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All years study > Year 3, Sem 2 > Flashcards

Year 3, Sem 2 Flashcards

1
Q

What are similarities and differences btwn primary and secondary acute apical periodontitis?

A

Primary: initial periapical response, so swelling or periapical evidence, vital or non-vital

Secondary: similar symptoms happened before, widening of PDL space at apex, discontinuation of lamina dura, tooth non-vital

BOTH: Pain of short duration, TTP

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2
Q

What is a periapical granuloma also known as?

A

Chronic apical periodontitis

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3
Q

What are characteristics of chronic apical periodontitis?

A
  • Asymptomatic
  • Well-defined radiolucency
  • <1cm
  • No corticated borders
  • Non-vital
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4
Q

How is a radicular cyst caused?

A

Rests of epithelial cells of Malassez in PDL are stimulated to proliferate and undergo cystic degeneration by inflammatory products from non-vital tooth

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5
Q

What are characteristics of radicular cyst?

A
  • No symptoms unless secondary infection
  • Large cysts can cause swelling
  • Feel bony hard if cortex intact, crepitant as it thins and rubbery/fluctuant as its lost
  • Located at apex of non-vital tooth
  • Common in mx anteriors
  • Well-defined radiolucency >1cm, with corticated borders (unless infected)
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6
Q

What are some side effects of large radicular cysts?

A
  • Displacement and resorption of nearby roots
  • Invaginate antrum
  • Outer cortical plates can expand
  • Displace IAN canal inferiorly
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7
Q

How to manage radicular cyst?

A
  • Exo, endo or apicoectomy
  • If large, can involve surgical removal/marsupialisation
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8
Q

What is a residual cyst?

A
  • Cyst that remains after incomplete removal of original cyst (same symptoms as radicular cyst)
  • More common in md
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9
Q

What are characteristics of acute periapical abscess?

A
  • Pus
  • Swelling
  • Severe pain & sudden in onset
  • No radiographic evidence or slight widening of PDL space
  • Non vital tooth
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10
Q

What are characteristics of chronic periapical abscess?

A
  • Pus
  • No/little pain
  • Swelling/sinus opening
  • Ill-defined radiolucency at apex of tooth
  • No corticated border evident
  • Non-vital tooth
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11
Q

What is an apical scar?

A

Normally surgical site fills with blood clot which mineralises and remodels like surrounding bone. In apical scar, this process fails to occur. If RCT was completed >8 months ago and there isn’t normal bone formation, it is considered apical scar.

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12
Q

Differentiate between periapical and periodontal abscess

A
  • Acute periapical: sharp shooting pain, caries/trauma hx, swelling w/ pus, vertical TTP, non-vital, tender in apical region of B sulcus, no/slight PDL widening, tx: RCT or exo
  • Chronic periapical: no pain, caries/trauma hx, sinus opening and pus, vertical TTP, non-vital, ill-defined radiolucency at apex, tx: RCT or exo
  • Periodontal: dull aching/gnawing pain, deep pocket & pus extruding from pocket, horizontal TTP, vital, tender in lateral tooth region of attached gingiva, ill-defined radiolucency at let aspect of root, tx: perio management and AB if required
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13
Q

What is condensing osteitis caused by?

A

If exudate from infected pulp is of low toxicity and long standing, the mild irritation may lead to circumscribed proliferation of periapical bone.

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14
Q

What are features of condensing osteitis?

A
  • Non-vital, large carious lesion
  • Widening of PDL space at apex, loss of lamina dura at apex
  • no/mild symptoms
  • Smooth, distinct periphery that blends into surrounding bone
  • Radiopaque internal structure
  • Can stimulate resorption or bone formation
  • Halo shadow if condensing osteitis lesion reaching mx antrum
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15
Q

How is condensing osteitis managed?

A
  • Endo or exo
  • Surgical removal of sclerotic bone not indicated unless symptomatic
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16
Q

Why does periapical cemental dysplasia happen?

A

Localised change on normal bone metabolism results in replacement of components of normal cancellous bone with fibrous tissue and cementum like material, abnormal bone or both.

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17
Q

What are clinical features of periapical cemental dysplasia?

A
  • Asymptomatic
  • Vital tooth
  • No TTP
  • Large lesions can expand bone
  • Middle age, females, md anterior region more common
  • Lesions are multiple
  • Well-defined radiolucency with varying radiopacities internally, surrounded by sclerotic border.
  • Loss of lamina dura, expansion of jaws if large and elevation of mx antrum.
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18
Q

What is this?

A

Early periapical cemental dysplasia

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19
Q

What is this?

A

Condensing osteitis

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20
Q

What is focal cemental osseous dysplasia?

A

Posterior counterpart of cemento-osseous dysplasia

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21
Q

What is florid cemento-osseous dysplasia?

A

Same as periapical cemental dysplasia but has extensive involvement in 2 or more quadrants

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22
Q

What is the tx for periapical cemental dysplasia?

A
  • Continuous observation
  • Surgical removal and microscopic exam for larger lesions
  • Rarely teeth exo required
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23
Q

What are aetiological factors for hypercementosis?

A
  • Ortho
  • Periapical inflammation
  • Unerupted tooth
  • Pagets disease
  • Idiopathic
  • Hyperpituitarism
  • Cleidocranial dysplasia
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24
Q

What are features of hypercementosis?

A
  • Asymptomatic
  • Vital
  • Non TTP
  • Most common in premolars, then molars
  • Normal lamina dura and PDL
  • Smooth/irregular outline
  • No tx required
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25
Q

What is this?

A

Late periapical cemental dysplasia

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26
Q

What is this?

A

Hypercementosis

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27
Q

What is this?

A

Hypercementosis

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28
Q

What is benign cementoblastoma?

A

Slow growing, mesenchymal neoplasm composed of cementum that attaches to apex of permanent tooth.

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29
Q

What is this? + how is it treated?

A

Benign cementoblastoma

Tx: exo

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30
Q

What are features of benign cementoblastoma?

A
  • Vital and painful
  • Slow growing and may displace teeth
  • Md molar/premolar area most common
  • Mixed radiopaque/lucent lesion with wheel spoke pattern, surrounded by radiolucent halo and corticated border
  • Can cause ERR or expansion of jaws
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31
Q

What is Garre’s osteomyelitis and what is it caused by?

A

Balance of bone metabolism is tipped toward inc bone formation, producing subsequent sclerotic radiographic appearance. Caused by dental infection or cellulitis involving perioteum.

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32
Q

What is this?

A

Garres Osteomyelitis

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33
Q

What are features of Garres osteomyelitis?

A
  • Non-vital tooth
  • Intermittent recurrent swelling, pain, fever, lymphadenopathy
  • Common in young adults
  • Mor common in md
  • Poorly defined borders when disease is active
  • Radiopaque lines parallel to cortical bone surface (onion skin appearance)
  • Roots may undergo ERR and lamina dura may be lost
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34
Q

How is Garre’s osteomyelitis treated?

A

Exo of affected tooth

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35
Q

What radiopaque structures are associated with non vital teeth?

A

Condensing osteitis

Garre’s osteomyelitis

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36
Q

What is periapical idiopathic osteosclerosis?

A

Localised growths of compact bones within the cancellous bone

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37
Q

What are clinical features of idiopathic osteosclerosis?

A
  • Asymptomatic
  • Normal overlying mucosa
  • Vital tooth
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38
Q

What are clinical features of idiopathic osteosclerosis?

A
  • Asymptomatic
  • Normal overlying mucosa
  • Vital tooth
  • Common around md premolars and molars
  • Borders well defined or ragged
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39
Q

What is this?

A

Idiopathic osteosclerosis

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40
Q

What are odontomas composed of? What is their impact on surrounding structures?

A
  • Mature components of dental hard and soft tissue
  • Can interfere with normal tooth eruption and can cause expansion of jaw
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41
Q

What are features of compound odontomas?

A

Collection of small radiopaque masses (denticles), most commonly in ant mx

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42
Q

What is the complex odontoma?

A
  • Irregular mass of calcified tissue with no resemblance to normal tooth.
  • May be missing tooth if it arises from normal tooth follicle.
  • Often found in post md
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43
Q

What is dilated odontoma?

A
  • Most severe expression of dens invaginatus
  • Found in anterior mx
  • Radiopaque with radiolucent central portion (donut form)
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44
Q

How are odontomas managed?

A

Surgical removal (no recurrence)

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45
Q

What are types of microdontia/macrodontia?

A

True generalised (assoc with pituitary gigantism or dwarfism)

Relative generalised

Focal/localised

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46
Q

What are DD of localised macrodontia?

A

Gemination, fusion

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47
Q

What do supernumerary teeth result from?

A

Continued proliferation of dental lamina to form 3rd tooth germ

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48
Q

What conditions commonly have supernumerary teeth?

A

Cleidocranial dysplasia

Aperts syndrome

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49
Q

What is a paramolar vs distomolar?

A
  • Paramolar: located B or L to mx molar
  • Distomolar: located D to 3rd molar
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50
Q

What are the most common missing teeth?

A
  • 3rd molar
  • 2nd premolar
  • Mx lat incisors
  • Md central incisors
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51
Q

What is oligodontia?

A

Lack of development of 6 or more teeth

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52
Q

What is fusion vs gemination?

A
  • Fusion: 2 tooth germs fuse to form one
  • Gemination: Single tooth bud attempts to divide
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53
Q

What syndromes is taurodontism associated with?

A
  • Downs syndrome
  • Klinefelter’s disease
  • Ectodermal dysplasia
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54
Q

What is talons cusp + concern?

A

Extra cusp found commonly on mx lat incisor. Cusp can have pulp horn so exposure possible in bruxism pts

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55
Q

What is dens evaginatus and clinical significance?

A

Tubercle of enamel on occlusal surface of premolars. Pulp can be present in tubercle so pulp exposure is high possibility.

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56
Q

What is dens invaginatus + clinical significance + tx?

A
  • Deep surface invagination of crown root lined by enamel.
  • Commonly found in mx lat incisors.
  • Debris can get caught and lead to caries
  • On radiograph can have inverted tear drop shape
  • Tx: place prophylactic restoration & monitor
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57
Q

What is this + disease associated?

A

Hutchinson’s incisors- associated with congenital syphillis

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58
Q

What are DD of enamel pearl?

A

If conventional film is used, air bubble artifact.

Calculus

Pulp stone

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59
Q

What is amelogenesis imperfecta + 3 types?

A

Developmental alteration in enamel structure in absence of systemic disease.

  • Hypoplastic
  • Hypomaturation
  • Hypocalcification
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60
Q

What are the differences between the 3 types of amelogenesis imperfecta?

A
  • Hypoplastic: hard, translucent, thin enamel, random pits/grooves, Square crowns, open contacts, lack of proper anatomy
  • Hypomaturation: adequate enamel thickness, pitted, snow capped, enamel wears rapidly, enamel exhibits radiodensity similar to dentin
  • Hypocalcified: adequate thickness of enamel, chalky appearance, yellow/orange, brittle, enamel, fractures off
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61
Q

What is dentinogenesis imperfecta?

A

Altered structural development of dentine in absence of systemic disease

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62
Q

What is the difference between type I, II and II dentinogenesis imperfecta?

A

Type I: assoc with osteogenesis imperfecta

Type II: not assoc with osteogenesis imperfecta

Type III: Bradwine type (racial isolate in maryland)- egg shell teeth

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63
Q

What is this?

A

Hypocalcified AI

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64
Q

What is this?

A

Hypomaturation AI

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65
Q

What is this?

A

Hypoplastic AI

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66
Q

What are similarities of the 3 types of DI?

A
  • Normal enamel but wears rapidly
  • Abnormal dentine and pulp
  • Translucent, opalescent appearance
  • Yellow-brown to grey in colour
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67
Q

What are radiographic features of type I and II DI?

A
  • Thin roots
  • Bulbous crown
  • Cervical constriction
  • Obliteration of pulp chamber
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68
Q

What are radiographic features of type III DI?

A
  • Egg shell appearance
  • Large pulp
  • Thin dentine
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69
Q

Tx for DI?

A

Jacket crowns anteriorly

SSC posteriorly

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70
Q

What are the 2 types of dentin dysplasia?

A

Type I Radicular

Type II Coronal

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71
Q

What are characteristics of type I dentine dysplasia?

A
  • Rootless teeth (W shaped molar roots)
  • Pulp obliterated
  • Teeth misaligned
  • Normal colour
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72
Q

What are characteristics of type II dentine dysplasia?

A
  • Normal roots (except for radicular pulp obliteration)
  • Large coronal pulp
  • Multiple pulp stones
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73
Q

What are characteristics of regional odonto-dysplasia (ghost teeth)

A
  • Thin rough enamel
  • More common in mx anterior region
  • Uncommon
  • Small
  • Thin enamel + dentine
  • Large pulp
  • Marked reduction in radiodensity
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74
Q

What is turners hypoplasia?

A
  • Local hypoplastic defect (brown spot) on permanent tooth as a result of periapical infection/trauma of primary predecessor.
  • Crown may appear as ill-defined radiolucent region
  • Mx incisors and premolars are most affected
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75
Q

What is this?

A

Dentinogenesis Imperfecta type I and II

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76
Q

What is this?

A

Type III dentinogenesis imperfecta

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77
Q

What is this?

A

Type I dentine dysplasia

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78
Q

What is this?

A

Type II dentine dysplasia

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79
Q

What is this?

A

Regional odonto‐dysplasia (Ghost teeth)

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80
Q

What is this?

A

Turners hypoplasia?

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81
Q

What is primary herpetic gingivostomatitis?

A
  • HSV-1
  • Common in children
  • Fever, malaise, lymphadenopathy
  • Vesicles on lips, tongue and cheek that rupture and form shallow ulcers
  • Difficulty in eating/swallowing
  • Tx: hydration, analgesics, CHX mouthwash 3/day
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82
Q

What is recurrent herpes labialis?

