Daily exam deck Flashcards

1
Q

What is the basic investigative process in oral pathology?

A
  1. Presentation of chief concers
  2. Information collection - medical history, patietn history, clinical examiantion and special tests
  3. Information collation
  4. Development of a differential diagnosis - list most likely diagnoses and do specific test to eliminate potential diagnoses
  5. Arrive to definitive diagnosis and commence treatment
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2
Q

What are the types of differential diagnosis?

A
  1. Clinical differential diagnosis
  2. Radiographic differential diagnosis
  3. Provisional/working/tentative diagnosis
  4. Histological differential diagnosis
  5. Definitive diagnosis
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3
Q

What is the step by step process to understand the arisal of a certain oral lesion?

A

Use this scheme

  1. Developmental origin
  2. Inflammatory origin
  3. Hyperplastic origin
  4. Degenerative origin
  5. Hormonal origin
  6. Neoplastic origin
  7. Idiopathic origin

DIHDHNI

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4
Q

How do we take history about a lesion?

A
  1. Duration when the patient first started seeing the lesion
  2. Variations in site and character of the lesion
  3. Symptoms - related to the lesion and any systemic symptoms
  4. Onset - any associated hsitorical events related to the lesion
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5
Q

What is the systematic way to examine a lesion?

A
  1. Site - using anatomical terminology
  2. Size - measure with a probe
  3. Morphology - elevated, flat or depressed
  4. Colour - compare to adjacent normal tissue
  5. Consistency - how it feels (ONLY CLINICAL DO NOT SAY THIS IN EXAM), texture - how the surface looks like (PHOTOS ARE APPROPRIATE :))
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6
Q

What are some of the terminology in a lesion with elevated morpholoy?

A

Blisters - Fuild filled masses:

  1. Vesicle - upto 0.5cm
  2. Bulla - more than 0.5cm
  3. Pustule - pus of any size

Non-blisters - not fluid filled elevations

  1. Papule - upto 0.5cm
  2. Nodule - from 0.5cm to 2 cm
  3. Tumour - more than 2 cm
  4. Plaque - more than 0.5cm but it is only clightly raised
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7
Q

What are some of the terminology of a lesion with depressed or flat morphology?

A

Depressed:
1. Ulcer (epithelium lost) - if it is yellow tissue more likely to be an ulcer

  1. Erosion (epithelium lost)/atrophy - if it is redness tissue more likely to be an erosion/atrophy

Flat:
1. Macule - discoloration (freckel)

  1. Patch - big discolouration
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8
Q

What kind of structure is this?

A

A brown macule - a flat discoloration

Site - RHS lower vermilion shifted around 10 mm from the midline of the lips

Size - measure with peiro probe - around 5-10mm

Morphology - flat, round, heart shapped

Colour - brown

Consistency - NOPE IT IS A PHOTO - Texture - maybe rough, defiantly different from the normal lip

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9
Q

What kind of structure is this?

A

It is a white polyp

Site - RHS buccal mucosa adjacanet to the buccal surface of 45

Size - measure with perio probe - around 10-15mm

Morphology - elevated, rounded, sphere like

Colour - white, opaque, with small amounts of pink

Consistency - NOPE IT IS A PHOTO - Texture - rubbery

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10
Q

What investigation do we have in oral pathology?

A
  1. Biopsy (taking the whole or some of the tissue) - histopathology (investigative process) and exfoliative cytology
  2. Adjunct diagnostic techniques - light-based and vital stains
  3. Other techniques - microbiology, biochemistry, serology
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11
Q

What are some of the types of biopsy?

A
  1. Scalpel biopsy - incisional or exitional - most common procedure
  2. Fine needle aspiration
  3. Core biopsy
  4. Exfoliative cytology - taking the gunk and spreading it over a film
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12
Q

What are the consideration during biopsy?

A
  1. The lesion in question
  2. Surrounding anatomy
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13
Q

What should you do with some of the lesions that you may encounter to understant if they are vascular?

A

Use a small, transparent plate and apply pressure - if the lesion stars to blanch, it is most likely to be vascular

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14
Q

What are some of the features of pathology that can be observed by a light based system such as Velscope?

A

In some instances, the pathological tissue may take up the light thus resulting in a shadowing of the structures.

Good adjunct but please do not use this as a basis of diagnosis.

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15
Q

What are some common stains in oral pathology?

A
  1. Haematoxylin and eosin
  2. Periodic Acid-Shiff - used for fungal infection
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16
Q

What is exfoliative cytology?

A

It is the examination of cells scraped from the surface of the lesion - great for fungal infection - it is quick and easy but may not be used to more complex lesions with pathology below the surface

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17
Q

What is fine needle aspiratin used for?

A

It is mostly used for intraosseous pathology and fluctuant soft tissue pathology and neck masses

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18
Q

What is core biopsy used for?

A

It is used to remove the core of some tissues - it is similar to scalpel biopsy but it has more complication than fine needle biopsy.

Mostly used in biopsy in the abdomen but also can be used on a lymph node

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19
Q

What is a smere vs a swab?

A

Swab - microbial analysis - need to send to a lab for something like PCR

Smere - do a cell analysis - straight under the microscope - think exfoliative cytology

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20
Q

What are the two basic types of mucosa present in the mouth?

A
  1. Attached, orthokeratinised mucosa
  2. Non-attached, non-keratinised mucosa
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21
Q

What are the four layer of the epithelium?

A
  1. stratum basale (D)
  2. stratum spinosum (C)
  3. stratum granulosum (B)
  4. stratum corneum (A)

E and F and the papillary and reticular layer accordingly

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22
Q

What are some the benign lesion of epithelial layer with idiopathic or developmental origin?

A
  1. Leukoedema
  2. White Sponge Nevus
  3. Epidermolysis Bullosa
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23
Q

What is a leukoedema?

A

It is a common developmental lesion of the oral mucosa. It is a variation of normal mucosa and it is more common in individuals with dark skin. Mainly in buccal mucosa

It can be implicated by the use of tobacco or alcohol.

They are asymptomatic, bilateral, poorly defined and it disappears when the mucosa is stretched or whipped with a gauze. Please consider not to stretched the attached gingiva!

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24
Q

What is the histology of leukoedema?

A

It appears in the supperficial half of the epithelium.

There are large vacuolated cells present with some Pyknotic nuclei.

Epithelial hyperplasia present as well as long elongated rete pegs

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25
Q

What is the management of leukoedema?

A

Unless there are any other worrying signs - no management is needed just monitoring

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26
Q

What is the White Sponge Naevus?

A

It is a rare inherited condition. It is autosomal dominants trait and it is early onset. Majority of cases present with oral lesion, other mucosal surface may be affected.

It is asymptomatic, diffuse, with white thickening and if irregular thickening

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27
Q

What is the histology of White Sponge Naevus?

A

It appears in the superficial layer of the epithelium.

Large vacuolated cells.

Pyknotic nuclei and thickened parakeratin layer

No dysplasia present

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28
Q

What is benign migratory glossitis?

A

It is also known as geographic tongue - it is quite common and the aetiology is well known

It is a result of loss (atrophy) of filiform papillae. Sometimes it can be sore but again not much can be done - if concerning please refer for biopsy

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29
Q

What can be commonly seen int eh benign migratory glossitis histologically?

A

Numerous microabscesses in the surface of epithelium filled with neutrophils and lymphocytes

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30
Q

What is hairy tongue (aka coated tongue)?

A

It is a condition with poorly understood aetiology and a result of increased length of filliform papilla.

May be initiated by heavy smoking, atiobiotics and other.

Usually asymptomatic.

Increased number of chromogenic microorganisms thus a change in colour to usually darker one

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31
Q

What do we do in the instance of hariy tongue, migratory glossitis or other benign developmental deviation?

A
  1. Ensure the patient that this is not something pathological
  2. Take a smear if needed
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32
Q

What is haemangioma?

A

It is a localised vascular proliferation that may be congenital or arise later in life.

Could be single or multiple and results in soft tissue lesions usually

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33
Q

What is the hsitological appearance of haemangioma?

A
  1. Layer of epileium
  2. Perforations of endothelial blood vessels and cells - forming capillaries
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34
Q

What type of haemangioma is this?

A

This is capillary haemangioma due to the small capillary vessels presence

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35
Q

What type of haemgioma is this?

A

This is cavernous haemangioma due to larger blood vessels present

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36
Q

What is lymphangioma?

A

It is a type of lesion that is present in tongue swelling. The epithelium lining is very thin with a large, lymph filled vascular spaces

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37
Q

What kind of condition is this?

A

This a lymphagioma of the tongue - due to the pink limp liquid being observed in the hghlighted areas

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38
Q

What conditions is this?

A

This is a caliber persistent labial artery.

It occurs when the inferior alveolar artery maintains it’s size after leaving the mental forament and becomes superficial in the lower lip.

It can present as a nodule. PLEASE PULPATE IT BECAUSE IT WILL PULSE

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39
Q

What is this condition?

A

Oral melanotic macule or focal melanosis or an intraoral freckle

It is a well demarcated, uniform in colour, asymptomatic and has the same consitency as the surrounding mucosa macule.

Histologically it is related to increase melanin deposition.

Sometimes can arise due to medication use specifically oral medications.

Remeber macules DO NOT CHANGE OVER TIME

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40
Q

What is this condition?

A

This iss a mucosal menocytic naevus.

It is a rare oral cavity lesion or patch.

It is bening proliferation of neaevus cells.

The lesion is not neoplastic but is a hamartomatous lesion

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41
Q

What is a hamartoma?

A

It is a tumour-like lesion.

Non-neoplastic proliferation of tissue.

It grows at the same rate as the surrounding tissue

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42
Q

What type of naevus is this?

A

This is a junctional naevus because is confined to the basal layer of the epithelium

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43
Q

What type of naevus is this?

A

This is intraomucosal naevus - because is is not in the epeithelium

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44
Q

What condition is this?

A

This is an amalgam tattoo - it is associated with some of the amalgam being incorporate into the adjcent soft tissue over time. PLEASE LOOK AT AMALGAM NEAR BY.

This lesion can grow but usually at a none alarming rate.

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45
Q

What does ectopic mean?

A

It is a tissues that are in an abnormal sire of position

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46
Q

What are Fordyce spots?

A

They are ectopic sebaceous glands that usually occur on the buccal mucosa - their instance increases with age.

They are slightly elevated yellowish nodules.

It arises due to the arisal of the tissue from the ectoderm during the embrio development

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47
Q

What are the histological features of the Fordyce spots?

A

They are very similar to sebaceous glands

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48
Q

What condition is this?

A

These are lingual tonsils.

This is part of the lymphoid tissue (Welder’s ring) that is used to fight infection.

The lymphoid tissue underneath the folliate papilla goes through lymphoid hyperplasia (growth) and result in an elevation on the postra-lateral tongue surface.

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49
Q

What type of nodules are theses?

A

This is lymphoid hyperplasia

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50
Q

What type of tissue is this?

A

This is lingual thyroid tissue

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51
Q

What are the Tori and exostoses?

A

They are bony protuberances.

Non-neoplastic.

Possibly inherited

Exotoses - multiple or single nodules at the buccal aspect of the alveolar bone

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52
Q

What type of cyst is this?

A

This is a nasopalatine cyst.

It is the most common non-odontogenic oral cyst.

It s asymptomatic unless secondarily inflamed.

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53
Q

What type of conditon is this and why?

A

These are fordyce spots

They are sebatious glands in the oral mucosa.

Do not biopsy and reassure the patient that this is normal.

Pathogenesis: ectoderm refrences

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54
Q

What is hyperplasia?

A

It is an increase in the size of a particular tissue by increase in cell number - it is reversible and stimulus dependent

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55
Q

What is hypertrophy?

A

It is an increase in the size of particular tissue by increase in cell size.

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56
Q

What are the two main origins of hyperplastic lesions?

A
  1. Predominantly epithelial in nature
  2. Predominantly connective tissue in nature
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57
Q

What are the two basic morphological potentials of a lesion?

A
  1. Senssile lesion - broad based lesion
  2. Pedunculatedlesion - on a stalk - use a perioprobe to see if a lesion has a neck
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58
Q

What are some of the other adjectives that can be used to describe a lesion?

A
  1. Papillary - any small growth projectin into a cavity
  2. Verrucous - warty surface appearance (small hyperkeratinised projections)
  3. Epulis - lump on the gum non-neoplastic
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59
Q

What is fibroepithelial hyperplasia?

A

It is a growth of fibrous connective tissue underneath an epithelium

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60
Q

WHat are the clinical features of fibroepithelial hyperplasia?

A

It is a exophytic lesion.
Site is a site of trauma

Size is around 1-2mm upto 1cm

Moprphology could be sessile or pedunculated

Colour is similar to normal mucosa but could look inflamed

Consistency could be soft to hard depending on the age of the fibrous tissue

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61
Q

What is the aetiology, pathogenesis and treatment of fibroepethilial hyperplasia?

A

Aetiology: Chronic physical trauma, cheek biting, irritation from broken teeth etc.

Pathogenesis - cellular proliferation and production of cell product - predominantly connective tissue

Treatment: Excision of the tissue and removal of the cause

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62
Q

What is papillary hyperplasiaof the palate?

A

It is a nodular overgowth that is associated with dentures and S.Candida infection.

Associated with nodular hyperplasia in histological samples

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63
Q

What is the common histological presentation of the S.Candida infection

A

It is a presented as a nodule appearance with chronic inflammatory cell infiltrate

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64
Q

What condition is this?

A

This is fibroepithelial polyp. It is a localised fibroepithelial hyperplasia. Can occur anywhere but commonly sites prone to trauma.

It is similar to the colour of the surroinding tissue but may appear a bit more inflammaed.

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65
Q

What is the histopathology of fibroepithelial polyp?

A

It is an overlying epithelium - hyperplastic or atopic or normal. Bulk lesion is made up of densely collagenous fibrous connective tissue.

MAY OCCUR WITH OSSIFICATION

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66
Q

What is the aetiology and treatment of fibroepithelial polyp?

A

Aetiology: chronic physical trauma and inflammation

Treatment: Excision

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67
Q

What condition is this?

A

This is pyogenic granuloma.

It is a localised soft tissue lesion that is common in people who are pregnant due to the hormone imbalance.

Site: Anywhere but classically arises from the interdental papilla

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68
Q

What are the clinical features of pyognic granuloma?

A

Usually sensile

Sudden onset and rapid growth

Bright red and haemorrhagic, ulcerated surface.

Tissue may mature thus becomes fibrosed

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69
Q

What is the hsitopathology of Pyogenic granuloma?

A

Many lesions are made up of exuberant granulation tissue. It is a very vascular lesion with large numbers of thin walled dilated blood vessels lined by endothelial cells

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70
Q

What is the treatment for pyogenic granuloma?

A

Excision and removal of causative factors

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71
Q

What are some of the differential diagnosis for pyogenic granuloma?

A
  1. Neoplasm
  2. Heamongioma
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72
Q

What is peripheral giant cell granuloma?

A

It is a similar lesion to the pyogenic granuloma but it also involves bone tissue

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73
Q

What is the histopathology of the peripheral giant cell granuloma?

A

It is a well vascularised cellular tissue with mononuclear cells.

If you see multinucleadted diant cells - probs a peripheral giant cell granuloma

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74
Q

What is the imortant aspect of the peripheral giant cell granuloma?

A

It is important to determine that the lesion is not an intra-bony or central lesion which has perforated cortical bone

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75
Q

What is ulcerated fibrous epulis with ossification? what are the clinical features?

A

It is a relatively common oral lesion. Presents as localised lesion of gingiva like fibrous epulis and pyogenic granuloma.

Clinical features:
1. Painless

  1. Relatively rapid growth
  2. Size usually less than 1 cm
  3. Sometimes - surface ulceration
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76
Q

What is the histopathology of ulcerated epulis with ossification?

A

It is a very cellular lesion - well vascularised and collagenous. IT CONTAINS CALCIFICATIONS.

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77
Q

What are generalised gingival hyperplastic lesions?

A

They are lesion that occur due to underlying factors such as plaque or use of certain medications such as hypertension medication (calcium channel blockers) or anti-covulsants or immunosupresants.

Drug Induced Gingival Overgrowth is one of them

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78
Q

What is a linea alba?

A

It is a lesion occurring on the buccal mucosa as a result of a local mechanical trauma

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79
Q

What is the clinical presentation of linea alba?

A

It is usually symptomless and is very very common.

It presents as a white, narrow, linear lesion on the buccal mucosa.

Could be unilateral or bilateral

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80
Q

What is the histopathology of linea alba? What is the management of linea alba?

A

A thichening of the prickle cell layer can be observed. Hyperkeratosis occurs. Nothing cna be done to manage it - just please do not bite your cheek.

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81
Q

What is morsicatio buccarum?

A

It is cheek biting which causes chronic mechanical trauma.

Clinical presentation is a unilateral or bilateral white patch on the buccal mucosa, which is rough and whitenned. Usually symptomless

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82
Q

What is the management of cheek biting?

A
  1. Control of habit
  2. Might need to treat the underlying stress
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83
Q

What is frictional keratosis?

A

It is similar to the cheek biting and linea alba but usually occurs on commonly traumatised sites such as the lips, lateral border of the tongue, buccal mucosa, edentulous alveolar ridge.

Appears as a poorly demarcated white lesion.

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84
Q

What happens histologically in frictional keratosis? What is the management?

A

Histological features:
1. Hyperkeratosis

  1. No dysplastic changes

Management:

  1. Identify and try and remove a cause - might be difficult with edentulous patients
  2. Always biopsy if in doubt :)
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85
Q

What is smoker’s keratosis?

A

It is a diffused, white, moderately thickened palate that can be sometimes roughened.

It usually involves the entire palate with characteristic, red, minor salivary gland dots.

Associated with tobacco smoking, especially reverse smoking.

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86
Q

What is the histopathology of smokers keratosis?

A

Hyperkeratosis is common. Thickening of stratum spinosum (prickle cell layer)

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87
Q

What is the management of smokers keratosis?

A
  1. Smoking cessation
  2. The lesion is usually not malignant but close monitoring is idea
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88
Q

What condition is this?

A

This chronic hyperplastic candidiasis.

It is usually a single, fixed, white or mix of white and red patch that syays when whipped.

May occur anywhere but common sites are the tongue and buccal mucosa.

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89
Q

What is the histopathological appearance of chronic hyperplastic candidiasis?

A

Thickening large bulbus epithelial with keratinisation

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90
Q

What are the three common oral HPV infections?

A
  1. Squamous papillomas/Oral warts
  2. Condyloma accuminatum
  3. Focal epithelial hyperpklasia
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91
Q

What are histopathological features of the giant cell fibroma? What are the clinical features?

A

The main difference between giant cell fibroma is the Giant Stellate Cells rather than the osteoclast like cells.

The clinical features are similar: small, raised, pedunculated lesion that is asymptomatic

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92
Q

What is the treatment for giant cell fibroma?

A

usually surgical excision.

The reoccurance of giant cell fibroma is relativley rare

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93
Q

What is traumatic neuroma? What are it’s clinical signs?

A

It is a lesion thatoccurs due to the damage of a nerve trunk following some sort of injury (like surgery or pressure on dentures).

Essenially - the repair of the axon does not go as planned and the lesion if fully comprised of the neural tissue.

Clinical features: small swelling or nodule on mucosa near mental foramen, alveolar ridge, lips or tongue. Pressure on the nodule cuases pain

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94
Q

What is histapathology and treatment of traumatic neuroma?

A

Histopathology: Presents as a mass of irregular bundle situated in variable amount of connective tissue stroma.

Treatment: surgical excision

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95
Q

What is this condition?

A

This is verruciform xanthoma, it is a rare lesion that mimic squamous cell carcinoma.

It is flat, velvety, pebbly.

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96
Q

What is the histopathological appearacnce of verruciform xanthoma?

A

It is usually associated with foamy, lipid filled marophages.

The lesion is bening

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97
Q

What are the principles of management of oral ulcers?

A
  1. Detect a lesion
  2. Health and lesion histories
  3. Examination - identify cause and remove if possible
  4. Differential diagnosis
  5. Monitor or Investigate - including biopsy/referral for biopsy
  6. Follow-up/referral
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98
Q

What is an ulcer?

A

An ulcer is the loss of contnues of epithelial linings and some fo the connective tissue. It is associated with colour yellow.

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99
Q

What are the parts of an ulcer?

A
  1. Border
  2. Depression
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100
Q

What are some of the oral ulcer that require urgent attention and referral?

A
  1. Long-standing ulcers with no obvious cause
  2. Indurated (hard) borders - PLEASE PALPATE
  3. Deep ulcers with rolled borders
  4. Ulcer that is fixed to underlying tissues - usually ulcers are mobile
  5. Painless ulcer
  6. Ulcers associated with lymphadenopathy - if there is a large swelling - EMERGENCY
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101
Q

What are the different sub types of ulcers that can occur?

A
  1. Reactive lesions
  2. Developmental
  3. Inflammatory/immunologic
  4. Infective
  5. neoplastic
  6. Idiopathic
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102
Q

What is a traumatic ulceration?

A

It is a type of ulceration from mechanical, chemical, thermal and radiation injury.

Please recall the patient in 2 weeks and during the session try to remove the cause.

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103
Q

What are the two types of traumatic lesions?

A
  1. Acute traumatic lesions - a lot of pain, surface covered by yellow fibrinous exudate and halo border
  2. Chronic traumatic lesions - minimal pain, elevated margins, fibroepithelial hyperplasia, epithelial hyperkeratosis, induration
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104
Q

What is a traumatic eosinophilic ulcer?

A

It is a bening chronic ulcer usually presenting on the tongue.

It is crateriform in shape.

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105
Q

What is the histopathological significance of eosinophilic ulcer and why should it worry us?

A

Eosinophilic ulcers are usually associated with an abnormal presentation of eosinophils thus it is important to send a biopsy sample of the ulcer for histopathological investigation to ensure it is not malignant

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106
Q

What is this condition?

A

This is a minor aphthous ulcer - which one of the most common ulcer of infectious origin.

It usually occurs in non-keratinised mucosa, it is shallow and rounded.

It has erythematous margins and yellowish floor

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107
Q

What is this condition?

A

This is a major Aphthous Ulcer - an uncommon ulcer of infectious origin.

It is usually very large and can involve keratinised mucosa. This need to be reffer for biopsy because this could be a melignancy.

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108
Q

What is this condition?

A

This is Herpetiform aphthous ulvers - it is an uncommon and are very very small.

Named herpetiform due to the resemblance of the ulcers to those of herpetic stomatitis

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109
Q

What are the basic management plan for aphthous ulcers?

A
  1. Accurate diagnosis
  2. Symptomatic treatment
  3. Steroid
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110
Q

What are the oral manifestations of Crohn’s disease?

A
  1. Diffuse lip swelling
  2. Coble stone thickening of the mucosa
  3. Ulcers
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111
Q

What is glossitis?

