?

A

Non-encapsulated, infiltrative of surrounding tissue, cribbform appearance and perineural involvement.

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34
Q

What are the components of odontogenic epithelium?

A

Dental lamina, residual enamel epithelium, rest of Serres and rest of Malassez.

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35
Q

What are the components of odontogenic mesenchyme?

A

PDL, pulp, follicle, papilla.

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36
Q

Differentials for multilocular ameloblastoma?

A

Odontogenic keratocyst, odontogenic myxoma, central giant cell granuloma.

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37
Q

Complications of odontomes?

A

Impede eruption, can painfully erupt themselves, can replace teeth, expand bone.

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38
Q

What does an ameloblastic fibroma resemble?

A

Cap stage tooth germ.

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39
Q

What odontogenic tumour is commonly associated with the roots of a tooth?

A

Cementoblastoma.

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40
Q

Name 3 hyperplasias related to dentures?

A

Denture hyperplasia, leaf fibroma, papillary hyperplasia.

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41
Q

Describe the appearance of a leaf fibroma?

A

Hyperplastic tissue beneath the denture form a leaf shape.

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42
Q

Name 4 types of epulis?

A

Pregnancy, giant cell, fibrous, congenital.

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43
Q

What is a fibroepithelial polyp?

A

A benign reactive swelling secondary to trauma.

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44
Q

Histological features of an epulis?

A

Hyperplastic epithelium, bundles of fibrous tissue, may/may not be ulcerated.

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45
Q

What is the histopathology of OLP?

A

Basal membrane immune mediated damage, sub-basal lymphocyte band, hyperkeratosis, rete ridges, hypokeratosis of surrounding tissues.

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46
Q

How does a viral papilloma form?

A

Hyperplasia, hyperkeratosis and papillomatous surface.

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47
Q

What is a cavernous haemangioma?

A

A haemangioma which has bony involvement (confirmed with radiograph)

  • Presents with:
    i. bony expansion
    ii. excessive gingival bleeding
    iii. excessive bleeding post XLA
    iv. in large lesions the involved deep may depress downwards upon direct pressure application and then return back to normal position soon after.

Appears as radiolucency

Tx:
i. surgical
ii. interventional radiological techniques e.g. embolisation to block blood supply to haemangioma.
iii. Radical surgery e.g. hemimaxillectomy in maxillary cavernous lesions.

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48
Q

What is a torus?

A

A benign bony outgrowth - can be found on the lingual surface of the mandible or on the palate.

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49
Q

How does a torus appear histologically?

A

Appears as normal lamellar bone.

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50
Q

What are the 2 forms of inflammatory collateral cysts?

A

Paradental and buccal bifurcation cyst.

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51
Q

What is the most common treatment for trigeminal neuralgia?

A

Carbamazepine tablets 100mg

10 day regimen: 1 tablet 2 times daily. Total 20

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52
Q

Infection of HPV is closely associated with development of what malignancy (type + location)?

A

HPV 16 + 18, oropharynx (includes tonsils and base of tongue)

Oropharyngeal squamous cell carcinoma.

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53
Q

What is the most effective mediation for treating recurrent aphthous ulceration?

A

Betnesol =

Betamethasone soluble tablets, 500micrograms.
1 tablet dissolved in 10ml as a mouthwash 4x daily.

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54
Q

What nerve supplies taste?

A

Facial nerve - chorda tympani

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55
Q

Where is head and neck cancer most commonly found?

A

Oral cavity, oropharyngeal and larynx.

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56
Q

Name 5 things that can increase your risk of cancer.

A

Tobacco, alcohol, ethnicity, premalignant lesions, diet.

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57
Q

What is extracapsular extension in lymph nodes?

A

When a tumour in the lymph node ruptures through the capsule of the node and spreads to surrounding tissues. Poor prognosis for tumour as is very aggressive.

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58
Q

How does HPV lead to uncontrolled cell replication?

A

HPV interrupts the cell cycle as its protein E6 inhibits p53 meaning the cell cycle continues.

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59
Q

What HPV is responsible for oropharyngeal cancer?

A

16 + 18

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60
Q

Overexpression of what molecule indicates HPV?

A

P16

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61
Q

What patients are at higher risk of developing Karposi’s sarcoma?

A

Immunocompromised patients.

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62
Q

What is the appearance of homogenous leukoplakia?

A

A white plaque with no other obvious cause except smoking, homogenous means it has a white and uniform appearance.

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63
Q

What areas of the mouth have higher risk of malignant transformation?

A

Tongue, floor of mouth, soft palate, retromolar pad.

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64
Q

What are the histopathological features of dysplasia?

A

Hyperplasia, change in size/shape of cells, increased mitotic activity.

  • Epithelial architecture: Disrupted layers. Basal cell hyperplasia (replaces prickle cell layers and produces drop shaped rete ridges).
  • Cytological features: change in cell size/shape, pleomorphic cells, loss of polarity, prominent nuclei.
  • Function aspects: Increased mitotic activity. Aberrant keratinistion (dyskeratosis where see keratin where it shouldn’t be)
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65
Q

How do odontogenic cysts expand?

A

Hydrostatic pressure. The jaw expands by resorption of the cortex and pushing out of the periosteum.

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66
Q

Why is enucleation not often chosen if cyst close to lower 7/8?

A

Risk of damage to IDN

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67
Q

What are the disadvantages of marsupilation?

A

Increased risk of infection, more than one appointment therefore have to be good attenders, shrinkage can be slow and not much tissue for histological review.

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68
Q

What occurs after prescription of azoles and erythromycin in patients taking statins?

A

Myopathy.

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69
Q

How do you tell the proximity of the IDN radiographically.

A

Darkening of roots, divergence of roots, narrowing of roots, loss of tram lines, black band over apex, divergence of canal, narrowing of canal, darkening of canal.

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70
Q

What can an adenomatoid odontogenic tumour be confused with?

A

Dentigerous cyst, however usually AOT often circulate the coronal and radicular portion of the tooth.

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71
Q

What is the classic radiographic appearance of an ameloblastoma?

A

Soap-bubble appearance. Well corticated, may resorb roots.

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72
Q

Where is an ameloblastoma commonly found?

A

Mandible around the region of the 8s.

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73
Q

Where are adenomatoid tumours commonly found?

A

Maxilla

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74
Q

Where are cementoblastomas most commonly located?

A

Mandible, associated with roots of teeth.

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75
Q

What are some clinical features of ameloblastic fibroma?

A

Slow growing, painless swelling that causes facial asymmetry.

Ameloblastic fibroma (AF) is an extremely rare true mixed benign tumor that can occur either in the mandible or maxilla.[1] It is frequently found in the posterior region of the mandible, often associated with an unerupted tooth.[2] It usually occurs in the first two decades of life with a slight female predilection.

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76
Q

What are some clinical features of an odontogenic myxoma?

A

Painless swelling of either jaw, most commonly around the molar region. They are locally aggressive and have a high risk of recurrence. Have lacy tennis racket radiographic appearance.

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77
Q

The mutation of what gene results in ameloblastoma formation?

A

V600E mutation in the BRAF gene.

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78
Q

Where is a compound odontome found?

A

Found around the canine region in the maxilla and contains tooth like structures known as denticles.

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79
Q

Where is a complex odontome found?

A

Found around the premolar/molar region and contains an irregular mass of enamel/dentine/cementum.

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80
Q

What are complications of complex odontomes?

A

They can impede eruption, they can replace teeth of normal series, they can erupt themselves and cause infection and pain.

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81
Q

What is a cemento-ossifying fibroma?

A

IT’s a fibrous-osseous lesion associated with the PDL of the teeth and is found in the maxilla or mandible around the tooth bearing areas. Radiographically a small radiolucency is seen usually with calcifications inside.

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82
Q

What should be prescribed within 72 hours of suspected giant cell arteritis?

A

60mg prednisolone

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83
Q

What should be prescribed for Bell’s palsy?

A

25mg prednisolone

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84
Q

What should be avoided when treating dry socket and why?

A

Using chlorhexidine as an irrigant can exhibit severe allergic reaction.

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85
Q

How should peri-implantitis be treated?

A

0.2% chlorhexidine rinse.

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86
Q

What should be prescribed for a patient with ulcers for less than 3 weeks?

A

Difflam = benzydamine

  • Benzydamine mouthwash, 0.15%. Rinse of gargle using 15ml every 1.5 hours as required. Not given for more than 7 days.
  • Benzydamine oromucosal spray, 0.15%. 4 sprays onto affect area every 1.5 hours.
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87
Q

When should treatment be carried out for patients on DOAC’s?

A

In the mornings

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88
Q

When should treatment be carried out for patients with Parkinson’s?

A

In the mornings - straight after medication.

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89
Q

What DOAC is taken twice a day?

A

Dabigatran and apixaban

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90
Q

What DOAC is taken once a day?

A

Rivaroxaban

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91
Q

How does warfarin work?

A

Vitamin K antagonist meaning clotting factors 2,7,9,10 are not produced. IT affects the extrinsic pathway so when looking at a clotting screen INR and PT should be observed.

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92
Q

How does dabigatran work?

A

Thrombin inhibitor

Anti-thrombin

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93
Q

How does rivaroxaban/apixaban work?