A
  • When HSV-1 is reactivated due to sunlight, fevers, trauma, immunosuppression
  • Tingling, burning
  • Vesicles on lip (cold sore) that rupture to form ulcers
  • Heals in 7-10 days
  • Tx: self limiting, acyclovir cream may reduce duration
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83
Q

What is recurrent intra-oral herpes?

A
  • Occurs of keratinised epithelium
  • Shallow, irregularly shaped clusters of surface erosion
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84
Q

What is varicella (chickenpox)?

A
  • Highly contagious
  • Malaise and fevere
  • Rash on trunk, then face, limbs
  • Macule/papule develop intro vesicle and can rupture
  • Tx: self limiting, antivirals
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85
Q

What is shingles?

A
  • Virus becomes dormant in dorsal root of trigeminal ganglia
  • Reactivation occurs in 5-7th decade
  • Dermatomal distribution
  • Pain and burning along nerve followed by vesicles in 24-48hours
  • Tx: systemic antiviral therapy (if within 72 hours), analgesics, specialist referral if immunocompromised
  • Tx: supportive, acyclovir
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86
Q

What is infectious mononucleosis?

A
  • Kissing disease
  • EBV
  • Malaise, fever, sore throat, lymphadenopathy
  • Mucosal petechiae (near vibrating line)
  • Enlarged tonsils with exudate
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87
Q

What is hairy leukoplakia?

A
  • Seen in immuno-compromised pts
  • Assoc with EBV
  • No malignant potential
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88
Q

What does cytomegalovirus cause orally?

A
  • Can infect major salivary glands and cause xerostomia
  • Ulcerations
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89
Q

What is kaposi sarcoma?

A

Seen in HIV pts

Vascular tumour (purplish, bleeds readily)

Found on palate

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90
Q

What are some examples of HPV infection?

A
  • Verruca vulgaris
  • Squamous papilloma
  • Condyloma acuminata
  • Focal epithelial hyperplasia
  • SCC
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91
Q

What is verruca vulgaris?

A
  • Appears on vermillion border or keratinised surfaces of gingiva and palate
  • Oval, white
  • Contagious
  • Common in children/adolescents
  • Tx: excision, recurrence uncommon
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92
Q

What is condyloma acuminatum (venereal wart)?

A
  • Sexually transmitted (suspect sexual abuse if found in young children)
  • Multiple/single lesions
  • Lips, commissures and gingiva
  • Common in homosexual males
  • Tx: excision, laser, cryotherapy
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93
Q

What is focal epithelial hyperplasia (heck’s disease)?

A
  • Rare
  • Predominantly children
  • Asymptomatic and contagious
  • Tx: spontaneous recover, laser, cryotherapy
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94
Q

What is squamous cell papilloma?

A
  • Single, <1cm
  • Painless
  • Pedunculated with numerous projections
  • Tx: excision, do not recur
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95
Q

What are characteristics of measles?

A
  • Highly contagious
  • Runny nose, cough, conjunctivitis, fever
  • Macullo-papular rash on skin
  • Koplik spots on B mucosa
  • Tx: OH, antipyretic
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96
Q

What are characteristics of mumps?

A
  • Highly contagious
  • Salivary gland enlargement
  • Fever, pain
  • Symptomatic management
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97
Q

What are characteristics of mumps?

A
  • Highly contagious
  • Salivary gland enlargement
  • Fever, pain
  • Symptomatic management
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98
Q

What are characteristics of hand, foot and mouth disease?

A
  • Coxsackie virus
  • Young children
  • Lesions of hand foot and mouth
  • Oral vesicles lead to ulcers with peripheral erythema
  • Symptomatic management
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99
Q

What is herpangina?

A
  • Coxsackie virus
  • systemic infection
  • Children
  • Fever
  • Vesicles rupture leaving ulcers
  • Tonsils, soft palate, uvula
  • Symptomatic management
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100
Q

What are features of homogenous leukoplakia?

A
  • Even colour and texture
  • Uniformly flat
  • Thin
  • Shallow cracks of surface keratin
  • Lower malignant transformation
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101
Q

What are characteristics of non-homogenous Leukoplakia and the 3 types?

A
  • Non uniform colour and texture
  • Higher malignant transformation
  • Speckled, nodular, verrucous
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102
Q

What is proliferative verrucous leukoplakia?

A
  • Affects older females
  • Covers wider area (usually gingiva and mucosa)
  • No strong association with tobacco or alcohol
  • Resistant to all tx
  • Recurrence common following excision
  • High malignant transformation (70-100%)
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103
Q

What are risk factors for malignant transformation?

A
  • Female
  • Long duration of leukoplakia
  • Leukoplakia in non-smokers
  • Tongue/FOM
  • Larger size
  • Non-homogenous
  • Present of dysplasia
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104
Q

How is oral submucous fibrosis caused?

A

Betel nut chewing- induces inflammation, inc collagen synthesis and dec collagen degradation leading to excessive fibrous tissue formation → fibrosis

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105
Q

What are characteristic of OSF?

A
  • Early: Burning sensation, depigmentation, de-papillation of tongue, leathery mucosa, vesicles
  • Late: fibrous bands in B mucosa and rima oris, trismus, narrowing of oropharyngeal orifice, distortion of uvula
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106
Q

What are issues with OSF?

A
  • Trismus
  • OH
  • Difficulty eating, OH
  • Poor nutrition
  • Malignant transformation
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107
Q

What are risk factors for malignant transformation of OSF?

A

Male, older age, low SES, presence of other OPMD.

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108
Q

What is actinic cheilitis?

A
  • Chronic inflammatory condition of lip arising from excessive solar UV radiation exposure
  • Malignant potential
  • Hyperplastic/atrophic changes with pigmentation and keratinisation
  • Risk factors include:
    • UV intensity
    • Age
    • Lack of lip protection
    • Genetic predisposition
    • Immunosuppression
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109
Q

What is palatal keratosis associated with reverse smoking?

A
  • Light end of cigar inside mouth
  • Exclusively on palate
  • Diffuse whitening of palatal mucosa
  • Elevated red nodules
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110
Q

What features indicate malignant transformation of OPMDs?

A
  • Quick inc size
  • Crack or fissure
  • Bleeding spots
  • Ulceration
  • Appearance of growth
  • Induration
  • Rolled edges
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111
Q

What are characteristics of pseudomembranous candidiasis?

A
  • White plaques/papules on surface of oral mucosa- may appear as milky curds
  • Can be wiped of, revealing erythematous mucosa
  • Found in immunosuppressed individuals
  • Risk factors: elderly, poorly controlled diabetes, HIV, corticosteroids, broad spectrum AB therapy
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112
Q

What are features of erythematous candidiasis?

A
  • Localised erythema of oral mucosa
  • May/may not have symptoms
  • Commonly on dorsum of tongue and palate
  • Risk factors: broad spectrum AB, corticosteroids, HIVS
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113
Q

What is denture associated erythematous candidiasis?

A
  • Affects mucosa in contact with fitting surface of denture
  • Erythema and oedema
  • Asymptomatic, mild discomfort or burning sensation
  • Risk factors: poor denture hygiene, ill fitting denture, denture wearing at night
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114
Q

What are features of angular cheilitis?

A
  • Chronic inflammatory lesion at labial commissure
  • Fissured erythematous lesion
  • Risk factors: reduced vertical height (dentures), wrinkling at angle of mouth, maceration with saliva, iron/B12 deficiency
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115
Q

What is median rhomboid glossitis?

A
  • Chronic erythematous lesion on tongue, affecting dorsum anterior to circumvallate papilla
  • Symmetrical
  • Rhomboid shape
  • Depapillation
  • Cause unknown
  • Candida hyphae growing to epithelium
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116
Q

What are features of hyperplastic candidiasis (isolated oral lesions)?

A
  • Can be isolated oral lesion or mucocutaneous candidosis
  • Appear as white patch affecting anywhere on oral mucosa
  • Common in post commissural area
  • Common among smokers
  • Higher risk of malignant transformation
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117
Q

What is the issue with candida hyphae invading epithelium?

A

Can lead to secretion of nitrous amides (carcinogenic), making epithelium more vulnerable to malignant transformation

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118
Q

What are features of mucocutaneous candidiasis?

A
  • Heterogenous disorder affecting mucosa, skin and nails
  • Often associated with endocrinopathies or immunodeficiency
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119
Q

How can you manage candida infecitons?

A
  • Identify predisposing factor and eliminate/control
  • Inspect denture for denture induced lesions
  • Denture hygiene advice
  • Reline or new denture if required
  • Correction of iron, B12 deficiency
  • If non-responsive or systemic antifungals are required (fluconazole), refer to specialist
  • Antifungal meds: topical or systemic
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120
Q

What is histoplasmosis?

A
  • Invasive fungal infection caused by histoplasma capsulatum
  • Causes chronic pulmonary infection- similar to TB
  • Need biopsy
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121
Q

What is scarlet fever?

A
  • Streptococcal infection
  • Begins as tonsillitis and pharyngitis
  • Most common children
  • Tonsils, pharynx and soft palate erythematous and oedematous
  • Palatal petechiae, strawberry tongue
  • High fever
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122
Q

What is erysipelas?

A
  • Superficial skin infection
  • Streptococcal and staph aureus
  • Affect young or elderly
  • Cheeks, nose affected
  • Bright red, painful, swollen, indurated, warm areas
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123
Q

What are features of neisseria gonorrhoea?

A
  • Involvement of oral cavity due to oral sex
  • Painful ulceration of lips, erythematous gingivae
  • Gonococcal pharyngitis
  • Vesicles or ulcers with gray/white pseudomembrane
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124
Q

What are features of mycobacterium tuberculosis oral lesions?

A
  • Oral lesions relatively rare
  • Secondary to pulmonary lesions (hx of TB useful)
  • Chronic ulcers on dorsum on tongue
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125
Q

What are characteristics of primary, secondary and tertiary syphilis lesions?

A

Sexually transmitted & caused by treponema pallidum

  • Primary: forms 3-90 days after exposure, primary chancre, heals in 3-8 weeks
  • Secondary: systemic symptoms, snail track ulcers, forms 4-10 weeks after initial infection
  • Tertiary: 1-30 yrs latency, syphilitic gumma
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126
Q

What are some oral manifestations of syphilis?

A
  • Screwdriver or peg shaped incisors
  • Mulberry molars
  • Hypoplastic teeth
  • Saddle nose
  • Atrophic glossitis
  • Post-rhagadic scars
  • High arched palate
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127
Q

What is actinomycosis?

A
  • Chronic, suppurative infection
  • Rare
  • Organism enters through area of trauma (exo socket)
  • Minimal/no pain
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128
Q

What is the definition of SSC?

A

Invasive epithelial neoplasm with varying degrees of squamous differentiation and a propensity to early and extensive lymph node metastases, occurring predominantly in alcohol and tobacco-using adults in the 5th to 6th decades of life.

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129
Q

What are the oral cancer burdens?

A
  • Require massive surgery
  • Disfugirement
  • Disability and rehab
  • COst/hospital stay
  • Social
  • Significantly affects quality of life
  • If uncontrolled- death
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130
Q

What is screening?

A

Method for detection of disease when it is not symptomatic

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131
Q

What are pros and cons of screeinng during conventual oral exam?

A
  • Pros: MI, high validity, short time, can be repeated, no special facilities required, can be undertaken during exams
  • Cons: depends on quality of examiner, training of screeners required, can’t distinguish between benign lesions, cancer and OPMD’s, may not turn up for next appt, cost effectiveness uncertain
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132
Q

What are adjunctive methods to oral cancer screening?

A

Vital staining

Autofluorescence

Brush biopsy

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133
Q

What are features of vital staining? How to use it?

A
  • Good in detecting SCC
  • High sensitivity and specificity
  • Detection of dysplasia doubtful
  • Cheap, simple
  • Clean surface with acetic acid, apply toluidine blue on lesion, remove excess stains with acetic acid. If blue still present, indicates carcinoma in situ or carcinoma
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134
Q

What are features of autofluorescence? How to use it?

A
  • Light of 400-500nm wave length
  • Loss of fluorescence/dark patch indicates presence of abnormal tissue
  • Does not diagnose any lesions and interpretation is required by specialist.
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135
Q

When does midline suture of md close?

A

1 year old

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136
Q

What are the aetiologies of posterior cross bite?

A
  • Genetics, environment, habits (thumb sucking)
  • Crowding, impaired nasal breathing, over retention of primary teeth
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137
Q

How can we examine transverse dimension?

A
  • Study models and I/O
  • Need to assess face and dentition in frontal, sagittal and transverse views
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138
Q

What is the rationale for early correction of posterior crossbite with functional shift?

A

Functional shift can cause adaptive remodelling of TMJ and asymmetric md growth. This can become a permanent skeletal asymmetry if not intercepted early.

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139
Q

What is the difference between relative and absolute transverse discrepency?

A

Relative: when teeth are in class I occlusion, there is no transverse discrepancy

Absolute: when teeth are placed in class I occlusion this is transverse discrepancy

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140
Q

What are methods to diagnose skeletal and dental transverse problems?

A
  • Andrews WALA ridge
  • Transpalatal width
  • Maxillomandibular transverse differential
  • CBCT’s
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141
Q

How does dental vs skeletal posterior crossbite appear?

A
  • Dental: Mx molars are tipped lingually with maxilla of normal width
  • Skeletal: Mx teeth are often tipped buccally to compensate for mx constriction
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142
Q

What are tx options for skeletal vs dental crossbites?

A
  • Skeletal: RME
  • Dental : tip mx posterior teeth buccally
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143
Q

Why is correction of dental crossbites recommended in mixed dentition?

A
  • Eliminates functional shifts and wear on erupted permanent teeth and possible dento-alveolar asymmetry
  • Increases arch circumference to provide more space
  • Simplifies future tx
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144
Q

How are dental crossbites treated?

A

Tipping teeth bucally

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145
Q

How can skeletal crossbites be corrected and when should this be done?