A

It is the atrophy of the lingual papilla

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112
Q

What is periodontitis?

A

Periodontists is a multi factorial, inflammatory diseases associated with dysbiotic microbial dental biofilms and characterised by non-reversible progressive periodontal tissue destruction. It manifests through: CAL, radiographically assessed alveolar bone loss, presence of periodontal pocketing, gingival bleeding and leads eventually to tooth loss.

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113
Q

What are the main points of the old, Non-specific Plaque Hypothesis?

A
  1. All plaque bacteria are equally pathogenic
  2. Quantity of plaque determines the pathogenicity
  3. Host has threshold capacity to detoxify bacterial products
  4. Disease develops if threshold is surpassed

Treatment: non-specific mechanical removal of total amount of plaque

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114
Q

What are the main points of the Specific Plaque hypothesis?

A
  1. Due to advancement of microbiological technologies, specific bacteria that are believed to be pathological to the periodontium were isolated
  2. Not all plaque is equally pathogenic
  3. Presence and increase of specific microorganism causes more destruction

Treatment: targeting and elimination of specific microoganisms using antimicrobials

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115
Q

What are the main points of the ecological plaque hypothesis?

A
  1. Disease is the result of an imbalance in the total micro-flora due to ecological stress
  2. Quantitative plaque increase changes local micro-environment promoting the growth of specific pathogens, qualitative shift
  3. Ecological factors such as the presence of nutrients and essential cofactors, pH and redox potential

Treatment: prevention of dental caries, modification of micro-environment to prevent nourishment of pathogens

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116
Q

Explain, briefly, the Yellow, orange and red groups that were suggest by Dr. Socranky research of 1998. Please include the names of at least 3 different bacteria in all of the groups.

A
  1. The yellow, orange and red groups are suggested groups of bacteria that are associated with periodontal health and pathology
  2. Yellow group - include: S. Mitis, S. Oralis and S, Snagius - are early coloniser groups that are related to healthy periodontium
  3. Orange group - include: P.Intermedia, P.Nigrescens and F. Nucleatum - are late coloniser that are believed to be an intermediate step and are able to facilitate red group (the most pathogenic group) in binding in the periodontal pocket
  4. Red group - include: P. Gingivalis, T.Forsythia, T. Denticola - believed to be the most pathogenic group
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117
Q

What is the microbial virulence?

A

Virulence is defined as the degree of pathogenicity of the ability of the organism to cause disease measured in experimental procedures.

Organism need to:

  1. Attach and colonise
  2. Multiply and gain access to appropriate nutrition
  3. Evade host defences
  4. Propagate
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118
Q

What is A. Actinomycetemcomitans?

A

A. Actinomycetemcomitans or AA is a gram negative anaerobe that is associated with localised aggressive periodontitis.
Able to produce high level os leukotoxins thus causes the lysis of PMNs.
It is equiped with adhesis and invasisn which means it can penetrate the tissue and attach to the space it has penetrated

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119
Q

What is P.Gingivalis?

A

P. Gingivalis is a gram negative anaerob that is associated with periodontits (around 79-90% of perio cases will have this bacteria)
Main cause of the inflammation to the tissue - release of endotoxin (name: P.Gingivalis LPS)
Contains invasins, adhesins and also collagenases which degrade connective tissue.

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120
Q

What are the main points of the Keystone Pathogen Hypothesis & Polymicrobial synergy and Dysbiosis Model?

A
  1. Keystone pathogens (e.g. P.Gingivalis) trigger inflammation even in low numbers
  2. Causes normal microbiome to become dysbiotic
  3. Manipulation of native immune responses of host
  4. Inflammatory byproducts sustain dysbiotic microbiota

Treatment: host modulation in adjunct to direct antimicrobial measures

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121
Q

What are the stages of the IMPEDE model

A

Stage 0 - gingival and periodontal health
Stage 1 - gingival inflammation
Stage 2 - Polymicobial emergence
Stage 3 - Inflammation - mediated dysbiosis - initial perio
Stage 4 - Late stage periodontitis

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122
Q

What is the consensus on how periodontal destruction actually occur?

A

It is widely believed that periodontal destruction occurs due to effects of the immune response and not directly due to bacteria. 80 immune response, 20 bacteria.

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123
Q

What is the aetiology of periodontitis?

A
  1. Predominance of PMNs in pocket epithelium/activation in connective tissue
  2. Elevated activity of macrophages
  3. Plasma cells dominate the infiltrate
  4. Increase of pro-inflammatory cytokine production (like IL-6 and IL-8 and more)
  5. This results in disturbed tissue homeostasis leading to destruction of collagen, connective tissue matrix and bone
  6. This results in true pocket development from the junction epithelium
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124
Q

What are MMPs?

A

Matrix metalloproteinases (MMPs) are a large family of calcium-dependent zinc-containing endopeptidases, which are responsible for the tissue remodeling and degradation of the extracellular matrix (ECM), including collagens, elastins, gelatin, matrix glycoproteins, and proteoglycan.

They are regulated IL-6 and IL- 8.

They are released by many cells like PMNs.

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125
Q

What causes bone resorption?

A
  1. RANKL - produced by osteocytes in large quantities, due to stimulation of pro-inflammatory cytokines like IL-6 and IL-8, able to activate osteo clasts - bone resorbing cells
  2. RANK - receptor on osteocalst - binding site of RANKL
  3. OPG - scavenger receptor that prevents RANKL binding thus preventing bone resorption

RANKL:OPG ratio: relative amount regulate the bone turn over

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126
Q

What is a risk factor?

A

Health risk factor are attributes, characteristics or exposures that increase the likelihood of a person developing a disease or health disorder.

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127
Q

What are some of the pre-disposing factors for periodontitis?

A

Any factor that result in retention of biofilm or prevents ts removal thus predisposing for disease progression.

E.g.:

Anatomical factors: root proximity, tooth malposition, concavities and furcation

Aquired/Iatrogenic factors: overhangs, open contacts and appliances

All this needs to happen in a susceptible host.

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128
Q

What are modifying or systemic factors?

A

They are factors that modify disease expression and may influence disease progression by altering host’s immune response
e.g. in periodontitis: smoking and diabetes

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129
Q

How does smoking increases the risk of periodontitis and by how much on average does it increase the instance of periodontitis according to latest studies?

A

The mechanisms:
1. Chronic reduction in blood flow and vascularity
2. Increase the prevelance of potential periodontal pathogens in the sulcus
3. Shift in neutrophil function towards destructive activities
4. Shift to a dysbiotic, pathogen enriched microbiome
5. Affects PMNs making them more aggrevated
6. Increase the number of aggravated T cells that produce inflammatory cytokines

It increases the risk of periodontitis by 85%!

Smoking cessation has beneficial effect on therapy outcomes and disease progression - this should be attempted for patient with nicotine dependence/

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130
Q

What are two useful statistics to give to a smoker patient in order to discourage them from smoking?

A
  1. Regular smokers have around 50% less improvement in clinical parameter after nonsurgical therapy
  2. Regular smoker have 2x implant failure rate compared to nonsmokers
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131
Q

How does diabetes increases the risk of periodontitis and by how much on average does it increase the instance of periodontitis according to latest studies?

A
  1. No solid evidence of causal relationship between poorly controlled diabetes and periodontal microbial dysbiosis in humans, but there some evidence in vitro thus it is biologically plausible
  2. Osteogenesis reduction due to apoptosis of osteoblasts and PDL fibroblasts
  3. Increase in RANKL expression and OPG expression is decreases
  4. Increase in collagenase activity

It increases the risk of periodontitis by 3x to 4x!

Multidisciplinary control and treatment of diabetes is ESSENTIAL to treatment of periodontitis.

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132
Q

What can be seen intraorally in a patient with diabetes and perio?

A
  1. No specific phenotypic features
  2. Pronounced clinical and radiographic signs
  3. Signs of progression
  4. Multiple reoccuring periodontal abscesses
  5. Unpredictable responses to therapy
  6. Increases risk of future attachment loss

If you suspect undiagnosed or poorly controlled diabetes, refer to GP for further investigations or management

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133
Q

What is the relationship between diabetes and periodontitis?

A

There is a bi-directional relationship between diabetes and periodontitis, meaning improvement in diabetes improve periodontitis but also improvement in periodontitis improve diabetes!

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134
Q

How do you write a diagnostic statement for periodontist modified by diabetes?

A
  1. Type of periodontal disease
  2. Disease extent
  3. Stage
  4. Grade
  5. Current disease status
  6. Risk factor profile

E.g.
Periodontitis: generalized (65%), Stage III (CAL <10 mm), Grade C (HbA1c 8.9%), currently unstable (PPD <8mm, BOP 45%).
Risk factors: uncontrolled diabetes (HbA1c 8.9%), smoking 20 cig/day, high strss levels (change in work)

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135
Q

How do we calculate clinical attachment loss?

A

Pocket depth + recession or pocket depth - over growth or pocket depth

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136
Q

Is periodontal disease rare ?

A

No - very very common - both gingivitis and perio are pretty common

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137
Q

What is prevalence?

A

It refers to the total number of individuals in a population who have a disease or health condition at a specific period of time, usually expressed as a percentage of the population.

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138
Q

What is incidence?

A

It refers to the number of individuals who develop a specific disease or experience a specific health-related event during particular time period.

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139
Q

What have the 70-80s research into Sri Lankan tea labourers showed us?

A
  1. 10-15% resist periodontitis
  2. 10-15% have rapid progression
  3. 70-80% have moderate progression
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140
Q

How can you link back the instances of severe periodontitis with the current classification standards?

A

It was discovered, that on avergaere, people with sever cases of periodontists have attachment loss of around 0.45mm per annum.

Thus in the new classification, Grade C (fast progressing) is considered to be when an individual has a rate of progression of more than 2mm per 5 years (5 x 0.45)

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141
Q

What is one of the findings from studies relating to periodontal health in Australia?

A

Rates of periodontitis have remained relatively the same yet the tooth retention rate has been improving

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142
Q

What levels are we aiming at when we are discussing a plaque index?

A

We are aming at below 20% as it is essential for stable periodontal and peri-implant health over the long-term.

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143
Q

What is the 2017 Periodontits Case definition?

A

1.Interdental CAL detectable at 2 non adjacent teeth

or

  1. Buccal or oral CAL above or equal to 3mm with pocketing equal or more than 3mm at 2 or more teeth

AND

OBSERVED CAL CANNOT BE ASCRIBED TO NON-PERIODONTITIS CAUSES: SUCH AS VERTICAL ROOT FRACTURE/S

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144
Q

What is one of the findings from studies relating to periodontal health in Australia?

A

Rates of periodontitis have remained relatively the same yet the tooth retention rate has been improving

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145
Q

What levels are we aiming at when we are discussing a plaque index?

A

We are aming at below 20% as it is essential for stable periodontal and peri-implant health over the long-term.

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146
Q

What BOP score are we aiming to achieve?

A

BOP score of less or equal to 20% because that is associated with significantly lower risk of CAL progression and want the score to decrease continuously and keep stable.

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147
Q

What the Community Periodontal Index of Treatment Needs codes and what treatment do they need?

A

Code 0 - healthy - treatment: home care
Code 1 - bleeding on probing but no attachment loss - treatment: oral hygiene instructions
Code 2 - calculus present + BOP - treatment: calculus removal and scaling + OHI
Code 3 - pockets of below 5 mm - treatment: calculus removal and scaling + OHI
Code 4 - pockets of above 6 mm - treatment: complex therapy + calculus removal and scaling + OHI

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148
Q

What is the second group of systemic disease and conditions that relate periodontitis?

A

They are some relatively common systemic conditions that have a moderate impact on prevalence / severity of priodontitis.

These diseases usually have an influence on the parthenogenesis of periodontal disease.

Some of these disease and disorders are:
1. Diabetes
2. Obesity
3. Osteoporosis
4. Arthritis - could through are process of inflammatory aggravation called citrulination
5. Stress and depression
6. Hypertension - maybe but probably not - but people with perio are more likely to have hypertension

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149
Q

What is the third group of systemic disease and conditions that relate to peridontitis?

A

They are systemic or local conditions that mimic periodontitis and cause destruction of periodontal attachment. They are independent of plaque induced periodontitis and cause periodontal tissue damage through other mechanisms.

Some of these disease and disorders are:
1. Neoplasm that originate from the gingival and may resemble perio
2. Giant cell granuloma and many other very rare diseases that may mimic symptoms and signs of perio

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150
Q

What is the theory of “direct pathway” that connects periodontal health with systemic health?

A

It believed that due to increased number of bacteria and smaller barrier to penetrate (ulcerated epithelial pocket lining).
1. The ulcerated periodontal pocket liing acts as a gate for viable bacteria, bacterial toxins/componetns
2. It results in frequent transient bacteremia
3. And could result in substantial systemic inflammatory response

This pathway also goes via other organs and systems like during swallowing or inhalation.

Important to understand that systemic bacteraemia as a result of periodontal infection is rare.

There is actually a way you can calculate periodontal inflamed surface area thus it is important to reduce that area with treatment.

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151
Q

What is the theory of indirect pathway?

A

It also relates to the periodontal inflamed surface area.

It is a theory that states that affects on the systemic health from periodontal disease result due to pro-inflammatory mediators that are involved in periodontitis.

Less plausible than the direct pathway.

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152
Q

What is the association between periodontitis and atherosclerotic coronary vascular disease?

A

AVD is the most common form of death worldwide.

It is a result of vascular inflammation and subintimal lipid accumulation which could result in build up of atheroma, stenosis of the valves, rupture of blood vessels and thrombosis.

There is some evidence to suggest there is association between the A.a. bacteria and P. Gingivalis being recovered from human atheromas. Thus an increase in those bacteria may result in increases risk of atheromas. These bacteria may effect the endothelia walls, immune function, impact macrophage function through different mechanisms.

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153
Q

What are some of the steps that need to be taken for a patient with AVD as soon as they have been diagnosed with the condition?

A
  1. Periodontal health needs to be assesed
  2. A treatment plan with focus on prevention should be constructed
  3. Combination of at home and in chair procedures must be performed to maintain good periodontal health thus reduce the risk of AVD worsening
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154
Q

What is the association between periodontitis and diabetes?

A

Periodontitis and diabetes have a bilateral relationship thus an improvement in one of them may result in improvement of the other

The process of periodontitis affecting diabetes:

  1. Periodontal infection causes elevation of serum pro-inflammatory cytokines
  2. Systemic inflammation leads to insulin resistance by blocking insulin receptors
  3. Bacterial dissemination may alter b cell secretion through b-cell dedifferentiation - also enzymes produced by P.Gingivalis may reduce glucose-induced insulin production
  4. There are also some evidence that P.Gingivalis may cause gut dysbiosis but take it with a grain of salt
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155
Q

What to do if a patient has uncotrolled diabetes?

A

You should do non-surgical treatment ad collaborate with GP and inform patient that perio help with diabtes

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156
Q

What is prognosis?

A

A prognosis s a prediction of the probable course duration, and outcome of a disease based on a general knowledge of the pathogenesis of the disease and the presence of is factors for the disease.

Prognosis is establish after diagnosis.

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157
Q

What s the difference between prognostic factors and risk factors?

A

Prognostic factors are characteristics that predict the outcome once the disease is present.

Risk factors are characteristics that put an individual at increased risk of developing a disease.

Sometime they are the same but sometimes they are different

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158
Q

How can we separate the types of prognosis?

A
  1. Overall prognosis - genetic conditions, patient compliance, age, patient expectation
  2. Individual prognosis - local prognostic factors (tooth positions, ppd, furcation etc.) and prosthetic/restorative factors (caries, endodontic status etc.)
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159
Q

What is the system of tooth prognosis by Nibali?

A

It is a very objective system that involves

  1. Bone loss
  2. Furcation and modbility
  3. PAI score
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160
Q

When should we extract a tooth?

A

Only teeth with hopeless prognosis and that are not favourable

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161
Q

When would you suggest an immediate extraction?

A
  1. Due to pain
  2. Due to acute abscesses
  3. If patient request due to other treatment like ortho
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162
Q

What is favourable periodontal disease progression?

A

It is when the periodontal status of the tooth can be stabilised with comprehensive periodontal treatment and periodontal maintenance. Future loss of periodontal supporting tissue in unlikely.

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163
Q

What is questionable periodontal disease progression?

A

It is when the periodontal status of the tooth is influenced by local and systemic factors that may or may not be able to be controlled. The periodontium can be stabilised.

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164
Q

What is unfavourable periodontal disease progression?

A

It is when the periodontal status of the tooth is influenced by local and/ or systemic factors that cannot be controlled.

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165
Q

What is the hopeless periodontal disease progression?

A

Only extraction may help

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166
Q

What are some of the goals of periodontal treatment?

A
  1. Absence of pain
  2. Reduction and elimination of infections and inflammation
  3. Cessation of attachment loss and gain of attachment
  4. Restoration of physiologic bone and gingival contour to aid plaque control
  5. Satisfactory function and aesthetic for the individual
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167
Q

How can you categories your perio treatment goals?

A
  1. Immediate goals
  2. Intermediate goals
  3. Long term goals

Remember - patient must know that periodontal treatment is not a one off - it is continuous

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168
Q

What are the steps of periodontal treatment for good and fair prognosis teeth?

A
  1. Initial therapy
  2. Revaluation or reassessment of prognosis
  3. Surgical or maintenance phase
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169
Q

What are the steps of periodontal treatment for questionable and unfavourable teeth?

A
  1. Plan potential abutment for rem/fixed prosthesis
  2. IF NOT, Initial therapy
  3. Revaluation or reassessment of prognosis
  4. Surgical (when pocket depth above 6mm) or maintenance phase (if pocket depth are below 6mm after treatment)
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170
Q

How to set up a case report for perio?

A
  1. Reason for referral
  2. CC
  3. MHx
  4. DHx
  5. Family Hx
  6. Diagnosis
  7. Oral hygiene
  8. Establishing goals and motivation
  9. Prognosis
  10. Treatment plan
    11 Treatment
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171
Q

How to set up a provisional treatment plan for perio?

A
  1. Emergency phase - e.g. exo
  2. Systemic phase - e.g. control systemic diseases
  3. Initial phase - e.g. testing and debridement
  4. Surgical phase - regenerative surgery
  5. Restorative phase - temporary crowns
  6. Maintenance phase - depending on risk close recall or normal recall
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172
Q

What are acute periodontal conditions?

A

They are conditions that are:
1. Rapid in development
2. Cause pain/discomfort
3. Rapid tissue destruction
4. Usually a result of infection

e.g. hepatic gingival stomtitis, necrotising gingivitis/periodontitis

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173
Q

What happens if a patient shows up to the initial treatment appointment with an active herpes cold sore?

A

Might need to postpone the treatment as the disease is in it’s most contageous stage - similar to other diseases like COVID 19

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174
Q

Would you give antibiotic prophylaxis to patient before root planing?

A

Yes you would if they have an underlying health condition.

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175
Q

What is the objective of the initial phase of therapy?

A

The objective is to achieve clean and infection free conditions for the oral environment by removal of soft and hard deposits and any retentive points and factors that might propagate them

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176
Q

What are the steps to the initial phase of treatment for Stage I-III of periodontitis?

A
  1. Patient self care and removal of biofilm by patient with - behavioral modification, mechanical (like brushing and using of inderdental brushes or other methods) and chemical (mouthrinse and oral irrigation)
  2. Supragingival scaling and reduce predisposing factors such as bad restorations - the evidence suggest that are not preffered way i.e 1 quadrant per session or half the mouth per session
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177
Q

What can you provide for pain management
for perio procedures?

A
  1. LA
  2. Topical
  3. Mouth rinse using cepacaine
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178
Q

What is the relationship between the pocket depth and the average percentage of root surface debrided?

A

With the increase of pocket depth - the amount of debridement usually goes down even with experienced operators

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179
Q

What are some of the difficulties with subgingival root plaining?

A
  1. Macromorphology of the roots - e.g. the mesial forcation of the upper sixes is quite deep and hard to get
  2. Micromorphology of the cellular cementum
  3. Irregular of the base of the pocket

Even with these problems, subgingival debridement seen to be incredibly useful in causing a reduction in bacteria levels and pathogenic bacteria like P.Gingivalis reduces

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180
Q

What are some of the factors that may impact outcome of non-surgical periodontal therapy?

A
  1. Smoking
  2. Number of roots on the tooth
  3. Plaque levels
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181
Q

What is one of the ways periodontal pocket repairs after the subgingival debridement?

A

Repair through long junctional epithelium:

It is a restoration of the continuity in the wound or defect area, without regeneration of the originally intact tissues from and function for example long junctional epithelial attachment with new collagen fibers parallel to it. Thus the periodontal pocket closes up.

Some of the tissue may actually reattach but it important for those tissues to not be infected.

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182
Q

What are some of the side effects of non-surgical therapy

A
  1. Reduction in gingival tissue due to reduced oedema - increase in th black triangle between teeth
  2. Increase in dentine hypersensativity due to damaged cementum that covers dentinal tubules
  3. OH may causes reduction in dentine like making those wedge like
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183
Q

What are some of the complexity factors could occur in the periodontium?

A
  1. Pocket depth and type (supraboney or infraboney)
  2. Vertical bone loss
  3. Furcation ivolvment
  4. Ridge defects
  5. Masticatory dysfunction
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184
Q

What are some of the common boney defects and how would you describe them?

A
  1. 3 Wall defect - balcony-like defect
  2. 2 wall defect - 2 roots of adjacent teeth are connected ( a little bit) or where is 2 walls of the defect
  3. 1 wall defect - might manifest itself as a v shape with a single wall

All defects must undergo non-surgical therapy.

The defects can be accessed using horizontal strokes, mini-currettes or special ultrasonic scalers.

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185
Q

What are some of the aetiology of furcation involvement?

A
  1. Periodontitis
  2. Endodontic infection
  3. Iatrogenic - rct perforation
  4. Anatomy - like enamel pearls
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186
Q

What are some of the anatomy that we must know for furcation involvement?

A
  1. Root fornix - the upper morst area of the furcation close to the crowns
  2. Root trunk - the area between the CEJ and the fornix
  3. Root divergence - the degree of separation between the roots
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187
Q

What is the disadvantage of a short root trunk length for furcation debridement?

A

A short root trunk length results in earlier furcation exposure but has better accessibility for treatment

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188
Q

Why do class 2 and 3 furcations have bad prognosis?

A

Because of biofilm accumulation and hardness of debridement

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189
Q

What are the advantages of access flap debridement?

A
  1. Improved access for professional instrumentation
  2. More efficient calculus removal
  3. Significant clinical improvements
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190
Q

What are other techniques that could be useful in improving the oral hygiene caee for furcations for a patient?

A

Tunneling technique - surgical exposure of inter-radicular space. Most common complication - root caries.

Root resection - for a patient with RCT and class 3 furcation

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191
Q

What occurs in the primary occlusal trauma and how does it affect the periodontal health?