A

Factor Xa inhibitor

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94
Q

How does heparin work?

A

Activate antithrombin

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95
Q

How does aspirin work?

A

COX inhibitor

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96
Q

What does APTT tell us?

A

Measures the intrinsic pathway and tells us how long the blood takes to clot.

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97
Q

What does PT tell us?

A

Measure the extrinsic pathway

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98
Q

How does clopidogrel work?

A

P2Y12 inhibitor

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99
Q

What is a radicular cyst?

A

A cyst that is formed from a non-vital tooth. It forms from the cell rests of Mallasez. They can be treated by treating the non-vital tooth (XLA or RCT).

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100
Q

What is a dentigerous cyst?

A

A cyst that forms from an unerupted tooth over the coronal portion.
They can sometimes be seen close to the surface as a blueish fluctuation swelling.
They come from reduced enamel epithelium and are attached at the CEJ.

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101
Q

What is a keratocyst?

A

A cyst that forms from the cell rests of Serres. It has parakeratinised lining and doesn’t resorb teeth. It often grows around the tooth.

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102
Q

What should you be aware of if a patient is on dual antiplatelet drugs?

A

Interactions between drugs that can lower coagulation levels.

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103
Q

How should you manage a patient with increased bleeding risk?

A

Pack and suture.
Make extraction as atraumatic as possible.
Staged approach - limit to 3 in 3 different places.
Give clear post op advise.

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104
Q

How should you manage a patient on dual antiplatelet and anticoagulants?

A

Be aware bleeding may last over an hour, consider staging treatment.

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105
Q

What stabilised a blood clot?

A

Fibrin

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106
Q

What stage of haemostasis do antiplatelets work on (primary or secondary)?

A

Primary

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107
Q

What stage of haemostasis do anticoagulants work on?

A

Secondary

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108
Q

When are DOACs prescribed?

A

To decrease the risk of PE, DVT. Patients who have had a stroke or TIA to prevent stroke. Patients who have had stents/heart valve replacements.

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109
Q

What does the term bleeding complications mean?

A

Prolonged or excessive bleeding or bleeding not controlled by initial haemostatic measures.

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110
Q

What is classed as a simple extraction?

A

1-3 teeth with restricted wound size.

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111
Q

What patients should you take precaution with when carrying out an IDB?

A

Patients on warfarin showing signs of unstable INR.

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112
Q

List 4 medical conditions that may increase bleeding risk.

A

Chronic renal failure, liver failure, recent/current chemotherapy or radiotherapy, vWF disease.

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113
Q

Apart from anticoags/platelets name 4 groups of drugs that can affect clotting?

A

Methotrexate
Biological Immunosuppresents
NSAIDs
SSRIs

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114
Q

In what patients should anticoagulant therapy not be stopped? (3)

A
  • Pt with prosthetic metal valve replacement or coronary stent.
  • Pt who has had PE or DVT in past 3 months.
  • Pt on anticoagulants for cardioversion.
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115
Q

When should the delayed morning dose be retaken?

A

4 hours after haemostasis has occured.

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116
Q

What does INR greater than 1 indiate?

A

Not clotting properly

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117
Q

What classifies a patient with a stable INR?

A

A stable patient is one who doesn’t require weekly monitoring and who has not had a reading above 4 in the last 2 month.

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118
Q

What is LMW heparin used for?

A

Used in hospital to prevent DVT.

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119
Q

What drugs increase bleeding risk of DOACs?

A

NSAIDs and erythromycin.

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120
Q

What drug decreases plasma concentration of DOACs?

A

Carbamazepine, therefore increases thromboembolic risk.

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121
Q

What drugs increases effect of warfarin - increases INR/incr anticoagulaiton effect?

A
  • Metronidazole.
  • Other antibiotics:
  • penicillins (phenoxymethylpenicillin, amoxicillin, co-amoxiclav)
  • macrolides (clarithromycin, erythromycin, azithromycin, clindamycin)
  • tetracyclines (tetracycline, doxycycline, minocycline)
  • NSAIDS: aspirin, ibuprofen, diclofenac
  • Azole antifungals: miconazole, fluconazole
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122
Q

What should not be prescribed with warfarin due to decreased effect of warfarin?

A

Carbamazepine.

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123
Q

If patients have stopped taking bisphosphonates should you still allocate them a risk group?

A

Allocate as if the patient is still taking.

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124
Q

If a patient has stopped taking denosumab should you still allocate them a risk group?

A

If has been taken in the past 9 months, allocate as if they are still taking??

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125
Q

How should low-risk MRONJ patients be managed?

A

Prior to treatment, patients should be made as dentally fit as possible, should be treated as high risk caries patients with constant personalised prevention given to them.
All risks should be explained to patients prior to extraction and a review should be carried out at 8 weeks.
Prioritise endo, change any dentures that may cause trauma to the bone.
Perform straightforward extractions and procedures that may impact bone in primary care.
DO NOT PRESCRIBE ABX OR ANTISEPTIC PROPHYLAXIS UNLESS REQUIRED FOR THER CLINICAL REASONS.

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126
Q

how should high risk MRONJ patients be managed?

A

Same as low risk however when it comes to extraction, all other options should be explored prior and should consider contacting an oral surgeon if you do not feel comfortable treating.

Aim to avoid procedures that impact bone by considering other tx options.
If extraction or other proceudre that impacts bone is most appropriate, discuss risks of procedure with patient to ensure valid consent.
Review healing: if extractions socket not healed at 8 weeks, and you suspect pt has MRONJ, refer to oral surgery/special care dentistry specialist as per local protocols.

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127
Q

What should not be prescribed to MRONJ patients following extraction?

A

Antibiotic or antiseptic prophylaxis.

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128
Q

What is the definition of MRONJ?

A

MRONJ is non healing bone that can be probed through a fistula 8 weeks after extraction, from a patient currently taking anti-resorptive/angiogenic drugs and no history or radiotherapy.

Exposed bone or bone that an be probed through an intra oral or extra oral fistula, in the maxillofacial region that has persisted for more than 8 weeks in patients with a history of anti-resorptive or anti-angiogenic drugs, where there has been no history of radiation therapy to the jaw or no obvious metastatic disease to the jaws.

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129
Q

What are the symptoms of MRONJ?

A

Delayed healing, pain, swelling, infection, numbness/altered sensation. Some people are asymptomatic therefore it is important to book in a review after 8 weeks to assess.

-Exposed bone, loose teeth, pain, tingling, numbness, altered sensation and swelling. (guidelines)

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130
Q

What is the risk of MRONJ in a cancer patient?

A

<5%

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131
Q

What is the risk of MRONJ in osteoporosis patients?

A

<0.05%

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132
Q

How is bone remodelled?

A

By osteoblasts which create bone tissue and osteoclasts which resorb bone tissue.

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133
Q

How do anti-resorptive drugs work?

A

Anti-resorptive drugs inhibit osteoclast differentiation and function leading to decreased bone resorption and therefore remodelling.

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134
Q

How do bisphosphonates work?

A

Bisphosphonates reduce bone resorption by inhibiting enzymes that are essential to osteoclast function.

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135
Q

How does denosumab work?

A

Denosumab binds to RANKL inhibiting osteoclast function.

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136
Q

How do anti-angiogenic work?

A

Anti-antiogenic drugs target the way new blood vessels are formed and are used in cancer treatment to restrict tumour vascularisation.

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137
Q

What is low-risk MRONJ?

A

-> Patients being treated for osteoporosis with bisphosphonates for less than 5 years no glucocorticoids.

-> Patients being treated for osteoporosis with IV bisphosphonates for less than 5 years with no glucocorticoids.

-> Patients being treated for osteoperosis with denosumab with no glucocorticoids.

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138
Q

What is high-risk MRONJ?

A

-> Patients being treated for osteoporosis with bisphosphonates (oral or IV) for more than 5 years.

-> Patients being treated for osteoporosis with bisphosphonates and glucocorticoids for any length of time.

-> Patients currently taking/taken in last 9 months denosumab and is concurrently being treated with systemic glucocorticoids.

-> Patients being treated for malignancy.

-> Patients with previous history of MRONJ.

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139
Q

How is MRONJ avoided?

A

Patient should be made as dentally fit prior to beginning drugs, regular radiographs to assess pathology, preventive advice should be given ofter, patients should be advised against extractions where possible.

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140
Q

What is the definition of conscious sedation?

A

A drug that causes CNS depression that allows treatment to be carried out whilst patient remains aware of instructions and reflexes and verbal contact can still be maintained.

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141
Q

What is the classification of child, young person and adult for conscious sedation?

A

Child 0-12
Young adult 12-16
Adult 16+

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142
Q

What are some indications for conscious sedation?

A

Medical conditions aggravated by stressful situation (IHD, epilepsy, respiratory conditions), patients with Parkinsons, patients with severe learning disabilities, phobias.

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143
Q

What is the responsibility of the referring practitioner for sedation?

A

To carry out an assessment, to explore other options (behaviour management/therapy), to ensure sedation is absolutely necessary, to include any details of medical history, to explain to the patient/carer why sedation is being offered and what it may include, provide preventative oral hygiene advice (wait list can be long).

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144
Q

What grade ASA should be carried out in primary care?