A

Mx:

  • Before age 14 ideal: can use any expansion device
  • If early adolescence: RME with heavy force
  • If suture has fused: camouflage tx or surgical mx expansion (if severe)

Md

  • Camouflage tx or surgical md constriction (if severe)
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146
Q

What are examples of SME appliances?

A
  • Quad helix
  • W arch
  • URA- Hawley
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147
Q

What are examples of RME appliances?

A
  • Hyrax
  • Haas
  • Tooth-bone or bone anchored RME
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148
Q

What are advantages of quad helix?

A
  • More flexible and greater range of action than W arch
  • Helices of anteriror palate are bulky so can help eliminate thumb sucking habit
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149
Q

What happens following opening of maxillary suture and formation of diastema?

A
  • Palatal suture fills with bone
  • Crowns tilt mesially to close gap
  • Roots shift mesially
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150
Q

What occlusion class is commonly associated with deep bite?

A

Class II

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151
Q

What are the 3 fundamental ortho tx approaches for deep bite correction (not including surgical options)?

A

Posterior extrusion

Anterior intrusion

Anterior teeth flaring

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152
Q

What are methods for extruding posterior teeth to correct deep bite?

A
  • Straight continuous arch wire
  • Step bend archwire
  • Bite plates in ant region
  • Md reverse curve of spee
  • Altering bracket placement heights
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153
Q

What patients are indicated for extrusion of posterior teeth to correct deep bite?

A

Short lower facial height

Excessive curve of spee

Moderate-minimal incisor display

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154
Q

What pts are indicated for flaring of incisors?

A

Pts with Class II div II deep bite or Class III

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155
Q

When is intrusion of incisors indicated for deep bite patients?

A

Long lower facial heights

Excessive incisor display

Overeruption of upper incisors

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156
Q

What effect does extrusion of posterior teeth have on md?

A

Moves md downward and backwards, increasing lower facial height and interfacial gap

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157
Q

What is the etiology of open bite?

A
  • Genetics
  • Environment (habits, mouth breathing)
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158
Q

What are effects of thumb sucking?

A
  • Narrow transverse width of mx
  • Anterior open bite
  • Proclination of upper incisors
  • Retroclination of lower incisors
  • Posterior cross bite
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159
Q

What are the 3 phases of thumb sucking?

A
  • Phase 1: normal process, birth-3yrs
  • Phase 2: 3-6/7 years, chil needs to break habit to prevent use of appliances, can indicate anxiety
  • Phase 3: intractable sucking, often require psychological assistance, usually goes beyond age 4-5
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160
Q

How should you intercept thumb sucking in 3-6 yr/olds?

A
  • Nail paint
  • Positive reinforcement
  • Finger splint
  • Gloves
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161
Q

What age can open bite spontaneously resolve if thumb sucking habit is ceased?

A

In primary dentition

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162
Q

When should appliance therapy be considered to prevent thumb sucking?

A

If other methods have ineffective by age 7, more definitive tx is required.

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163
Q

What should happen if pts open bite closed after abandoning habit but their tongue now has functional problem?

A

Speech therapy and appliance to correct tongue posture

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164
Q

How does removable tongue crib work?

A
  • Prevents tongue pressing against teeth and seating on palate
  • Prevents thumb/pacifier entering mouth
  • Effective until permanent incisor root apices have fully developed
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165
Q

Does tongue thrust cause open bite? Why/why not?

A

No, it is secondary to thumb sucking. It just prevents it going back to normal

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166
Q

What open bite measurement in mixed dentition warrants immediate appliance therapy?

A

If greater than 2mm

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167
Q

At what stage of tooth development can spontaneous open bite correction no longer occur?

A

If central incisor apices are already formed

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168
Q

How long each day does a removable appliances need to be worn to impact position of teeth?

A

At least 6 hours

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169
Q

What are indications for removable vs fixed appliances for open bite pts?

A
  • Removable: once habit is already stopped and you need to correct tongue posture
  • Fixed: to stop habit
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170
Q

After open bite correction, what should be used to help correct the tongue in rest position? How long for?

A
  • Hawley plate with tongue crib and posterior bite block
  • Hawley plate with incisive orifice
  • 6 months
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171
Q

What is orthodontic anchorage?

A

Preventing tooth movement in one group of teeth while moving the other group of teeth.

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172
Q

What is group A anchorage?

A

75-100% movement from anterior segment and the rest from posterior segment to close extraction space

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173
Q

What is group B anchorage?

A

50% movement from anterior and posterior segments

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174
Q

What is group C anchorage?

A

75-100% movement from posterior segment and the rest from anterior segment to close extraction space

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175
Q

What are the 5 types of anchorage control according to Angle?

A
  • Occipital (headgear)
  • Intermaxillary (elastics)
  • Stationary (reinforcement of anchorage units through banding of multiple teeth)
  • Simple (relied on competing support of dentition to affect tooth displacement)
  • Reciprocal (as above)
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176
Q

What is simple anchorage?

A

Use of larger tooth or teeth to move smaller tooth using tipping movement

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177
Q

What is stationary anchorage?

A

Anchorage teeth move bodily while the movement teeth are allowed to tip.

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178
Q

What is reciprocal anchorage?

A

Teeth of equal size are moved together by same amount

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179
Q

What is reinforced anchroage?

A

Utilises extra forces to limit/eliminate movement in one segment and promote movement in other segment

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180
Q

What are methods off reinforced anchorage?

A

Utilising 7’s

Incorporating more teeth for anchorage

Reducing number of teeth to be moved

Elastics

Headgear

Implants/miniscrews

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181
Q

How can maximum anchorage be achieved?

A

Implants and ankylosed teeth

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182
Q

Planning to extract upper 1st premolars. What kind of anchorage do we need? What % of extraction space should be closed by movement of canine vs posteriors?

A

Type A (75% canine, 25% molar)

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183
Q

Pt missing upper 1st premolar. Planning to extract lower 1st premolar. Molars almost in class I relationship and canines in class III. What anchorage is required?

A

Type A (90-100% anchorage required)

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184
Q

Would like to extract upper 1st premolar to resolve crowding. What anchorage is required?

A

Type B (50% of each to make molar full unit class II and canine class I)

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185
Q

When does mandibular growth catch up to maxilla?

A

When adolescent growth spurt is completed

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186
Q

How does growth of mx occur?

A

Intramembranous ossification

  • Apposition of bone at sutures
  • Surface remodelling

Until 7 years, growth is predominantly forwards from the cranial base pushing it forwards. When the cranium ceases its growth, maxilla growth is from sutural growth on the posterior and superior aspects. This growth pushes mx downwards and forwards. Resorption of anterior surface occurs

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187
Q

What are sites of growth on md?

A

Posterior md ramus

Condyle

Coronoid process

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188
Q

Describe remodelling of the palatal vault

A

There is resorption of the nasal floor and apposition of bone on the palate

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189
Q

When does termination of mx growth occur in girls vs boys?

A

Boys: 17

Girls: 15

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190
Q

What direction does the md grow?

A

Downwards and forwards

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191
Q

Why does increased chin prominence occur?

A

There is forward translation of chin resorption above chin (no bone apposition occurs on chin)

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192
Q

When does cranial base finish growth?

A

7 years

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193
Q

What age is it too late to treat mx skeletal deficiency? What is the ideal age?

A
  • 10 years is too late and will need to be treated with surgery
  • Ideal age is around 7 as you want pt after eruption of incisors
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194
Q

What is the issue with excessive mandibular growth pattern patients?

A

Difficult to treat. Often require surgery.

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195
Q

What structures are involved in equilibrium?

A

Tongue

Lips/cheeks

PDL

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196
Q

How long must force be placed against a tooth to impact its position?

A

6hours each day

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197
Q

Describe balance between tongue and lip/cheek during swallowing

A

Tongue exerts more force against the teeth than the lip and cheek. However, this is only a very short amount of time and isn’t enough to cause tooth movement

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198
Q

How does the PDL affect equilibrium?

A

At rest, there is around 5g more force coming from the tongue than the lips/cheek. The PDL is able to withstand 5g of force to prevent tooth movement. Therefore the PDL is able to resist movement and teeth remain in equilibrium

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199
Q

What is the threshold for orthodontic force?

A

5-10g

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200
Q

How does mobius syndrome affect equilibrium?

A

In mobius syndrome, there is underdevelopment of cranial nerves 6 and 7. This can result in facial paralysis and inability to move eyes side to side. As there is paralysis of orbicularis oris muscle there is no force coming from the lip side, while there is still forward pressure from the tongue. This disrupts equilibrium and causes teeth to procline.

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201
Q

How does thumb sucking affect arch width?

A

Tongue isn’t sitting high against palate so mx posterior teeth are not supported with tongue pressure anymore. Increased pressure against teeth from cheek side due to sucking, results in palatal tipping of mx posteriors. Can have narrow mx arch and posterior cross bite.

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202
Q

What is maximum anchorage?

A

By definition means no anchorage loss. The only true maximum anchorage can be achieved with skeletal anchorage systems.

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203
Q

What is normal swallowing habit in children 2-4years?

A

Pushing tongue against lower lip

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204
Q

What can be used for treatment of open bite in early mixed dentition?

A

Tongue spurs and TPA

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205
Q

When do teeth start forming?

A

20 weeks in utero

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206
Q

What syndromes are assoc with missing teeth?

A

Ectodermal dysplasia

Ellis Van Crevald

Downs Syndrome

Crouzon

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207
Q

What should you do if there is no permanent successor and the tooth is infraoccluded?

A

Can build up tooth or crown it

Can extract and orthodontically close the space.

Can extract and place implant or bridge

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208
Q

What happens if implants are placed prior to alveolar growth ceasing?

A

They will become submerged as the bone continues to grow around it.

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209
Q

What syndromes are associated with supernumerary teeth?

A
  • Cleidocranial dysplasia
  • Ehlor danlos syndrome
  • Ellis-van Creveld
  • Apert syndrome
  • Gardener syndrome
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210
Q

How are supernumerary teeth managed?

A

Can be extracted

They can be left if not causing any harm

If spacious arch, they may fit in

If crowded arch, may erupt and then extract.

If it doesn’t erupt, surgically extract at later stage

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211
Q

How do you label supernumerary teeth?

A

Inverted/non inverted

Erupted/non erupted

Type (mesiodens, distomolar etc)

Tooth number closest to

S

E.g. inverted non-erupted mesiodens 11S

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212
Q

What conditions are sometimes associated with microdontia?

A

Ectodermal dysplasia

Pituitary dwarfism

Ellis-van crevald

Downs syndrome

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213
Q

What conditions are sometimes associated with macrodontia?

A

Pituitary gigantism

Klinefelters disease

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214
Q

If pt presents with pulpally involved (abscessed) premolar with no history of caries/trauma what could the diagnosis possibly be?

A

Dens invaginatus

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215
Q

What is the early intervention treatment for dens evaginatus?

A

Protection of the tubercle by placing composite resin around it. Best done before the tooth comes into occlusion. Avoid grinding of tubercle and sealing as it can expose pulp.

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216
Q

Why may first permanent molars (6’s) have radiolucencies and no other teeth have issues (2)?

A

PEIR

Hypoplasia

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217
Q

What is PEIR?

A
  • Pre-eruptive intracoronal resorption.
  • Lesion located within dentine that presents as radiolucency adjacent to the DEJ in a radiograph.
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218
Q

What are neonatal lines?

A

If there is a disturbance during birth, teeth can exhibit a linear defect on the tooth crown. Often found on primary incisors and molars as they are developing at this time.

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219
Q

If you see hypocalcified E’s, what other teeth are likely to be affected?

A

C’s (calcification takes place from birth-1st year)

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220
Q

What is rickets and the 2 types?

A

Lack of mineralisation in growing body

  • Vit D dependent rickets
  • Hypophosphatemia rickets: inability to absorb vit D
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221
Q

What hx questions need to be asked about trauma?

A
  • Med hx: allergies, transmissible disease, bleeding disorders
  • Have they had tetanus immunisation (if wound has been contaminated with soil)
  • Prev trauma hx
  • When, what, how, where?
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222
Q

What injuries have greatest effect on permanent successor?

A
  • Intrusion
  • Lateral luxation
  • Avulsion
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223
Q

What is the difference between sensibility and vitality testing?

A
  • Sensibility testing measures neural supply. If a tooth is sensible we often assume it is vital and has adequate blood supply.
  • Vitality testing measures blood flow.
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224
Q

What does dull vs ankylotic sound indicate upon percussion?

A
  • Dull: PDL is present and intact
  • Ankylotic/higher: loss of PDL
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225
Q

What is enamel infraction and tx?

A
  • Incomplete fracture of enamel (crack)
  • No tx required unless present with other injury
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226
Q

What is enamel fracture + how is it managed?

A
  • Loss of enamel without visible signs of exposed dentine.
  • Recontour any sharp areas or restore. Follow up.
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227
Q

What is complicated crown fracture and how is it managed?

A

Enamel + dentine fracture with pulp involvement

Tx:

  • Pulp capping if exposure occurs straight away and is pinpoint
  • Pulpotomy or pulpectomy
  • Exo may be indicated
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228
Q

How is uncomplicated crown root fracture managed in primary teeth?

A
  • Fracture extends subgingival but does not involve pulp
  • TTP
  • Tx: depends on location and extent of fracture- fragment removal and resto OR exo. POI and review also important
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229
Q

How is complicated crown root fracture managed in primary teeth?

A
  • Fracture extends subgingival and involves the pulp. Crown can be split into 2 or more fragments with possibility of loose fragment.
  • TTP
  • Can sometimes do pulpotomy or pulpectomy and then resto with strip crown. Often indicated for exo. POI and review
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230
Q

What is root fracture + management in primary teeth?

A
  • Coronal fragment may be displaced and mobile. Can be discoloured
  • TTP
  • If no significant mobility, no tx. If coronal segment is displaced or mobile, do exo. POI and review
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231
Q

How is concussion managed?

A

Observation only, soft diet, OH, poss complications, review

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232
Q

What is subluxation + how is it manged in primary dentition?