A
  1. There is excessive occlusal force
  2. This results in acute inflammation and compression
  3. This lead to bone resoprtion and widening of the PDL with no clinical attachment loss
  4. When occlusal forces removed - PDL goes to normal
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192
Q

What occurs in the secondary occlusal trauma and how does it affect the periodontal health?

A
  1. Excessive occlusal force applies to healthy teeth, healthy gingiva on a reduced periodontium
  2. SImilar addaption and widening of the PDL with no clinical attachment loss
  3. When forces removed some bone apposition might occur

BUT when untreated periodontitis is involved:

  1. The occlusal forces may cause damage to the connective tissue supporting the teeth
  2. When occlusal trauma remove attachment is lost
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193
Q

What are clinical signs of occlusal trauma?

A
  1. Increased tooth mobility
  2. Tooth migration
  3. Fremitus positive
  4. Wear facets disproportionate to age or diet

Radiographicaly:
1. Widened PDL space
2. Angular bone loss
3. Thickened supporting alveolar bone

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194
Q

How should we treat mobile teeth?

A
  1. Treat the cause
    2.Periodontal surgery
    3.Splinting - remember to adjust the occlusion
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195
Q

What are the 2 main ways to apply antibiotics for periodontitis?

A
  1. Local - to the site
  2. Systemic - through the blood stream
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196
Q

What are the disadvantages of supragingival antibiotic application?

A

It does not create subgingival penetration thus will not greatly affect bacteria which affect periodontal disease.

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197
Q

What are the advantages and disadvantages of subgingival antiobitc application?

A

Advantages
1. high local concentration
2. Fewer side effect
3. Improved compliance

Disadvantages:
1. GCF clearance
2. Reinfection from untreated sites
3. Limited product availability

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198
Q

What are the advantages and disadvantages of systemic administration of antibiotics

A

Advantages:
1. can reach periodontal tissue
2. Easily available

Disadvantages:
1. Variable local concentration
2. Resistance
3. Systemic side effects

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199
Q

What is the recomendation in terms of use of oral antiseptics in conjunction with periodontal treatment?

A

They may be considered, in some cases, as adjuncts to mechanical debridement - cases like patient who cant perform proper mechnanical plaque control post surgery or necrotising periodontal disease or people with saviour arthritis

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200
Q

What are some of the challenges faced with use of antibiotic therapy on periodontal bacteria?

A
  1. There are thousands different types of periodontal bacteria present - hard to choose one antibiotic
  2. The bacteria reside within a biofilm thus they are harder to reach - THUS BIOFILM NEEDS TO BE REMOVED AND ANTIBIOTICS ADMINISTERED 24 HOURS POST DEBRIDEMENT
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201
Q

What is the common combination of anti-biotics used to treat periodontal disease?

A

Metronidazol & amoxicillin which is known as Winkelhoff cocktail - it is the most researched combination and also does produce clinically significant improvements

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202
Q

What are the recommendations of anti-biotic prescription for periodontal disease in Australia?

A

Amoxicillin 500 mg orally, 8-hourly for 7 days PLUS Metronidazole 400 mg orally, 12-hourly for 7 days

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203
Q

What patient should get anti-biotic therapy?

A
  1. Young patient
  2. Generalised severe periodontitis patient
  3. Patients with systemic diseases
  4. Rapidly progressing form
  5. Refractory/therapy-resistant forms of periodontitis
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204
Q

When should you recall the patient after completion of the innital phase of dembridment and provision of at home OHI?

A

After around 12 weeks in order to give the periodontium the chance to heal

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205
Q

What should you do after the patient has come back after the 12 weeks?

A
  1. Review MHx and risk factors
  2. Assess the OH performance
  3. Periodontal examination
  4. Re-evaluation - caries check, restorative and implant status
  5. Supportive periodontal therapy session - the aim of therapy is to have pocket of no more than 4 mm
  6. The third step can be taken aswell after another reassessment - this involves teeth that did not respond to therapy well and may need to address those remaining point of biofilm accumulation
  7. If the pocket are more than 6mm, surgeyr may be needed
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206
Q

What is supportive periodontal treatment?

A

It is treatment that plans to maintain already achieved goals with improvement of periodontal health. Patient should come back for assessment every 3-12 months depending on their risk profile )high risk - come every 3 months, low risk - every 12 months)

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207
Q

How can we evaluate risk of periodontal disease progression in the patient?

A

There dirrent matrix you can use to determine the recall frequency - a common one is the PRA (periodontal risk assessment) and it can be accessed online.

Preio-tools.com seems like the website to go to to find different matrix that may assist you.

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208
Q

What are the steps to a good supportive periodontal treatment session?

A
  1. Patient greeting and interview
  2. Review of medicla history
  3. Existing factors evaluation and counselling
    4, Clinical examination and re-evaluation: Oral Path, OH status, Perio exam, Caries check, fix-pros check
  4. Hygiene
  5. Motivation
  6. ALWAYS BOOK ANOTHER APPOINTMENT
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209
Q

Shouldyou probe all the teeth at SPT session

A

YES of course you should to understand the health of pockets - but you can choose not to do a brand new perio chart unless you find some findings

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210
Q

What would you mention to a patient who has periodontitis?

A
  1. Periodontitis - a disease that destroys the bone underneath the tooth
  2. Usually occurs from bacteria aggrevating the gums
  3. Aggrevating the gums leads to inflammatory condition - gingivitis
  4. When gingivitis is present with some underlying risk factors such as smoking, diabetes or immunuesupressed organism - periodontitis is caused
  5. Periodontitis is caused by the immune system trying to fight off the bacteria in the plaque - but not bring very mindful of the surrounding tissue
  6. Unfortunatley periodontitis is irreverisble - but if proper treatment - it can be slowed down or even arrested - thus we need to collaborate on this issure
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211
Q

What kind of model of progression is periodontitis believed to be?

A

Linear destruction model or burst destruction modle.

Phases of remission and exacerbation.

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212
Q

What are some of communication pathways between the pulp and periodontium?

A
  1. Apical foremen
  2. Dentinal tubules
  3. Accessory canals
  4. Lateral canals
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213
Q

What is the primary aetiology factors of endo-perio lesions?

A
  1. Endo or perio infection
  2. Trauma an/or iatriogenic trauma - like perforation during root canal treatment or root fracture or crack post RCT or root resorption
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214
Q

What is an endo-perio lesion?

A

An EPL (endo-perio lesion) is a pathological communication between the pulpal and periodontal tissues at a given tooth accompanied by a deep periodontal pocket and altered pulp sensitivity test that may occur in (symptomatic) acute or chronic (asymptomatic) form.

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215
Q

What is the endo-perio aetiology?

A
  1. Primary endo infection - carious lesions affect the pulp and secondarily affect the periodontium
  • Inflamed pulp exerts little or no effect on the periodontium
  • Necrotic pulp cause bone resorption
  • Sinus tract drain through PDL into gingival sulcus
  • Isolated periodontal defect
  1. Primary perio - periodontal disease introduces bacteria through different channels of communication in
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216
Q

What are some of the diagnostic hints that might lead us to see that the lesion is a primary endo secondary perio lesion?

A
  1. Pulp test negative
  2. Compromised coronal integrity
  3. Isolated deep narrow peridontal pocket - might need to use a guttapercha and take a PA
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217
Q

What is the treatment of primary endo secondary perio lesion?

A
  1. RCT
  2. No immediate scaling and root instrumentation - please await healing first - 3-6 months should be enough for healing and reassessment
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218
Q

What are some of the diagnostic hints that might lead us to see that the lesion is a primary perio secondary endo lesion?

A
  1. Sever periodontitis
  2. Pathological changes occur in pulp
  3. Retrograde pulpitis - acute pain for long duration
  4. Pulp test incoclusive
  5. Coronal integrity intact
  6. Deep periodontal pockets around the tooth
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219
Q

What is the treatment of primary perio secondary endo lesion?

A
  1. Scaling and root instrumentation needs to be done together with the root canal treatment

or

  1. Extraction depending on prognosis
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220
Q

What is the diagnostic clues of a combination endo-perio lesion?

A
  1. Pup test is negative
  2. Deep peridotnal pockets on multiple sites
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221
Q

What is the treatment for a combination endo-perio lesion?

A
  1. Scaling and root instrumentation needs to be done together with the root canal treatment
  2. Possible resective surgery
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222
Q

What is the treatment of fractures teeth?

A
  1. Do nothing
  2. Extraction
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223
Q

What is usually associated with hopeless prognosis of EPL?

A

EPLs that are related to aitriogenic damage.

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224
Q

How to write a diagnostic statement for a endo-perio lesion?

A
  1. Write that it is a endo perio lesiom
  2. Root damage extent
  3. Perio status of the patient
  4. Grade of the problem
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225
Q

What are the classifications of periodontal pockets associated with an endo-perio lesion associated with periodontitis patients?

A

Grade 1 - narrow and deep periodontal pocket in 1 tooth surface

Grade 2 - wide deep periodontal pocket in 1 tooth surface

Grade 3 - wide deep periodontal pocket in more than 1 tooth surface

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226
Q

What are the classifications of periodontal pockets associated with an endo-perio lesion associated with non-periodontitis patients?

A

Grade 1 - narrow deep periodontal pocket in 1 tooth surface

Grade 2 - wide deep periodontal pocket in 1 tooth surface

Grade 3 - deep periodontal pockets in more than 1 tooth surface

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227
Q

What are the difference between the periodontium in children comparing to adults?

A
  1. Gingival colour more reddish because of the thinness
  2. Rounded gingval margins
  3. Looser consistency
  4. Smoother surface
  5. Increase in attached gingiva
  6. Sulcus depth shallower
  7. Wider PDL space
  8. Prominent lamina dura
  9. Distance between CEJ to alveolar crest is less
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228
Q

What decreases the susceptibility to gingivitis in children?

A
  1. Thicker junctional epithelium
  2. T-cell dominated response
  3. Few B lymphocytes
  4. Less calculus build up thus less niches for bacteria to propagate
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229
Q

Why is there around 100% occurrence rate of gingivitis in kids going through puberty?

A

There is a theory that during puberty when tooth exfoliation occurs, due to some discomfort that may occure during the process - the brushing habit worsen in kids thus resulting in gingivitis.

Also fixed and removable orthodontic appliances contirute to this.

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230
Q

What are some of the other systemic factors that may contribute to development of gingivitis in young patients?

A
  1. Smoking
  2. Hyperglycemia
  3. Nutritional factors
  4. Pharmacological factors
  5. Sex steroid hormones
  6. Hematological factors like leukemia
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231
Q

How do we treat primary herpetic gingivostomatitis?

A

Primary herpetic gingivostomatitis is a disease that occurs after primary infection with herpes simplex virus

Treatment:

10-14 day duration

Control fever, pain and hydration

DO NOT TOUCH THE ULCERS

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232
Q

What do we classify any fast-progression periodontitis in young patients?

A

Grade C and we look at the underlying systemic conditions or genetic factors.

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233
Q

What is the BPE and how do we use it for paediatric patients?

A

BPE stands for basic periodontal examination and we use it as a code system similar to PSI!

Children with codes 0,1,2 should just have routine exams

While children with codes 3 & 4 should be undergoing consistent periodontal care to improve their condition

Note that some times Code 3 in a mixed dentition could be just erupting teeth so please be considerate.

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234
Q

What caution should we have in terms of perio and orthodontics?

A

The actual orthodontic process do not cause attachment loss but:
There needs to be cautious approach for patient with with thin periodontium phenotype as labial orthodontic movement in thin periodontal phenotype may result in bone dehiscence.

And presents of gingival inflammation or trauma may result in CAL.

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235
Q

What is pathological tooth migration (PTM)?

A

In significant periodontitis, the arch integrity may be compromised due to destruction of Sharpay fibres thus resulting in migration of the teeth.

The symptoms may be increase diastemas, drifting of teeth or collapsing of occlusal vertical dimension

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236
Q

What is the treatment of pathological tooth migration?

A
  1. Periodontal therapy - treating of Stage 4 perio is successful
  2. During ortho therapy - after periodontal stabilityis achieved - patient periodontal status needs to be closely managed by a periodontist - maintenance and interruption of ortho treatment is possible
  3. Life long orthodontic and periodontic care needs to be provided for the patient
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237
Q

What kind of instrument could you use of disturbing the biofilm in a patient with orthodontic appliances?

A
  1. Airflow instrument
  2. Different ultrasonic scalers
  3. Hand instruments - use appropriate size because it is generally difficult to debride
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238
Q

What is the supracrestal attached tissues?

A

It is the combination of junctional epithelium width and connective tissue attachment width

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239
Q

What happens when you place the restoration subgingivally inappropriately?

A

It results in violation of supracrestal attached tissues resulting in chronic inflammation and bone loss because the body ants to maint that SAT at around 2mm

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240
Q

How do we assess the SAT violations?

A
  1. Radiographic findings
  2. Clinical assessment - beeding on probing int he area, clinical attachment loss and pocket formation - debridement does not help the lesion
  3. Bone sounding - pass through the attached tissues witha
    sterile probe should be around 3mm from gingival margin - if the margin of the restoration and the alveolar crest have a distance of less than 2mm it is considered as a SAT violation - note that this is a guide, healthy alveolar crest could be upto 3mm below CEJ
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241
Q

What are the treatments of SAT violations?

A
  1. Consider restoring appropriately - please do not damage the tissues, remove the cement properly
  2. Re-establish SAT width by surgical crown lengthening or orthodontic extrusion
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242
Q

What are the steps to make a gingiva friendly temporary crown?

A
  1. Mark cervical margin and contact point
  2. Polish it
  3. Consider interdental papilla
  4. Polish it
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243
Q

How should you design a pontic?

A

It need to be hygienic in order to be cleaned.

Tell your patient to use super floss to clean under the bridge

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244
Q
A
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245
Q

What is this condition?

A

This is necrotising gingivitis. It is usualy caused by a presence of an opportunistic bacteria and an underlying stress factor.

Clinical features: necrosis of the papilla, sudden onset, ulcer covered by greyish pseudomembrane from surrounding mucosa

Treatment:

  1. OHI
  2. Debridement
  3. CHx
  4. Metronidozole 400mg 6 hourly for 5-7 days
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246
Q

What is this condition?

A

This is cancrum oris (noma) - it is a destructive condition involving oral soft tissues and jawbone.

Usually associated with children who are malnourished and have lower immunity due to systemic infections.

Thought to arise from NG

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247
Q

What is this condition?

A

This is actinomyces - an infection characterised by multiple foci of chronic suppuration.

Patient present with firm swelling commonly in the submandibular region with variable pain symptoms.

Treatment: prologned antimicrobial treatment after cultures

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248
Q

What are the histological features of Actinomyces?

A
  1. Chronic granulomatous inflammation surrounded by abundant granulation tissue and fibrosis
  2. Granules consisting of tangled meshes of organisms may be seen
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249
Q

What is syphilis and what are the 2 common types of syphilis?

A

It is a sexually transmitted disease that is cause by T. Pallidum

Two common types

  1. Congenital
  2. Aquired
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250
Q

What are some of the oral manifestations of congenital syphilis?

A
  1. Notched permanent incisors
  2. Hypoplastic first molars
  3. Saddle bone deformity
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251
Q

What are the lesion of the primary syphilis?

A

It is a chancre - which occurs at the site of primary inoculation 3-4 weeks after infection.

Lesions are high infectious - be careful!

Heals naturally

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252
Q

What are the lesion of the secondary syphilis?

A

They are usually described as some mucous patch, rash or condyloma lactum.

Usually occur 6-8 weeks after primary stage.

Still infectious - please be careful

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253
Q

What are the lesion of the tertiary syphilis?

A

They are called Gumma - they usually involve the hard palate perfiration or syphilitic glossitis

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254
Q

What are the oral manifestation of Tuberculosis?

A

Mulitlobular ulcerated growth due to immundeficency - histologically it is associated with granuloma inflammation.

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255
Q

What are the oral manifestations of Leprosy?

A

Nodular mucosa lesions are present in 20-60% of the patient

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256
Q

What are the aitological factors to Oral Candidosis?

A

Local factors:
- Poor denture hygiene
-Reduced vertical dimension
-Reduced salivary flow

Systemic factors:
-Extreme of age
-Endocrine disturbances
-Malnutrition
-Antibiotic therapy

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257
Q

What are the classifications of oral candidosis?

A
  1. Acute:
    - Atrophic (denture or antiotic-associated)
    - Pseudomembranous condidosis - thrush
  2. Chronic
    -Atrophic
    -Hyperpastic
  3. Mucocutaneous
    - Usually T cell deficiency
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258
Q

What is an Acute Atrophic Candidosis? What is the management?

A

It is a generalised, red focal area of red/inflamed oralmucosa.

This condition has no other specific symptoms other than pain.

Management:
-Correct diagnosis
-Oral denture hygiene
-Antifungal agents

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259
Q

What is the acute pseudomembranous candidosis or thrush?

A

it is most common type of acute candidiasis.

This is a lesion/lesions that is associated with soft, white/yellow plaque that can be lifted off the mucosa.

These plaques represent inflammatory exudate, dead cells and fungal colonies

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260
Q

What is the management of acute pseudomembranous cndidosis?

A
  1. Base your diagnosis on oral features and cytology smear
  2. Managment depedns on sverity of symptoms and predisposing factors:
  • for simple case - antibiotic therapy, topical antifungal agents and oral hygiene instructions
  • for a complex case e.g. patient with immunosuppression - medical consultation and topical/systemic antifungal agents
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261
Q

What is chronic atropic candidosis?

A

Chronic Atrophic Candidosis - is a non-specific red area in the mouth.

Some of the example of it is angular cheilitis

Take a smear.

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262
Q

Whatis a Chronic Hyperplastic Candidosis?

A

It is lesion/lesions that may occur anywere but are common to the tongue and buccal mucosa.

Present as white or mixed white/red patches or plaques on the mucosa.

THIS LESION CAN RESEMBLE OTHER PATHOLOGY - like lichen planus or early squamous cell cercinoma biopsy and re-biopsy after antifungal treatment

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263
Q

What can exfoliative cytology be used for?

A
  1. Fungal infections
  2. Bacterial infections
  3. Viral infections
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264
Q

What is one of the treatment of oral candidosis?

A

Miconazole 2% gel 2.5 mL topically (then swallowed), 4 times daily, after food, for 7 to 14 days; continue treatment for at least 7 days after symptoms resolve

Or Amphotericin B 10 mg lozenge sucked (then swallowed),4 times daily, 7 to 14 days; continue treatment 2 to 3 days after resolved

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265
Q

What is a treatment for a patient with angular cheilitis?

A

Miconazole 2% gel 2.5 mL topically (then swallowed), 4 times daily, after food, for 14 days; continue treatment for at least 14 days after symptoms resolve

or

Chlorimazole 1% cream topically to the angles of the mouth, twice daily for at least 14 days; continue treatment for 14 days after symptoms resolve

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266
Q

What are quite common viruses with oral manifestations?

A
  1. Herpes labialis
  2. HPV
  3. HIV
  4. Hep C
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267
Q

What is the basic progress of infection and manifestations with a herpes simplex virus?

A
  1. An inividual is seronegative
  2. Exposure to the virus occurs
  3. Primary disease - Subclinical Gingivostomatitis is considered to be primary disease
  4. An inidividual becomes seropositive
  5. Reactivation of the diseases (aka Secondary disease) may occur due to stressors - usually results in a cold sore
  6. Resolution of the cold sore - return to being seropositive
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268
Q

What is gingivostomatitis?

A

It is a widespread vesicular eruption involving skin, vermillion and mucosa.

It results in painful widespread infection that can be observed in the photo.

It is associated with young children or older adult who are immunocomprimised

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269
Q

What is recurrent herpes simlex vitus?

A

It is a vesicular eruption affecting perioral skin, lips, gignivae and palate - knowns as harpes labialis

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270
Q

What are the histological features of herpetic lesions?

A
  1. Intraepitheial vesicle formation - aka acantholysis
  2. The vesicles contain inflammatory cells and exudate
  3. Destruction of epithelial cells
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271
Q

What is the varicells virus?

A

It is also known as chicken pox!

It is a vesicular infection that migh have some oral mucosal involvement

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272
Q

What does the reactivation vericells virus lead to?

A

It leads to shingles.

Shingles may result in oral manifestations like vesicular lesiosn aorund the oral cavity.

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273
Q

What is a dermatome?

A

A dermatome is an area of sking that is associated with a root of a single neural connection to the spine or orofacial (cranial) nerves

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274
Q

What is Oral Hairy Leukoplakia?

A

It is a oral manifestation that relates to the Epstein Barr Virus and is associated with HIV invection

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275
Q

What is this condition?

Extra information: The patient is from Greece?

A

This a kaposi’s sarcoma - an oral lesion associated with Herpes Virus 8 - it is very aggresive in it’s course

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276
Q

What are the two conditions related to Coxsackie virus infections?

A
  1. Hand-foot-and-mouth disease
  2. Herpangina

Both are self limiting infections that effect children more than the adults

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277
Q

What do you usually associate infections with?

A

Systemic symptoms such as fever and enlarged tender lymph nodes.

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278
Q

What is the difference between true herpes infection ulcer and a herpetiform apthous ulcer?

A

True herpes infections come with systemic symptoms herpetiform does not

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279
Q

What are the most common origins of tumours in the oral cavity?

A
  1. Epithelial - related to the epithelial lining of the oral cavity, salivary gland, oeontogenic epithelium
  2. Mesenchymal
  3. Haemotlymphoid
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280
Q

What is a meaning of tumour?

A

Tumour - means swelling above the size of 2cm.

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281
Q

What is a meaning of a neoplasm?

A

Neoplasm - is a tumour that does not stop growing

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282
Q

What are the terminology of the bening and malignant tumours?

A
  1. Bening tumours have the suffix “…oma”
  2. Melignant tumours:
    - Epithelial tumours are “carcinoma”
    - Mesenchymal tumour have a suffic “…sarcoma”

The exeptions are: melanoma and lymphoma which are both malignant

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283
Q

What is the orgini of most benign fibromas in the oral cavity?

A

Most of them arise from fibropepithelials polyps and fibroepithelial hyperplasia

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284
Q

What is a solitary fibrous tumour?

A

The solitary fibrous tumours are benign neoplasms that arise from combination of altering hypocellular and hypercellular areas.

It consists of bands of hyalinised collagen in between spindle shaped cells.

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285
Q

What is a myxoma?

A

It is an uncapsulate lesion with infiltrative growth and stellate and spindle.

Occurs as bubbly in appearance.

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286
Q

What is a lipoma?

A

It is an uncommon lesion in the oral cavity - most commonly filled with adipose tissue (fat cells)

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287
Q

What are some muscle tumours?

A
  1. Leiomyoma - smooth muscle, benign neoplasm
  2. Leiomyosarcoma - smooth muscle, malignant neoplasm
  3. Rhabdomyosarcoma - skeletal muscle, malignant neoplasm
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288
Q

Whats is neurilemmoma?