A

ASA1&2, 3 can be treated in primary care dependent upon facilities and operator.

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145
Q

What patient factors may influence the provision of sedation?

A

Overly-anxious patients, patients with phobias, patients with severe learning disabilities and are unable to cooperate.

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146
Q

What are common features of a benign tumour?

A

Benign tumours are often painless, slow growing, mobile.

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147
Q

What are common features of malignancy?

A

Malignancy is suspected through pain, ulceration, fixed, can cause altered sensation and mouth eaten bone radiographically. They are fast growing and can cause loose and displaced teeth.

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148
Q

What are pre-op instructions for sedation?

A

Light meal 2 hours before, no alcohol before, take medication as usual, escort required, consent required.

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149
Q

What are the post-op instructions for sedation?

A

Escort, don’t drive/operate machinery for 24 hours, don’t go to work next day, no familial responsibility or sign important documents, take medication as usual, no drinking/alcohol.

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150
Q

What is preferred drug for inhalation sedation?

A

Nitrous oxide.

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151
Q

What is preferred drug for intravenous sedation?

A

Midazolam

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152
Q

When might transmucosal midazolam sedation be used?

A

Patients with special care requirements and extreme needle phobic patients.

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153
Q

How is MRONJ treated?

A

0.12% chlorhexidine, debridement, good oral hygiene, hyperbaric oxygen, pentoxyfiline/tocopherol, 0.9% saline irrigation.

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154
Q

What are sialoliths?

A

Build up of calcium in salivary glands usually due to decreased salivary flow.

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155
Q

Name 3 benign salivary gland tumours.

A

Pleomorphic adenoma Warthins tumour
Canalicular adenoma.
(PWC!)

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156
Q

Name 4 malignant salivary gland tumours.

A

Acinic cell carcinoma
Mucoepidermoid carcinoma
Adenoid cystic cell carcinoma
Ex-pleomorphic adenoma carcinoma

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157
Q

What are concerns of a pleomorphic adenoma?

A

Risk of recurrence and can become malignant.

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158
Q

What are 8 potentially malignant lesions of the oral cavity?

A

Leukoplakia
Proliferative verrucous (warty) leukoplakia
Erythroplakia
Oral lichen planus (OLP)
Oral submucous fibrosis
Discoid lupus erythematosus (DLE)
Actinic cheilitis - sun damaged lips
Chronic hyperplastic candidosis.

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159
Q

What should a patient still be able to do under consious sedation?

A

Retain protective reflexes and be able to understand verbal communications.

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160
Q

What conditions are aggravated by dentistry?

A

IHD, asthma, epilepsy, hypertension.

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161
Q

What conditions affect co-operation in dentistry?

A

Spasticity disorders, Parkinsons, learning difficulties.

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162
Q

What psychosocial issues can indicate sedation?

A

Phobias, gagging, fainting, lack of response to LA.

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163
Q

What dental procedures may require sedation?

A

Ortho extractions, implants, wisdom teeth removal.

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164
Q

Name 5 absolute contraindications for sedation?

A

Severe systemic disease
Mental/physical handicap.
Severe psychiatric disorders.
Narcolepsy.
Hypothyroidism.

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165
Q

What are contraindications for benzodiazepines?

A

Intracranial pathology, COPD, myasthenia gravis, hepatic insufficiency, pregnancy/lactation.

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166
Q

What are contraindications for inhalation sedation?

A

Blocked nasal airway, COPD, pregnancy.

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167
Q

What are the clinical effects of benzodiazepines?

A

Anxiolysis, anti-convulsive, slight sedation, amnesia, complete sedation, muscle relaxation, anaesthesia.

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168
Q

What are the mechanisms of action of benzodiazepines?

A

GABA inhibitors (work on GABA-A receptors), mimics effect of glycine.

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169
Q

How is cardiac output maintained during IV sedation?

A

BP decreases triggering the baroreceptor reflex causing heart rate to increase therefore cardiac output remains of net 0.

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170
Q

What occurs with patients of benzos and opioids?

A

Enhanced respiratory depression.

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171
Q

What is rebound sedation?

A

When the reverser drug (flumazenil) has a shorter half life than the benzo leading to the patient to become re-sedated.

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172
Q

How is midazolam able to cross the blood brain barrier so quickly?

A

Lipid soluble at physiological pH.

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173
Q

What is the reverser drug used in IV sedation?

A

Flumazenil

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174
Q

What are the contraindications for flumazenil?

A

Patients with benzo allergy, patients on benzos for epilepsy, patients dependent as can cause acute withdrawal.

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175
Q

What is the MDAS?

A

Modified Dental Anxiety Score. A score of over 15 indicated anxiety.

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176
Q

What are the risks of obesity and conscious sedation?

A

Air compromisation, co-morbidities such as heart disease and sleep apnoea, resuscitation risks.

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177
Q

What patient management options are availalbe?

A

Behaviour management, behaviour therapy, conscious sedation, general anaesthesia.

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178
Q

List 6 safety features of the Quantiflex MDM (Monitored Dial Mixer). (oxygen/nitrous oxide flow tubes)

A

Pin index system, diameter index system, scavenger system, reservoir bag, minimum oxygen is 30%, when oxygen is low N2o2 automatically turns off.

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179
Q

Advantages and disadvantages of inhalation sedation?

A

Advantages: rapid onset, rapid recovery, rapid peak action, drug not metabolised.

Disadvantages: expensive, requires nasal breathing, not very potent.

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180
Q

What are signs of adequate sedation?

A

Patient is comfortable, verbal contact maintained, protective reflexes maintained, gag reflex lessened, vitals maintained, reduced blink rate.

181
Q

What should be monitored during sedation?

A

Consciousness, oxygen saturation, respiratory rate, pulse.

182
Q

What is von Willebrand disease?

A

Congenital bleeding disorder that results in reduced level of von willebrand factor.

183
Q

What is von willebrand factor required for?

A

Crucial to primary haemostasis through platelet adhesion and to to the intrinsic coagulation cascade through factor 8 stabilisation.

184
Q

What are oral signs of vWD?

A

Purpura and petechiae, prolonged bleeding post XLA, gingival bleeding.

185
Q

What factor is deficient in Haemophilia B?

A

Factor 9

185
Q

What factor is deficient in Haemophilia A?

A

Factor 8

186
Q

What factor is deficient in Haemophilia C?

A

Factor 11.

187
Q

What are 2 examples of haemostatic cover?

A

Tranexamic acid and desmopressin.

188
Q

What is infective endocardititis?

A

Inflammation of the endocardium, build up of bacteria form vegetations. Patients present with flu like symptoms such as fever, chills, headaches and muscle pains.

189
Q

Who is at high risk of infective endocarditis?

A

Those with heart valve replacements, congenital heart disease and previous history of IE, damaged heart valves, hypertrophic cardiomyopathy.

190
Q

Is antibiotic cover required for dental procedure for IE?

A

Antibiotic cover is not generally advised for dental procedures however if ever unsure contact the patients cardiologist.

191
Q

What are the 5 principles of MCA?

A
  1. Assume all patients have capacity until proven otherwise.
  2. Do everything to support them to have capacity.
  3. Just because they make a bad decision doesn’t mean they lack capacity.
  4. All treatment should be carried out in the patients best interest.
  5. All treatment done should infringe on their rights as little as possible.
192
Q

What is required for valid consent?

A
  • Patient must have capacity (understand, retain, weigh up, communicate).
  • Consent must be specific to treatment proposed.
  • Patient should be adequately informed (material benefits and risks).
  • Patient must be free to make decision without pressure from others.
193
Q

Why should supportive oxygen often not be given to COPD patients?

A

Increased oxygen can decrease their respiratory drive leading to an accumulation of CO2.

194
Q

What increases the risk of OAC?

A

Root form, well pneumatised sinus, sinusitis, cysts, lone standing tooth, excessive luxation, any posterior upper tooth, radiographically close.

195
Q

Why do abscesses form in the buccal sulcus for a maxillary molar?

A

Due to the thin buccal cortical plate and the high attachment of the buccinator.

196
Q

How does the infection from pericoronitis spread?

A

Infections spreads into the buccal sulcus or past the buccinator into the cheek. In more serious situations can spread into the lateral pharyngeal or pterygoid space allowing it to then travel to the mediastinum.

197
Q

What is Ludwigs angina?

A

Bilateral swelling of the submandibular and sublingual spaces due to infection. Can potentially be life threatening due to closure of the airways and/or sepsis.
Tongue may be raised and protruded, drooling, floor of mouth raised, hot potato voice, difficulty breathing and swallowing, swelling.

198
Q

What is osteomyelitis?

A

Infection of the bone through bone marrow spaces. Patients with decreased vascularity or certain systemic diseases are predisposed.

199
Q

What is cavernous sinus thrombosis?

A

It is when a blood clot forms in the cavernous sinus stopping the jugular vein return and presses on the optic nerve. It can be caused by infection in the canine that spreads into the sinus and facial nerve.

200
Q

When is actinomycosis suspected, what is it and how is it treated?

A

It is a rare subacute to chronic infection caused by gram-positive bacteria, Actinomyces.

When there is a persistent draining sinus that remains after removal of a tooth, usually around the angle of the mandible. It is treated by incision of by penicillin based antibiotics.