A
  • Bleeding from sulcus if seen promptlty after
  • Mobile + TTP
  • Tx: observation only, soft diet, OH, poss complications, review
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233
Q

What is extrusive luxation + how is it managed in primary teeth?

A
  • Mobile and TTP
  • PDL is wider apically
  • Tx: do NOT reposition. If only slightly mobile, monitor. If fairly mobile, exo. Soft diet, OH and poss complications, review.
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234
Q

What is lateral luxation + how is it managed for primary tooth?

A
  • Tooth may be proclined or retroclined
  • Usually jammed into bone so non-mobile
  • Ankylotic sound present. TTP
  • Shortened if proclined, elongated if retroclined
  • PDL space wider apically
  • Can leave to spontaneously erupt if no excessive mobility and not in traumatic occlusion. If in slight traumatic occlusion and minimal mobility can grind tooth slightly to remove occlusal interference. If excessive mobility, exo indicated. Soft diet, OH, poss complications, review
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235
Q

What is intrusion + how is it managed for primary tooth?

A
  • Short crown/may appear missing
  • Jammed into bone and non mobile
  • TTP and ankylotic sound
  • If toward bone, can leave to erupt spontaneously. If alveolar fracture or toward successor, exo.
    • < ½ crown: leave to spontaneously erupt over next 3 months
    • ½ crown: monitor closely. May erupt or may need exo.
    • 75%: exo indicated
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236
Q

How is avulsion managed for primary tooth?

A
  • Do not reimplant. Soft diet, OH, poss complications.
  • Review 1 week, 6months, 1 year
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237
Q

How is complicated root fracture managed in permanent teeth?

A
  • Clean, reposition coronal fragment and splint
  • If coronal ⅓ fracture and not too mobile, can do flexible splint for around 4 months (poor prognosis- exo likely)
  • Fractures more apically, can be managed by flexible splint for 3-4 weeks.
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238
Q

How is extrusion managed in permanent teeth?

A

Mobile, TTP, usually -ve sensibility

  1. Clean area
  2. Reposition
  3. flexible splint for 10-14 days
  4. POI
  5. Review (check RR and vitality)
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239
Q

How is lateral luxation of permanent tooth managed?

A

Usually jammed into bone, -ve TTP, usually -ve sensibility, wider apical PDL space

  1. Clean, LA
  2. Reposition tooth with finger pressure or forceps
  3. Reposition displaced bone with finger presser if fractured
  4. Splint for 4 weeks if bone fracture otherwise splint for 2 weeks
  5. POI, review
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240
Q

How is intrusion managed for permanent tooth?

A

Non-mobile, TTP, -ve sensibility, loss of PDL space

  • If immature tooth or 12–17-year-old with <6mm intrusion, leave to spontaneously erupt. If no change in position after 1 months, do ortho traction.
  • In pts 12-17 years with >6mm of intrusion or pt >17 years, perform ortho or surgical repositioning, splint for 4 weeks and perform RCT within 3-4 weeks.
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241
Q

How is avulsion managed for permanent tooth?

A
  1. Clean, reimplant tooth
  2. Flexible splint for 10-14 days
  3. RCT within 7-10 days if mature tooth. If immature tooth, see how tooth responds- if no response in 3-4 weeks do RCT
  4. AB/tetanus, POI
  5. Review (every week for 4 weeks, 2 months, 3 months, 6 months, 1 year)
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242
Q

What are the 3 signs of immature teeth?

A

Open apex

Short root

Thin dentinal walls

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243
Q

What are the types of healing with fractured roots?

A
  • Calcified tissue
  • Connective tissue
  • Bone and connective tissue
  • Granulation tissue
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244
Q

What does granulation tissue healing for root fracture indicate? How should this be treated?

A

Indicates, coronal part of fractured root is non vital as the pulp has been severed. Can root fill the coronal section and the radiolucency should resolve with bony healing. Fracture line acts as apical stop. Place MTA plug, obturate and then assess for healing.

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245
Q

What are the 3 outcomes of pulp healing?

A

Revascularisation

Pulp canal obliteration

Necrosis

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246
Q

What are the 3 forms of external root resorption and which is most concerning?

A
  • Surface root resorption (repair related)
  • Replacement root resorption (ankylosis)
  • Infection related inflammatory root resorption (most concerning- rapidly progresses)
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247
Q

What are the review times for trauma and what should be done at each review appt?

A
  • 1 week: soft tissues
  • 3-4 weeks: PDL (if you see resorption, do pulp therapy to halt resorptive process)
  • 6-8 weeks: Pulp
  • 6 months: Review
  • 1 year: review
248
Q

What is the checklist for post op instructions?

A
  • Soft diet
  • OH- CHX swab if child under 6, otherwise CHX mouthrinse.
  • Analgesics as indicated
  • AB as indicated
  • Tetanus prophylaxis as indicated
  • Follow up
249
Q

What shape do bruises from slips and trips occur as? What structures are commonly involved?

A

T shaped

  • Forehead, nose, upper lip, chin
250
Q

What are characteristics predictive of abuse (TEN-4-FACES)?

A
  • In children < 4years, injury to trunk, ears or neck.
  • Any bruising in infant <4months old as they can’t move.
  • Frenulum
  • Auricular area
  • Cheek
  • Eyes
  • Sclera
  • Patterned bruising
251
Q

What are characteristics of non-accidental injury?

A
  • Injury that doesn’t match history
  • Bilateral injury
  • Untreated injury
  • Injuries with particular patterns
252
Q

What is the primary eruption sequence?

A

RULE OF 4’s
Central Incisors: 7 months
Lateral Incisor: 11 months
First Molar: 15 months
Canine: 19 months
Second molar: 23 months

253
Q

What are the 3 factors of eruption to look for?

A

Sequence
Age
Symmetry

254
Q

When should delayed eruption be investigated?

A

After 12 months (med syndrome, missing permanent successor?)

255
Q

What are symptoms of teething?

A
  • No excessive symptoms –only drooling
  • Might get irritability, rise in temperature, loss of apetite, runny nose
  • Only get symptoms day or 2 before tooth erupts.
256
Q

How can teething discomfort be alleviated?

A
  • Rubbing or cooling the gums (teething rings, fruits & veggies)
  • Topical anaesthetic
  • Analgesic –for babies (paracetamol)
  • Alternative therapies (amber beads, clove oil/ointment)
257
Q

What is the presentation of natal/neonatal teeth and what can they cause?

A
  • Normal crown shape
  • Undeveloped, loosely attached root
  • Gingival inflammation
  • May cause trauma to tongue (Riga-Fede) and/or to mother’s breast with feeding,
258
Q

What systemic diseases/syndromes are associated with delayed eruption?

A
  • Endocrinopathies
  • Downs syndrome
  • Rickets
  • Cleidocranial dysplasia
  • Gingival hyperplasia
  • Mx & md hypoplasia
  • AI, ED
  • Disturbance of bone metabolism
259
Q

What local factors are associated with delayed eruption?

A
  • Fibromatosis of the gingiva
  • Supernumerary
  • Tooth/ root formation anomaly
  • Crowding
  • Cyst
  • Ankylosed primary tooth may delay eruption of successor
260
Q

What is the chance of a canine coming into position (after extracting the primary canine) if its cusp tip overlaps the distal aspect of the lateral incisor root?

A

91%

261
Q

What is the chance of a canine coming into position (after extracting the primary canine) if its cusp tip overlaps the midline of the lateral incisor root?

A

64%

262
Q

How can you diagnose impacted maxillary canines?

A
  • At 9yrs, palpate canine bulge
  • Obtain OPG if absence of canine bulge or anomalous upper lat incisor
  • If cusp tip of canine lies over distal half of lat incisor root.
263
Q

What is the management of impacted maxillary canines?

A
  • Early intervention
  • Extraction of primary mx canines to provide room (9-10yrs age)
  • Surgical exposure of canine (can have ortho bracket) if diagnosed at later stage
264
Q

What is the management of ectopic first permanent molars?

A
  • Self correction possible between 6-7yrs
  • Placement of separating elastics between the teeth
  • If mild, distal grinding of second primary molar to free permanent molar.
  • Distalisation of permanent molar
265
Q

How long can be allowed for normal variation in exfoliation time of primary teeth?

A

18 months

266
Q

What conditions are linked to premature exfoliation of primary teeth?

A
  • Hypophosphatasia
  • Prepubertal periodontitis
  • Cherubism
  • Acrodynia
  • Rickets
  • Cyclic neutropenia
  • Downs sydrome
  • Ehlor Danlos syndrome
  • Juvenile diabetes
  • Papillon Lefevre syndrome
  • Leukaemias
267
Q

What are oral impacts of hypophosphatasia?

A
  • Spontaneous exfoliation
  • Deficient cementum
  • Root not completely resorbed (roots can be intact as attachment of PDL to bone and tooth is impaired)
  • Lack of severe gingival inflammation
  • May have decreased alveolar height
268
Q

How can ankylosis affect adjacent and opposing teeth?

A
  • Tilting of adjacent teeth
  • Infraocclusion of tooth in growing child
  • Over-eruption of opposing teeth
  • Deficient vertical height of alveolar bone in area of ankylosed tooth.
269
Q

What is the management of ankylosis of primary teeth?

A
  • Monitor (ankylosed primary molars with successor usually exfoliate)
  • May be built up/place crown if to be kept and if infraoccluded
  • May need exo if severe infraocclusion, tipping, if ortho plan involves exo, vertical bone loss
270
Q

What is the rationale for overdentures?

A
  • Alveolar bone preservation
  • Proprioception
  • Masticatory performance
  • Inc occlusal forces
  • Retention, support, stability
  • Psychological advantages
  • Tooth mobility greatly reduced
271
Q

What are grades 1-4 mandible?

A
  • Grade 1: well-rounded slightly atrophic alveolar ridge with slight reduction in height
  • Grade 2: knife edge with only slight vertical bone loss. Reduce height to create flatter bone surface
  • Grade 3: height of md if reduced significantly but well rounded
  • Grade 4: height and width reduced significantly
272
Q

Why does alveolar bone resorption continue after fabrication of complete denture?

A

Mucosal receptors under denture are unable to stimulate bone with occlusal overloading

273
Q

What are disadvantages of overdentures?

A
  • More expensive
  • Frequently need perio therapy
  • Bulkier
  • If overdenture and teeth are not kept clean, caries and perio can progress
  • Secondary caries under margins of copings
274
Q

What are indications for overdenture?

A
  • Pt has some stable remaining teeth
  • Pt with badly attritted down teeth
  • Pt with congenital or acquired I/O defect of cleft palate, oligodontia, microdontia or cleidocranial dysplasia
275
Q

What are 4 classes of over dentures?

A
  • Immediate: fabricated immediately after removal of natural teeth- it has minimal discomfort and interference with function
  • Transitional: made by converting existing RPD to a full denture as a temporary appliance
  • Definitive
  • Overlay
276
Q

How many teeth should be retained in md ach for overdenture?

A

Ideally 4 (one canine & one molar/premolar each side)

277
Q

How are teeth prepared to be abutments for overdenture?

A
  • Endo tx
  • Tooth reduced to 1-2mm above gingival margin
  • Amalgam placed in access to root canal and dentine
  • Coping placed if indicated (prev caries/resto below gingival margin or if natural teeth present in opposing arch)
278
Q

What are the variations in abutments?

A
  • Cast post and tall core
  • Cast post and short core
  • Amalgam in prepared tooth
279
Q

What are impacts of bone loss?

A
  • Drifting/rotation of teeth
  • Change of facial structure
  • Jaw line can recede
280
Q

What are contraindications/disadvantages for implants?

A
  • Can’t afford it
  • Can take several months to compete
  • May be emotionally challenging
  • Implant may loosen and require replacement
  • Risk for infection greater with implant than fixed bridge
  • Severely immunocompromised
  • Pts with diseases of CV, respiratory and GI systems
281
Q

What is the difference between implant mucositis and peri-implantitis?

A
  • Implant mucositis just involves soft tissues surrounding the implant
  • Peri-implantitis is more severe and involves loss of surrounding bone
282
Q

What are the 3 types of dental implants?

A
  • Endosteal: placed directly into bone
  • Subperiosteal: placed below periosteum but on top of bone
  • Transosteal: inserted through inferior border of md
283
Q

What should clinical do as part of initial diagnostic assessment for implants?

A
  • Get accurate, well extended and articulated diagnostic casts
  • Wax up
  • Consider protocol for rehabilitation
284
Q

What is osseointegration?

A

Direct structural and functional connection between ordered, living bone and the surface of a load bearing implant

285
Q

what are the 3 overlapping steps of osseointegration?

A
  • Early immune inflammatory response
  • Angiogenesis
  • Osteogenesis
286
Q

Describe healing after implantation of dental implant?

A
  • Within 24hrs: neutrophils infiltrate, blood clot forms, neovascularization happens
  • 2-4 days: macrophages and monocytes infiltrate which removes blood clot and debris. Large secretion of cytokines and growth factors help mesenchymal cells differentiate into osteoblasts. There will be osteogenesis and vascularization happening
  • 5-7 days: new bone formation on implant surface with calcification from host bone onto implant
  • By 4 weeks: implant surface will have osteogenesis and osteoblastic activity on it
  • After 8-12 weeks: initial phase of osseointegration completed. Quite soft and not fully mineralized. Peri-implant interface is replaced by mature lamella bone
287
Q

What are the 2 impression techniques for implants and indications/features for each?

A
  • Closed tray: easier to use, lack of draw so can lock impression in mouth if implants are misaligned
  • Open tray: multiple implants, more accurate
288
Q

What are sustained vs controlled release local drug delivery devices?

A
  • Sustained: provide drug delivery for <24hours
  • Controlled: duration of drug release exceeds 1 day
289
Q

What are some examples of local drug delivery systems for management or perio?

A
  • Actisite
  • Periochip
  • Elyzol
  • Arestin
  • Atridox
  • Periocline
290
Q

What is the antimicrobial concentration and delivery system of periochip? How is it placed?