A

They are benign neoplasm associated with schwann cells.

Could occur as a asymptomatic, submucosal mass

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289
Q

What is neurofibroma?

A

It is usually a multiple lesion - it is asymptomatic and is related to neurofribromatosis

This lesion could turn malignant

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290
Q

What is a granular cell tumour?

A

It is a painless smooth swelling on the tognue related to large granular cells.

Histologically it relates to hyperplasia in an odd way where it looks like it’s invading other tissue

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291
Q

What are oral potentially malignant disorders?

A

It is a clinical presentation that carry a risk of cancer development in the oral cavity whether in a clinically definable precursor lesion or in clincally normal oral mucosa.

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292
Q

What are risk factors for cancer?

A
  1. Tobacco
  2. Alcohol
  3. Betel-quid (tobaco in a different form) - bucal sulcus
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293
Q

What is the cinical spectrum of normal mucosa to erythroplkia?

A
  1. Normal mucosa
  2. Thin, smooth leukplakia
  3. Thick, fissured, leukoplakia
  4. Granular, verruciform leukoplakia
  5. Red tissue - erytholeukoplakia
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294
Q

What is a leukoplakia?

A

It is a predominantly white plaque of questionable risk having excluded other known diseases or disorders that carry no increased risk of cancer

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295
Q

What is proliferative verrucous leukoplakia?

A

Proliferative verrucous leukoplakia is a progressive, persistent and irreversible disorder characterized by the presence of multiple leukoplakia that frequently become warty.

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296
Q

What is eryhtroplakia?

A

Erythroplakia is a predominantly fiery red patch that cannot be characterized clinically or pathologically as any other definable disease

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297
Q

What is lichen planus?

A

A lichen Planus is a chronic inflammatory disorder of uknown etiology with characteristis relapses and remissions, displaying white reticular lesions, accompanied or not by atrophic, erosive and ulcerative and/or plaque type areas. Lesion are frequently bilaterally symmetrical.

Desquamative gingivitis may be a feature.

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298
Q

What condition is this?

A

This is an oral lichenoid lesion - which is similar to oral lichen planus but is usually around a single site.

Usually associated with medications and go away when medication is stopped

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299
Q

What is oral submucous fibrosis?

A

Oral submucous fibrosis is a chronic, insidious disease that affects the oral mucosa, initially resulting in loss of fibroelasticity of the lamina propria and as the disease advances, results in fibrosis of the lamina propria and the submucosa of the oral cavity along with epithelial atrophy.

Associated with tobaco products that stay in the crevaces of the oral cavity for a long time

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300
Q

What is actinic cheilitis?

A

Actinic cheilitis is a disorder that results form sun damage and affects exposed areas of the lips, most commonly the vermillion border of the lower lip.

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301
Q

What is dysplasia?

A

It is the presence of cells of an abnormal type within a tissue, which may signify a stage preceding the development of cancer.

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302
Q

What are some of the architectural changes that occur in dysplasia?

A
  1. Drop shaped rete pegs
  2. Irregular eppithelial stratification
  3. Loss of polarity in basal cells
  4. Increased number of mitotic figures
  5. SUPERFICIAL MITOSES
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303
Q

What are the cytological changes in dysplasia?

A
  1. Nuclear pleomorphism

2.Cellular pleomorphism

  1. Increased nuclear size
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304
Q

What are the the different types of dysplasia?

A
  1. Mild (grade I) - dysplasia is in the first third of the pithelium
  2. Moderate (grade II) - dysplasia entering the middle third of the epithelium
  3. Severe (grade III) - dysplasia near the basal layer
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305
Q

What is carcinoma in situ?

A

It is when dysplasia that has been only registered in one layer of the tissue but is through out the whole layer - the epithelium have not yet created island in the connective tissue below thus the basal layer has not yet been breached

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306
Q

How do you manage dysplastic lesions?

A
  1. Observation:
    - Mangaing lifestyle risk factors
    - Regular follow-ups
    -Clinical risk assessment

Excision
- Cold-knife excision
- Cryosurgery
- CO2 laser ablation
- Photodynamic therapy

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307
Q

What are risk factors for cancer

A
  1. Tobacco
  2. Alcohol
  3. Betel-quid (tobaco in a different form) - bucal sulcus
  4. Human Papillomavirus (HPV) types 16 and 18
  5. Ultraviolet radiation
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308
Q

What is the parthenogenesis of cancer?

A
  1. Loss of cell cycle control through loss of apoptosis proteins (p53) and up regulation of proliferation proteins - cell communication occurs
  2. Invasion and metastasis - through breach of basement membrane and over expression of oncogenic enzymes - metastasis could be distant
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309
Q

What is the clinical presentations of malignant lesions?

A

RULE acronym:

  1. Red/white
    2.Ulcer
    3.Lump

Exceeding 3 weeks in duration

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310
Q

What are some of the other presentations of oral cancer coudl arise?

A
  1. Non-healing extraction socket
  2. Pigemented lesion (melanoma) with irregular borders
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311
Q

What are the common sites for squamous cell carcinoma?

A
  1. Lower lip
  2. Tongue
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312
Q

What is the pathology of squamous cell carcinomal?

A
  1. Invasion of malignant epithelial
  2. Localised tissue destruction like bone erosion - floating tooth on the radiograph (primary intraosennous carcinoma
  3. Spread to the lymphatic system
  4. Distant metastasis
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313
Q

What is the grading of tumours?

A

It is a process of examining the degree of differentiation of cells

Grade 1 - well differentiated squamous cell carcinoma

Grade 2 - moderately differentiated squamous cell carcinoma

Grade 3 - Poorly differentiated squamous cell carcinoma

Grade 4 - anaplastic - fucked

The greater the grade the worst a prognosis

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314
Q

What are the 4 pathways of spread of an oral carcinoma?

A
  1. Direct extension into adjacent tissue
  2. Perineural infiltration
  3. Vascular invasion
  4. Lymphatics
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315
Q

What is the staging system used for oral cancers?

A

Based on TNM system
T is size
N is invasion of surrounding tissue
M is distant malignancies

Minimum is Stage 1: T1N0M0

Max Stage 4 : Any M

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316
Q

What is the survival rate of each stage of oral cancer?

A

Stage 1 and 2 - around 50% over 5 years

Stage 3 - 15-20% over 5 years

Stage 4 - less than 5% over 5 years

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317
Q

What is main treatment for patient with oral cancer?

A
  1. Initial diagnosis
  2. Definitive treatment
  3. Management of complications and monitoring
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318
Q

What are the actual treatment options for oral cancer?

A
  1. Surgery
  2. Radiotherapy
  3. Chemotherapy
  4. Combination of treatments above
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319
Q

What is the role of a general denstist for a patient with oral cancer?

A
  1. Detection of potentially problematic lesions and referral
  2. Management role - for any other oral concern, including complications from treatment of oral cancer
  3. Ongoing screening
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320
Q

What is the advantage of radiotherapy?

A

Radiation affect the ability of rapidly dividing cells to replicate, thus a tumour can not grow.

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321
Q

What is the disadvantage of radiotherapy?

A

Radiotherapy may also affect the salivary gland and mucosa - causing it to become atrophied and ulcerated

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322
Q

What is the effect of radiotherapy on salivary glands?

A
  1. Loss or atrophy of acini
  2. Inflammation
  3. FIbrosis
  4. Dilation of ducts
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323
Q

What is the effect of radiotherapy of the bone tissue?

A
  1. Endarteritis obliterans - destruction of blood vessels thus making the tissue depleted of oxygen and nutrients
  2. Osteonecrosis
  3. Infection and pain
  4. Can be potentially life threatnening
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324
Q

What is the common condition that may be caused by radiotherapy?

A

Radiation mucositis

325
Q

What are the side-effects of chemotherapy on the oral environment?

A
  1. Oral mucositis is common
  2. Salivary glands impairment
  3. Increase the rate infections and decreased rate of healing due to supressed immunity
326
Q

What is the management of side effects related to chemotherapy?

A
  1. Prevention of oral infections
  2. Maintenance of oral hygiene - basic oral care
  3. Supportive treatment
327
Q

How do we prevent a patient from having sever cancers?

A
  1. Primary prevention - reducing the risk factors - tobacco control, healthy eating, reduced exposure to sunlight, inherited risks
  2. Secondary prevention - early detection
328
Q

What are the 5 categories of most frequent lesions of the oral cavity?

A
  1. Apthous ulcers
  2. Herpex simplex lesions
  3. Trauma associated lesions
  4. Migratory glossitis
  5. Candidiasis infection lesions
329
Q

What is oral granulomatosis?

A

It is a process where multiple granulomas can be seen in the oral cavity.

Associated with:

Crohn’s disease

Leprosie

TB

330
Q

Give 5 differential diagnosis for a white lesion

A
  1. Leukodema
  2. Leukoplakia
  3. Lichen Planus
  4. Frictional keratosis
  5. Oral squamous cell carcinoma
331
Q

Give 5 differential diagnosis for red lesions

A
  1. Pyogenic granuloma
  2. Haemangioma
  3. Peripheral Giant Cell Granuloma
  4. Erythroplakia
  5. Oral squamous cell carcinoma
332
Q

Give 5 differential diagnosis for a pigmented lesion?

A
  1. Oral melanotic macule
  2. Mucosal melanocytic naevus
  3. Amalgam tattoo
  4. Malignant melanoma
  5. Smokers melanosis
333
Q

Give 5 differential diagnosis for a gum lump?

A
  1. Haemangioma

2.Fibroepithelial polyp

  1. Pyogenic granuloma
  2. Peripheral giant cell granuloma
  3. Calcifying fibroblastic granuloma
334
Q

Give 5 differential diagnosis for an ulcer?

A
  1. Herpetiform ampthous ulcer
  2. Mild amthous ulcer
  3. Major ampthous ulcer
  4. Traumatic acute ulcer
  5. Traumatic chronic ulcer
335
Q

What lesion is associated with human papilloma virus?

A

Squamous papilloma.

An asymptomatic, solitary lesion that is associated with cauliflower like apperance

336
Q

What are the histological features of squamous papilloma?

A

Exaggerated growth of usually parakeratinsed benign squamous epithelium.

Finger-like projections of epithelium with central cres of fibrovascular tissue

337
Q

What is the link between HPV and cancer?

A

Sometimes HPV can playe a role in oropharyngeal carcinoma - which is a basaloid subtype of squamous cell carcinoma.

338
Q

What is another type of lesion that can be caused by HPV?

A

Genital warts in the mouth or Oral Condyloma Accuminatum.

It is an infections lesion that can cause transmission through direct contact.

It presents as a broad based pink nodule that grows and coalesce (come as one)

339
Q

What are the two haematolynphoid tumours?

A
  1. Non-Hodgkin lymphoma
  2. Hodgkin lymphoma
340
Q

What are the oral manifestation of non-hodgkins lymphoma?

A

Large ulceration, swelling, pain, paraesthesia and losse teeth
Aetiology is unknowns

341
Q

What is the main feature of oral malignant melanomas?

A

They have a defused appearance

342
Q

What does lichen planus mean?

A

Flat fungus - it is originally a tree disorder and IS NOT A FUNGUL INFECTION IN THE MOUTH

343
Q

What are the most common lichen planus lesion appearances

A
  1. Striated lesions
  2. Erosive/ulcerative lesions - THESE ARE PAINFUL
  3. Atrophic lesion
344
Q

What is lichen planus in oral pathology terms?

A

Oral lichen planus is a common immune-mediated (NOT AUTOIMMUNE) mucosal disease. It has an incidence of around 2.2%.

It is a chronic disease, often bilaterla and symmetrically distributed.

Common sites: buccal mucosa, dorsal surface of tongue and gingiva.

Could be triggered by medication, dental materials, mints and cinnamon

345
Q

What are clinical features of oral lichen planus?

A
  1. Striae - most common, sharply defined and do not disapear when whiped
  2. Atrophic areas - read areas and thin mucosa
  3. Erosive areas - shallow area of ulceration
  4. White plaque - think about leukoplakia
346
Q

White kind of appearance can the gingiva be if it is affected by lichenoid inflammation?

A

Desquamative gingivitis appearance - atrophic and “raw”.

Remember that this is not exclusive to lichen planus

347
Q

What are some of the other, extraoral signs of lichen planus?

A

Cutaneous lesion on the flexour surfaces of the body.

Purple papules, scaly lesions.

Look at patients wrists

348
Q

What is the pathology of lichen planus?

A
  1. Migration of T-lymphocytes into the epithelium
  2. Epithelium basal cell layer destruction - the stems cells within the basal cells are lost
  3. Epithelium becomes thinner and keratinised
  4. Further lymphocytes recruitment forms dense infiltrate below the epithelium
  5. Immune reaction leading to keratinocyte destruction
349
Q

What are the option of clinical diagnosis of lichen planus?

A
  1. Very good medical history - all contact reactions, time noticed
  2. Histopathology - request histopathology after biopsy
  3. Immunofluorescence studies - pathology LAB ONLY - in lichen planus it is deposition of fibrinogen along the basement membrane - it appears shaggy

But the most important part - DISCLUDE ALL OTHER WHITE LESIONS THAT ARE SIMILAR

350
Q

What is immunofluorescence or immunohistochemistry?

A

It is a test that can be used for autoimmune disease as well immune mediated conditions (such as lichen planus).

For this test - pathology lab needs to pick u the sample on the day or you need to do it asap with prior fixing in paraformaldehyde 4% at room temperature

351
Q

What do we look for in autoimmune diseases?

A

Auto-antibodies - self anti-bodies that attack self cells.

352
Q

What is the aetiology of lichen planus?

A

The main factor and process is not known but we have some associations.

353
Q

What are the differential diagnosis for a lesion that is similar lichen planus?

A
  1. Lichen planus
  2. Lupus eythematosus
  3. Cheek biting/ frictional keratosis
  4. Graft versus host disease
  5. Candidosis
  6. Idiopathic leukoplakia
  7. Squamous cell carcinoma
  8. Chronic ulcerative stomatitis
354
Q

What are the steps to diagnosis of lichen planus?

A
  1. History of drugs and/or systemic illness
  2. Location/pattern of lesions
  3. Histopathology and immunofluorescense
355
Q

What is the reported rate of transformation rate of lichen planus into a malignancy?

A

Around 0.44%.

356
Q

What do you do if you confirm lichen planus?

A
  1. Long term monitoring
  2. Reducing factors associated with lichen planus such as tobaco or other
  3. Control of symptoms - use CHx and maybe avoid certain foods. Use Corticosteroids, topical injection, antifungal therapy.
357
Q

What are the topical steroid used for lichen planus?

A

Betamethasome dipropionate 0.05% cream or ointment topically to the lesions, twice daily after meals, until symptoms resolve

358
Q

What is lupus erythematosus?

A

It is an autoimmune disease.

Two main forms: Systemic lupus erythematosus and discoid (cutaneous) lupus ertyhematosus

359
Q

What can you see histologically around lichen planus?

A

Melanin continetns - proliferation of melanin around the lichen planus.

This may be also een clinically - post inlammation pigmentation

360
Q

What is aetiology of lupus?

A

Unclear but it does have auto antibodies circulating and it is genetic in nature

361
Q

What is the common presentation of discoid lupus eythematosus?

A

They appear disc in shape and similar in appearance to lichenoid lesions but with some epidermal lesions also present in sun exposed areas.

362
Q

What is some of the common aspects of discoid lupus erythematosus lesions orally?

A

Common in buccal mucosa, gingiva and vermillion.

Plaque or erosions

White keratotic stria

363
Q

What are some of the common aspect of histology of discoid lupus erythematosus lesions?

A

Similar to lichen planus but the sub-epithelial band is not as uniform than in lichen planus.

Also - lupus band test that is shown in immunoflurescence due to deposition of immunoglobulin and C3 - very very distinct unlike the shagging like in lichen planus

364
Q

What are the clinical features of systemic lupus erytehmatosus?

A

Butterfly rash in young woman - could be the first sign.

Oral ulcers - pretty common

365
Q

What is the most important difference between discoid and systemic lupus erythematosus?

A

In discoid lupus erythematosusthere are no major systemic sympotms while the systemic one ususally present with systemic symptoms

366
Q

What is erythema multiforme?

A

It is a self limiting hypersensitivity reaction which presents itself as recurrent oral ulceration and blistering.

Cell-mediated hypersensitivity reaction - usually trigered by drugs and viruses.

367
Q

What some of the intra-oral and extra-oral manifestations of erythema multiforme?

A
  1. Oral lesions - swollane and crusted lips that are bleeding - widespread erosive lesions and lots of pain
  2. Cutaneous lesions - “target lesions”
368
Q

What is the histology of erythema multiforme?

A
  1. Keratosis at the top
  2. Apoptosis of basal keratinocytes
  3. Intraepithelial vesicle formation
  4. Lymphocyte and macrophage perivascular inflitrate in connective tissue
369
Q

What is important to ask a patient that you suspect has erythema multiforme?

A

Previous virus or drug use history

370
Q

What is Steven Johnson syndrome?

A

It is a more advanced systemic form of erythema multiforme and it can progress. PLEASE LET THE GP KNOW DUE TO SIGNIFICANT RISK OF DEATH

371
Q

For which drugs could there be a lichenoid drug reaction?

A

ACE inhibtors, NSAIDS, Tetracyclines and many more

372
Q

What oral lichenoid contact lesions?

A

They are lichenoid lesions that may occur due to contact with dental materials.

HISTORY and EXAMINATION is essential

373
Q

What do autoantibodies attack?

A

The usually attack desmosomes that combine cells - and create blister or vesicles

374
Q

What is a vesicle?

A

It is a blister less than 5mm in diameter

375
Q

What is a bulla?

A

It is a blister more than 5 mm diameter

376
Q

What is acantholysis?

A

It is a blister that separates keratinocytes

377
Q

What is pemphigus vulgaris?

A

Pemphigus is a group of potentially life threatening disease that has an autoimmune basis.

The autoantibodies attack the desmosomes (desmoglein 1 & 3 types) between the cells.

Clinical features - very fragial oral mucosa - think Nikolsky sign and widespread painful erosion.

Very bad because they may cause infection

378
Q

What is mucous membrane pemphigoid?

A

It is a chronic subepidermal/subepithelial blistering, scarring autoimmune disease with a predilection for stratified squamous mucous membranes and occasionally skin.

This conditions attacks hemidesmosomes - the conectors between the basal epithelium and the connective tissues.

This conditions can result in OCULAR SCARRING - VISION WILL BE AFFECTED.

379
Q

What are the clinical features of pemphigus?

A
  1. Very fragile blistering intraepithelialy
  2. Residual erosion
  3. Nikolsky sign - rub the tissue and blister signs appears
380
Q

What are some of the other signs of pemphigus extra-oraly?

A
  1. Erisions and crusts on the face
  2. Extensive denudation of the entire neck and back
  3. Distal onychodystrophy and transverse Beau’s line of the thumb nails
  4. DIrect immunofluorescence microscopy of a perilesional biopsy soecimen shows intercellular deposits of IgG in the epidermis - CHICKEN WIRE PATTERN
381
Q

What are some of the histological features of pemphigus?

A
  1. Loss of intercellular adhesion
  2. Acantholysis
  3. Tzanck cells - detached epithelial cells
  4. Intraepithelial blisters
382
Q

What is the management of pemphigus vulgaris?

A
  1. Early diagnosis is important - differentiation from other veisculobullours diseases. Biopsy of perilesional mucosa with immunofluorescence studies -INCISIONAL BIOPSY OF NON-ULCERATED TISSUES
  2. Topical steroids in combination with systemic treatments
  3. Systemic steroid and immunosuppressive agents
383
Q

What are the clinical features of mucous membrane pemphigoid?

A
  1. More common in females
  2. Oral ucosa often first site of involement erosion on non-keratinised mucosa desquamative gignivitis.
384
Q

What is histology pemohigoid?

A

There is a large loss of attachment and separation of full thickness of pithelium from connective tissue at the basement membrane. With the epithelium forming the rooft of the blister

385
Q

What is the treatment of mucous membrane pemphigoid?

A

For only oral lesions:
Topical steroid

For widespread lesions:
1. Systemic steroids
2. Immunosuppressive medication

Referral to the specialist

386
Q

What are diagnostic steps of mucous membrane pemphigoid? Why should we refer these patient to a specialist?

A

Incisional biopsy of non-affected area - looking for gravestone appearance. This occurd due to binding of immunoglobulin to the basement membrane.

Because MUCOUS MEMBRANE PEMPHIGOID MIGHT EFFECT THE EYES.

387
Q

Where are the minor salivary glands?

A
  1. Oral mucosa
  2. Pharynx and tonsillar area
  3. Larynx, trachea, major bronchi
  4. Nasopharynx, nasal cavity and paranasal sinuses
388
Q

What are some reactive salivary gland lesions?

A
  1. Mucoceles:
    - Mucus extravasation mucocoeles
    - Mucus retention cyst
  2. Necrotising sialometaplasia
  3. Radiation related lesions
  4. Salivary gland obstruction
389
Q

What are some infective salivary gland lesions?

A
  1. Mumps
  2. Bacterial parotitis
390
Q

What are some of the miscellaneous salivary gland lesions?

A
  1. Age-related changes to the salivary gland
  2. Sialadenosis
391
Q

What is mucoele?

A

It is a clinical term that includes mucus extravasation pehnomenon and mucus retention cyst

392
Q

What are the histological differences between serous and mucus acinii?

A

Serous - more purple like shown in picture on the left

Mucus - more pale and bubbly like shown on the right

393
Q

What is ranula?

A

It is a clinical term that includes mucus extravasation phenomenon and mucus retention cyst - however it occurs specifically in the floor of the mouth

394
Q

What are clinical features of mucus extravasation mucocoele?

A
  1. Most common in the lower lip
  2. Painless smooth-surfaced mass
  3. May have bluish colour
  4. consistency - fluid like
  5. Associated with trauma
  6. NOT A TRUE CYST - granulation tissue capsule
395
Q

What is the most basic explanation of formation of a cyst from a salivary gland?

A
  1. The duct of the salivary gland is damage
  2. The saliva in able to float in the surrounding tissue - mucus extravasation
  3. Saliva accumulates
  4. Inflammatory reaction begins - granulation tissues forms - reactive change to saliva gland occur (acinar atrophy and inflammation)
396
Q

What a cyst?

A

It is a fluid filled cavity that may or may not be lined an epithelium (true cyst have an epithelium) that is abnormal in nature.

Note - the fluid is not puss -

397
Q

What is a mucous retention cyst?

A

It is a cyst that occurs during the obstruction of salivary flow

It is less common than extravasation mucocoeles.

The mucosa is intact and the cyst is not surrounded by granulation tissue.

Acinnar inflammation will still occur.

398
Q

What is meal time syndrome?