201
Q

What is sialolithiasis and what can it lead to?

A

They are the formation of calcifications in the salivary gland and can lead to sialadenitis (an infection of the salivary glands). They are caused by drugs that cause hypo salivation, dehydration, and reduced food intake.

202
Q

How does a patient with sialoliths tend to present?

A

Present as a painful lump on the floor of the mouth which are usually worse upon eating.

203
Q

Why do salivary gland cysts often present in babies?

A

Issues related to ear development lead to cysts around the parotid gland.

204
Q

How does a patient with Sjogren’s present?

A

Swelling of the salivary glands, dry eyes, dry mouth, patient may also present with another form of autoimmune conditions (secondary Sjogrens e.g. SLE or RA)

205
Q

What is sialadenosis?

A

bilateral painless swelling of the salivary gland with no obvious cause.

206
Q

How is salivary gland function tested and measured?

A

Sialometry

207
Q

Where does the parotid gland empty into the mouth?

A

Stensons duct by the upper 7.

208
Q

What should be screen for in a pateint with sialadentitis?

A

Screen the patient for TB or HIV.

209
Q

What 3 systemic conditions is a build up of salivary calculi associated with?

A

Diabetes, hypertension, liver disease.

210
Q

What should you be careful of with a tumour in the parotid gland?

A

Facial nerve lies within the parotid so perineural involvement/changes in sensation.

211
Q

What is frey’s syndrome and what does it lead to?

A

Increased sweating, especially when eating, due to damage to the auriculotermporal nerve.

A rare, neurological disorder that causes a person to sweat excessively while eating. Is diagnosed based on medical history (e.g. history of surgery or trauma).

212
Q

What are the signs and symptoms of TMJD?

A

Crepitus, trismus (less than 40mm), pain, pain on release, deviation, locking, aching.

213
Q

How can you distinguish between Ramsay Hunt and Bell’s Palsy?

A

Bell’s palsy is milder than Ramsay hung. Ramsay hunt is also usually preceded by a rash in the ear.

214
Q

How is Ramsay Hunt Syndrome treated?

A

Prednisolone and acyclovir within the first 3 days has the best chance of reversal.

215
Q

How is TMJ managed first line?

A

Education and reassurance, soft splint, diet advice/behaviour changes, physiotherapy, CBT, analgesia advice, TCAs can be given.

216
Q

What is the difference between fibrous and bony ankylosis?

A

Ankylosis is abnormal union across a joint space, fibrous is joint to joint and bony is joint to bone.

217
Q

What pain is perceived by A delta fibres?

A

Sharp, shooting pain - thicker fibres that are myelinated.

218
Q

What pain is perceived by C fibres?

A

Dully achy pain - thinner fibres that are not myelinated.

219
Q

What is gate control theory, when can it help clinically?

A

It’s the idea that pain can be reduced by activating a non-noxious stimuli (touch) as larger nerves have more activity than the thinner, smaller ones. This can be useful when anaesthetising a patient as you can add in that element of distraction.

220
Q

What theory describe dentine hypersensitivity?

A

The hydrodynamic theory, changes in the environment increase fluid flow through the tubules therefore increasing the excitement of the mechanoreceptors.

221
Q

What are the special investigations that should be carried out when diagnosing?

A

TTP, sensibility (PE), mobility, pocketing, colour, appropriate radiographs (in acute pain this tends to be a PA of tooth).
Photographs and study models can be taken for cases where aesthetic treatment will be done or in trauma.

222
Q

How is periodontal pain managed?

A

Analgesia advice, oral hygiene advice (brush twice a day, fluoride toothpaste, correct size TePe brushes), local debridement under LA. IF tooth has become an abscess then options are drainage, PMPR, antibiotics or extraction.

223
Q

How does a pt with cracked tooth present?

A

Pain on release, sharp pain, discomfort, pain from grinding/cold.

224
Q

What are the 4 causes of cracked tooth?

A

Habits, developmental (AI), large restorations (less enamel or removed pulp chamber causes a weaker tooth), occlusal trauma.

225
Q

What are the symptoms of sinusitis?

A

Headaches, pain around the ears and upper molars, fever, purulent discharge, cough and halitosis.

226
Q

What are the symptoms of pericoronitis?

A

Halitosis, pain, trismus, bad taste, swelling, inflammation.

227
Q

How does a patient with necrotising gingivitis present? Who is at higher risk?

A

Necrosis and ulceration of the interdental papilla and the gingival margin with a grey pseudomembrane around these necrotic areas. Patients present with pain, bleeding, ulceration, halitosis, bad taste, lymphadenopathy.

There are 6 causes: immunosuppression, poor diet, smoking, poor oral hygiene, stress and vitamin deficiencies. Patients who smoke and have HIV are at higher risk.

228
Q

How do we treat sinusitis?

A

If bacterial can prescribe pen V, analgesics, decongestants (ephedrine 0.5%), mucolytics, steam inhalation.

229
Q

How would a patient with trigeminal neuralgia present?

A

Spontaneous pain that lasts a couple of seconds to 2 minutes along the trigeminal distribution. The pain is an electric shock like pain.

230
Q

What are the 3 steps of planning a surgical XLA?

A
  1. Path of withdrawal
  2. Avoidance of obstacles
  3. Path of elevation
  4. Bone removal
  5. Flap design
231
Q

What are the 6 principles of flap design? Why do we have them?

A
  1. Broad base
  2. Intact papilla
  3. Incision over sound bone
  4. Full thickness flap
  5. Surgical access
  6. Avoid vital structures.
    It’s all done to improve healing.
232
Q

How does wound healing occur?

A

Haemostasis, followed by inflammation (neutrophils phagocytose any necrotic tissue, then macrophages remove RBCs and release growth factors), maturation and then differentiation.

233
Q

What is the role of growth factors in wound healing?

A

Growth factors support angiogenesis, fibroblast proliferation and smooth muscle production.

234
Q

Why would listening to a suspected Grave’s disease lump help?

A

Helpful for diagnostic purposes as if there is a beat it means there is increased blood flow.

235
Q

What is Grave’s disease?

A

An autoimmune condition that leads to hyperthyroidism, bulgy eyes.

236
Q

What does the IDN supply?

A

The lip, chin and teeth.

237
Q

What occurs during primary haemostasis?

A

Blood vessels vasoconstrict, VWF binds to collagen, platelets adhere and form a platelet plug.

238
Q

What occurs during secondary haemostasis?

A

Activation of the clotting factors in the clotting cascade, each clotting factor is an enzyme that activates the next until fibrin is activated, fibrin stabilises the clot.

239
Q

What is the role of plasminogen?

A

Plasminogen is responsible for fibrinolysis which is where the clot is broken down into normal tissues again.

240
Q

What is the role of von Willebrand factor?

A

VWF is required for platelet adhesion and is the carrier for Factor 8.

241
Q

What is the role of vitamin K in clotting?

A

Vitamin K is required for carboxylation of factors 2,7,9,10.

242
Q

What blood tests should be done for alcoholics?

A

Liver function test, Full blood count, Clotting screen (INR, APTT, PT).

243
Q

What is thrombopoietin and where is it produced?

A

It’s a hormone that regulates platelet function and is found in the kidney, this is why renal disease can lead to clotting problems as primary haemostasis is affected.

244
Q

How does renal disease cause bleeding issues?

A

These patients require dialysis which they are usually on high dose heparin for which increases bleeding risk, also due to decreased thrombopoietin.

245
Q

What is stored in the spleen?

A

Red blood cells and platelets. Spleen disease can lead to thrombocytopenia.

246
Q

What is immune idiopathic thrombocytopenia and how is it managed?

A

Where the immune system breaks down platelets, it can be caused by pregnancy, idiopathic or post viral infection. It is managed by corticosteroids, immunosuppression and splenectomy.

247
Q

What antibiotic is given for Ludwig’s angina?

A

1.2g IV co-amoxiclav.

248
Q

What features of an extraction make an OAC more likely?

A

Complex root formation, well pneumatised sinus, sinusitis, cysts, posterior upper teeth, excessive luxation, lone standing teeth, radiographically close.

249
Q

Signs of an OAC?

A

Bubbles from extraction site when breathing or when blowing (if you get patient to blow, be careful as too much pressure can lead to expansion of the OACs, whistling sound, may have discharge coming from the hole.

250
Q

What 2 flap designs are used for OAC?

A

Buccal advancement flap (with or without fat bad) and palatal rotation flap.

251
Q

How is an OAC managed (generally)?

A

Dependent on size.
If less than 5mm, then leave with advice given to patient not to blow or increase pressure in oral cavity, use decongestants, can irrigate with 0.9% saline if signs of infection, can consider a removal obturator to cover hole, referral.

252
Q

What increases risk of maxillary tuberosity fracture?

A

Bulbous roots, multi-rooted teeth, hypercementosis, well pneumatised or infected sinus.

253
Q

Why should surgicel not be placed on the IDN?

A

Can cause altered sensory nerve function and sensation.

254
Q

How is IDN damage managed?

A

Ice pack for 24 hours then for a week, high dose NSAIDs or 1mg/kg prednisolone, 6 hr post op review (over phone) then 2 weeks later. If damage severe, refer.