A

CHX gluconate 2.5mg, chip

Placed directly into pockets _>_5mm following SRP

291
Q

What is the antimicrobial concentration and delivery system of arestin?

A

Minocycline HCL 10%, microspheres

292
Q

Why is actisite no longer available?

A

Non restorable fibres can lead to infection if left in pocket

293
Q

What are sites of action for LDD?

A
294
Q

What is the antimicrobial concentration and delivery system of elyzol? How does it work?

A

Metronidazole benzoate 25% gel

Gel placed in pocket where it is liquidized by body heat and then hardens, forming crystals in contact with water

295
Q

What is the antimicrobial concentration and delivery system of atridox? How does it work + advantage?

A

Doxycycline 10% gel

Solidified upon contact with GCF allowing for controlled release for 7 days.

It is considered equally as effective as monotherapy compared to SRP alone

296
Q

When should local AMA be used (3)?

A

During active phase as adjunct to active therapy

During evaluation in non-responding site

During maintenance phase

297
Q

What situation may clinicians consider use of LDD’s in perio pts as adjunct to SRP?

A

When localised recurrent and/or residual PD at least 5mm with inflammation is still present following conventional therapies

298
Q

When is LDD’s not useful?

A

Multiple sites > 5mm

Use of LDD’s has failed to control periodontitis

Anatomical defects are present (intrabony defects)

299
Q

Describe how bacteria can cause periodontal infection?

A
  • Periodontitis bacteria can cause disease without entering tissue
  • Bacteria in subgingival plaque and their products interact with host tissues without direct tissue penetration
300
Q

What is the limitation of antimicrobials for periodontal therapy?

A
  • They do not remove calculus and bacterial residues
  • High dose required to be effective against biofilm microbes
301
Q

What are differences between local and systemic drug delivery?

A
  • Local:
    • Narrow range
    • High dose at treated sites, low levels elsewhere
    • May act better locally on biofilm associated bacteria
    • Reinfection from non-treated sites
    • Limited to treated sites
  • Systemic:
    • Wide range
    • Variable levels in diff areas
    • May reach widely distributed organisms better
    • Systemic side effects
    • Requires good pt compliance
302
Q

What are advantages of systemic over local AB therapy?

A
  • Simple and easy administration
  • Economical
  • Target multiple perio sites of higher disease severity
  • inhibit microbes on oral mucosa and other tissues
303
Q

Who are ideal candidates for systemic antimicrobial therapy?

A
  • NUG (if systemic signs exist)
  • Stage III-IV periodontitis (if non responsive to perio therapy)
  • NUP
  • Periodontitis as a manifestation of systemic disease
304
Q

What is augmentum?

A

Clavulanic acid + amoxicillin

305
Q

What perio indications is metronidazole used for?

A
  • More effective with mechanical therapy
  • Specifically useful in NUG
  • Refractory cases (with amoxicillin or augmentum)
306
Q

What are characteristics of azithromycin, dose and danger associated?

A
  • Effective against anaerobes and G -ve bacilli
  • Higher levels in diseased vs healthy perio tissues
  • Penetrates fibroblasts and phagocytes
  • 250mg/day for 5 days after initial loading of 500mg
  • Can alter heart electrical activity (prolonged QT interval- avoid in pts with heart conditions)
307
Q

What is the benefit of combining antimicrobial agents?

A
  • Wider spectrum of activity than single agent
  • May reduce development of bacterial resistance
  • May have synergistic action against target organisms, allowing lower dose of each AMA
308
Q

What is used to treat molar incisal periodontitis?

A

Tetracycline 250mg qid

309
Q

What is host modulation and who is it useful in?

A
  • Modifying host reaction to bacteria
  • Useful in patients with non-modifiable risk factors e.g. genetic defect in neutrophils
310
Q

What is the only FDA approved systemically administered HMT?

A

Tetracycline (sub antimicrobial dose doxycycline 20mg 2x daily for 3 months)

311
Q

How does sub-antimicrobial dose of doxycycline work as HMT?

A

Blocks destruction of tissue

  • Reduces osteoclast activity and bone resorption
  • Stimulates osteoblast activity and bone formation
312
Q

What should the pt be made aware of before scaling teeth?

A
  • Spaces between teeth after calculus removal
  • Inc sensitivity
  • Teeth may become mobile
  • Black triangle
313
Q

What are the aims and rationale of phase I periodontal therapy (5)?

A
  • Reduction of etiological factors
  • Elimination of predisposing factors
  • Suppression/elimination of pathogens
  • Return of inflamed to healthy gingiva
  • Shrinkage of swollen inflamed tissue
314
Q

What is the sequence of phase I?

A

1: Plaque control instructions
2: Removal of supragingival & subgingival plaque biofilm and calculus.
3: Recontour defective restos and crowns
4: Management of carious lesions
5: Tissue re-evaluation

315
Q

What is the rationale for full mouth disinfection vs quadrant wise disinfection?

A

Full mouth disinfection prevents reinfection of treated sites from untreated sites.

316
Q

What are the clinical results after phase I periodontal therapy?

A
  • Reduction in pocket depth and inflammation.
  • Deepest pockets show highest improvements.
  • Shift in flora from G-ve to G+ve microbes in the subgingival area.
  • No osseous repair
317
Q

What are the 4 types of cells that can potentially heal area after being cleaned?

A
  • Junctional epithelium
  • Gingival connective tissue
  • PDL cells
  • Bone cells
318
Q

What are features of good, fair, poor, questionable and hopeless prognosis?

A
  • Good: control of etiologic factors and adequate periodontal support
  • Fair: approx 25% AL and/or class I furcation
  • Poor: 50% AL, class II furcation involvement (location & depth make maintenance possible but difficult)
  • Questionable: >50% AL, poor crown-root ratio, poor root form, class II or III furcation, >2+ mobility
  • Hopeless: exo indicated
319
Q

What are systemic and environmental factors to consider for periodontal disease?

A
  • Smoking
  • Systemic disease
  • Genetic factors
  • Stress
320
Q

What are local factors to consider for perio?

A
  • Plaque/calculus
  • Subgingival restos
  • Overhangs
  • Abnormally placed denture clasps
321
Q

What are anatomic factors to consider for perio?

A
  • Short tapered roots
  • Cervical enamel projection
  • Enamel pearls
  • Bifurcation ridges
  • Root concavity
  • Developmental grooves
  • Root proximity
  • Furcation involvement
  • Tooth mobility
322
Q

What are overall clinical factors to consider for perio?

A
  • Age
  • Disease severity
  • Plaque control
  • Pt compliance
323
Q

What are prosthetic and restorative factors for perio?

A
  • Abutment selection
  • Caries
  • Non vital teeth
  • Root resorption
324
Q

What is more favourable- shallow poclets + severe AL/BL OR deep pockets and little AL/BL?

A

Deep pockets and little AL and BL

325
Q

Where are root concavities most common?

A
  • Mx first premolars
  • MB root of mx first molar
  • Both roots of md first molars
  • Md incisors
326
Q

Where is a palato-gingivo groove present + significance?

A
  • Mx lateral and central incisors
  • Can lead to necrosis of pulp without symptoms of caries.
327
Q

What is difference between gingival enlargement/overgrowth and gingival hyperplasia?

A
  • Enlargement/overgrowth: clinical term
  • Hyperplasia: histological assessment
328
Q

What are the grades of gingival enlargement?

A
  • Grade 0: no signs of gingival enlargement
  • Grade 1: enlargement confined to interdental papilla
  • Grade 2: enlargement involves papilla and marginal gingiva
  • Grade 3: enlargement covers ¾ or more of crown
329
Q

What are the different classifications of gingival enlargements?

A
  • Inflammatory
  • DIGO
  • Systemic conditions
  • Systemic disease
  • Other forms
330
Q

What systemic conditions are associated with gingival overgrowth?

A
  • Puberty
  • Pregnancy
  • Vit D deficiency
  • Plasma cell gingivitis
331
Q

Which systemic diseases are associated with gingival overgrowth?

A

Leukaemia

Wegener’s granulomatous

332
Q

What are characteristics of acute inflammatory enlargement?

A
  • Painless but can become painful if it develops into gingival abscess
  • Occurs due to trauma from foreign object getting stuck in gingiva e.g. bristle of toothbrush
  • Localised enlargement
333
Q

What are characteristics of chronic inflammatory enlargement?

A
  • Plaque induced
  • Progresses slowly
  • Occurs due to ortho appliances, irritation from resto’s, poor OH
  • Can be localised of generalised
  • Painless unless complicated by acute infection or trauma
334
Q

How does mouth breathing cause gingival enlargement and how does it present?

A
  • Dryness causes irritation to mucosa
  • Presents as red, oedematous, shiny gingiva
  • Occurs in mx anterior region
335
Q

What classes of drugs cause gingival overgrowth? Provide examples of each.

A
  • Anticonvulsants (phenytoin, Lamotrigine)
  • Calcium Channel Blockers (nifedipine, amlopidine)
  • Immunosuppressants (cyclosporine)
336
Q

What are clinical features of DIGO? Does it recur? Where is it most prominent?

A
  • Generalised but more prominent anteriorly.
  • Starts out in interdental gingiva and then spreads to marginal gingiva. They unite and cover the portion of the crown.
  • It recurs after surgery.
  • Pale pink, mulberry shaped gingiva.
  • No tendency to bleed unless there’s plaque or secondary inflammation
337
Q

What is the impact of plaque on DIGO?

A

When gingiva is non inflamed, fibroblasts are quiescent and do not respond to circulating levels of phenytoin. Rare to get DIGO if there’s no plaque presence

338
Q

What is the histopathology of DIGO?

A
  • Elongated rete pegs
  • Abundance of amorphous ground substance
  • Abundant collagen bundles
  • Hyperplasia of connective tissue and epithelium
339
Q

What is severity of overgrowth in patients taking phenytoin related to?

A
  • Decrease in collagen degradation.
  • Decrease in salivary IgA.
  • Lack of OH increases severity of growth.
340
Q

What are features of DIGO caused by immunosuppressive drugs (cyclosporine)?

A

More vascularised than phenytoin enlargement.

More frequent in children.

341
Q

What is the possible etiological mechanism of calcium channel blockers?

A

Defect in collagen degradation due to reduced folic acid uptake.

Upregulation of KGF

342
Q

What are clinical features of idiopathic gingival enlargement?

A
  • Cause is unknown, but hereditary basis
  • Pale, firm, leathery gingiva
  • Can cover large portion of crown
  • Can impact eruption of teeth due to dense, fibrous gingiva.
  • Affects interdental, marginal and attached gingiva.
343
Q

What are the histopathology features of idiopathic gingival enlargement?

A
  • Dense collagen bundles
  • Elongated rete pegs
  • Relatively avascular
344
Q

What is conditioned gingival enlargement and the 3 types?

A

Systemic condition of pt exaggerates normal gingival response to plaque.

  • Nutritional
  • Hormonal
  • Allergy
345
Q

Describe features of enlargement in puberty?

A
  • Affects marginal and interdental gingiva in areas of plaque accumulation.
  • Occurs in both sexes
346
Q

Describe features of enlargement in pregnancy. What are the hormonal changes brought about?

A
  • Marginal enlargement (usually generalised)
  • Increase in progesterone and estrogen
    • Vascular changes (dilated capillaries)
    • More anaerobic bacteria and p.intermedia.
347
Q

What is tumour-like gingival enlargement or pregnancy tumour?

A
  • Highly vascular solitary tumour
  • Sessile or pedunculated
  • Mushroom shaped mass from IP space
  • Painless, superficial
  • Smooth glistening surface with red pin-points.
  • Painless
348
Q

What are characteristics and clinical features of plasma cell gingivitis?

A
  • Increase in plasma cells.
  • Gingiva becomes red and friable
  • Intense oedema, inflammation and hyperaemia
  • More prevalent in young females.
  • Involves marginal, interdental and attached gingiva.
  • May be allergic
349
Q

Where is plasmacytoma more commonly found? What is it?

A
  • Nasopharynx
  • Solitary plasma cell tumour
  • Pink and smooth
  • Slow growing
  • Pedunculated
  • Oral manifestation of multiple myeloma in rare cases.
350
Q

What are clinical features of gingival overgrowth associated with leukaemia?

A
  • Haemorrhagic tendency
  • Friable
  • Buish red and shiny
  • Acute necrotising painful ulcers
  • Chronic inflammation with leukocytes
351
Q

What is an epulis?

A

Solitary benign tumour of gingiva

352
Q

What is a fibroma?

A
  • Slow growing, solitary, spherical mass
  • Normal colour
  • Firm & nodular
  • Arises from gingival connective tissue
  • Bundles of well-formed collagen fibres with variable vascularity
353
Q

What is the difference between scaling and root planing?

A
  • Scaling involves plaque, stain and calculus removal from crown and root surface.
  • Root planing involves removing contaminated and rough cementum from root
354
Q

What is the frequency of ultrasonics?

A

20 000 cycles per sec

355
Q

What are advantages of ultrasonic instruments as opposed to hand scaling?

A
  • More efficient
  • Thinner tip > more comfortable
  • Water flushing effect
  • Less pressure applied
  • Multiple surfaces of tip are capable of removing calculus
  • Less tissue destruction
  • No need to sharpen
  • Less chance for repetitive stress injuries
356
Q

What are disadvantages of ultrasonic instruments?

A
  • Aerosol production
  • Can’t be transported easily
  • Louder
  • Less tactile sensation
  • More precautions and limitations
  • Reduced visibility
357
Q

What’s the difference between magnetostrictive and piezoelectric ultrasonics?

A
  • Piezoelectric range is uniform, it uses scraping or tapping motion and has linear pattern
  • Magnetostrictive range is uniform, uses scraping motion and has elliptical pattern
358
Q

What are contraindications if ultrasonic scaling?

A
  • Pt with communicable disease
  • Pt with pacemaker
  • Young pt
  • Pt with deglutination problems
  • Porcelain or bonded restos
359
Q

What are 2 types of genes that prevent malignant transformation?