A

A sialolith is present in the salivary gland - during meal time salivary flow increases - resulting in a mucus retention cyst - this condition is known as sialadenitis

399
Q

What is the treatment for sialoliths?

A

Surgical removal of stone with/without gland

400
Q

What is necrotising sialometaplasia?

A

It is one of the mimics of oral cancer but it is a benign condition which usually affect the palate.

Aetiology - slaivary gland ischaemia due to local trauma - LOCAL ANAESTHETIC - salivary gland inferction characterised by loss of acini and inflammation with ductal mataplasia - cuboidal and columnar epithelium becomes squamous

401
Q

What is the histological appearance of necrotising sialometaplasia?

A

Squamous metaplasia of ducts mimicking invasive squamous cell carcinoma - but main difference is there no major cellular atypia

402
Q

What is mumps?

A

It is a disease that mainly affect the parotid gland.

It is caused by a paramyxovirus

Acute onset with pain and bilateral parotid swelling, difficulty swallowing and fever.

Management: rest, lots of fluid, management of pain and antipuruetic

403
Q

What is acute bacterial sialadentitis?

A

It is bacterial infection of the salivary glands that may be caused by xerostomia or sialoliths.

Might have systemic symptoms

Management: Antimicrobilas and drainage of the puss

404
Q

What is the most common salivary gland to get a sialolith?

A

Submandibular, because:

  1. The duct is bent
  2. Gravity - the duct that come out sublingually is affected by it
  3. Content is mainly serous
405
Q

What are some of the age related changes of the salivary glands?

A
  1. Acinar atrophy
  2. Fibrosis
  3. Fatty infiltration
  4. Diffuse chronic inflammatory infiltrate
406
Q

Why is there high risk of xerostomia post head and neck radiation therapy?

A

Patient with head and neck cancer that recieved radiation therapy may have atrophy of acini - thus are unable to produce saliva

407
Q

What is xerostomia?

A

It is the experience of a patient associated with dry mouht - aka it is a symptom

408
Q

What is salivary gland hypofunction?

A

It a decreased flow rate of saliva due to a multitude of factors - aka it is sign

409
Q

What are the three main causes of xerostomia?

A
  1. Organic cause - disease
  2. Functional cause - dehydration and so on
  3. Drugs - like diuretics, SSRIs and other
410
Q

How can you investigate salivary gland disease?

A
  1. Salivary flow test - unstimulated flow of less than 0.1-0.2mL/min , stimulated less than 0.7mL/min
  2. Labial salivary gland biopsy - particularly Sjogren’s syndromes
  3. Ultrasound
  4. Sialogram - injecting contrast medium
  5. CT scan - VERY COOL
411
Q

What is the management of a patient with xerostomia?

A
  1. Investigate underlying systemic disease
  2. Always get the diagnosis
  3. Palliative/symptomatic care and control other diseases and conditions - think mucosal trauma and caries
412
Q

What is Sjogren’s syndrome?

A

It is an autoimmune diseases that affects the eyes and the salivary glands.

Sometimes it occurs with other diseases like rheumatoid arthritis or other connective tissue disease - known as secondary Sjogren’s syndrome

413
Q

What is important to keep in mind with Sjogren’s syndrome?

A

They need to be seen by a specialist because there is a chance to develop lymphoma

414
Q

What are the steps to diagnosing Sjogren’s syndrome?

A
  1. Ocular symptoms
  2. Oral symptoms
  3. Occular signs
  4. histopathology - minor salivary glans
  5. Salivary gland testing/salivary gland involvement
  6. Autoantibodies presence in serum
415
Q

What is the histological features of Sjogren’s syndrome

A
  1. Lymphocytic periductal infiltration of slivary glands
  2. Acinar cell destruction
  3. Proliferation of ductal elements to form islands of epithelium
416
Q

What is the management of patient with Sjogren’s syndrome?

A
  1. Opthalmological review
  2. Palliate dry mouth
  3. Prevention and control of caries
  4. Dietary advice
  5. Management of infection - candidosis
  6. Need multidisciplinary management
417
Q

What is associationg between Sjogren’s Syndrome and MALT?

A

Sjogren’s syndrome may cause B cell lymphomas in mucous associated lymphoid tissue

418
Q

What is Scleroderma?

A

Scleroderma is a chronic, autoimmune connective tissue disorder that is primarily characterized by thickening and hardening of the skin and other tissue

419
Q

What are some oral manifestations of scleroderma?

A
  1. Widening of periodontal ligament space
  2. Tooth resorption
  3. Can be concurrent with Sjogren’s syndrome
420
Q

How do you manage scleroderma as a dentist?

A
  1. Oral hygiene
  2. Management of concominant conditons
421
Q

What are the steps to describing radiographic lesions?

A
  1. Relative radiodensity - mixed, radioopaque or radiolucent - CONSIDER SOFT TISSUE SHADOWS
  2. Site
  3. Size
  4. Shape
  5. Outline or border
  6. Effects on adjacent structures
422
Q

How do we describe the size of a boney lesion?

A
  1. Measuring dimension in centimeters
  2. Describing boundaries in two dimension - e.g. extending from (blank) to (blank)
423
Q

How do we describe the shape of a boney lesion?

A
  1. Round, oval, kidney like or irregular
  2. Unilocular or Multilocular
424
Q

How do we describe a border of a boney lesion?

A
  1. Well or poorly defined
  2. Smooth, ragged, corticated or indistinct
425
Q

What are some of the structure a boney lesion can effect?

A
  1. The teeth
  2. The bone
  3. Displacement or destruction of other structures
426
Q

Where do majority of salivary gland tumour occur?

A

They are mostly found in the major salivary glands

427
Q

What are some of the general categories of neoplastic lesions that are associated with salivary tissue?

A
  1. Malignant tumours
  2. Benign tumours
  3. Non-neoplastic epithelial lesions
  4. Benign soft tissue lesions
  5. Haematolymphoid tumours
428
Q

What are the most common well defined tumour for the upper and lower lips?

A

Upper - salivary gland neoplasm

Lower - mucococeal

429
Q

What are the main features os benign salivary gland tumours and malignant salivary gland tumours?

A

Benign (on the left):

  1. Slow-growing
  2. Soft and rubbery
  3. Common in parotid tumours
  4. DO not ulcerate
  5. No associated nerve signs

Malignant (on the right):

  1. Many slow growing
  2. Sometimes hard consistency
  3. Rare
  4. May ulcerate and invade bone

5, May cause cranial nerve palsie

430
Q

What kind of investigation can be used for salivary gland neoplasm?

A

Fine needle aspiration and cytology, incisional biopsy or excisional biopsy

This leads to processed that are able to tag genes of different tumours:

  1. In-situ hybridisation
  2. Fluorescent in-situ hybridisation
431
Q

What are adenomas?

A

It is a type of benign neoplasm

432
Q

What is a pleomorphic adenoma?

A

It is a type of benign neoplasma that is the most common one - histological presentation are the pleomorphic cells, it comes in blobes and is usually incapsulated.

It is non-ulcerated, slow growing and painless

433
Q

What is a basal cell adenoma?

A

Basal cell adenoma is a rare benign neoplasm characterised by the basaloid appearance.

It is a slow growing neoplasm.

It is monomorphic - single cell type involved

434
Q

What are the the 2 most common malignant types of salivary gland tumours?

A
  1. Mucoepidermoid carcinoma
  2. Adenoid Cystic Carcinoma
435
Q

What is a mucoepidermoid carcinoma?

A

It is a malignant glandular epithelial neoplasm characterised by mucous, intermediate and epidermoid cells with columnar clear cell and oncocytoid features.

This is the most common malignant salivary neoplasm.

Cystic and solid area mixed in

436
Q

What is adenoid cystic carcinoma?

A

Adenoid cystic carcinoma is a basaloid tumour consisting of epithelial and myoepithelial cells in variable morphology, It has a relentless clinical course and usually a fatal outcome.

It is slow growing and it may ulcerate or be painful.

Histologically: solid islands, crods, strands of darkly staining epithelial cels in delicate fibrous connective tissue stroma - perineural invasion is common

437
Q

What is the basic histology of the cyst?

A
  1. Lumen on the inside

2/ Epithelial lining surrounding the lumen

  1. Capsule around the epithelium and lumen that may be inflamed or may not be inflamed
438
Q

What are key features of jaw cysts?

A
  1. Well-defined raiolucencies with radiopaque borders
  2. Apsiration test can confirm fluid contents - if fluid comes out it is probably a cyst
  3. Superficial cysts may clinically appear bluish and may be transilluminated
  4. Usually asymptomatic
439
Q

Where do most jaw cyst arise from?

A
  1. Reduced enamel epithelium
  2. Rests of Serres - remenants of the odontogenic epithelium that are retained in the gingiva
  3. Rests of Malassez - remenants of the odontogenic epithelium that are retained in the periodontal ligament
440
Q

What do cysts mimic sometimes on radiographs?

A
  1. Anatomic structures: maxillary sinus and foramina
  2. Periapical granulomas
  3. Odontogenic tumours - ESPECIALLY AMELOBLASTOMAS
  4. Solitary and aneurysmal bone ‘cysts’
  5. Giant cell lesions
  6. Cherubism
441
Q

What are the three categories of inflammatory jaw cysts?

A
  1. Radicular cyst
  2. Residual cyst
  3. Inflammatory collateral cyst
442
Q

What is the pathogenesis of radicular cyst?

A
  1. Epithelial lining is derived from remanants of the root sheath
  2. Inflammation in the periodontal ligament initiates proliferation of epithelial cells
  3. Inflammation usually occurs as a result of pulp necrosis
  4. Cyst enlargement occurs as a result of hydrostatic pressure
  5. Bone resorption occurs in surrounding area
443
Q

What are the clinical features of radicular cyst?

A
  1. They are asosciated with roots of non-vital tooth
  2. Radiographically it presents as a well defined radiolucency
  3. Histologically the lumen contains debris
444
Q

What are residual cyst?

A

Radicular cysts that are “left” within the jawbones after extraction of tooth.

Histologically similar to a radicular cyst but it may have less inflammatory cells

445
Q

What are inflammatory collateral cyst?

A

It is a buccal or distobuccal aspects of the roots of partially or recently erupted teeth.

It is well defined, corticated radiolucency on the lateral root surface

Histopathology - similar non-keratinised squamous epithelium with fibrous connective tissue capsule

Treatment: curettage of the bony cavity or to extract the tooth

446
Q

What are the common developmental odontogenic cysts?

A
  1. Lateral periodontal cyst
  2. Odontogenic keratocyst - second most common
  3. Dentigerous cyst - most common one
  4. Nasopalatine cyst - not dontogenic tho
447
Q

What word would you use to describe a cyst that is around the coronal part of the tooth?

A

Peri-coronal radiolucency

448
Q

What is a dentigerous cyst?

A

It is a developmental odontogenic cyst of the jaws surrounding the crown of an unerupted tooth, the lining attached to the cementoenamel junction

449
Q

What is an eruption cyst?

A

It is a variant of a dentigerous cyst found in soft tissues overlying an erupting tooth.

Clinical significant sign: presents as a bluish soft tissue swelling of the mucosa

Important: eruption cyst and dentigerous cyst are the same thing - please do not put the in a differential

Treatment: make an incision and make the tooth come through

450
Q

What is an odontogenic keratynocyst?

A

It is a genetic mutation of PTCH1 gene that activates cell proliferation. It is an aggressive cyst. IT CAN EXPAND THE JAW and IT CAN RE-OCCUR.

It arises from dental lamina and is significant due to active epithelial growth rather than take up of water.

There is a risk of recurrence and occurs in the posterior body and the ramus.

Associated with Gorlin Syndrome or Naevoid Basal Cell Carcinoma Syndrome (same thing).

It could present as a multi-locular appearance

451
Q

What is the lining of odontogenic keratynocyst histologically?

A

Thing lining of parakeratinised stratified squamous epithelium with palisading hyperchromatic basal cells

452
Q

What naevoid basal cell carcinoma syndrome?

A

It is a rare autosomal dominant trait.

It is characterised by multiple odontogenic keratocysts, multiple basal cell carcinomas and skeletal anomalies.

453
Q

What is a latral periodontal cyst?

A

It is a developmental odontogenic cyst lined by non-keratinised epithelium occuring on the lateral aspect or between the roots of erupted teeth

It is uncommon and is treated by enucleation please make sure that the PULP IS VITAL.

Clinical feature: they can be botryoid or come in a bunch

454
Q

What is a gingival cysts?

A

They are rare, asymptomatic and dome-shaped projection of gingival mucosa that arise from dental lamina.

455
Q

What are calcifying odontogenic cyst?

A

It is a developmental odontogenuc cyst characterised histologically by ghost cells, which often calcify.

Common in young patients.

Radiographic appearance - most lesion present as well-defined radiolucnecny containing verying amounts of radiopaque material.

456
Q

What are odontogenic tumours?

A

A diverse group of neoplasms which derive from the epithelium and/or etomesenchyme normally associated with tooth formation.

Therefore all odontogenic tumours arises in the tooth bearing areas of the jawbones

457
Q

What are the benign epithelial odontogenic tumours?

A

A group of neoplasms cosnisting of proliferating odontogenic epithelium without ectomesenchymal tissue

458
Q

What is ameloblastoma?

A

Ameloblastoma is a benign but locally infiltrative epithelial odontogenic neoplasm of the jawbones characterised by ameloblas-like cells.

MOST COMMON ODONTOGENIC TUMOUR - most common in the mandible

459
Q

What are clinical features of ameloblastomas?

A
  1. Slow destructive area
  2. Expansion rather than perforation
  3. Seldom painful
  4. Somehow it can mestasise but it is very rare

Radiographically:

  1. Typically well defined, multilocla radiolucency
  2. FLOATING TOOTH APPEARANCE
460
Q

What is the histology of ameloblastoma?

A

Core components: Outer layer adjacent to CT resembling pre-ambeloblasts and centra, more loosely organised zone like stellate reticulum cystic breakdown

*there is no mineralised dental tissues or matrices

461
Q

What are the two main histological types ameloblastomas?

A
  1. Folicular - discrete islands of tumour
  2. Plaxiform - irregular masses or strands
462
Q

What are the two different types of ameloblastomas depending on cell type?

A
  1. Acanthomatus - folicular and may produce keratin
  2. Basal - basal, cuboidal cells present
463
Q

What are the two types of ameloblastomas according to behaviour?

A
  1. Unicystic ameloblastoma
  2. Peripheral or multicystic ameloblastoma
464
Q

What is a Unicystic ameloblastoma?

A

It is an ameloblastoma with a single cystic cavity with wall tissue being the worst clinically.

More likely to be unilocular and may be enucleated

465
Q

What is a
Peripheral or multicystic ameloblastoma?

A

It is an ameloblastoma with multiple cystic cavity.

It is worst than unicystic ameloblastoma.

This requires excision.

466
Q

What are the treatment for ameloblastoma?

A
  1. Local surgical resection
  2. Radio-resistant - because it is a slow growing tumour
  3. Good prognosis although regular follow up is essential
467
Q

What is clacifying epithelial odontogenic tumour?

A

It is also known as Pindborg tumour

It is a bening epithelial odontogenic tumour that secretes amyloid protein and tends to calcify.

Radiographic appearance: Radiopacity inside the radiolucency

468
Q

What is adenomatoid odontogenic tumour?

A

It is a benign encapsulated epithelial odontogenic tumour that contains rosette or duct-like structure and has an indolent behaviour.

Treatment with enacliation

469
Q

What are odontomas?

A

Odontomas are mixed odontogenic hamartomas that mature from soft tissues.

IT IS MOST COMMON IN YOUNG PATIENTS.

Two types:
-Complex - irregular mass of calcified material - top image

-Compound - variable number of small tooth-like structues - bottom image

Treatment: Surgical enucleation

470
Q

What is odontogenic myxoma?

A

It is a benign neoplasm histologically resembling odontogenic extomesenchyme and chracterised by sparse spindle.

Radiographic features: Soap bubble appearance - very multilocular, may be well or poorly defined

Treatment: resection

471
Q

What is cementoblastoma?

A

It is a distinctive benign tumour that is intimately associated with the roots of the teeth.

It is characterised by formation of calcified cementum like tissue which is deposited directly on tooth root.

Radiographic appearance: well-defined radiopaque mass closely associated with tooth root and often surrounded by radolucent halo.

Treatment: extract tooth and enucleate or locally resect tumour

472
Q

What are fibro-osseous lesions?

A

They are lesions where bone is replaced by cellular fibrous tissue and is characterised by gradual deposition of woven bone which matures overtime to form lamellar bone.

Diagnosis depends on clinical and radiographic feature of the different lesions

473
Q

What is fibrous dysplasia?

A

It is a genetically based sporadic disease of bone that may affect single or multiple bones. Fibrou dysplasia occuring in multiple adjacent craniofacial bone is referred to as craniofacila fibrous dysplasia.

Main types: monostotic (single bone) or polyostotic (multiple bones)

474
Q

What are the clinical features of fibrous dysplasia?

A

Radiological:
Radiolucency or mixed appearance, ill-defined margins and narrowing of the periodontal ligament

475
Q

What is the histology of fibrous dysplasia?

A
  1. Well vascularised fibrous cellular connective tissue
  2. Irregular trabeculae of immature woven bone - osteoid bone is the precursur
476
Q

What are the affects of firbous dysplasia on the patient?

A

Skeletal deformities in the mpatient

477
Q

What is the treatment of fibrous dysplasia?

A
  1. Time the skeletal maturation
  2. Orthodontic +/- conservative surgical recontouring
  3. May turn into a sarcoma so NO IRRADIATION
478
Q

What is cemento-ossifying fibroma?

A

It is the bening fibroosseous neoplasms affecting the jaws and craniofacial skeleton

479
Q

What are key features of cemento-ossifying fibroma?

A

It is rare and ususally occurs in tooth bearing areas of the jaws.

480
Q

What are the clinical features of cemento-ossifying fibroma?

A

Clinical
1. Painless
2. Slow growing

Radiographic
1. Well demarcated
2. Mixed radiopacity/lucency

481
Q

What is the histopathology of cemento-ossifying fibroma?

A
  1. Well defined, sometimes encapsulated lesion
  2. Hypercellular fibrous tissue
  3. Variable amounts of calcified tissue
482
Q

What is the treatment of cemento-ossifying fibroma?

A

Conservative surgical excision.

Juvenile form have a higher tendency to recur

483
Q

What a cemento-ossseous dysplasia?

A

It is a non-neoplastic fibro-osseous lesion of the tooth bearing regions of the jaws.

It is not common

484
Q

What are the 3 variant of cemento-osseous dysplasia?

A
  1. Periapical cemento-osseous dysplasia - apical areas of mandibular anterior teeth
  2. Focal cemento-osseous dysplasia - association with a single tooth
  3. Florid cemento-osseous dysplasia - multifocal involvement
485
Q

What are the radiologic features of cemento-osseous dysplasia?

A
  1. Radiolucent and than mixed lesions
  2. Well defined
  3. Thin radiolucent rim
  4. Lesions that are not fused to roots of the teeth
486
Q

What is a simple bone cyst?

A

It is an intraosseous cavity that is devoid of an epithelial lining and can be empty, blood filled or serous fluid filled.

Also know as a traumatic cyst.

It is pseudo cyst, because it is essentially some blood vessels and inflammed tissues - surgical intervention usually results in positive outcomes.

487
Q

What is a Tori?

A

It is a non-neoplastic, localised hyperplasia of dense lamellar bone.

Usualy in the palatle midline or mandible.

488
Q

What is a chondrosarcoma?

A

It is rare malignant bone tumour that produces cartialaginous matrix. THIS IS A TRUE NEOPLASTIC TUMOUR.

489
Q

What is osteosarcoma?

A

It is a group of malignant bone tumours. Creates bone expansion. Grows fast and could be ulcerated. THIS IS A TRUE NEOPLASTIC TUMOUR.

490
Q

What does osteomayalitis mean?

A

It means the inflammation has extended into the bone marrow

491
Q

What is alveolar osteitis?

A

It is a complication of tooth extraction - aka dry socket.

Localised inflammation of the bone, due to lack of blood clot formation or early lysis of clot.

It can progress to osteomayalitis.

Clinical signs: PAIN

492
Q

What is focal sclerosing osteitis?

A

It is asymptomatic condensation of the bone also known as condensing osteitis.

Maybe included in a differential of cemento-ossifying fibroma.

493
Q

What are the predisposing factors to the oseomyelitis of the jaws?

A
  1. Periapical infection
  2. Pericoronitis
  3. Compound fractures of the jaw
  4. Penetrating injuries
  5. Local damage to the jaws
  6. Impaired immune function
494
Q

What are the two different types of osteomyelitis?

A
  1. Acute - painful
  2. Chronic - not so painful
495
Q

What are the common clinical signs of acute oseomyelitis?

A

Requires some time to develop rediographically.

Loss of trabeculae, formation of necrotic bone sequestra - radiopaque areas within the jaws.

496
Q

What are histopathological signs of acute osteomlyolitis - particularly dead bone?

A

A lot of bacterial colonies and empty lacunae.

497
Q

What are the clinical signs of chronic osteomyalitis?

A

Persisten pain

Draining pass

In the areas of avascular bone

498
Q

What are the radiographical features of chronic osteomyelitis?

A

Radiolucency with focal areas

Moth eaten appearance

499
Q

What is the management of the chronic osteomyelitis?

A
  1. Aggressive, prolonged antibiotic treatment
  2. Removal of the cause
  3. Removal of dead bone
500
Q

What is osteoradionecrosis?

A

It is a form of ostemyalitis. It occurs in patient undergoing radiotherapy or post radiotherapy.

Aetiology: radiotherapy causes endarteritis of vessels - reducing bone vascularity - leading to bone hypoxia.

Remember: only directly irradiated bone is affected.

501
Q

What is the treatment for osteoradionecrosis?

A
  1. Prevention
  2. Removal of teeth that are grossly carious
  3. Managing sources of infection
  4. INTENSE ORAL HYGIENE
502
Q

What is MRONJ?

A

It is the medication-related osteonecrosis of the jaw.

It is related to antiresorptive, immune modulators or antiangiogenic medications.

Susceptible sites: Exposed bone

503
Q

What does radiopaque border of the lesion signinify?

A

It means that the lesion is slow progressing

504
Q

What are the most common site of salivary gland tumour? WHat is the most malignant site?

A

Most common site is related to parotid salivary gland.

Most malignant is sublingual gland.

505
Q

What are the geneneral clinical differences between a bening salivary gland tumour and malignant salivary gland tumour?

A

Both grow slowly usually

But malignant once are hard, can ulcerte and may cause ner palsie

506
Q

What are some of the common investigation we can use for salivary gland tumour?

A
  1. Excisional biopsy
  2. Fine needle aspiration an cytology
507
Q

What is pleomorphic adenoma?

A

It is a tumour of variable capsulation characterised microscopically by architectural pleomorphism.

It is very common bening neoplasm and occurs mostly in parotid gland. Painless for the patient.