255
Q

What are the symptoms of ORN and MRONJ?

A

Exposed non-healing bone, pain, pus, sequestra, swelling.

256
Q

What is Garre’s osteomyelitis and how does it appear radiographically?

A

Chronic osteomyelitis with proliferative periostitis that present in children, appears as onion skin radiographically.

257
Q

What should be checked in a systems review?

A

Head to toe: brain, skin, heart, lungs, stomach, kidneys, urine - general health (weight loss, malaise)

258
Q

What are the oral manifestations of anaemia?

A

Atrophic glossitis
Angular cheilitis
Aphthous like ulcers
Oral dyskinesia

259
Q

When thinking about how a patient would be treated in secondary care what 4 options for extra investigations are available?

A

Radiographically, blood test, special diagnostic tests - swab or biopsy.

260
Q

What 2 neurotransmitters are involved in the pain buffering system?

A

Noradrenaline and serotonin (hence why antidepressants often work for chronic pain).

261
Q

What are 3 examples of immunosuppressents?

A

Corticosteroids, azathioprine, and mycophenolate, monoclonal antibodies.

262
Q

What are patients on long term steroids at higher risk of developing?

A

Prone to infections, ulcers and infection.

263
Q

What is a steroid crisis?

A

When patients that are dependent on steroids stop producing their own and then abruptly stop (SECONDARY). can also occur in pts with Addisons in stressful situations (PRIMARY).

264
Q

How does cyclosporin work?

A

Inhibits calcineurin so prevents the production of IL-2 leading to stopped replication of T cells.

265
Q

How can dry mouth be managed topically, what are these patients at higher risk of developing now?

A

Can be managed with glandosone - this however is acidic so these patients can be at higher risk of TSL.

266
Q

What is the common clinical presentation of cyclosporin induced gingival hyperplasia?

A

commonly seen in younger patients in the anterior region.

267
Q

What 3 drugs can cause gingival hyperplasia?

A

Cyclosporin, phenytoin, calcium channel blockers (amlodipine).

268
Q

How does a patient with acute pseudomembranous candida typically present, local and systemic factors, how is this treated?

A

Creamy white non-adherent patches that can be wiped off to reveal erythematous areas which may bleed. Can affect any oral site, but frequently soft palate and tongue, often w steroid inhaler use.
Local factors: poor denture hygiene, dry mouth, steroid inhaler.
Systemic factors: immunocompromised, antibiotics, anaemia, diabetes.
Tx: Systemic antifungal: fluconazole 50mg/day - 7 days. Correction of local factor (if no obvious cause, investigate for immunocomp, anaemia, diabetes, HIV screen).

269
Q

How does acute erythematous candida present and how is it managed?

A

Antibiotic sore mouth. Erythematous areas of reddness that are normally painful. On dorsum of the tongue. Worse when eating spicy, acidic foods.
Tx: address underlying issue (rinse after steroid inhaler, stop antibiotics, new antibiotics), if this doesn’t correct it consider fluconazole.

270
Q

How does chronic hyperplastic candida present and how is it managed?

A

Candida leukoplakia. A chronic low level fungal infection which causes hyperplasia and keratosis. Most suffers are smokers. Tend to present with bilateral white adherent plaques in commissures of the mouth.
Do incisional biopsy as has close association with dysplasia and low risk of malignant change.
Smoking cessation. Systemic fluconazole 50mg daily for 7 days.

271
Q

What is seen histopathologially for chronic hyperplastic candida?

A

Hyperkeratosis, OLP with candida invasion (candida hyphae) into the epithelium.

272
Q

What are 4 risk factors for chronic hyperplastic candida?

A

Smoking, COPD, diabetes and complete dentures.

273
Q

How does chronic erythematous candida present and how is it managed?

A

Denture stomatitis. Erythematous areas on denture bearing surface, typically under acrylic denture. Usually non painful, unless severe. Caused by poor denture hygiene.
Manage with denture hygiene instructions and topical miconazole placed on the denture bearing surface 4 times a day. IF pt is on warfarin then nystatin suspension should be used.

274
Q

What is angular cheilitis?

A

A candida infection which causes bilateral erythematous areas at angles on mouth. Is painful and sore and may accompany any form of intra-oral candidosis. Often with ill-fitting denture, overclosed with folds of skin due to reduced vertical dimension.
Treat underlying cause: new denture. Topical microbial gel : miconazole.

275
Q

How does median rhomboid glossitis present and how is it managed?

A

Red and papillated areas on central dorsum of tongue. Usually painless. May be corresponding palatal area of erythema “kissing lesion”. A form of chronic erythematous candidosis.
Associated with steroid inhaler use, denture wearers, immnodeficiency and smokers.
Rule out underlying cause: anaemia, deficiencies, diabetes.
Treat w antifungals: systemic fluconazole 5mg. Treat underlying cause otherwise will reoccur.

276
Q

With most fungal infections what special investigations should be carried out?

A

Microbial swab to culture and sensitivity test.

Bloods: FBC, Haematinics, Random glucose, HIV testing.

Screen for HIV/immunocompromised/anaemia.
Identify local/systemic factors.

277
Q

What is cellulitis and what can it lead to?

A

It is an infection of the skin, with a severe systemic reaction where the body is failing to respond to the organism. Presents as swelling of tissues, no suppuration, redness, pain.
Can spread through adjacent spaces/facial planes, dictated by local anatomy. If spreads into fascial spaces of neck, can cause difficult swallowing and compromise airway. If severe can lead to septicaemia.
Tx with antibiotics.

278
Q

What is an alveolar abscess?

A

Localised collection of pus/bacteria found around the alveolar bone. It is usually preceded by chronic infection in a now non-vital tooth.
Can result in tissue destruction or the infection can spread if the bone is perforated leading to cellulitis - so need to remove tooth.

279
Q

What are the clinical features of necrotising gingivitis?

A

Necrosis and ulceration of the interdental papilla with grey pseudomembrane around this area. Patient with present with pain, halitosis, bad taste, inflammation and submandibular lymphadenopathy. Punched out ulceration. Mainly affects lower anterior region.

280
Q

What patients are at higher risk of developing necrotising gingivitis?

A

HIV, smokers.
Poor hygiene, diet, stress and lifestyle.

281
Q

What bacteria causes necrotising gingivitis?

A

Fusiformis fusiform. Spirochete species.
(check this answer)

282
Q

How does TB present orally?

A

Chronic ulcer on dorsum of tongue.

283
Q

What are the four stages of syphilis and how do they present clinically?

A

Primary: primary chancre
Secondary: snail track ulceration
Latent
Tertiary: gumma on palate and leukoplakia on tongue.

284
Q

How is syphilis managed?

A

Benzathine penicillin, GUM clinic, contact tracing sexual partners.

285
Q

How does primary herpetic gingivostomatitis present and how is it managed?

A

Crusting of the lips, pain, fever, malaise, lymphadenopathy, acute gingivitis, ulceration - managed with analgesia, increased fluid intake, 0.2% chlorhexidine mouthrinse (immunocompromised pts can be prescribed 200mg acyclovir). Will return as herpes labials when triggered by UV, stress, pregnancy, cold.

286
Q

What topical tx is given in herpes labialis that isn’t given in primary herpetic gingivostomatitis?

A

Acyclovir 5% cream

287
Q

How does chickenpox become shingles and how does shingles present?

A

The VZV virus lies latent in the body and when remerges will produce ulceration along sensory distribution with prodromal burning.

288
Q

How is shingles managed?

A

Analgesia and systemic acyclovir 800mg or valacyclovir 1g.

289
Q

What is glandular fever?

A

EBV/HHV-4. Cells of the virus replicate and spread to B lymphocytes and the bloodstream. Causes fever, fatigue, swollen glands and sore throat.

290
Q

What infection will HHV-8 cause? How is this then treated?

A

Karposi’s sarcoma - a type of cancer that forms in the blood cells and lymph nodes and presents as a blue/red nodule. Treated with local radiotherapy, systemic chemo, intralesional chemo.

291
Q

What oral problems can persist in immunocompromised patients?

A

Increased risk of infection, increased risk of opportunistic infection, poor wound healing, increased risk of malignancy, may need antibiotic cover.

292
Q

What is oral hairy leukoplakia caused by?

A

Painless white patch found on lateral border of tongue. Caused by EBV/HHV-4, HIV, organ transplant.

293
Q

How does hecks disease present and what is it caused by?

A

HPV 13+32. Presents as pink papules on the tongue and buccal/labial mucosa. As doesn’t cause any problems treatment is just for aesthetic concerns.

294
Q

What are 5 symptoms of xerostomia?

A

Dry sticky mucosa, problems eating, salivary gland swellings, altered taste, fissured tongue, presence of candida, increased plaque, increased caries.

295
Q

What is Sjogren’s syndrome - what can it lead to?

A

Autoimmune condition that’s characterised by the presence of dry eyes and dry mouth as it acts on exocrine glands - lymphocytic infiltration on the salivary and lacrimal glands.
Can cause B-cell non-hodgkins lymphoma.

296
Q

What tests are done in secondary care for Sjogren’s?

A

Schirmer, sialography, antibody (SS-A, SS-B), sialometry (unstimulated salivary flow rate), biopsy.