A
  • Proto-oncogenes: controls normal cell growth
  • Tumour suppressor genes: regulate mitosis- p53, Rb
360
Q

What is stage vs grade of cancer?

A
  • Stage: progression or spread in body
  • Grade: cell differentiation (how many mutations)
361
Q

What are the top 3 anaemias?

A
  • Iron deficiency
  • Megaloblastic anaemia
  • Immune haemolytic anaemia
362
Q

What are clinical features of anaemia?

A

· Pale
· Dizzy
· Extreme fatigue
· Chest pain
· Shortness of breath,
· Tachycardia

363
Q

How do RBC appear in megaloblastic anaemia?

A
  • Macrocytic
  • Very few and very large
364
Q

How do RBC appear in iron deficiency anaemia?

A
  • Microcytic hypochromic
  • Small and pale. Fewer RBC present too.
365
Q

Diagnosis if MCV is lower and higher than average (whole volume of one RBC)?

A
  • Lower - Iron def
  • Higher - megaloblastic & haemolytic anemias
366
Q

What are features of leukemia?

A

Cancer of bone marrow blasts.

  • Inc blast (cancer) cells
  • Dec RBC, WBC and platelets
  • Anaemia, fever and bleeding
367
Q

Most common type of Leukaemia

A

Chronic lymphatic leukaemia

368
Q

What is multiple myeloma?

A
  • Malignancy of mature B cells.
  • Tumour produces plenty of monoclonal antibodies
  • Blood becomes thick
  • Symptoms: multiple punched out bone lesions, infections, renal failure
369
Q

What are the 4 top bleeding disorders?

A
  1. Thrombocytopenia
  2. Vit K deficiency
  3. Haemophilia (A&B)
  4. Von Willebrand Disease
370
Q

What do prothrombin time (PT) and partial thromboplastin time (PTT) tests measure?

A

PT - tests extrinsic pathway (7)

PTT - tests intrinsic pathway (8, 9, 12)

371
Q

What is Von Willebrand Disease?

A

Von Willebrand Factor carries and protects factor 8. Deficiency results in lack of platelet function.

  • Normal platelet count but not functional so increased bleeding time.
  • Normal PT but PTT is increased
372
Q

What is disseminated intravascular coagulation?

A

Extensive activation of coagulation all over the body. Consumption of coagulation factors and platelets lead to severe bleeding.

373
Q

What is biological width?

A

Combined heights of connective tissue and junctional epithelium attachment to a tooth. If you invade biological width you can get permanent gingival inflammation around crown.

374
Q

What are dental applications of electrosurgery?

A
  • Crown lengthening
  • Gingival recontouring
  • Excision of hyperplastic gingival tissue
  • Haemostasis
  • Exposing of tooth margins
375
Q

What are therapeutic objectives of electrosurgery?

A
  • Electrosection
  • Electrocoagulation (white coagulation, dessication, black coagulation)
376
Q

What electrosurgery waveform ensures the most efficient cutting?

A

Fully rectified wave forms

377
Q

What are the 3 levels of coagulation in electrosurgery?

A

White coagulation
Dessication
Fulguration (tissue left charred)

378
Q

What are precautions with ESU?

A
  • CI in cardiac pacemaker pts.
  • CI in radiation therapy and acutely immuno-compromised pts.
  • Don’t use near alveolar bone or flammable vapours/liquids
  • Do not contact tooth or alloy restos
  • Do not use with N2O2 or O2.
  • Do not retract tissues with metal instruments
  • Avoid prolonged tissue contact.
  • Have good ventilation
  • Adjust current for optimal use
379
Q

What is the issue with retraction cord containing epinephrine?

A

A 2.5cm length of cord contains just less than the amount of epinephrine in 4 LA carpules. This is about 2x the allowable dose for a cardiac pt.

380
Q

What is expasyl?

A

Clay material that you place in gingival tissue margin, leave for 5 minutes and wash off. Will retract gingival tissue

381
Q

What are indications for full gold crown?

A
  • When most or all axial surfaces of a posterior tooth are weakened or are restored.
  • When there is insufficient interocclusal distance
  • Heavy bruxism
  • Bridge abutment
382
Q

What are the reduction measurements for full gold crowns?

A
  • Functional cusp: 1.5mm
  • Non-functional cusp: 1mm
  • B and L walls: 0.5mm chamfer
  • B seating groove
383
Q

What is centric relation?

A

Also known as RCP. Relationship of md to mx when condylar head is situated in the most anterior superior position within the glenoid fossa. It is a reproducible position.

384
Q

What is group function?

A

Premolar and molar takes over the lateral excursion (rather than canine discluding posterior teeth)

385
Q

What is a clue to a potential steep curve of spee?

A

Excessive wear on O surface of molars

386
Q

Differentiate between plane line and semi adjustable articulators

A
  • Semi-adjustable: simulates anatomy slightly better
  • Plane line: smaller radius of closure so posterior teeth tend to get premature contacts on restos. Also, lateral jaw movements cannot be simulated so posterior restorations should be fabricated on semi-adjustable articulators.
387
Q

What’s the difference between red wax and pink wax?

A
  • RED: known as boxing wax. Place wax around tray to make box and this is where you can pour your stone into.
  • PINK: bite registration wax. Not as soft as red wax. Requires to be heated up with hot water or gas flame.
388
Q

What are the consequences of a lost temporary restoration?

A
  • Tooth sensitivity
  • Bacterial ingress/pulpitis
  • Proximal tooth drift
  • Over-erupted prepared tooth
  • Eruption of opposing teeth
  • Compromised appearance
  • Prep prone to damage
389
Q

How can temporary cement be removed?

A
  • Instrument (carver, scaler, excavator tip)
  • Cotton pledget soaked in CHX
  • Ultrasonic tip
390
Q

What factors can prevent seating in trial insertion?

A
  • Tight proximal contacts
  • Undercuts and very parallel prep walls
  • Flaws in resto fitting surface
391
Q

How is the fitting surface of crowns checked?

A
  • GC Fit Checker
  • Artispot fit checker.
  • Paint red on fitting surface of crown.
  • Put crown on tooth
  • Pull crown off tooth
  • Adjust when the red is gone.
    (if there is risk of perforation it may be necessary to minimally alter the tooth.
392
Q

What is the solution for not being able to seat the crown?

A

Adjust proximal contacts
Alter taper of prep
Alter fitting surface of resto

393
Q

What is the solution for poor fit (margins, rocking) of crown?

A
  • Retake impression
  • Remake crown
394
Q

What is the solution for unsatisfactory shade of crown?

A
  • Remake without impression
  • Alter shade in lab with low fusing ceramic addition.
  • Alter shade with indirect resin
395
Q

What cement is often used for Maryland bridges

A

Resin cements (Panavia)

396
Q

What are characteristics of polycarboxylate cements?

A
  • Adhesion to enamel/dentine
  • Well tolerated by pulp
  • Mix is sticky
  • Contains fluoride (caries resistance)
397
Q

What are characteristics of zinc phosphate cement?

A
  • Good film thickness
  • Poor strength
  • High solubility
  • Nil chemical adhesion
  • Easy to use
  • Minimal sensitivity
398
Q

What is a resin-bonded cast alloy bridge?

A

Fixed prosthesis with alloy frame, bonded to abutment teeth with resin cement via an acid etch technique

399
Q

What are problems with bonded pontics? What was solution to this problem?

A
  • Fracture through proximal contact area.
  • Metal mesh incorporated into prosthesis and placed on lingual aspect (rochette bridge) to strengthen connector areas
400
Q

What is the mechanism of bonding for ‘maryland’ bridge?

A

Electrolytic etching of alloy fitting surface and cementation with panavia resin cement

  • Basically same as rochette bridge. However, maryland bridge doesn’t use holes in framework for retention. Instead, bridge fitting surface is electrolytically etched and CR bonds nicely to it.
401
Q

Pros/cons of electrolytic etching vs sandblasting?

A
  • Electrolytic: less safe, better retention, voids trap air, technique sensitive, air inhibits resin polymerisation
  • Sandblasting: safer, less retention, less air entrapment, good oxide layer for adhesion
402
Q

What are indications for resin-bonded cast alloy bridges?

A
  • Short edentulous span
  • Stable abutments
  • Sound coronal tooth structure
  • Good ridge form
  • Open bite
  • Cuspid guidance
  • Ortho space maintainance
  • Splinting
  • Protection against tooth surface loss
  • Interim fixed option before implants
403
Q

What are contraindications for resin-bonded cast alloy bridges?

A
  • Long edentulous span
  • Poor ridge form
  • Severe tooth rotations or angulations
  • Deep bite
  • Bruxer
  • Mobile abutments
  • Heavily restored tooth
  • Alloy hypersensitivity
404
Q

Why is base metal alloy used for backing of bridge rather than gold?

A

Base metal alloys can be cast to 0.3mm whereas gold requires 0.5mm. Thicker material can prevent posterior teeth occluding (don’t want to place metal on occlusal contact areas)

Get pt to bite on articualting paper. Don’t want to place metal on occlusal contact areas bc when pt bites down they won’t be able to get posterior teeth together.
Tend to use . That’s why base alloy is good for maryland bridge.

405
Q

How are resin bonded cast alloy bridges fabricated?

A
  • Wax up
  • Investing
  • Casting
  • Trimming- surface treatment
  • Ceramic or resin addition
406
Q

What is connector and retainer thickness for resin bonded cast alloy bridge?

A
407
Q

What is the bridge cementation process for resin bonded alloy bridge?

A

Panavia system

Place rubber dam
Clean abutments with pumice and water
Apply etchant and self etching primer to tooth
Place alloy primer on metal fitting surface
Mix resin pastes and apply to retainers only
Seat bridge, wipe away excess cement
Apply Oxyguard II
Finish metal margins

408
Q

What tooth preparations need to be made for a bridge?

A
  • Lingual rest seat
  • Lingual reduction
  • Proximal groove
  • Proximal reduction
  • Chamfer
409
Q

What are problems with resin-bonded cast alloy bridges?

A
  • Partial or total debond
  • Secondary caries
  • Pontic movement
  • Pontic fracture
  • Hyperocclusion
  • Gingival inflammation
410
Q

What are safety precautions for bridge removal?

A
  • Protect pt nasogastic passage
  • Tie floss around bridge
  • Have HVE to suction bridge fragments
411
Q

What are advantages of resin bonded cantilever prosthesis opposed to fixed-fixed bridge?

A
  • Less tooth preparation (only one side)
  • Avoids caries under a debonded retainer
  • Less expensive
  • Lasts longer than fixed fixed as the pontic moves with tooth
412
Q

What is the strength of monolithic zirconia compared to emax?

A
  • Zirconia: 750MPa
  • Emax: 360MPa
413
Q

How are zirconia crowns cemented onto the tooth?

A
  • Rely x unicem
  • Ivoclar SpeedCem Plus
414
Q

What is speed cem cementation procedure for zirconia crown?

A
  1. Wash and dry restoration
  2. Apply Ivoclean for 20 seconds-then wash and dry again
  3. Apply Ivoclar SpeedCem Plus dual cure cement (transparent) to the crown or bridge fitting surface. Apply with a micro-brush to ensure all margins are covered.
  4. Seat the restoration and use dental floss inter-proximally.
  5. Tack light cure margins for 5-10 seconds and remove excess. The material will self- cure in 3- 4 minutes
415
Q

How does speedCEM plus bond to zirconia curface?

A

SpeedCEM Plus cement contains MDP which bonds to the tooth and zirconia surface by means of PO4 groups

416
Q

How do you adjust zirconia?

A

High speed fine diamond bur to adjust zirconia. Will then need to polish with ZirconBrite otherwise will wear adjacent tooth rapidly as it is harder than enamel

417
Q

How are Emax veneers and onlays bonded onto the tooth?

A
  1. HF acid etch in lab
  2. Apply 3M Scotchbond Universal onto the fitting surface of the restoration and tooth prep for 35 secs (silanates fitting surface and etches tooth surface)
  3. Apply Nexus 3 (shade clear) to the restoration and seat.
  4. Clear contacts with floss and tack cure for 5-10 seconds.
  5. Remove excess resin.
  6. Check occlusion
417
Q

What are clinical applications of PFM?

A
  • Splinting of perio teeth
  • Single anterior and posterior crowns
  • Full coverage for fractured teeth
  • Abutment for RPD
  • Retainer and pontics for fixed bridgework
  • High stress situation (deep overbite or bruxer)
418
Q

What thickness of metal and porcelain is required for PFM crown?

A
  • Base metal: 0.2mm- issues bonding to porcelain, casting diffiulties
  • Nobel metal: 0.3-0.5)- superior bond with porcelain
  • Porcelain: 0.7mm
420
Q

What temp are PFM crowns placed in the vacuum? What is the purpose of placing PFM crown in vacuum?

A

980 degrees which melts the ceramic particles, forming a composite structure of crystals within a glass matrix. Vacuum removes air bubbles

421
Q

How much does PFM crown shrink in vacuum?

A

30-40%

422
Q

What are the 4 mechanisms of metal ceramic bonding?

A
  • Micromechanical
  • Molecular
  • Chemical
  • Compressive
423
Q

What is the process of fabricating a PFM crown?

A
  • Tooth prep
  • Impression
  • Die
  • Wax up
  • Cast metal
  • Oxidise surface of metal
  • Placement of opaque layer
  • Place body and enamel porcelain
  • Heat 980 degrees and place in vacuum
424
Q

What are cons of metal ceramic crowns?

A
  • More expensive
  • More destructive preparation
  • Less aesthetic due to reflectance from opaque layer
425
Q

What are the reduction measurements of PFM crown?

A
  • Incisal : 2mm
  • Occlusal: metal + ceramic: 2mm, metal alone on non-functional cusp: 1mm, metal alone on functional cusp: 1.5mm
  • Labial/incisal ⅔: 1.5mm
  • Labial/gingival ⅓: 1.3mm
  • Proximal: 0.5-1mm
  • Gingival/cingulum wall: 0.5mm
  • Lingual concave surface
    • Metal + ceramic: 1mm
    • Metal only: 0.5-0.8mm
426
Q

What are the 4 possible facial margins for PFM crown?