508
Q

What is the histology of pleomorphic adenoma?

A

The histoloy might be marked variation. Usually involves squamous metaplasia, keratin and sebaceous glands

509
Q

What is the management of pleomorphic adenoma?

A

Careful excision

Monitoring

510
Q

What is basal cell adenoma?

A

It is a rare bening neoplasm characterised by basaloid appearance of the tumour cells

511
Q

What are two common carcinomas of the salivary glands?

A

Mucoepidermoid carcinoma

Adenoid cystic carcinoma

512
Q

What is mucoepidermoid carcinoma?

A

It is a malignant glandular epithelial neoplasm characterized by mucous, intermediate and epidermoid cells with columnar clear cell and oncocytoid features.

It is most common malignant neoplasm of salivary glands.

513
Q

What is the histology of mucoepidermoid carcinoma?

A

Usually they are charecterised as low, medium or high grade. the most cystic it is the lower the grade.

Usual suspects - mucous cells and infiltrative appearance

514
Q

What is adenoid cystic carcinoma?

A

It is a basaloid tumour consisting of epithelial and myopethelial cells in different structural configurations. IT IS USUALLY FATAL

515
Q

What is the histology of adenoid cystic carcinoma?

A

Solid islands, cords, strands of darkly tained epithelial cells in fibour connective tissues.

Swiss-cheese pattern

516
Q

What are the 4 giant cell lesions of the bone?

A
  1. Central giant cell grnuloma
  2. Hyperparathyroidism
  3. Aneurysmal bone cyst
  4. Cherubism
517
Q

What are the clinical features of central giant cell granuloma?

A

Most common in anterior mandible

Radiographic appearance:

  1. Uniform radiolucency
  2. Often multilocular
518
Q

What are the differential diagnosis for central giant cell granuloma?

A
  1. Hyperparathyroidism
  2. Cherubism
  3. Aneurysmal bone cyst
519
Q

What is the treatment for central giant cell granuloma?

A

Surgical enucleation.

It has tendency to recur

520
Q

What are the radiographic appearance of hyperparathyroidism?

A
  1. Clear bone resorption and replacement
  2. Cystic change within bone - formation of Brown Tumours
  3. Pulpal obliteration
521
Q

What is an aneurysmal bone cyst?

A

It is a bone cyst that may occur due to trauma in molar/ramus lesion and may be painful

522
Q

What are the features of the aneurysmal bone cyst?

A

Radiographic:
1. Cystic radiolucency, multiloculated

Histologically

  1. A lot of multinucleated giant cells and fibrous tissues
523
Q

What is the treatment for aneurysmal bone cysts?

A

Surgical enucleation

Be careful of acess bleeding

524
Q

What is cherubism?

A

It is an inherited condition where soft tissue replaces normal bone tissue

525
Q

What are the clinical signs of cherubism?

A
  1. Loosening of teeth
  2. Facial swelling
  3. Hypodontia
  4. Usually occurs in posterior mandible and is bilateral
526
Q

What is the treatment of cherubism?

A

Cosmetic facial surgery and dental management

Conditions regresses with age

527
Q

Why is open disclosure important?

A
  1. Patient has a right to be informed of what is happening to them
  2. To minimise harm to the patient
  3. We have a duty of care to the paitnet
  4. To maintain trust in the dentist-patient relationship
  5. To gian informed consent for any further treatment related to the incident
  6. To prevent a recurrence of the incident to others
  7. To possibly avoid formal complaint
528
Q

What are the elements of open disclosure?

A
  1. An apology or expression of regret
  2. A factual explanation of what happened
  3. An opportunity for the patient to relate their experience
  4. An explanation of the steps being taken to manage the event and prevent recurrence
529
Q

What is the definition of open disclosure?

A

Open disclosure is the process of providing an open, consistent approach to communicating with patients/consumers, their family, carer and/or support person following a patient incident. The process includes expressing regret or saying sorry.

530
Q

What are two separate but linked process are initiated in SA dental post patient incident?

A
  1. Open disclosure
  2. Incident reporting
531
Q

What are the steps for open disclosure?

A
  1. Acknowledgement of the incident, and offering initiating or signalling the need for open disclosure
  2. Preparing for, and engagin in open disclosure discussion, including expressing regret
  3. Providing follow up to patient and family/caregiver, including actions taken as a result of the investigation
  4. Completing process and maintaining documentation
532
Q

How do we express regret? Give an example.

A

I am sorry that this has happened to you.

533
Q

Why can be difficult to say sorry at times?

A
  1. Innate fight or flight response
  2. Vulnerability aspect
  3. Fear
  4. Self-image issues
  5. Worry that patient might still file a complaint
  6. Lack of confidence
534
Q

What are some of the risk factors for root caries and why?

A
  1. Root surface exposure - cementum and dentine are less minirelised thus begin to demineralise at a higher salivary pH comparing to enamel
  2. Very poor saliva quality and/or quantity - REALLY IMPORTANT FACTOR
  3. Wearing of partial dentures
  4. Other factors are similar to normal caries factors
535
Q

What are some of the key questions we should ask a patient who we think has root caries?

A
  1. What is going on? - Diagnosis + evaluation of specific risk factors
  2. Evaluation of disease state - understanding of remin/demin balance
  3. Impact and implications of disease
  4. Risk and benefit analysis
  5. What are the patient expectations?
  6. What is the plan for monitoring and ongoing care?
536
Q

Can a root caries lesion be restored or remineralised?

A

In all situations, try to avoid operative interventions before prevention has been given a chance to work

  1. Address risk factors
  2. Apply needed chemicals for remin
  3. Consider silver fluoride
  4. Restorative work might be needed in some cases

Because root caries restoration have a really poor prognosis

537
Q

What are the basic steps to preventing root caries?

A
  1. Identifying cariogenic biofilm with tri-plaque disclosing gel
  2. Disrupt the biofilm mechanically
  3. Disrupt the biofilm chemically - high strngth fluoride or chlorexedine
  4. Evaluate saliva - replace the building blocks of tooth structure - MORE FLUORIDE
  5. Raise the pH
538
Q

What are some of the silver fluoride products available in Australia?

A
  1. Creighton Dental CSDS silver fluoride
  2. SDI Riva Star
  3. SDI Riva Star Aqua (ammonia free - thus does not irritate soft tissue as much)
539
Q

What determines the effectiveness of silver fluoride?

A
  1. Site consideration - type of lesion and size
  2. Material selection - concentration
  3. Control of caries risk factors
  4. Monitoring and reapplication
540
Q

What are the key considerations to understand when restoring a root caries lesion?

A
  1. Size and type of lesions
  2. Extent and rate of caries activity
  3. Physical and mental condition of the patient
  4. Aesthetic requirements
541
Q

What are the basic outcomes of endodontic treatment?

A
  1. Maintain the health of all or part of the dental pulp
  2. Preserve the normal periradicular tissues
  3. Restore the periradicular tissues health
542
Q

What is the most common cause of endodontic problems?

A
  1. Caries
  2. Trauma
  3. Others
543
Q

What is tertiary dentine?

A

Tertiary dentine represents the more or less irregular dentine formed focally in response to noxious stimuli such as tooth wear, dental caries, cavity preparation and restorative procedures.

It is also known as reactionary dentine or reparative dentine - depending on the type of stimulus.

544
Q

What is reactionary dentine?

A

Reactionary dentine is defined as a tertiary dntine matrix secreted by surviving postmitotic odontiblast cells in response to an appropriate stimulus, Typically, such a response will be made to milder stimuli and represents up-regulation of the secretoy activity of the existing odontoblat responsible for primary dentine secretion.

545
Q

How can you describe dentine according to Dr. Rossi?

A

Dentine is like Swiss cheese - it is pour-us - the closer you are to the pulp the bigger the holes.

The permeability properties of dentine regulate the rate of diffusion of irritants that initiate pulpal inflammation.

546
Q

What are the indication of indirect pulp capping?

A
  1. Deep lesions likely to result in pulp exposure
  2. No history of subjective pretreatment symptoms such as spontaneous pain or provoked pulpal pain
  3. Pulp should test vital
  4. Pre-treatment radiographs should exclude apical pathosis
547
Q

What are the three treatments for endodontic problems?

A
  1. Extraction
  2. Root canal treatment
  3. Vital pulp therapy
548
Q

What are the requirements for successful vital pulp therapy?

A
  1. Pulp is not inflamed
  2. Haemorrhage is controlled
  3. Non-toxic caping material is applied
  4. Good seal provided by capping material and restoration to prevent influx of bacteria - MOST CRITICAL FACTOR
549
Q

What material is used in vital pulp therapy?

A

MTA or Calcium Hydroxide but MTA is better

550
Q

What are the three different types of vital pulp therapy?

A
  1. Direct pulp capping - no pulp is removed as pulp is not inflamed during mechanical pulp exposure
  2. Partial pulpotomy - a little pulp removal to stop the bleeding in inflamed pulps
  3. Full pulpotomy - removal of the entire pulp in the pulp chamber
551
Q

How often do you wanna recall your patient after vital pulp therapy?

A

1, 3, 6 and 12 months

552
Q

What are the steps for direct pulp capping?

A
  1. Consent, LA and appropriate rubber dam isolation
  2. Tooth disinfection with CHx post removal of all caries
  3. Control of haemorrhage from the pulp
  4. Application of calcium hydroxide liner or MTA
  5. Tooth restoration
  6. Recall every pattern: 1, 3, 6 and 12 months
553
Q

What are indications for partial pulpotomy?

A
  1. Traumatic exposure
  2. In immature permanent tooth or mature permanent tooth with simple restoration needs
  3. Patient who can not affor root canal therapy
554
Q

What are the steps for partial pulpotomy?

A
  1. Consent, LA, Appropriate rubber dam
  2. Disinfect the tooth after caries removal with CHx
  3. Remove 1-2mm of superficial pulp tissue
  4. If extensive bleeding observed , extend the preparation apically
  5. Use preassure yo facilitate haemostasis
  6. Calcium hydroxide liner or MTA use
  7. Restore tooth
  8. Recall every pattern: 1, 3, 6 and 12 months
555
Q

What are the indication for a full pulpotomy?

A
  1. Traumatic exposure
  2. In immature permanent tooth or mature permanent tooth with simple restoration needs
  3. Extensive pulpal inflammation or small coronal pulp
  4. Patient who can not afford root canal therapy
556
Q

What are the steps for a full pulpotomy?

A
  1. Consent, LA, Appropriate rubber dam
  2. Disinfect the tooth after caries removal with CHx
  3. Remove entire mass of coronal pulp tissue to level of canal
  4. If extensive bleeding observed , extend the preparation apically
  5. Use preassure yo facilitate haemostasis
  6. Calcium hydroxide liner or MTA use
  7. Restore tooth
  8. Recall every pattern: 1, 3, 6 and 12 months
557
Q
A
558
Q

How to write a diagnosis for endodontic diagnosis?

A
  1. Pulpal and root canal condition - aka irreversible pulpitis, necrotic pulp, reversible pulpitis
  2. Periapical status - clear periapical radiolucency with a corresponding draining sinus or no periapical radiolucency
559
Q

What factors should you consider before endodontic treatment?

A
  1. Strategic value of the tooth
  2. Periodontic factors
  3. Patient factors - MHx, age, compliance
  4. Restorability options - consider oral hygine - and consider teeth that are not restorable
560
Q

What system is used for case selection in endodontics?

A

American Association of Endodontists Endodontic Case Difficulty Assessment Guidlines

The following considerations are used:

  1. Patient considerations
  2. Diagnostic & treatment considerations
  3. Other considerations

Tally the numbers:
1. Easy - less than 20
2. Moderate - 20-40
3. Hard (refer) - above 40

561
Q

When accessing a tooth - what is a good guide for access cavity location?

A

A good guide - bitewings!

They will show you that the pulp chamber is situated in the middle thus by drilling in the middle of the tooth - less tooth structure is destroyed comparing to the traditional shape outline method. Remember - long axis of the tooth is an important guide

Remember - traditional shape method does not consider a lot of factors such as the shape of the tooth, caries condition and restorations.

562
Q

What is the objective of initial access?

A

Just to reach the roof of the pulp chamber.

If you do not sense the “pin drop” of the bur - stop and re-assess - you don’t want a perforation

563
Q

What bur should you do after initial access?

A

A non end-cutting bur in order to extend the pulp chamber access without removing extra tooth structure from the pulpal floor.

564
Q

How many canal does upper first premolar have?

A

2 usually

565
Q

How many canals does upper first and second molar have?

A

Usually 4 - remember MB2

566
Q

What is the purpose of an endoprobe?

A

Endoprobe is used to assist in identification of root canals

567
Q

What is a good radiographic hint pointing that a lower incisor might have 2 different canals?

A

If in the radiograph - pulp chamber suddenly thins out or becomes smaller (suddenly) - that means that the tooth might have 2 canals

568
Q

What is the aim of chemo-mechanical debridement?

A

Aim is to gradually increase the size of the canal to allow for adequate penetration of irrigants/medicaments and to facilitate obturation

569
Q

What are the types of irrigants used in chemo-mechanical debridement?

A
  1. EDTAC - 15% commonly used as a removal of smear later and to increase permeability of dentinal tubules
  2. Sodium hypochlorite - 1% commonly used, dissolves organic matter - DANGEROUS
570
Q

What is a good way to ensure you dont push sodium hypochloride through the root apex?

A

Bend the needle but not at the hub and measure it - so it is far from the apex!!!!

571
Q

What are the number on the file represent?

A

The diameter of the file

572
Q

Why files need to be curved?

A

Real canals are never straight - a curved file means it follows the natural anatomy of the file.

573
Q

What bur can be used for coronal preparation?

A

Gates-Glidden burs - they are used coronaly in order to make the canal access easier

You distinguish them by number of slots - 2 slots is size 2, 3 slots is size 3

574
Q

How do you determine root canal lengths?

A
  1. Know average lengths
  2. Measure from pre-operative radiographs
  • Estimate working length
  1. Use electronic apex locator
  2. Confirm with radiograph
  • Correct working length established
575
Q

How to use dentaport ZX?

A
  1. Moisture in canals but not too much
  2. Attach the lip clip
  3. Attach the file clip
  4. Advanced the file until the read is “Past apex” withc careful watch-winding movement
  5. Come back to “Apex” reading
  6. Measure the file
576
Q

What is important for file size increase?

A
  1. First - make sure that the smaller file goes to length and is LOOSE - remember circumventional filing (going on all border of the root canal)
  2. Irrigate
  3. GO to next file
577
Q

What is the master apical file?

A

It is the largest file that goes to the correct working length

578
Q

Why going above a size 25 may complicate thing during root canal preparation?

A

Files above size 25 may be too stiff and create iotriogenic errors due to it’s straightness.

Ledges might form or strip perfirations.

579
Q

Why is ledermix bad?

A

It stains teeth because it is a tetracyclin derivative

580
Q

What is the aim for interim restoration?

A
  1. To prevent bacterial ingress
  2. Maintain function of the tooth
581
Q

What material are available for interim restorations?

A
  1. Cavit for initial layer
  2. GIC/RMGIC on top
582
Q

What are the reasons for obturation?

A
  1. Remove remaining bacteria
  2. Stop nutrients from apical tissues getting into root canal system
  3. Stop bacterial from coronal aspect getting into root canal
583
Q

What is the objective of a lateral spreader?

A

To condense the master GP and create space for accessory GPs - it has one end unlike endo probe

584
Q

What is the objective of an endodontic plugger?

A

It has a stopper to go to appropriate length - it is used to heat the GP point and burn them off

585
Q

What is working length?

A

It is the distance from a coronal reference point to the point at which canal preparation and obturation should terminate.

586
Q

What are some of the complication could occur if the correct working length is not calculated?

A
  1. Iatrogenic perforation
  2. Patency at apical terminus
  3. Extrusion of root fillings
587
Q

What are some of the technique that can be used to determine working length?

A
  1. Software
  2. Radiographic
  3. Electronic
  4. Paper point
588
Q

Why is the desired working length is 1-2 mm away from radiographic apex?

A

Because we looking at a 2D representation of a 3D object and the natural anatomy of the root may have a curvature thus if the working length taken for the entirety of root length - it may create a perforation

589
Q

What is the rule of tube shift in endodontics?

A

SLOB - (Same lingual opposite buccal) - usually the tube shift goes lingual

590
Q

What are the steps to an initial endodontic procedure?

A
  1. Consent, LA, rubber dam isolation
  2. Removal of caries and access to the pulp
  3. Idenitifcation of the appropriate access using radiographs
  4. Identification of canals using endo probe
  5. Using a small size file a few milimeters into a precieved canal in order to confirm that it is actually a canal
  6. Irrigation with a bent needle for safety
  7. Flaring of the coronal protion of each canal using Gate-Glidden burs
  8. Irrigation
  9. Estimationg of working length of each canal.
  10. Determination pf correct working length with appropriate file, raiographs and apex locators
  11. Apical preperation of each canal. Pre-curved files, watch-winding technique performing circumferential filing
  12. Recapitulate with a size 10 file between each file and irrigate well between each file
  13. Work up until file 25 -take radiograph to check the master apical file is at an appropriate length
    • irrigate and try master gutta percha of the the biggest size possible
  14. Place medicaments with lentulo spiral
  15. Resore with cavit and GIC
591
Q

What are the steps to root canal obturation?

A
  1. Consent, LA, Rubber dam isolation
  2. Re-access tooth and remove caivt safeyl
  3. Irrigate
  4. Check master apical file goes to correct working length
  5. Select master GP largest size that goes to correct working length
  6. Take radiograph to confirm
  7. Dry canals with paper points
  8. Place the sealer with lentulo spiral
  9. Coat master GP with sealer and place into the canal
  10. Use lateral spreader to condense the master GP
  11. Place accessory GP into space create
  12. Continue with lateral spreader until the space is filled
  13. heat the end of the endodontic pluger and burn off GP points
  14. FInal level of root-fillin should bet at or below CEJ
  15. Clean pulp chamber and reestore.
592
Q
A
593
Q

What are some of the common consequences of tooth loss?

A
  1. Bone resorption - can lead to high frenum/muscle attachment
  2. Overreruption of opposing tooth
  3. Medially/distally drifting/tilting of adjacent tooth/teeth
  4. Occlusal disharmony affecting function
  5. Change in speech and aesthetic
  6. General affects on general health as well as quality of lfie
594
Q

What are some of the way we can classified removable dentures?

A
  1. Based on location of missing teeth - partial vs comlete
  2. Based on materials - acrylic, valplast, crhome
  3. Based on support - tissue or tooth or combined
  4. Construction methods - immediate vs conventional
595
Q

What are the aims of a removable dentures?

A

Restore:

  1. Aesthetics
  2. Function
  3. Speech
  4. Preserving remaining soft and hard tissues
596
Q

What are indications for a removable dentures?

A
  1. Replacing single or multiple missing teeth
  2. Temporary space maintenance in congenital missing teeth
  3. Obturation of hard palate after removal or oral cancer
597
Q

What are contraindications for partial dentures?

A
  1. Lack of suitable abutmnet teeth
  2. Rampant caries
  3. Severe periodontal diseases
  4. Poor oral hygiene
  5. Patients who cannot tolerate dentures
  6. Patient who recently received head and neck radiation treatment
598
Q

What should we consider before making a denture for a patient?

A
  1. Patient oral hygiene
  2. Existing oral health conditions: caries, perio, pathologies, salivary flow and quality
  3. GIngivae and abutment tooth/teeth
  4. Gagging issues patient might have
  5. Patient’s perception
599
Q

What codes are there for dentures?

A
  1. Codes starting with 7
  2. Denture reline
  3. Denture repair
600
Q

How many appointments do you need for a general denture?

A
  1. Denture consult + primary impressions
  2. Secondary impressions
  3. Bite registration + shade mould selection
  4. Denture try on
  5. Denture insert
  6. Review denture
601
Q

What will the patient feel when they get a new denture?

A
  1. Excessive saliva
  2. Change in speech
  3. Feeling of bulkiness
  4. Food might get stuck under denture
  5. Denture moves to some extend
  6. Remove denture to clean
  7. Might have a sore spot or ulcer
  8. Might have a high spot
602
Q

How do they care for their denture?

A
  1. Remove dentures and clean after meals
  2. Brush dentures as brushing your teeth
  3. Brush and remove dentures at night and keep in denture container
603
Q

What is the difference between an overlay and overdenture?

A

Overlay - the denture sits around the tooth

Overdenture - the chrome part of the denture sits on top of teeth

604
Q

What are the standard steps for a chrome denture construction?

A
  1. Denture consult + primary impressions
  2. Secondary impressions
  3. Frame try in + bite registration + shade mould selection
  4. Trial denture - aka wax
  5. Denture insert
  6. Review denture
605
Q

What do you do in the consultation appoitmnet?

A
  1. Take all histories
  2. Do a specialised limited exam - extra oral exam, intraoral exam, occlucal exam
  3. Take alginate impressions
606
Q

What is the purpose of alginate impression?

A

To make a study cast and fabrication of a special trays - preforated (for secondary alginate) vs non perforated (for rubber based material)

607
Q

What do you write in a lab prescription after completing primary impression with alginate?

A
  1. Please pour up alginate impressions for study models
  2. Please construct a CCA special tray for upper or lower arch
608
Q

What is an occlusal stop?

A

It stops the tray from touching the teeth. Similarly - the gingival stopper will stop at the gingival thus making your impression better

609
Q

What materials could you use for secondary impressions?

A
  1. PVS
  2. PE
  3. Alginate
610
Q

What to do if the patient has no teeth and you still need a bite registration?

A

Record centric relation

611
Q

What are the indications for temporary denture? How many appointment does a construction require?

A

As an interim denture or immediate partial denture

Usually 3 appointments:

  1. Denture consult, alginate impression + shade selection
  2. denture try in
  3. Denture insert (after extractions)

+

Review

(Can’t be chrome or varplast)

612
Q

What is edentulism?

A

It is the state of being edentulous, without natural teeth

613
Q

What is edentulous?

A

It means “without teeth”. It could be partial or complete

614
Q

What are some of the reasons for tooth loss?

A
  1. Decay and periodontal disease
  2. Trauma
  3. Orthodontic extractions
  4. Congenital missing teeth
  5. Impacted teeth
  6. Pathologies
  7. Radiation therapy to treat head and neck cancers
615
Q

What are the Kennedy’s classifications of partial edentulous arch?

A

Class I - bilaterla edentulous areas located posterior to the remaining natural teeth

Class II - A unilateral edentulous area located posterior to the remaning natural teeth

Class III - A unilateral edentulous area with natural teeth remaining both anterior and posteror

Class IV - A single, bilaterla edentulous crossing mid line

616
Q

What are the 3 main categories of changes following tooth loss?

A
  1. Morphological changes - extra and intra oral changes
  2. Neuromuscular changes
  3. Functional changes
617
Q

What are some of the extra oral changes that occur due to tooth loss?