297
Q

What is the mechanism for halitosis?

A

Gram negative anaerobic bacteria produce volatile sulphur compounds that accumulate.

298
Q

What can cause halitosis?

A

Smoking, decreased eating, not drinking enough.

299
Q

What are red flags of TMJD?

A

History of malignancy, persistant or unexplained neck lump, neural involvement, facial asymmetry, recurrent epistaxis, unexplained fever/weight loss, patient over 50 with unilateral headache.

300
Q

What is secondary trigeminal neuralgia compared to primary?

A

Secondary is when a cyst/tumour is compressing the trigeminal nerve leading to sharp shock like pain - therefore another disease is causing it.

301
Q

How is trigeminal neuralgia managed?

A

Carbamazepine, can also have surgical therapy.

302
Q

Where does the glossopharyngeal nerve supply?

A

Throat/tonsils.
(look up better answer pls)_

303
Q

What is burning mouth syndrome and how is it managed?

A

Burning sensation that affects the tongue and buccal mucosa, can be made worse by stress/fatigue and doesn’t tend to affect them lying down. Managed by CBT, ruling out other symptoms, amitriptyline and difflam.

304
Q

How does giant cell arteritis present and what causes it?

A

Large vessel vasculitis affecting branches of the external carotid artery resulting in ischaemia, patients presenting with gangrene tongue, throbbing headaches at temples, vision loss, systemic unwellness.

305
Q

How does chronic idiopathic facial pain present and how is it managed?

A

Gnawing, dull pain that presents either unilateral or in the maxilla. It is poorly localised and has no other causes therefore is a diagnosis by exclusion. Managed by amitriptyline from 10mg to 70mg.

306
Q

Why is managing a patient with chronic idiopathic facial pain difficult?

A

As there is no real cause it is about controlling the patients expectations and managing the perceived symptoms.

307
Q

What is angioedema and how is it managed?

A

Severe local swelling of the skin caused by type 1 hypersensitivity (mast cells degranulate and release histamine).

308
Q

What is the histological appearance of orofacial granulomatosis?

A

Noncaseating granulomatous inflammation

309
Q

What are the signs and symptoms of oral chrons?

A

Lip fissuring, cobblestone mucosa, pyostomatitis vegetans (snail track ulceration), swelling of the mucosa, angular cheilitis, staghorning of the submandibular glands, mucosal tags, severe aphthous ulceration

310
Q

How is orofacial granulomatosis managed?

A

Diet advice (avoid benzoate and cinnamon), intralesional steroid, topical/systemic steroids or immunosuppressants. For Chron’s anti TNF alpha drugs can also be used.

311
Q

How does sialadenitis form?

A

An acute infection due to build of calcification or strictures in the salivary gland openings. Can be caused by xerostomia.

312
Q

What is a pyogenic granuloma?

A

A benign fibro vascular proliferation of capillary blood vessels commonly found on the tongue. It is different to a fibrous overgrowth due to how vascular it is and how quickly it develops. Can be associated with chronic trauma or hormones.

313
Q

What is the classic presentation of an eruption cyst?

A

Blue-ish, fluctuant swelling that presents 2-3 weeks prior to eruption.

314
Q

What is Wegner’s and how does it present?

A

Systemic condition that results in inflammation of blood vessels presents with strawberry gingivitis.

315
Q

How do you test for a haemangioma?

A

When you press on it, it should go white then when you release red again (blanching test).

316
Q

What is an extravasation mucocele, what is a retention mucocele?

A

Extravasation is caused by trauma to a minor salivary gland and the fluid is released into the connective tissues - more common to lower lip.
Retention is due to blockage where there is no break in the epithelium, so the mucin pools into a cyst - more common upper lip.
They are more fluctuant, soft swellings.

317
Q

What is Addison’s and how does it present orally?

A

Addison’s is a primary adrenal gland disease that leads to insufficient production of cortisol and aldosterone. It leads to excess ACTH production due to negative feedback leading to increased melanocyte production causing endogenous pigmentation orally. It can be caused by TB, malignancy, autoimmune or idiopathic.

318
Q

What is the role of BP180?

A

It is a protein that holds the basement membrane to the epithelium, it is the protein targeted in mucous membrane pemphigoid.

319
Q

What is the definition of an ulcer, what is the definition of erosion?

A

Oral ulceration is a break in the epithelial continuity with damage to the lamina propria.
Erosion is a break in the epithelial continuity but with no break to the underlying lamina propria.

320
Q

How can you tell if there is desquamation of gingiva?

A

Desquamation is thinning of the epithelium therefore when minimal pressure is applied the epithelium will slide off causing a break resulting in bleeding.

321
Q

If aphthous like ulcers are suspected what should be carried out?

A

Full blood count, haematinic assays (B12, Ferritin, Folate), coeliac disease screen, auto antibody profile.

322
Q

How can recurrent aphthous ulcers be managed?

A

Prior to treatment but address underlying cause/predisposing factors (trauma, stress, food, SLS, smoking cessation).
Then pt can be managed with topical steroids (beclometasone), antiseptic preparations (0.2% chlorhexidine) or systemic mediation (prednisolone/mycophenolate mofetil).

323
Q

What is the MOA of RAU?

A

Immunologically mediated T cell reaction with a humoral component.

324
Q

What can predispose a pt to erythema multiforme?

A

Microbial (HSV), drugs (penicillin/carbamazepine), food (benzoate/cinnamon).

325
Q

What is erythema multiforme caused by and how does it present?

A

It is an immunologically mediated disease that results in destruction of the epithelium, it involves one or more mucous membrane and sometimes the skin. It can present with widespread ulceration, desquamative gingivitis, target lesions and can involve the eye. Can have minor (one mucosa + skin) or major (two mucosa + one skin).

326
Q

How can you treat erythema multiforme?

A

Referral to specialist care. Supportive care (hydration, chlorhexidine, pain, relief), eliminate trigger, drug therapy (if caused by HSV).

327
Q

What is mucous membrane pemphigoid, how does it present?

A

MMP is an autoimmune condition in which antibodies target the BSP180 protein in the basement membrane leading to erosion, ulceration, atrophic inflammation, desquamative gingivitis, bullous lesions and scarring of the eyes, oral, skin and genitals. Can lead to blindness.

328
Q

How can both pemphigoid and pemphigus be treated?

A

Both are diagnosed through histopathology and direct/indirect immunofluorescence. Can be treated by topical or systemic steroid/immunosuppressants.

329
Q

What is the role of desmoglein 1+3?

A

Holds to epithelium cells together.

330
Q

What is pemphigus vulgaris, how does it present?

A

PV is an autoimmune condition in which antibodies target desmoglein 1+3 in the epithelium leading to erosion, ulceration, scarring, atrophic inflammation, bullous lesions, and desquamative gingivitis. It can affect the oral cavity, pharynx, skin and genitals. It is characterised by it presenting with oral lesions and then skin lesions later.

331
Q

What are Fordyce spots?

A

Enlarged minor salivary glands.

332
Q

What is the clinical presentation of geographic tongue?

A

Loss of papillae that creases lacy white and red patches on your tongue.

333
Q

What is white sponge nevus, what are some differentials?

A

Bilateral patches along the buccal surfaces that present in childhood/young adulthood. It is a hereditary disease in which no treatment is required.
Differentials: leukoplakia, OLP, sub-mucous fibrosis.

334
Q

What is trauma along the posterior buccal mucosa due to bruxism called?

A

Linea alba.

335
Q

What is the clinical presentation of oral lichen planus?

A

OLP is an autoimmune condition in which lymphocytes target keratocytes leading to patches which appear reticular, plaque like or ring like. It can also lead to bullous lesions, erosive/ulcerations, atrophic inflammation and desquamative gingivitis.

336
Q

What is oral hairy leukoplakia associated with?

A

Associated with EBV and HIV.

337
Q

What are 2 systemic causes of white patches that can be differentials to OLP?

A

Discoid lupus erythematosus and Graft Versus Host Disease (GVHD)

338
Q

How does extra oral lichen planus present?

A

Purple purpura with white striations, Wickham striae.

339
Q

What is oral lichen planus and what causes it?

A

Cell mediated autoimmune condition that targets oral keratinocytes. It can be idiopathic in nature but can get drug induced OLL or mercury OLL.

340
Q

What drugs can cause lichenoid lesions?

A

Anti-hypertensives, hyperglycaemics and steroids.

341
Q

What special investigations can be used to differentiate between OLP and hep C?

A

HCV serology (looks for antibodies to hep C)

342
Q

What are the complications with OLP?

A

Painful lesions can affect quality of life, periodontal attachment loss due to compromised OH and malignancy risk.

343
Q

What are the 2 different immune systems - what is the difference between them?

A

Innate and adaptive.

344
Q

What is the difference between Hodgkins and non-hodgkins lymphoma?

A

Hodgkins lymphoma contains Reed-Sternberg cells whereas NHL does not contain Reed-Sternberg cells.
NHL majority pts over 55. HL median diagnosis 39.
NHL may arise in lymph nodes anywhere in body whereas HL typically begins in upper body, such as neck, chest or armpits.

345
Q

How long should you postpone dental treatment for post transplant?

A

6 months.

346
Q

How does HIV attack the body?