A
  • Ceramic radial shoulder
  • Ceramic heavy chamfer
  • Heavy chamfer with gold collar
  • 45 degree beveled shoulder with gold collar
427
Q

What is the role of opaque porcelain in PFM crown?

A

Covers the metal so the tooth won’t appear as grey in colour. Also helps the ceramic and metal bond.

428
Q

What can happen if 1.3mm is not reduced on gingival margin for PFM crown?

A
  • Metal collar
  • Overbuilt crown
429
Q

What can happen if 1.3mm is not reduced on gingival margin for PFM crown?

A
  • Metal collar
  • Overbuilt crown
430
Q

Why is a heavy chamfer with gold collar sometimes necessary?

A

If margins terminate on root and not much tooth structure can be drilled away

431
Q

What are the 5 layers of a PFM crown?

A
  • Body porcelain
  • Incisal porcelain
  • Opaque layer
  • Unveneered metal
  • Veneered metal
432
Q

What is E max made of?

A

Lithium disilicate glass

433
Q

For tissue health, how should the portion of the pontic touching the ridge be shaped?

A

As convex as possible

434
Q

What are the 3 classes of endentulous space?

A
  • Class I: Reduced B-L dimension but normal ridge height
  • Class II: Reduced ridge height but normal width.
  • Class III: Reduced ridge height and width.
435
Q

What are the 5 pontic classifications?

A
  • Sanitary
  • Conical
  • Ovate
  • Modified ridgelap
  • Saddle ridgelap
436
Q

What are characteristics of sanitary pontics?

A

Easy to clean
Poor aesthetics
Generally posterior mandible
Not used anteriorly

437
Q

What are characteristics of ‘saddle’ ridgelap pontics?

A

Good aesthetics
Difficult to clean
Generally not recommended

438
Q

What are characteristics of conical pontics?

A
  • Poor aesthetics
  • Food entrapment in undercut areas
  • Good access for cleaning
  • Generally for molars with non aesthetic requirement
  • CI in pts with poor OH and highly aesthetic situation.
439
Q

What are characteristics of modified ridgelap pontics?

A
  • Easy to clean
  • Some food packing in undercut area
  • Good aesthetics
440
Q

What are characteristics of ovate pontics?

A
  • Excellent aesthetics
  • May require minor surgical preparation
  • Fairly easy to clean
  • Minimal food entrapment
  • Primarily for upper anteriors
441
Q

What are the primary functions of a post?

A

Retain & stabilise the core
Obturation of post canal

442
Q

What are the design parameters for posts and post holes?

A
  • Post at least crown length
  • Retain apical seal
  • Correct angle in root canal
  • Do not over prepare canal
443
Q

What are contraindications for posts?

A
  • Non-restorable tooth
  • Short roots, thin roots, carious roots
  • Existing root pathology
  • Poor periodontal support
  • If core can be retained and supported without post
  • Endo filled canals without coronal seal (3 months or longer)
444
Q

What are different post shapes?

A

Tapered

Tiered

Parallel

445
Q

What is the function of serrations of the paraposts?

A

Ribs on post cut into dentine. Divets are where the cement flows and holds post against dentine of root canal

446
Q

What are the 2 post placement techniques?

A
  • Passive: post placed without actively cutting into dentine surface.
  • Active: Placed and cemented with post actively engaging dentine.
447
Q

How much GP should remain at the apex of the tooth when placing post?

A

4-5mm

448
Q

What are issues with gates glidden and para post drills?

A

GG: can fracture

PP: can perforate

449
Q

How should fibre posts vs paraposts be cut?

A
  • Fibre posts: Diamond bur and water spray. Don’t cut with scissors as glass fibers will fracture.
  • Parapost: Cut from apical end. Sharp edges smoothened with diamond bur.
450
Q

What is the procedure for placing rely x fibre post?

A
  1. Remove GP with universal drill, leaving a minimum 4 mm of filling apically
  2. Select post size and matching drill. Use appropriate drill to widen and shape the root canal.
  3. Insert post to check the fit in the prepared canal. Should be able to easily remove the post.
  4. Shorten post to the required length using a diamond disk and Suction system
  5. Disinfect the post with alcohol and dry it with air free of water and oil.
  6. Disinfect the root canal with 2.5-5.25% NaOCl. Rinse immediately with water and dry with paper points
  7. Begin apically in the root canal and dispense RelyX Unicem cement. Keep elongation tip immersed in the cement initially and during the entire cement application process to avoid trapped air in the cement
  8. Seat the post immediately. Twist slightly and apply moderate pressure to hold in position. Remove excess cement
  9. Light cure cement for 40 seconds or allow to self-cure for 5 minutes from start of mix
451
Q

What can be used for alloy post cementation?

A

GIC
Auto-mix self etching resin cement

452
Q

What is Naayer technique?

A

Direct restorative material placed into root canal (e.g. amalgam, CR). Difficult and rarely used.

453
Q

What is the benefit of anti-rotation design for posts?

A

If you just have post stick in the hole without a key/notch, there is propensity for composite resin crown to rotate around tooth. Core will be retained better with anti-rotation design. Use in ovoid or asymmetrical root canals.

454
Q

What is the process of taking impression of root canal?

A
  1. Go in with gates glidden burs with stopper (WL-5mm)
  2. Cut post
  3. Place light body material and plastic post down root canal to take impression (plastic post is mechanically retained in impression to prevent distortion of silicon upon removal)
455
Q

Plastic post is mechanically retained in impression to make sure silicon doesn’t distort in removing it from root.

A

Up to but no more than ⅓ of root width

456
Q

What are some goals for posts?

A
  • Conserve as much dentine as possible.
  • Don’t over prepare root canal.
  • Adequate post lengths to achieve core retention.
  • Keep cement within root canal.
  • Preserve apical seal.
457
Q

What are problems with post retained restorations?

A
  • Loss of retention
  • Secondary caries
  • Root fracture
  • Post fracture
  • Post bending
  • Root resorption
  • Apical infection
458
Q

How can you remove alloy posts?

A
  • Create space around post (fine diamond, Masseran Kit)
  • Ultrasonic agitation
  • Post-puller
459
Q

How can you remove a temporary crown from a pt?

A

May need LA if tooth is vital.

Can use spoon excavator under margin to lift off

Otherwise can drill small hole in buccal surface and use spoon excavator to twist off.

460
Q

What are indications for porcelain laminate veneers?

A
  • Removal of enamel defects
  • Diastema closure
  • Tooth colour correction
  • Alter shape of teeth
461
Q

What are advantages of porcelain laminate veneers?

A

Highly aesthetic

Minimally invasive

Good clinical record

Good colour stability

Well tolerated by gingiva

462
Q

What are limitations of porcelain laminate veneers?

A
  • Hard to block out dark stains
  • Difficult for severe tooth angulation and position
  • Fragility
  • Sensitivity
463
Q

What teeth are the 0.3mm vs 0.5mm burs used for veneer prep?

A
  1. 3mm: md incisors
  2. 5mm: everywhere else
464
Q

How can a porcelain laminate veneer be repaired with fractured segment is not salvagable?

A
  1. Isolate fracture site with RD
  2. Bevel fracture margin with HS diamond
  3. Etch porcelain with 9.5% HF acid gel and wash + dry
  4. Etch enamel/dentine and wash +dry
  5. Apply silane primer to porcelain edges
  6. Wait 60 seconds
  7. Apply Optibond Solo Plus and LC
  8. Repair with resin composite LC
  9. Recontour and polish
465
Q

How can a porcelain laminate veneer be repaired with fractured segment is salvagable?

A
  1. Isolate fracture site with RD
  2. Bevel fracture margin with HS diamond
  3. Etch porcelain and fragment with 9.5% HF acid and wash + dry
  4. Etch enamel/dentine and wash + dry
  5. Apply silane primer to porcelain and fragment, wait 60 seconds
  6. Apply Optibond Solo Plus to tooth and porcelain margin and LC
  7. Apply Nexus 2 cement to fractured piece and seat correctly. LC
  8. Recontour and polish
466
Q

What are causes of marginal leakage with porcelain veneers?

A
  • Margin contamination during etching, bonding
  • No enamel adhesion
  • Poor cementation technique
  • Tooth flexure
467
Q

What are indications for porcelain veneer shell crowns?

A
  • Diastema closure
  • Conservative full coverage restoration
  • Alter tooth shape (peg lateral, microdontia)
  • Correct angulation or tooth form
  • Sufficient area for adhesion
468
Q

What are advantages of porcelain veneer crowns (shell crowns)?

A

Less invasive than full crown

Aesthetic

469
Q

What is the procedure for repairing fractured porcelain/ceramic on PFM crowns?

A
  1. Roughen surface of the metal with high speed diamond bur
  2. Bevel edges of porcelain
  3. Place Panavia alloy primer over exposed metal and porcelain (use an applicator to apply primer) and let dry
  4. Place scotch bond over the metal and porcelain, air dry and light cure
  5. Place opaquer or shade modifier on the metal and light cure
  6. Place appropriate shade resin composite over the opaquer and light cure
  7. Finish and polish
470
Q

What are pt factors for planning fixed bridgework?

A

Motivation

Financial status

Caries experience

Salivary flow

Perio status

471
Q

What features of an edentulous ridge need to be considered before bridge placement?

A

Length of span

Height and width of ridge

Over erupted opposing tooth

Inter arch distance

472
Q

What is a consequence of bridge flexure?

A

Can cause secondary caries under margin bc gap is formed

473
Q

What is a precision attachment and its purpose?

A

Attachment placed on pier abutment that allows the posterior segment to move independently from the anterior segment. Reduces load on whole bridge

474
Q

What are problems with tilted abutments for bridges?

A
  • Need to take off substantial amount of tooth structure to be able to seat the bridge
  • Can cause pulp exposure
  • Mesioangular 3rd molar
  • Over tapered, non-retentive prep
475
Q

Should cantilevers be M or D?

A

Mesial

476
Q

What can cause root fracture?

A
  • Overprepared root canals.
  • Heavy forces
  • Perio involved roots
  • Absence of ferrule
  • Sharp post tip
  • Active post
477
Q

Why do RCT teeth sometimes have greater loads placed on them?

A

Mechanoreceptors regulate the amount of pressure placed on teeth so when they are removed, there is greater force placed on them

478
Q

How does salbutamol work?

A

Beta 2 receptor agonist for asthmatics. Causes bronchodilation to relax airway muscles irrespective of the spasminogen causing the attack. It is a physiological antagonist.

479
Q

What are the effects of adrenaline?

A
  • B2- Bronchodilation and vasodilation (perfusion of vital organs)
  • B1- Increase heart rate
  • A1- vasoconstriction to prevent CV collapse and venoconstriction to force blood back to the heart
480
Q

How does aspirin produce its effect?

A

It is a selective antiplatelet drug. It produces its effect by preventing coagulant effects of TXA2 and retaining anti-coagulant effects of PGI2

481
Q

What should be done for adrenal insufficiency patients undergoing a procedure with significant stress? (e.g. Addisons disease)

A

Give pt supplemental dose of corticosteroid prior to treatment as they could otherwise become hypotensive under stress.

482
Q

What is an impairment, disability and handicap?

A
  • Impairment: any loss, abnormality or defect in structure or function
  • Disability: any restriction or lack of ability to perform activity due to impairment
  • Handicap: disadvantage resulting from impairment or disability that limits fulfilment of role considered normal for that individual
483
Q

What are medical issues/disability than can arise from patients with down’s syndrome?

A
  • Epilepsy
  • Sleep apnoea
  • Brachycephalic skull with delayed closure of fontanelles
  • > risk infections, eczema.
  • > risk of childhood leukemia
  • Cardiac problems (teratology of fallot)
  • Intellectual disability
  • Altered speech
  • Sight and hearing issues
  • Dementia
  • Atlanto-axial instability
484
Q

What are features of teratology of fallot?

A
  • Pulmonary stenosis
  • Aorta emerges from both ventricles
  • Ventricular septal defect
  • Ventricular hypertrophy
485
Q

What needs to be kept in mind for dental patients if they have atlanto-axial instability?

A

There is instability between C1 and C2 so need to be aware of this when adjusting chair and head rest.

486
Q

What are oral features of pts with downs syndrome?

A
  • Mouth breathing
  • Drooling
  • Angular cheilitis
  • Chapped, everted lower lip
  • Tongue: scalloped, fissured, macroglossia, geographic tongue, tongue thrusting
  • V shaped high vault palate
  • Teeth: microdontia, peg laterals, hypodontia, supernumeraries, hypoplasia and hypocalcification, taurodontism, spacing, reduced risk of dental caries, delayed eruption
  • More susceptible to perio
487
Q

Why do some patients with downs syndrome have reduced risk of dental caries?

A

High salivary pH
High bicarbonate levels
Lower strep mutans levels

488
Q

What are the take home messages for managing patients with downs syndrome in dental setting?

A
  • Hypotonia
  • Periodontal disease
  • Diet and OH
  • Positioning neck (atlanto-occipital instability)
  • Cardiac defects
  • Consent
489
Q

What is cerebral palsy

A

A non-progressive motor disorder caused by brain injury prior to completion of maturation of CNS (in utero or before age 4)

490
Q

What disability is associated with cerebral palsy?

A
  • Intellectual disability
  • Seizure disorders
  • Speech difficulties
  • Visual problems
  • Hearing problems
491
Q

What are the dental issues of patients with CP?

A
  • Drooling
  • Dental trauma (falls)
  • Attrition
  • Malocclusion
  • Caries
  • Enamel hypomineralisation & hypoplasia
  • Mouth breathing
  • DIGO
  • Tongue thrust
  • Poor swallow reflex
  • Hyperactive gag reflex
  • Erosion (GI reflux)
492
Q

3 types of cerebral palsy + which type can benefit from N2O or benzos?