A
  1. FLat philtrum and deep nasolabial grooves
  2. Hollow cheeks
  3. Decreased columella-philtrum angle
  4. Narrowing of the lips
  5. Decrease face height
  6. Commissures drop
  7. Lost support for facial muscle
  8. Reduced facial height
618
Q

What are some of the intra-oral changes that occur due to tooth loss?

A
  1. High frenal attachment due to bone loss
  2. Bone resorption
  3. Traumatised neuromascular structure under denture
  4. Atrophic mucosa - can cause pain due to proximity of the denture to the nerves
  5. Class III skeleton relationship will develop eventually
  6. Decrease in occlusal vertical dimension
619
Q

What are some of the occlucal changes that occurs due to tooth loss?

A
  1. Occlusal disturbances
  2. Lost of occlusal vertical dimension
  3. Increase in parafunctional habits
620
Q

What are psychological changes following tooth loss?

A
  1. Emotional effects of tooth loss
  2. May increase stress levels
  3. Social-disability
621
Q

What are current and future treatment options for edentulism?

A
  1. Prevention of edentulism - MAIN STRATEGY - think about biopsychosocial approach
  2. Monitor alveolar ridge resorption
  3. Monitor oral mucosa health and screening oral mucosa lesions
  4. Rem. Pros.
  5. Consider implant retained overdenture or implat supported overdenture where appropriate
622
Q

What are the standard appointments for a valplast denture contruction?

A
  1. Consult, alginate impressions, bite reg, shade selection adn mould
  2. Dentur try in
  3. Denture insert
  4. Review
623
Q

What is complete denture retention?

A

Complete denture retention is the resistance to displacement of the denture base away from the ridge. It provides psychologic comfort to the patient.

624
Q

What is denture stability?

A

Stability is the resistance to horizontal and rotational forces. Stability has been cited as the most significant property in providing for physiologic comfort.

625
Q

What is denture support?

A

Support is the resistance to vertical movement of the denture base towards the ridge.

626
Q

What are some of the important aspect of the denture that promote retention?

A
  1. Proper contour and design of polish surface - harmonising with function of tongue, lips and cheeks
  2. Contour and thickness
  3. Smoothness
627
Q

What are some of the aspect that de-promote denture retention?

A
  1. Overextension of denture base
  2. Overcontour of polished surface
628
Q

What is the neutral zone?

A

It is a virtual potential denture space with a dynamic equilibrium forces of the tongue, cheeks and lips.

If denture seats in a neutral zone - denture is more retentive.

629
Q

What are some of the physical factors affecting retention?

A
  1. Adhesion
  2. Cohesion
  3. Surface tension created at the meniscus of the denture border
  4. Gravity ( think better for lower and worse for upper)
  5. Atmospheric pressure
630
Q

How to maximise denture retention by managing physical factors?

A

Good primary and secondary impressions - good accuracy, tissue contact and adequate periphery seal - remember special tray needs to have near perfect coverage and cover all hard tissues such as the tuberosities

631
Q

What are some of the biological factors affecting retention?

A
  1. Height of bone ridge
  2. Shape and width of bone
  3. Muscle attachment
  4. Neuromuscular control - muscle movement diseases such as Huntington’s disease may cause some problems
632
Q

What are some of the other method of providing retention for complete denture?

A
  1. Adequare extension and shape of the falanges of the denture
  2. Adequare saliva to provide adhesion, cohesion and surface tension - water can be used before insert
  3. Mechanical - overdentures using implants or root stumps
633
Q

How you tell a contact is high?

A

A ring shape with hollow middle - means contact is too high.

If it does not follow that round shape - it is not too high

634
Q

What are some of the factors that affect stability?

A
  1. Firm keratinised tissue
  2. Ridge height
  3. Ridge contour
  4. Ridge stability
  5. Intimate base adaptation
  6. Adequate extension
  7. Occlusal harmony
  8. Neuromuscular control
635
Q

How do we provide better stability and support to a denture?

A
  1. Maximise denture base extension
  2. Bilateral balance of occlusion
  3. Consider mono-occlusion
636
Q

What is the primary support areas for the dentures?

A

Upper - primary support area is the hard palate

Lower - retromolar area and buccal shell

637
Q

What provides retention, stability and support in partial dentures?

A
  1. Clasp units
  2. Major connectors
  3. Intra/extra coronal attachments
  4. Implant locator attachment
  5. Locator attachment on root
  6. Survey crown
638
Q

What are some of the other methods of achieving retention acrylic dentures?

A
  1. Clasps
  2. Acrylic dental papilla - soft tissue support
639
Q

What are the ideal properties for impression materials?

A
  1. Accuracy
  2. Elastic recovery
  3. Dimensional stability
  4. Viscosity that allows a flow into minute details
  5. Flexibility
  6. Workability
  7. Patient comfort
640
Q

What can you use the copper wax for?

A

You can use copper wax for bite registration

641
Q

What can you use modelling (red) wax for?

A

Wax rim or was bite registration

642
Q

When would you use Zinc Oxide Eugenol (ZOE) in rem pros?

A

Only use in edentulous patient because it is very very very rigid.

Please apply vasaline to patient face because it may burn the patient

643
Q

Why to do with alginate impression after you taken them?

A

After taking the impressions make sure you wrap it in a damp towel!

644
Q

What are the alginates that are available at the ADH?

A
  1. Halas Alginate - very dimensional stable
  2. Kromopan Alginate - EXTREMLY DIMENSIONALLY STABLE WOW
645
Q

What can you use alginate for in rem pros?

A
  1. Primary impression
  2. Secondary impression - for mobile teeth
  3. Valplast denture impressions
  4. Obturator of cleft palate
646
Q

Why don’t we use polysulfieds anymore?

A
  1. Long setting time
  2. Smells real bad
647
Q

Where do you use light body and heavy body?

A

Light body - gingival sulcus

Heavy body - everywhere else and to push the light body

DONT USE WITH LATEX

648
Q

What do we use PVS for in rem pros?

A
  1. Seondary impressions for all impression
  2. Wash impressions for reline
  3. Impressions for obturators for cleft palate
649
Q

What are some of the applications for Coe-soft and Coe-comfort in rem pros?

A
  1. Impressions for reline
  2. Impression for obturators of cleft palate
  3. Functional/neautral zone impressions
  4. Temporary reline
  5. Tissue condition impression
650
Q

What are some of the aspects to consider when selecting impression materials?

A
  1. Biocompatibility
  2. Accuracy
  3. Elastic recovery
  4. Hydrophilic or hydrophobic properties
  5. Working time and setting time
  6. Tear strength
  7. Dimensional stability
  8. Ease of use and delivery system
  9. Cost
651
Q

What are components of the dentures?

A
  1. Denture base
  2. Denture teeth

Denture connectors:
3. Major connect
4. Minor connector
5. Clasp unit

652
Q

What materials can be used for a denture base?

A
  1. Polymethyle methacrylate (PMMA) and it’s modifications- also know as acrylic
  2. Rubber reinforced Lucitone 199 - a type of acrylic that is specifically used at ADH
  3. Polyamides like Valplast - good for aesthetics for short saddles
  4. Formlabs denture resin
653
Q

What materials can be used for a denture teeth?

A
  1. Polymethyle methacrylate (PMMA) and it’s modifications - also know as acrylic
  2. Formlabs denture resin
  3. Sleeve crown (cobalt/chrome)
  4. Porcelain teeth
654
Q

What are the disadvantages of porcelain teeth for rem pros?

A
  1. They can not be adjusted or need glaze after occlusal adjustment
  2. They cause significant wear to opposing teeth
  3. They are quite brittle and easy crack or chip
655
Q

What material can you use for denture frame?

A
  1. Cobalt chrome - Remanium+ is used at ADH
  2. Titanium - for patient alergic to cobal chrome or other materials
  3. HPPE frame
656
Q

What is the centric relation?

A

It is the retruted contact position. It is the maxillo-mandibular relationship independent of tooth contact. This CAN BE RECORDED IN EDENTULOUS PATIENT. You can ensure that the patient is in centric relation by asking them to go through repeated movement of protrusion and retrusion in order to arrive at the centric relation.

657
Q

What is centric occlusion?

A

It is the intercuspation position. It is the occlusion of opposing teeth when the mandible is in centric relation. This may or may not coincide with maximum intercuspal position

658
Q

What is posselt’s envelope of motion?

A

The posselt’s envelope of motion looks at the following aspects of incisor potion through the movement of the mandible?

  1. Intercuspal position (ICP) aka cnetric occlusion
  2. Retruted contact position (RCP) aka centric relation
  3. Edge-to-edge articulation (E)
  4. Maximal opening without condylar translation of the condyle (rotation only)(R)
  5. Maximal mandibular opening with translation of condyle (T)
  6. Protrusion (Pr)
659
Q

What are clinical applications of centric relationship

A

When you have a full denture:

During bite registration you need to take an impression of the centric relation

While in try in and insert you need to assess the centric occlusion

When you have a partial denture:

During bite registration you need to take an impression of the centric occlusion

While in try in and insert you need to look at centric occlusion or maximal intercuspal position

660
Q

What is the natural rest position?

A

It is the occlusal vertical dimension + 2-4 mm

661
Q

What determines the OVD?

A

OVD is determined by the contact between natural teeth. If there is no natural teeth - please estimate OVD by subtracting from natural resting position

662
Q

What are the 3 types of occlusion?

A
  1. Balanced occlusion - the best type of occlusion - when is a balanced intercuspal position on anterior and posterior teeth - best of denture stability and create pressure to retain the bridge.
  2. Monoplane occlusion
  3. Lingualised occlusion - the elimination of buccal cusp contact - may be used if the patient has a modified occlusion due to skeletal and other reasons
663
Q

What are the difference between natural and artificial occlusion?

A
  1. Natural teeth retained by periodontal tissue - denture teeth are not
  2. Natural teeth move independently - denture teeth move as a unit
  3. Malocclusion in natural dentition may not cause any symptoms for yeras - in denture teeth there will be an immediate response
  4. In natural teeth, second molar is one of the power points of mastication - in denture teeth this may cause a shifting of the denture base
  5. Bilateral balance during excusrion is rare in natural teeth - in dentured teeth it is required for stabilisation of denture base
  6. Proprioceptors guide neuromuscular control during function, meaning mandible return to centric occlusion - if any interference occurs in dentured teeth, denture base shift and may be dislodged
664
Q

What is centric postion?

A

It is position of the mandible when the jaws are in centric relation

665
Q

What is the clinical significance of curve of Spee and Curve of Wilson in dentures?

A
  1. Curve of Spee os designed to permite protrusive disocclusion of the posterior teeth by combination of anterior and condylar guidance
  2. Curve of Wilson permits lateral mandibular excursion free from posterior interference
666
Q

When would you select no-anotomical teeth for a denture?

A

For partial: If anatonical teeth have been severley worn

For full: If the alveolar ridges are poor and there is uncoordinated jaw movements

667
Q

Can you state that “caries is a multifactoria disease”?

A

In a sense - no.

Because caries is primarily driven by free sugars - remove the sugars and there will be no caries.

But only because there other modifying factors - we claim that caries is a multi-factorial disease.

This is an argument made by Aubrey Sheiham, a dential rsearch of University College London

668
Q

What is the potential issues with increasing the oral health workforce in order to improve overall oral health in global population?

A
  1. Logistic challenge with the geographical distribution of dental practitioners
  2. Dentist-to-population ratios are only a crude measure of oral health-care service availability, and are not correlated to disease prevalence
  3. Individual actions in clinical settings are unlikely to prevent future disease
669
Q

What is the potential issues with increasing awareness about oral health-related behaviours in the population to improve overall oral health in global population?

A
  1. If this worked (alone) and actually changed behaviours, we would have different figures by now
  2. Dental education campaigns, when not articulated with other actions may not be effective overall and may also increase inequalitie
670
Q

Why behavioral interventions that do not take into account the social determinants of health are unlikely to work?

A
  1. Since patterning of health behaviours reflects underlying inequalities in material and social resources, it is unlikely that the growing inequality in health behaviours can be addressed without tackling these social factors
  2. The likelihood of adhering to health-related behaviours following universal education campaigns is also shaped by the social determinants of health
671
Q

Please describe the health impact pyramid from least population impact to most population impact.

A
  1. Counseling & Education
  2. Clinical interventions
  3. Long-lasting protection interventions
  4. Changing the context, so the defaul choice is healthy
  5. Socioeconomic factors
672
Q

What is an example of increased indivdual effort and low population impact activity?

A

Counselling & education of an individual in regards to caries.

It result in the ost benefit to the individual but the efforts by the individuals must be high, it is more suseptible to socio-economic difference and has minimal impact on overall population.

673
Q

What is an example of low level individual effort and high impact on population?

A

Universal water fluoridation to prevent caries.

This is an example where an individual needs to put low effort, yet statistically we have evidence of high impact on populations.

These universal adjustments also help to deal with socio-economic inequalities as we can regulate the aount of fluoridation depending on the gneral community need.

674
Q

What are some of the pre-requisites for health according to the Ottawa Charter?

A
  1. Peace
  2. Shelter
  3. Education
  4. Food
  5. Income
  6. A stable exosystem
  7. Sustainable resources
  8. Social justice and equity
675
Q

What are some of the action areas of health promotion according to Ottawa charter?

A
  1. Build healthy public policy - think sugar tax
  2. Create supportive environments - think ban of sugary foods in schools
  3. Strengthen community action - support your local dental programs such as the indigenous oral health unit
  4. Develop personal skills - raising awareness with patients
  5. Reorient health services - focus on both high risk and popuation approach
676
Q

What are the different types of “needs”?

A
  1. Normative need - expert opinion on needs of an individual
  2. Perceived need - based on the individual’s perception
  3. Expressed need - defined based on people’s use of service
  4. Comparative need - when different types of need are interpreted considering other populations’ standards
677
Q

What are the components of an oral health needs assessment?

A
  1. Systematic approach
  2. Normative/ preceived/ expressed needs addressed
  3. Likelihood of engaging in interventions
  4. Workforce and skills requirement
  5. Effectiveness of interventions
678
Q

What are three aspect of pubic health that helps us to view it?

A
  1. Disease prevention - action to reduce or eliminate or reduce the onset, causes, complications or recurrence of disease
  2. Health protection - crafting a safe environment
  3. Health promotion - process of enabling people to increase control over and to improve their health
679
Q

What is the main difference between high risk approach vs the population approach?

A

The main difference are:

  • Exposures with high individual risk can have a small impact on population risk if the exposure is rare (aka people with sever conditions are very rare - thus intervention is not as widespread)
  • Exposures with low individual risk can have a big impact on population health if exposure is widespread (aka people with not so severe conditions are common - thus intervention is more widespread)
680
Q

What are the advantages of high risk approach?

A
  1. Beneficial for the individuals
  2. Important in addressing inequalities
681
Q

What are the disadvantages of high risk approach?

A
  1. Does not change population levels of disease
  2. Issues in identifying who is at risk
  3. Does not change the drivers in the population
682
Q

What are the advantages of population approach?

A
  1. Tries to remove the reason why the disease is common
  2. Almost everyone benefits
  3. May have a large impact at a population level
683
Q

What are the disadvantages of population approach?

A
  1. May not address health inequalities
  2. Does not represent a large benefit to the individual
684
Q

What are some of the levels of prevention?

A
  1. Primary prevention
  2. Secondary prevention
  3. Tertiary prevention
685
Q

What are some of the example of secondary prevention?

A

Secondary prevention occurs to treat asymptomatic disease - example: small restorations

686
Q

What are some of the example of primary prevention?

A

Primary prevention occurs to stop the disease - example: water fluoridation

687
Q

What are some of the example of tertiary prevention?

A

Tertiary prevention occurs in established diseases or established disease with complications - example: full mouth rehabilitation

688
Q

What are the basic principles that evaluate health promotion strategies?

A
  1. Evaluate needs - assessing the need for it and evidence of previous intervention
  2. Evaluate the process - is the intevention intervented as reuqired - are the people involved happy
  3. Evaluate impact - hort term evaluation of the outcomes
  4. Evaluate outcome - long term evaluaton of the outcomes
689
Q

What is a good book to have for reference for pahrmacology?

A

Australian Medicines handbook

690
Q

Why do we need to know about drugs?

A
  1. We prescribe them
  2. For the one we dont prescribe - patient may want to have info about them or drugs they are taking may affect your approach to their dental treatment
691
Q

What are the four right for drug prescribing?

A
  1. Right drug
  2. Right dose
  3. Right frequency
  4. Right duration and deprescribing
692
Q

What does drug therapy hope to achieve?

A
  1. Prevent diseases
  2. Cure a disease
  3. Decrease mortality
  4. Decrease sickness
  5. Decrease symptoms of illness
693
Q

What is a xenobiotic?

A

It is a substance that is not synthesized in the body but must be introduced into the body from outside.

694
Q

How would you try to explain the relationships between substrates and their target molecules/active sites?

A

Lock & key relationship

695
Q

What is pharmacodynamics?

A

It is the effect of drug on bod. Like paracetamol relieves pain and is antipyretic (lower body temp)

696
Q

What is pharamacokinetics?

A

Effects of body on the drug. Like absorption and distribution and elimination. It looks at the how it is done and the rate at which it is done

697
Q

What do we need to remember about drug nomenclature?

A

Always use the GENERIC NAME. Because that way when prescription is getting fulfilled - it is not dependent on the supply of a certain brand name.

698
Q

What are the potential clinical consequences of this difference (ibuprofen vs aspirin) in inhibition for a patient requiring 3rd molar extraction?

A

Due to affect on platelets by aspirin, by irreversible inhibition of platelets, there needs to be extra caution in planing and use of extra tools such as mucoperiosteal flap use due to increase risk of inability to achieve adequate haemostasis.

Please ensure use of local haemostatic measures and remember that temporary interruption is not required.

699
Q

What are the two functional types of meidctions?

A
  1. Agonists - drugs that elicit response
  2. Antagonist - drugs that bind but do not elicit response - essentially just occupy the space on the receptor by being competetive
700
Q

Why are pharamacokinetics important?

A
  1. Adverse harmful effect to a medicine in people oftent due to altered pharmacokinetics - e.g. kidney disease
  2. Patient does not get better or gets worse on a medicine often due to altered pharamacokinetics 0 e.g due to genetic factor or taking other medicines
701
Q

What is the important aspects of pharmacokinetics in prescription?

A

Same drugs do not suit all patient. There is a difference in doses due to age, weight, pregnancy, environment, diet and use of other medications.

702
Q

Your prescribe the antibiotic metronidazole 200 mg twice a day for a spreading odontogenic infection and it has no effect. WHat could be a pharmacokinetic reason?

A
  1. Not dosing properly
  2. The drug is broken down too fast and it can not reach appropriate blood levels
  3. The drug is not being absorbed properly due to nausea and vomiting
703
Q

Your prescribe the antibiotic metronidazole 200 mg twice a day for a spreading odontogenic infection and it has no effect. What could be a pharamacodynamic reason?

A
  1. Metronidozale can not affect the bacteria that is responsible for the odontogenic infection
  2. Bacterial resistance
704
Q

What are some of the ways we can introduce the drug to the organism?

A
  1. Enteral - through the intestine - oral, sublingual and rectal
  2. Parentral - everything else due to them being sensative to gastric juices or we need a quick effect - injections basically - intravenous, intramuscular or subcutaneous
  3. Other routes - inhalation, tranasal, topical, transdermal patches and other other like eyes, nose, ears drops
705
Q

What are some of the factors that effect the gastrointestinal absorption?

A
  1. Blood flow
  2. Surface area of the intestines - remember stomach does not matter intestine is due to increased surface area of the intestine - microvilli and villi.
  3. Gastric emptying - e.g. codeine slows down the emptying of the stomach thus may increase the time that the drug may take to the site of absorption - water pormmotes stomach emptying 200ML OF WATER IS GOOD
706
Q

Why do some medicine should be taken with food?

A
  1. To reduce side effects
  2. To reduce side-effects of stomach upset
  3. To treat heartburn/indigestion
  4. To ensure the medicine is absorbed into the blood stream: like very water soluble drugs
  5. To help process the meal - like for diabetes medication
707
Q

Why do some drugs have bioavailability of less than 100%

A
  1. Insufficient time for absorption
  2. Decomposition in gut lumen
  3. Liver and first pass effect - portal vein passes through the liver thus the drug might be over processed there and it does not really reach systemic circulation
708
Q

What are the steps of drug distribution?

A
  1. Initially drug enters the blood stream and makes it to the capillaries around the organ tissue in the body
  2. Capillary endothelium is very “leaky” which means certain molecules can pass through. Exception: blood-brain barrier which is actually less permeable
  3. Drugs need to be lipid soluble to defuse into the target cell if not they can interact with receptors on the cell membrane
709
Q

Whatis the interaction between cliclosporin and Saint John’s wort?

A

Ciclosporin is an immunosupresant that is able to aid in organ transplants.

St John’s Wort is a over the counter herb that cna aid in depression.

St John’s Wort is able to trigger an increase production of an enzyme that metabolises ciclosporin.

Thus decreasing long term plasma concentration leading to transplant organ rejetion by the body.

710
Q

What determines the dosing regiment?

A

Pharmacokinetics control the dosage regiment.

711
Q

What is the therapeutic concentration range?

A

It is when the optimal concentration is reached, meaning the concentration of a medication is not too low to be ineffective and not too high to cause toxicity.

712
Q

What is a therapeutic index?

A

The ratio of the dose that produces toxicity to the dose that produces a clinically desired or effective response.

Essentially drugs with a large therapeutic index are more safe and harder to get an overdose on.

Example of low therapeutic index - morphine 70:1 index

Example of high therapeutic index - remifantanil 33000:1

713
Q

What are some of the targets for drugs?

A
  1. Non-specific targets
  2. Proteins - the most common
  3. RNA/DNA
  4. Lipid cell membranes
714
Q

What are some of the receptors that are targeted by medications?

A
  1. Ligand-gated ion channels (ionotropic receptors
  2. G-protein-coupled receptors (metabotropic)
  3. Kinase-linked receptors
  4. Nuclear receptors
715
Q

How long does it take for ligand-gates ion channels to respond?

A

Miliseconds

716
Q

What are some of the examples of ligand-gated ions channels? What are some of the drugs that bind to them?

A

Nicotinic receptors and ACh receptors.

Benzodiasapine like xanax

717
Q

What are some of the examples of G-protein-coupied receptors (metabotropic)? What are some of the drugs that bind to them?

A

Muscarinic receptors, ACh receptors

Opiod agonists like morphine

718
Q

How long does it take for Kinase-linked receptors to respond?

A

Hours

719
Q

What are some of the examples of Kinase-linked receptors? What are some of the drugs that bind to them?

A

Cytokine receptors

Methotrexate

720
Q

What are some of the examples of Nuclear receptors? What are some of the drugs that bind to them?