A

It attacks and destroys the CD4 T helper cells leading to immunocompromisation.

347
Q

How does radiotherapy work and help to treat cancer?

A

It is the application of radiation to help destroy malignant cells. It works by creating free radicals in the cancer cells which causes cell death when dividing. As it targets cells with rapid turnover, it also affects osteoclasts and mucosa.

348
Q

What are the 5 oral complications of radiotherapy?

A

Radiation caries, mucositis, periodontitis, ORN, hypersensitivity, loss of taste, dysphagia, opportunistic infections.

349
Q

What is the definition of ORN?

A

The presence of exposed bone or bone that can be probed through a fistula 8 weeks after extraction with history of radiotherapy but no history or anti-resorptive/angiogenic drug therapy.

350
Q

How long is treatment for radiotherapy, what should be done in this time?

A

6 weeks. Do not treat within this period.

351
Q

How long is the treatment block for chemotherapy, what shouldn’t be done in this time?

A

Course lasts 28 days with highest risk of bleeding/infection 14 days after dose. Therefore, treat just before or just after.

352
Q

What are the features of chronic leukaemia?

A

Patients tend to present later and are harder to cure due to the cells being more mature and having more function.

353
Q

What is a multiple myeloma?

A

A blood cancer arising from abnormal plasma cells and affects many bones within the body. It is characterised by relapsing as it is incurable.

354
Q

How do you describe a lesion?

A

Size, site, shape, margins, surrounding tissues, palpate, type.

355
Q

What 2 things can cause pigmentation and what are they?

A

The amount of melanin being produced by melanocytes or the number of melanocytes (specialised pigment producing cells found in the basal cell layer and mucous membrane).

356
Q

If a pigmented patch is found closer to the surface what colour is it?

A

Brown is surface, blue is deeper.

357
Q

What is the difference between focal and a diffuse pigment?

A

Localised is focal, diffuse means kind of scattered about.

358
Q

What drugs can cause exogenous focal pigmented patches?

A

Drugs (contraceptive, anti-virals), foreign bodies (amalgam, ink), and tobacco use.

359
Q

What drugs can cause exogenous diffuse pigmented patches?

A

Heavy metal, drugs (antimalarials/antibiotics), tobacco.

360
Q

What is black hairy tongue and how is it managed?

A

Elongation of filiform papillae on the dorsum of the tongue that gets stained by food, it is managed by brushing the tongue twice a day.

361
Q

Why does smoking lead to smokers melanosis?

A

Inflammation from smoking stimulates melanin production leading to discrete, brown macules.

362
Q

How would a melanotic macule present?

A

Small, brown spots usually round on lip/mouth due to increased melanin deposition.

363
Q

If there is an area with an increase in the number of melanocytes what is seen and what is it called?

A

Oral nevi are due to increase in melanocytes and they are seen as small, well circumscribed, brown/black raised patches. They are often found on the palate.

364
Q

How are oral melanocanthomas caused?

A

A rare benign pigmented patch caused hyperplasia of spinous keratocyts and dendritic melanocytes.

365
Q

Malignant melanomas require what to happen to all pigmented patches?

A

Biopsied.

366
Q

Where do malignant melanomas commonly present?

A

Hard palate or gingiva.

367
Q

Where is cortisol produced?

A

In the zone of fasciculata of the adrenal gland upon stimulation of ACTH.

368
Q

What regulates blood pressure and where is it produced?

A

RAAS system. Aldosterone which is made in the zona glomerula of the adrenal gland.

369
Q

How is cortisol produced?

A

By negative feedback and production of ACTH in the pituitary gland which stimulates cortisol in the adrenal gland.

370
Q

What is secondary adrenal gland insufficiency - what can cause it?

A

Patients who are on long term steroids as the body loses the feedback loop and the ability or produce cortisol. Also if there is a hypothalamus tumour and the body stops making ACTH.

371
Q

How does Addison’s present?

A

Tiredness, oral skin pigmentation (ACTH stimulates melanocytes), dizziness, loss of appetite and weight loss.

372
Q

What stimulates melanocyte production?

A

ACTH

373
Q

What are the main causes of Addison’s?

A

Idiopathic, TB, autoimmune or malignancy.

374
Q

How can you test for Addison’s?

A

Synachten test - patient is given ACTH and then cortisol levels are monitored, if none is produced then Addison’s.

375
Q

What is seen in primary adrenal gland insufficiency that is not seen in secondary?

A

There is an increase in pigmentation seen in primary due to excess ADTH.

376
Q

What should you be wary of with a patient with PEutx-jeghers?

A

It is genetically inherited syndrome in which patients can present with polyps and mucocutanous melanocytes. Diagnosis is key as patients are at higher risk of developing bowel cancer.

377
Q

What must be assessed when discussing a third molar on a radiograph?

A

Extent of eruption, coronal angulation, occlusal bony coverage/distal bone loss, caries, number of roots, angulation of roots, proximity to ID canal and adjacent teeth.

378
Q

What can be seen radiographically that is a signs of previous pericoronitis?

A

Distal bone loss

379
Q

What is parallax?

A

The use of 2 different angles of radiographs and depending on if the tooth reference point moves position between the two views will help to determine the placement of the tooth. SLOB (same lingual, opposite buccal). Definition: apparent displacement of an object because of the altered position of the observer.

380
Q

What is a supplemental tooth?

A

An extra tooth of normal anatomy

381
Q

How can we categorise supernumeraries?

A

Conical, Tuberculate, Odontome (complex or compound), Supplemental

382
Q

Name 5 features of cleidocranial dysplasia

A

Failed fontanelle fusion, clavicle aplasia, light bulb head, supernumeraries, dentigerous cysts, retained primary, failure of eruption of permanent.

383
Q

What are 4 conditions associated with hypodontia?

A

Gorlin goltz, cleft palate/lip, Downs syndrome, ectodermal dysplasia.

384
Q

What does fusion of the primary B and C indicated?

A

The permanent lateral may be missing.

385
Q

What is concresence, how is it diagnosed?

A

Concrescence is when the cementum of 2 teeth join together, cannot tell until you go to extract as looks like superimposition on a radiograph.

386
Q

Failure of what tissue to invaginate results in taurodontism?

A

Hertwigs root sheath cells at the correct level.

387
Q

What is dilaceration and what can it be caused by?

A

A disturbance in tooth formation that results in a sharp bend between the crown and root. It can be either developmental or due to trauma.

388
Q

What is the difference between dens evaginatus and dens invaginatus?

A

Invaginatus is where the cingulum pit folds into the tooth (pulp, enamel, dentine found within the tooth).
Evaginatus is when it folds out (an example of this would be a talon cusp).

389
Q

What has the classic bullseye radiographic appearance?

A

A dilated odontoma.

390
Q

Who are talon cusps on maxillary incisors more common in?

A

Cleft palate patients.

391
Q

How do pulp stones appear radiographically?

A

Calcifications that form within the pulp chamber and the chamber conforms to their shape so you will see it change.

392
Q

What can pulp stones be confused with?

A

Enamel pearls

393
Q

How can you tell the difference between type 1 amelogenesis and type 2/3/4?

A

Type 1 radiographically there will be a density difference between the enamel and dentine (however the enamel will be much thinner than normal). In the other types the density difference will not be as great due to the enamel being of poorer quality.
Clinically type 1 is thin, yellow enamel that may be quite shiny and has loss of interproximal points. The other types has enamel that breaks down easily and can range from cloudy to brown in colour.

394
Q

What is the clinical presentation of hypoplasia amelogenesis?

A

Flat cusps and loss of interproximal points. Thin, yellow enamel that is shiny.

395
Q

What is the radiographic appearance of hypomatured amelogenesis?

A

Pulpal sclerosis, same density enamel and dentine and snow-capped teeth.

396
Q

What is osteoporosis and how does it present?

A

Hereditary disease that results in a formation of defective type 1 collagen. Patients present with long slender bones, blue sclera and osseous fractures.

397
Q

What is the clinical presentation of Dentinogenesis imperfecta?

A

Teeth erupt amber but then become blue/grey over time. Enamel fractures and crown wear easily due to being unsupported and the dentine stains easily. Radiographically the crowns are tulip shaped with flame shaped pulps and pulpal sclerosis.

398
Q

How is the maxillary sinus assess radiographically?

A

You should compare the air shadows on both side, trace the outlines of the wall to look for any disruption and see if there are any soft tissue opacities.

399
Q

What epithelium lines the maxillary sinus?

A

Pseudostratified ciliated columnar epithelium.

400
Q

Who is at increased risk of polyposis?

A

Asthmatics

401
Q

How does rhinosinusitis appear radiographically?

A

A sinus cavity opacification or mucosal thickening with sclerosis of the sinus.

402
Q

What is a benign mucous retention cyst and how does it appear radiographically?

A

A benign cyst that originates from the accumulation of fluids inside the sinus membrane. Appears as a well-defined, domed radiopacity with intact walls.

403
Q

Who is at higher risk of developing a Warthin’s tumour?

A

Smokers, EBV patients and those exposed to radiation.

404
Q

What does condylar hyperplasia result in?

A

Enlargement and deformity of the condylar head and therefore the glenoid fossa it sits in, resulting in posterior open bite, chin deviation (is usually unilateral).