A

Oestrogen receptors

721
Q

What are the two drugs of asthma therapy? How do they work?

A
  1. Relievers - bind to G protein-coupled receptors for relaxation
  2. Preventers - bind to nucleus to alter ntranscription of inflammatory mediators
722
Q

What is drug elimination?

A

It is irreversible loss of drug from blood through use of metabolism (drug is converted to another chemical - done by liver) or excretion (loss of the chemically unchanged drug - done by kidneys)

723
Q

What kind of drugs are metabolised by the liver?

A

Lipid soluble drugs like local anaesthetics

724
Q

What kind of drugs are processed by the kidneys?

A

Water soluable drugs like anti-biotics

725
Q

What is drug clearance?

A

It is the measure of rate of elimination. Drugs could be totally cleared or partially cleared

726
Q

What are the steps to drug elimination in the kidneys?

A
  1. Afferent arteriole caries the blood to the glomerulus - drugs are than filtered as plasma water
  2. The plasma enters into the proximal tubules in which the drug is secreted via active pumps that pup the drug into the kidney lumen
  3. Lumen moves through the proximal tubule into the dital tubules and collecting duct where some rebasorption could occur but most emportantly water is removed and lipid soluble drugs will be diffused back into the blood stream - thus they need to metabolised by the liver
727
Q

How does the liver metabolise drugs?

A
  1. Enzymatic conversion of drug to another chemical form in order to make it more water soluble so kineys can excreate them
  2. Remember - liver processes most of the medication
728
Q

What are some of consequences of metabolism?

A

Usually, the metabolites have no pharmacological activity but:

  1. Some may act as parent drgus
  2. Some may be antagonistic - causing convulsions or nauses/vomiting

Concept - active metabolites is clinically important for elderly and patients with renal disease - because some patient may not be able to excrete the metabolite at the same rate thus the metabolite may have a toxic effect.

729
Q

What are 2 phases of metabolism?

A

Phase I: Oxidation - depends on Cytochrome P450 largley - binds the drugs and important in binding of steroid - essentially all drugs endogenous and exogenous - VERY IMPORTANT

Phase 2: Conjugation - polar chemical group is “added on or transferred” - Enzyme are called transferases

730
Q

What is the metabolic pathway of paracetamol and hepatotoxicity?

A
  1. Paracetamol enters the liver where 55% of it is turned into water soluble Paracetamol Glucuronide, 40% of it is turned into water soluble Paracetamol Sulphate and 5% is turned into Reactive Electrophilic metabolite
  2. This reactive electophilic metabolite than can turne into paracetamol glutathione and be excreted in the kidneys or it may bind with metabolite-proteins and cause hepatic cell death

Now in overdose:

  1. There is not enough sulphate to turn paracetamol into paracetamol sulphate so more paracetamol is trned into a reactive electrophilic metabolite thus increasing binding to metabolit-protein and cause more heaptic cell death
  2. The way to help a patient in this situation - measure blood and introduce a N-acetylcysteine (NAC) which will hel with conversion thus stop metabiolite-protein bindings
731
Q

Why might some people get an overdose with the “therapeutic dose” of paracetamol?

A

They taking paracetamol from different sources like regular paracetamol + Cough & Cold tablets + nurimol

732
Q

What are the treatments of SAT violations?

A
  1. Consider restoring appropriately - please do not damage the tissues, remove the cement properly
  2. Re-establish SAT width by surgical crown lengthening or orthodontic extrusion
733
Q

What is this condition?

A

This is necrotising gingivitis. It is usualy caused by a presence of an opportunistic bacteria and an underlying stress factor.

Clinical features: necrosis of the papilla, sudden onset, ulcer covered by greyish pseudomembrane from surrounding mucosa

Treatment:

  1. OHI
  2. Debridement
  3. CHx
  4. Metronidozole 400mg 6 hourly for 5-7 days
734
Q

What are the four concepts we need to understand in pharmakokinectics?

A
  1. Clearance
  2. Half life
  3. Volume of distribution
  4. Bioavailability
735
Q

What does the shape of the curve of plasma concentration over time depend on?

A
  1. Dose
  2. Route of administration
  3. Single dose versus chronic dose
  4. Patients’ elimination and distribution rates
736
Q

What is bioavailability?

A

It is how much of the drug enters the blood stream and how much can actually be used.

Usually calculated by finding the difference of plasma concentration betwene oral ingestion and with use of IV

Good drugs - bioavailabiltiy 100%

Symbol on graphs - F

737
Q

What is the stead-state condition?

A

When we can achieve the balance between the rate of elimination and plasma concentration

738
Q

What does clearance rate determines?

A

It determines the dose rate.

It is important to know that clearance is an independent pharamakokinetic parameter.

If clearance is higher than concentration in the plasma should be higher.

If clearance is lower than concentration in plasma is higher.

739
Q

How do we know that we are at the steady state?

A

Half-life - time for blood concentration/amount of drug in body in half.

Half-life is very useful because it tells us when we are in the steady state. E.g. if half-life 97% is achieved in 5 doses - means it takes 5 half-lifes to get to the steady state.

It will also take 5 half-lifes to clear the drug.

740
Q

What are some of the important aspects of Drug-Drug interactions?

A

Pharamacokinetic:
Interacting drug alters the plasma concentrations of index drug.

Usually also alters the hepatic clearance, could up or down shift it.

Commonly, renal clearance is down regulated.

Pharamacodynamically - some drugs may make the reaction to other drugs more potent

741
Q

What is drug enzyme induction?

A

When a drug stimulates gene transcritption that makes of a certain enzyme in general resulting in need in higher dose.

E.g. St Johns Wort

742
Q

A patient is taking some wafarin 3 mg daily and felodipine. They have candidiasis infection. You start them on fluconaole 100mg daily. Their candidiasis infection clears up but they starting to experience major gingival bleeding and bruising. Why?

A
  1. Fluconazole is an aenzyme inhibitor which prevents warfarin to be metabolised
  2. Thus decreasing the clearance of warfarin and increasing plasma concentration
  3. Increased plasma concentration results in toxicity which leads to increase in bleeding and bruising
743
Q

What is a triple wammy?

A

It is a pharmacodynamic problem which occurs with use of ACE inhibitor, diuretic and NSAID and can result in Acute Kidney Injury (AKI)

Process:

  1. ACE inhibitors preserve renal function and also cause relaxation of efferent renal arteriole - reducing the GFR
  2. NSAID are able to increase the vasoconstriction of the afferent arteriole by inhibiting the production of prostoglandins - a potent afferent arteriole dilator - reducing GFR
  3. Dirutetic drive the increase exertion of water through the renal system thus increasing the amount of blood that is carried to the glomerulus through the afferent arteriole - reducing GFR
  4. All three factors compound reduce the GFR significantly to cause kidney injury
  5. Solution - avoid NSAIDs
744
Q

How to avoid drug interactions?

A
  1. Thorough history
  2. Check the list with the datatbases
  3. Remember of the over-the-counter and herbals
745
Q

What is an adverse drug reaction?

A

Any response to a drug which is unintended, harmful and which occurs at a dose usually given to humans for management of disease.

This does not include: Overdoes or Error in dosing

746
Q

What is an adverse drug effect?

A

An injury resulting from medical intervention related to a drug - includes wrong dose or device malfunction

747
Q

What are major types of ADRs?

A

Type A - Exaggerated response to medication even tho the dose is normal - it is usually predictable with dose decrease should fix it

Type B - BIZARRE effect - not predictable - high risk of death - need to stop the drug - ALWAYS ASK THE PATIENT IF THEY ARE ALLERGIC BEFORE ANY PRESCRIPTION ESPECIALLY WITH ANTI-BIOTICS

Type C - long term affects - tolerance like for caffeine

Type D - delayed effect - thalidomide with babies

Type other - unavoidable toxicity - cancer chemotherapy

748
Q

Who is more at risk of ADRs?

A
  1. Elderly
  2. Infats and children
  3. Women
  4. People with history of multiple allergies
  5. People with other diseases
  6. Certain ethnicity and pharmacogenetics
749
Q

What are some of the oral reaction to drgus?

A
  1. Local reaction such as chemical irritation or suppression of oral flora
  2. Systemic reaction like from bone marrow depressor or immune suppressors
  3. Stevens-Johnson syndrome - lots of ulcers - could be caused by ibuprofen
  4. Lichen planus - can be caused by allopurinol
  5. Gingival bleeding - SSRIs
  6. Xerostomia - polypharmacy
750
Q

How are drugs discovered?

A
  1. Purification from natural sources through tradition medicine and chance observation - aspirin
  2. Screening of biological sources such as soil, microbes or marine organisms
  3. Chemical modification of active and known drugs
  4. Rational Drug Design depending on the disease - custom designs by manipulation or proteins etc - SSRIs
  5. Pure chance (Srendipity) - Aspartame
  6. New Indications from clinical observation
  7. Recombinant proteins - using bacteria to make endogenous proteins
751
Q

What are the steps of pre-clinical drug development?

A
  1. Laboratory tests in vitro - through use of high throughput screening
  2. Whole animal testing
  3. Phase I trials - is it immediatley safe?
  4. Phase II trials - trials in the target illness - can it work?
  5. Phase III trials - large scale clinical trials - is it effective?
752
Q

What are the steps of approval of a drug in Australia?

A
  1. Aims - to protect public from drugs that are: unsafe, ineffective and poor quality
  2. Process - TGA is presented data
  3. Evaluation of quality, safety and efficacy
  4. Registration
  5. Movement to the market
753
Q

What are the two types of products that are listed on the website of TGA known as the ARTG?

A

AUST L - listed produucts with little side effects - like sports supplements

AUST R - registered products with side effects - think all other proper medicines

754
Q

What are the schedules of drugs?

A
  1. Schedule 1 - unscheduled drugs - paracetamol
  2. Schedule 2 - Pharmacies only - Telfast
  3. Schedule 3 - Pharmacist Only medicines - Morning-after pill
  4. Schedule 4 - Prescription only - Antibiotics
  5. Skip all other schedules
  6. Schedule 8 - Drugs of addiction dependence - Morphine
755
Q

Define the following:

Infection

Colonisation

Bacteraemia

Septicaemia

Sepsis

A

Infection - invasion & multiplication of pathogenic microorganism in body tissue

Colonisation - localised presence of microorganisms

Bacteraemia - presence of viable bacteria in circulation

Septicaemia - systemic infection caused by microorganisms multiplying in circulation

Sepsis - multiple organ involvement from organisms

756
Q

What are antibiotics?

A

They are drugs that stop the spread and multiplication of bacteria in the body that are causing harm.

They come under general term of anti-infectives and antimicrobials.

757
Q

What some of the other anti-infective and anti-microbials?

A
  1. Antibacterials - bacteria
  2. Antivirals - viruses
  3. Antifungals - fungal infections
  4. Antimycobacterials - for TB
  5. Antiprotozals - malaria medication
  6. Anthelminitics - againts worms
758
Q

What is important to understand about antibiotics?

A

Antibiotics do not cure infections - our immune system does. Antibiotics just needed for their bactericidal or bacteriostatic functions.

Antibiotics give immune system more time to mobilise more effectivley

759
Q

How do antibiotics work?

A
  1. Inhibit metabolism of a bacteria (folic acid blockage) - trimethoprim - bacteriostatic effect
  2. Inhibit cell wall synthesis - penicillins - bacteriocidal effect
  3. Disrupt cell membrane - both bacteriostatic abd bacteriocidal
  4. Inhibit protein synthesis - metronidazole inhibits DNA synthesis
760
Q

What are the different efficacy of antibiotics?

A
  1. Narrow spectrum - a few species - benzylpenicillin
  2. Moderate spectrum - several species - amoxicillin
  3. Broad spctrum - many species - tetracyclines
761
Q

What are the 2 concepts that determine anti-biotic efficacy?

A
  1. Time-dependent killing - time in the blood where drug is above MIC - MIC can change with resistence - penicillins
  2. Concentration-dependent killing - the higher the peak concentration the more it will kill - prologned duration of killing - aminoglycosides
762
Q

What are some of the resistance pathway for the bacteria?

A
  1. Bacteria produce enzymes that inactivate the drug
  2. Bacteria changes drug binding site
  3. Drug is pumped out of microbe
  4. Microbe makes alternative enzyme bypass pathway

Example: MRSA - multiresistant Staphylococcus aureus

763
Q

What is the “creed” of antibiotic therapy?

A

In dental clinics - primary removal of infection is essential

M - microbiology guides therapy
I - indications should be evidence-based
N - narrowest spectrum required
D - dosage appropriate to the site & typ of infection

M - minimise duration of therapy
E - ensure monotherapy in most situations

764
Q

What are the principles of antimicrobial selection?

A
  1. Use narrowest antibiotic to treat disease
  2. Use the safest
  3. Avoid topical administration of a drug used systemically
  4. Don’t use combinations
  5. Don’t give prophylactically
  6. After considering all theses factors - choose lowest coast
765
Q

What should the dentist put on the prescription sheet to make sure that pharmacist does not dispense too many antibiotic capsules?

A

Number of days and numbers of pills

766
Q

What is the difference between the reliever and a preventer?

A

Preventer is taken before to lower the chance or severity of asthma through different vasodialating effect. Usually a low dose of corticosteroids

Reliever - is usually just use for quick relaxation of smooth muscles.

767
Q

Neostigmine is a competitive inhibitor of cholinesterase. Why is it useful in the treatment of Myasthenia Gravis?

A

Myasthenia Gravis is a auto-immune disease that affect acetylecholine receptors on skeletal muscles - thus affecting the contraction of said muscles. It is an inhibitor.

Neostigmine inhibits the enzyme acetylcholine esterase which breakswdown acetylcholine thus increasin it’s number in synaptic cleft.

this results in improvemenet in the condition due to greater numbers of acetylecholine.

768
Q

Rank the following in terms of speed of onset action when an agonist occupis the receptor?

GABBA receptor

Opiod receptor

Glucocorticoid receptor

A
  1. GABBA receptor - inhibitory receptor in the nerve - very quick because it is an ion channel
  2. Opiod receptor - G protein-coupled receptors - moderatley quick
  3. Glucocoricoid receptor - nuclear receptor superfamily of transcription factors - very slow
769
Q

What drug should you not give to pregnant women?

A

Category C drug like ibuprofen.

Aloso Category D drugs but they are pretty rare!

770
Q

What is a good principal of drug dosing for older patients?

A

SRTART LOW & GO SLOW

BUT DON’T STAY LOW if chronic dosing.

771
Q

What is an example of potentiation effect of medications?

A

Warfarin and iboprofen/aspirin - increase bleeding significantly

772
Q

If a mouthrinse claims that is is for treatment of “gingivitis” but you can buy it at Woolworths, what type of listing is it and what type of schedule is it?

A

AUST R listing

Shedule 1 or unscheduled

773
Q

How do antiobitcs have a bacteriostatic effect?

A

Sulfanilamide antibiotics have a bacteriostatic effect by targeting synthesis of folica acid - an important component of bacterial RNA and DNA

Sulfanilamide can completitivley inhibit enzymes that are used in production of folic acids, thus slotwing the synthesis thus slowing growth of bacteria due to reduced production of plasmids (circular DNA in bacteria).

774
Q

How do antiobtics have a bacteriocidal effect?

A

By inhibiting cell wall synthesis through rapid depolarization.

Beta-lactam - like amoxycillin - able to bind to bacterial cell walls causing repid depolirasation resulting in loss of membrane potential leading to inhibition of protein synthesis and destruction of DNA.

775
Q

What are the main drivers for ortho treatments?

A
  1. Aesthetics
  2. Functional reasons: increased overjet, crossbites
  3. Societal and cultural pressures
776
Q

What is interceptive orthodontis?

A

Interceptive orthodontics or primary orthodontics is an approach that uses phased treatments to manipulate growth, and particularly common growth patterns and correct developmental occlusion problems.

777
Q

What should a graduate dentist be able to do in terms of orthodontics?

A
  1. Distinguish abnormal development and growth from that which is normal
  2. Perform an orthodontic examination and explain the diagnosis, then devise treatment options, detailing the benefits and risks of each
  3. Commence, monitor and complete interceptive orthodontic treatment in a patient
778
Q

What is the difference between growth and development?

A

Growth - is an increase in size

Development - is an increase in complexity

779
Q

What to do if you find growth is abnormal?

A
  1. Establish possible aetiological factors
  2. Seek assessments
  3. Understand suitable options for intervention
780
Q

What is a cephalocaudal gradient?

A

It is a chart of proportional growth.

Structures towards to head grow first

781
Q

What are growth curves?

A

Scammon’s curves They are graphs that represent that different tissues grow at different rates

782
Q

What is more useful - developmental or chronological age?

A

Developmental. It is more useful to know stage of growth, rather than age, that specific growth occurs for orhtodontics.

783
Q

What are the peaks of growth in people?

A
  1. Childhood peak at about 5 years
  2. Juvenile peaks at about 7 and years old
  3. Adolescent peak at about 11-13 years for females and 13-15 years in males
784
Q

When do you want to catach potential orthodontic case for interceptive treatment?

A

Class II treatment are most effective when you detect that the patient cephalogram is at CS 1 or 2 and you able to utilise maximum mandibular growth.

Class III treatment is most eefective when it is broken down itno two distinct stage: Maxillary expansion before maximum mandibular growth AND mandibular manipulation during pre-pubertal/pubertal stages.

785
Q

What is the use of lateral cephalometry?

A

Lateral cephalometry standardised, reproducible radiograph used primarily for orthodontic diagnosis and treatment planning.

It is used to compare jaw growth over time thus is a good guide in orthodontic treatment.

It is able to assist with cervical vertebrae maturation which is a type of biological indicator of skeletal maturity. The vertebrae C2-C4 is assessed.

786
Q

What type of growth is responsible for ossification of the cranial vault?

A

Intramembranouse ossification - which is a direct transition of the mesenchymal tissue into bone due to osteoblasts deposition. This usually occurs in non-load bearing areas csuch as the cranial vault, maxilla and mandible (body)

787
Q

What type of growth is responsible for ossification of the cranial base?

A

Endochondral ossification - where bone develops from carilagious precursor. It is usually occuring in load bearing areas like cranial base, long bone and mandibular condyle.

788
Q

How does naso-maxillary complex grow?

A

It grows downwards & forwards in relation of the cranial base.

789
Q

How does the mandible grow?

A

The mandible grows up and back.

It occurs via the bone remodelling via subperiosteal resorption & deposition.

Cartilaginous growth occurs in the condyle

790
Q

Why is bone resorption in certain areas of the mandible essetial?

A

Bone resorption creates space for the eruption of teeth that don’t have of decidious pre-cursor - thus lower the probability of impacted molars (think surgical extraction or third molars)

791
Q

What are the key points to craniofacial growth in orthodontics?

A
  1. Much of the vertical face height increase due to tooth eruption + alveolar bone production
  2. Mx & Md + dentitions desplaced down and forward relative to the cranial base
  3. Individuals experience differing amounts and direction of facial growth
  4. Around adolescence, slight differential growth of Md relative to Mx - meaning mandible tries to catch up
  5. Facial growth dependent on idividual growth patterns
  6. Factors infleuncing growth & development: genetics, SES, neural control, exercise, neural control, hormones and more.
792
Q

Which structures make up the cranium?

A
  1. Cranial vault akak calvarium
  2. Cranial base
793
Q

What structure make up the face?

A
  1. Naso-maxillary complex
  2. Mandible
794
Q

How does the cranium grow?

A

2 distinct methods of growth:

  1. Intramembrenous ossification - provides gross growth
  2. Ectocranial resorption and remodeling - localised growth - the inner cortical plate resops and the outder cortical plate experiences deposition due to local growth of brain - think about all the cruves and bumb the brain has
795
Q

From which branchial arch does the mandible originate?

A

1st Branchial arch.

796
Q

What is an apical base?

A

It is the junction of alveolar & basal bones of the maxillary & mandible in the region of the apices of the teeth.

It is important for dento-alveolar compesation - which means that tooth eruption and alveolus dvelopment compensate for apical base dimension - making the teeth look “out of place slightly”

797
Q

What is malocclusion?

A

It is a failure of the dento alveolar compensatory mechanism.

798
Q

What is crowding and what types of crowding are there?

A

Crowding - the discrepancy between tooth size & jaw size that results in the misalignment teeth.

Primary crowding - genetic origin

Secondary crowding - environmental factors such as extraction as a child

Tertiary crowding - occurs in the post adolescent period

799
Q

At 10 years old - what sould you do to the patient in order to recognise appropriate tooth growth and positioning?

A

Palpate around the areas that are distal and lingual of the primary canines in order to feel the permanent canines - because they are the most impacted teeth besides third molars.

800
Q

What is a length of a dental arch?

A

It is the approximate distance from central incisors to most distal point of 2nd primary molars

801
Q

What is dental arch circumference?

A

Distance measured round the arch from the mesial contact of first primary molar to the mesial contact of the other first primary molar

802
Q

What is the inter-canine width?

A

The horizontal distance between cusp tips of the upper and lower canines

803
Q

What is the inter-molar width?

A

The horizontal distance between the righ and left central fossae of the upper and lower first primary molars

804
Q

What is leeway space?

A

It is the difference between the combined mesio-distal width of the permanent canine & premolars and the width of the corresponding precursors.

This space is eventually lost as mesial drift of first primary molars occurs following eruption of permanent canine & pre-molars

805
Q

What is incisor liability?

A

It is the difference between the total mesio-distal dimensions of the decidous and permanents incisors

806
Q

How do permanent incisors have enough space to fit in the arch during eruption?

A

Space is gained from:

  1. Residual spacing between deciduous incisors
  2. Permanent incisors erupt into more labial position and occupy a great arch perimetes
  3. Deciduous canines move distally as incisors erupt
  4. Transvers increase in intercanine arch width
807
Q

WHat is a physiological explanation of a common upper midline spacing aka “ugly duckling gap?

A

It is a variation of normal dental development

It arises as the effcts of:
- incisor apicies initially close together as incisors erupt
- lateral pressure from erupting laters and canines

Diastema may close after laterla incisors erupt

Diastema may persist if:
- deciduous canines have been lost
- upper incisors are flared labially

808
Q

What are the factors that facilitate dental arch allignment?

A
  1. Use of interdental, primate and leeway spaces
  2. Increased inter-canine width; mainly due to transverse growth
  3. Proclined eruption of permanent incisors, forming a wider arch & increases dental arch length
  4. Appositional growth of alveolar processes in 3 planes
  5. Appropriate size of apical base and teeth
809
Q

What are the factors that hamper dental arch alignment?

A
  1. Lack of interdental, primate and leeway spaces
  2. Reduction in dental arch length after permanent incisors erupt
  3. Dento-alveolar disproportion (mismatch between tooth & jaw size)
  4. Early loss of primary teeth
  5. Soft tissue issues - low frenal attachment resulting in midline diastema
  6. Oral habits such is sucking on a pacifier or suck on a thumb