405
Q

On extra oral examination how can you distinguish between condylar hyperplasia and hypoplasia?

A

Hyperplasia, the chin deviates to the opposite side.
Hypoplasia, it deviates to the affected side.

406
Q

Describe disc displacement with reduction?

A

Closed jaw - condyle seated in fossa with disk anteriorly.
Condyle begins translation - as mouth opens, click/pop sound as disk returns to normal position in relation to condyle.
During closing - disc becomes anteriorly displaced sometimes with secondary sound (reciprocal click).

407
Q

Describe disc displacement without reduction?

A

When articular disc is displaced anteriorly to the condyle when mouth opening and closing.

408
Q

What is the difference between rheumatoid arthritis and osteoarthritis?

A

Rheumatoid is an autoimmune condition whereas osteoarthritis is degenerative.

409
Q

How does cleft lip form?

A

Cleft lip is the failure of fusion of the medial nasal process with the maxillary process.

410
Q

How does cleft palate form?

A

Failure of fusion of the palatal shelves.

411
Q

What are the dental features of cleft lip/palate?

A

Hypodontia, hyperplastic teeth, supernumeraries.

412
Q

Name 5 clinical features of Down syndrome.

A

Bifid uvula, short trunk, small hands, macroglossia, class 3, hypodontia, peg shaped laterals, high palate.

413
Q

List 5 clinical features of ectodermal dysplasia.

A

Hypodontia, sparse hair, thin nails, reduced sweating, peg shaped teeth, reduced salivary flow.

414
Q

List 5 clinical features of gardners syndrome.

A

Multiple polyposis, multiple osteomas, dense bony islands, epidermoid cysts, hyperdontia.

415
Q

What is Paget’s disease?

A

Systemic bone disease where there is increased bone remodelling due to increased activity of osteoclasts. Can be confirmed by seeing an increase in serum alkaline phosphatase.
Patients present with malocclusions and hypercementosis.

416
Q

What is acromegaly and how can it appear?

A

Excessive growth hormone (primary - just excess, secondary - due to pituitary tumour).
Clinically seen with teeth spacing, anterior open bite, larger mandible, larger teeth and large sinus.

417
Q

What is sickle cell anaemia and what can it lead to?

A

A genetic disorder that effects the shape of red blood cells. Sickle cell crisis can occur when under stress and the RBC’s change shape even more and carry even less oxygen.

418
Q

What can thalassaemia lead to and why?

A

It’s a disease that leads to abnormal haemoglobin resulting in a destroyed spleen and anaemia. Loss of maxillary sinus and maxillary hyperplasia with a rodent face.

419
Q

What is a dilated odontome?

A

A very large supernumerary with an external ring of enamel and pulp with a donut like appearance.

420
Q

What is fibrous dysplasia and how does it appear radiographically?

A

Replacement of normal bone with fibrous tissue containing immature, woven bone. Ground glass fibre trabeculation.

421
Q

How does cherubism present and what can it cause?

A

Bilateral enlargement of maxilla/mandible and upturned eyes.

422
Q

What is the radiographic appearance of metastatic cancers?

A

Moth eaten lytic bone, loss of cortication, loss of anatomy.

423
Q

Multiple myeloma patients are at higher risk of what (usually)?

A

Patients usually on bisphosphonates so higher risk of MRONJ.

424
Q

How does an osteosarcoma appear radiographically?

A

Bony proliferation, PDL widening, sunburst appearance.

425
Q

What is myasthenia gravis?

A

Long-term neuromuscular disease where patients develop skeletal weakness due to breakdown of nicotinic receptors. Do not use midazolam.

426
Q

What is an IMCA?

A

Independent mental capacity advocate.
Listens to a patient and advocates for them when they lack capacity but have no one close to help.

427
Q

What is seen in a dysplastic cell growth?

A

Increase in size, pleomorphic cells, lots of mitochondria, loss of polarity, increase in vascularity and broken through basement membrane.

428
Q

How does LA work?

A

Local anaesthetic agents suppress action potentials in excitable tissues by blocking voltage-gated sodium channels. In doing so they inhibit the action potentials in nociceptive fibres and so block the transmission of pain impulses.

429
Q

What are the benefits of articaine over lidocaine?

A

More lipid soluble therefore greater potency, it works quicker due to superior diffusion through bone and articaine is not reliant on liver metabolism.

430
Q

What is the role of dressings in post-op wound management?

A

Keep wound in warm moist state, hide wound whilst healing, apply pressure to prevent haematoma, protect delicate tissue, absorb tissue exudate.

431
Q

How does the HPA axis work?

A

Body senses stress: hypothalamus release CRH to the pituitary gland which in turn releases ACTH to the adrenal glands which then produce cortisol (behaviour, immune system, blood pressure, metabolism).

432
Q

What is cortisol?

A

Mainly controls metabolism by getting cells to release more glucose/fat. It also causes adrenaline to be released (HPA system not cortisol).

433
Q

What is an adrenal crisis?

A

Life threatening hypotension leading to shock. People at risk are those who have primary adrenal insufficiency (Addison’s) and secondary (long term steroid therapy - immunosuppressed patients).

434
Q

What is the guidance for minor dental procedures regarding steroid crisis?

A

Before patients should take an extra tablet 60 mins prior and then after only take an extra dose if hypotensive symptoms show.

435
Q

Who is at risk of adrenal crisis?

A

Patients with primary adrenal insufficiency and those with secondary who have been taking prednisolone 5mg (or equivalent) for 1 month or longer.

436
Q

What is guidance for dental surgery regarding steroid crisis (RCTs)?

A

Double oral dose (up to 20mg hydrocortisone) one hour prior to surgery and then double oral dose for 24 hours, then return to normal.

437
Q

What is guidance of major dental surgery regarding steroid crisis?

A

100mg hydrocortisone IM just before anaesthesia and then double oral dose for 24 hours, then return to normal.

438
Q

What is the histological difference between extravasation and retention mucocele?

A

Extravasation are lined by granular tissue however retention are lined by epithelium.

439
Q

Describe an ameloblastoma.

A

Benign epithelial tumour commonly found around the region of the 8s in the mandible. It is asymptomatic until a swelling is noticed which can cause disfiguration. It has slow enlargement but can perforate the buccal plate. Radiographically it is seen as a well circumscribed radiolucency that can exhibit buccal/lingual expansion and can cause root resorption. Managed via simple excision with 10mm.

440
Q

Describe an adenomatoid odontogenic tumour.

A

Benign epithelial tumour that commonly presents in the anterior region of the maxilla. It may mimic a dentigerous cyst and is managed by simple enucleation.

441
Q

Describe an odontogenic myxoma.

A

Benign mesenchymal tumour commonly found in the molar region of either jaw and presents as a painless swelling. Radiographically appears similar to an ameloblastoma however displaces roots instead of resorbing. Histologically has randomly orientate stellate, spindle shaped cells, resembles dental papilla of developing tooth and permeates medullary bone. Managed by enucleation with currettage.

442
Q

Describe a cementoblastoma.

A

Benign mesenchymal tumour closely associated with the roots of teeth (especially posterior mandible). Radiographically is seen as a radiopaque mass with thin radiolucent margins, closely associated with teeth, causes resorption and can expand buccally/lingually. Histologically will see formation of calcified cementum like material. Managed by extraction of associated tooth and enucleation with curettage.

443
Q

Describe an ameloblastic fibroma.

A

Benign mixed tumour found in the posterior mandible. Can either expand slowly and displace teeth or be destructive of facial bones. Histologically may look like a cap stage tooth germ due to dental papilla, ameloblasts and stellate reticulum. Managed by conservative resection as can become a sarcoma.

444
Q

Describe a pleomorphic adenoma.

A

Benign salivary gland tumour found commonly in the parotid gland. Presents as soft, mobile, smooth growing lump that can push ear forward or present in the palate that is painless and well demarcated. Histologically you will see a fibrous capsule with a bosselated surface with the presence of both epithelium and connective tissues.

445
Q

Describe a warthin’s tumour.

A

Benign, circumscribed, mobile, slow growing, painless lump. Found on the lower portion of the parotid gland. Histologically seen as double layered, oncocytic, columnar lined epithelium. Contains glandular and cystic structures with papillary cystic arrangement. Risk factors are EBV, smoking and irradation.

446
Q

Where is a canalicular adenoma commonly found?

A

upper lip

447
Q

What are the risks of acinic cell carcinoma and what cells does it contain?

A

Serous cells in solid sheets. Has a high risk of reoccurrence and loco-regional metastasis.

448
Q

Describe an adenoid cystic carcinoma.

A

Malignant tumour that presents as ulcerated, slow growing, bone destruction and facial nerve palsy. Contain duct lining and myo-epithelial cells. Histologically seen as non-encapsulated, infiltrative, cribriform appearance with perineural involvement. Exhibits late metastasis, perineural involvement, lymph node involvement and extensive local invasion.

449
Q

Describe a mucoepidermoid carcinoma.

A

Malignant. Can present either high grade (fast growing, ulcerative, fixed) or low grade (soft, mobile, slow growing, smooth). Histologically squamous cells, mucous secreting cells and intermediate cells are seen.

450
Q
A

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