A
  • Ataxia
  • Athetoid (benefit from N2O or benzos)
  • Spastic
493
Q

Why is hypoplasia and hypomineralisation common in patients with cerebral palsy?

A

If there’s hypoxic event during birth or brain damage from infection in first 4 yrs (that has resulted in CP), ameloblasts are susceptible to alterations from oxygen levels.

494
Q

What is recommended for dental treatment for CP patients?

A
  • Early contact from young age.
  • Malocclusions can be reduced by oral stimulation and training from early age, sometimes with palatal plates and meds.
  • Regular follow ups.
495
Q

What is spina bifida?

A

Defective closure of the vertebral column due to defect of skin, vertebral arches and neural tube.

496
Q

What is the disability associated with spina bifida?

A
  • Complete paralysis of lower limbs and sphincters of bladder and bowel.
  • Club foot.
  • Dislocated hip.
  • Links with folic acid deficiency during pregnancy.
497
Q

What are dental tx considerations for patients with spina bifida?

A
  • May require AB prophylaxis id shunt is in place
  • May be in wheelchair
498
Q

What should be done prior to dental appointment for pt with disability?

A
  • Obtain med hx (contact GP or carer)
  • Discuss management strategies with carer/pt
  • Ask carer for level of tolerance
  • Find out who legally gives consent
  • Who pays?
  • Transport
499
Q

What are essential preparations for patients with disability while in the chair?

A
  • Obtain hx and level of independence
  • Understand emotional context of pt
  • Explain what are are doing at appropriate level for pt
  • Explain equipment
  • Evaluate reflexes
  • Evaluate meds
500
Q

What are issues to consider in formulating tx plan for patient with disability?

A
  • Ability to carry out OH
  • Level of interest in oral care
  • Urgency of medical condition
  • Medical treatment planned
  • Urgency of dental tx
  • Any necessary planned surgical procedures
  • GA?
501
Q

What are the prevention strategies for patients with disability?

A
  • Involve carer where appropriate (diet, OH advice)
  • Modified toothbrush
  • Fluoride in surgery and home (esp neutrofluor 5000)
  • Reward with non carious food
  • Shorter dental recalls (3-6 months)
  • Pit and fissure sealants
  • CPP-ACP
  • CHX
502
Q

What is the stereotyped behaviour associated with Autism?

A
  • Repetitive or ritualistic movement, posture or utterance.
  • Rigidly following routines
503
Q

What are features of Autism (13)?

A
  • Range in intelligence
  • Physically normal (may have difficulties)
  • Inability to relate to ppl (reduced social skills), variable ability to form emotional relationships
  • Unable to interpret language
  • May dislike physical contact
  • Lack of eye contact
  • Lack of response
  • Usually immersed in activity that interests them
  • Attuned to routine & lists
  • Abnormal facial perception
  • Selective attention
  • Altered sensory perception
504
Q

What are early signs and symptoms of autism?

A
  • No big smiles
  • No back and forth sharing of sounds or facial expressions by 9 months
  • No babbling by 12 months
  • No back and forth gestures (waving, pointing) by 12 months
  • No words by 16 months
  • Any loss of speech, babbling or social skills at any age.
505
Q

What are characteristics of ADHD?

A

Disorder of DOING- they know what to do but can’t manage to do it.

  • Impulsive
  • Hyperactive
  • Poor mood regulation
  • Easily distracted
  • Can’t sort out what to attend to.
506
Q

What medication is prescribed for ADHD vs ASD

A
  • ADHD: Ritalin (dec hyperactivity and impulsivity, improve alertness & concentration)
  • ASD: only for certain aspects- difficulty sleeping. Last resort after behaviour intervention failed.
507
Q

What should you do prior to appt with ASD pt (5)?

A
  • Obtain med hx
  • Discuss management strategies with carer
  • Ask carer level of tolerance
  • Who gives consent?
  • Need for chemical restraints?
508
Q

What should be done at the dental appt with ASD pt?

A
  • Should not be kept waiting
  • Short, regular appts
  • Desensitising appts
  • Keep instructions brief and simple
  • Be consistent
  • Minimise distractions
  • Tell-show-do
509
Q

What are oral issues of ASD (7)?

A
  • Epilepsy meds can cause gingival hyperplasia, delayed eruption.
  • Trauma- head banging, falls, accidents, seizures assoc w/ epilepsy
  • Oral habits- self mutilation, lip/cheek biting, pica.
  • Bruxism
  • GORD- erosion
  • Dental caries- cariogenic foods as reward for behavioural management
  • Periodontal disease- poor OH, poor compliance.
510
Q

Are serous or mucous acini more affected from chemoradiotherapy?

A

Serous acini

511
Q

How much radiation reduces salivary flow within 24 hours and causes permanent hyposalivation?

A
  • 2.2Gy reduces salivary flow within 24 hours
  • 40Gy causes permanent hyposalivation
511
Q

How much radiation reduces salivary flow within 24 hours and causes permanent hyposalivation?

A
  • 2.2Gy reduces salivary flow within 24 hours
  • 40Gy causes permanent hyposalivation
512
Q

How does saliva appear in patients with salivary gland dysfunction?

A

Thick, ropey or aerated

513
Q

What are the functions of saliva?

A

Lubrication
Cleansing
Antimicrobial
Remin
Buffering
Mucosal integrity
Digestion & taste

514
Q

When do taste buds recover following radiation?

A

Partial restoration of taste 20-60 days post RT.
Full restoration after 2-4 months.
Some report long term changes.

515
Q

What is graft vs host disease?

A

Donor T cells react against pt tissues directly or through exaggerated inflammatory responses following HCT.

516
Q

What are the oral manifestations and symptoms of graft vs host disease?

A
  • Pseudomembranous ulceration
  • Erythema and atrophy (acute)
  • Lichenoid hyperkeratotic changes (chronic)
  • Dysgeusia
  • Salivary gland dysfunction
517
Q

Why does radiation caries occur?

A
  • Shift to cariogenic flora
  • Reduced salivary antimicrobials
  • Loss of bioavailable calcium phosphate
  • Weakens dentine-enamel bonds
  • Alters prismatic enamel structure
  • Denatures collagen in dentine
  • MMPs hydrolyse dentine bonding agents
  • Can alter pulp vascularity & capacity to repair
518
Q

Where does radiation caries occur?

A
  • Different locations than common dental decay.
  • Labial surfaces
  • Incisal/cuspal tips
  • Proximal surfaces of lower anteriors
519
Q

Why is radiation caries common in lower anteriors?

A

Usually lower anteriors are bathed in saliva so they aren’t susceptible to caries. However, with salivary gland dysfunction, caries can occur frequently here. Distance between proximal surface and pulp is small for md anteriors.

520
Q

What toothpaste is recommended for patients at risk of radiation caries?

A

Neutrofluor sensitive (low in SLS) as it is less irritant to mouth.

521
Q

What are issues with composite in patients with radiation caries?

A

High rates of loss and recurrent caries.

522
Q

Why is GIC used in patients with radiation caries despite its high chance of crazing and getting lost in dry environment?

A

Potential to release fluoride so it’s unlikely to get recurrent caries.
Also, better to loose resto than get recurrent caries. Not always bad to lose the filling as the pt keeps coming back.

523
Q

Why are dentures contraindicated in patients undergoing chemo-radiotherapy?

A

Can compromise plaque control and increase risk of ORN. Avoid in partial dentate unless essential aesthetics and function.

524
Q

What are issues with performing endo in patients undergoing chemoradiotherapy?

A

Trismus complicates endo- rubber dam, access cavity, instrumentation. Access cavities through incisal or labial aspect or decoronating tooth may improve access.

525
Q

What happens if TMJ or muscles of mastication are in field of radiation?

A

Fibrosis and damage

526
Q

How can trismus be managed?

A
  • Early tx can prevent/minimise effects
  • Stacking wooden tongue depressors together 3-4x/day (add more over time)
  • Therabite device or Dynasplint Trismus system
  • Trigger point injections
  • Analgesics
  • Muscle relaxants
  • Botulinum toxin
  • Heat pack
527
Q

What are the phases of mucositis?

A

1st: Inflammatory/vascular (initiation)
2nd: epithelial (messaging, signalling and amplification)
3rd: ulcerative/bacteriological (pseudomembranous)
4th: healing

528
Q

What are the 4 grades of mucositis?

A

Grade 0: none
Grade 1: mild (sore mouth)
Grade 2: moderate (ulcers)
Grade 3: severe (can only swallow liquids)
Grade 4: life threatening (can’t eat or drink)

529
Q

What is the impact of oral mucositis on QoL?

A
  • Pain
  • Poss oral bleeding
  • Impact on communication, speech and expression
  • Difficultly with denture use, OH, dysgeusia, bad breath, dysphagia.
  • Poor nutrition and hydration
  • Oral medication difficult to take
  • Portal for systemic infection
  • Hospitalisation
  • Increased cost of care
530
Q

What is the typical mucositis and caries management for pts undergoing chemoradiotherapy?

A
  • MUCOSITIS MANAGMENT: Start difflam oral rinse at commencement of chemoradiotherapy (delays mucositis onset). If they get mucositis, switch to 0.12% Curasept (helps keep mouth clean).
  • CARIES RISK MANAGMENT: Get them to use CCP and high fluoride toothpaste
531
Q

What is the typical prevention regime for patients undergoing chemoradiotherapy?

A
  • Topical fluoride followed by CPP-ACP, starting 1 week before radiotherapy & continued
  • Foam brushes and rinses to reduce risk of microtrauma.
  • Avoid removable prosthesis (except while eating)
  • Refrain from smoking and food/drink that can cause irritation.
  • Saliva substitutes
  • Bicarb rinse after eating
  • Difflam, curasept
  • Natural yoghurt
  • Xylocaine gel
532
Q

How should candidosis be treated?

A

Miconazole

533
Q

How can pain relief be provided for patients with mucositis?

A
  • Topical anaesthetics
  • Difflam (anti-inflamm)
  • Bicarb/salt rinse
  • Systemic analgesics
  • Cryotherapy (causes vasoconstriction so may reduce amount of chemotaxic agent being delivered to oral mucosa)
534
Q

What is osteoradionecrosis?

A

Exposed and necrotic bone associated with ulcerated or necrotic soft tissue which persists for >3months in an area that has been previously irradiated

535
Q

What are the 3 classes of ORN?

A
  1. Notani I: confined to dentoalveolar bone
  2. Notani II: ORN limited to dentoalveolar bone &/or mandible above the inferior dental canal
  3. Notani III: ORN involving the md below the inferior dental canal or pathological fracture or skin fistula.
536
Q

What are the effects of ORN?

A
  • Pain
  • Infection
  • Loss of function
  • Malodour
  • Pathological md fracture
  • Disfigurement
  • Social isolation
537
Q

Where is bacteria present in ORN?

A

Only present on surface of bone and not in the necrotic area.

538
Q

What are the theories for pathogenesis of ORN

A
  • Radiation induced fibroatrophic theory (Pentoclo used to treat ORN)
    • activation and deregulation of fibroblastic activity creating imbalance btwn tissue synthesis and tissue degradation (fragile healed tissue)
  • Hypoxic-hypocellular-hypovascular theory ((hyperbaric oxygen is used to treat ORN)
539
Q

Why is the buccal cortex of the mandible the most common place of ORN?

A

Dense bone and higher mineral content absorb a higher radiation dose.

540
Q

What are risk factors for ORN?

A
  • Location (tongue, FOM, alveolar ridge, retromolar pad, tonsil)
  • Stage of cancer
  • Dose of radiation (>60Gy)
  • Prior surgery for tumour in jaw
  • Having teeth
  • Poor OH
  • Smoking & alcohol
  • Poor nutrition
541
Q

How can you prevent ORN post radiotherapy?

A
  • Dental exam prior to radiotherapy
  • Perform exos 2-3 weeks prior to tx
  • Management of OH and preventative strategies
  • Dietary advice
  • Regular dental recalls
542
Q

What the are the guidelines for management of patients who require dento-alveolar surgery and have previously had radiotherapy or been diagnosed with ORN? (tx planning, preop, peri-op, post op).

A
  • Tx planning: informed consent, place on operating list with senior staff.
  • Pre-op: rinse with mouthwash containing CHX, prophylactic AB.
  • Peri-op: Conservative surgical technique, primary closure of soft tissues where poss.
  • Post-op: CHX rinse for 2 weeks, post op antibiotics for 5 days.
543
Q

How should ORN be managed conservatively?

A
  • Systemic AB saved for episodes of acute infection.
  • Gentle removal of sequestra.
  • Reduction of local irritants (smoking, alcohol)
544
Q

Why are e. faecalis and c. albicans problematic?

A

Resistant against Calcium hydroxide
High Penetration into Tubuli
Biofilms

545
Q

When can radiographs reveal local inflammatory processes?

A

If more than 40% of bone structure is demineralised

546
Q

What is meant by the term “puffing” in endodontics?

A

Sealer being pushed out of foramen

547
Q

What ISO size should steel files be for length determination?

A

At least ISO size #15 (K files more visible than H)

548
Q

How long does it take for damaged periapical bone to completely heal?

A

Can take 1-3 years

549
Q

Why is rubber dam important for endo treatment?

A

Protect airway from files

Prevent saliva contamination

550
Q

What solutions can remove the smear layer?

A

16% EDTA

Citric acid

551
Q

How long does it take for EDTA to work?

A

4 minutes (use during terminal rinse)

552
Q

What are the effects of sodium hypochlorite at high vs low concentrations? Which comes first?

A

High: tissue dissolving, comes first

Low: disinfection, comes second

553
Q

What happens if the needle binds in the canal?

A

It can form a high pressure system, and extrude out of the apical foramen, burning the mucosa.

554
Q

What is the standard rinsing procedure?

A

Sodium hypochlorite (5ml per canal) in between instrument changes

16% EDTA

Sodium hypochlorite final rinse

Dry with paper points

CHX for problem cases

555
Q

What does ledermix contain?

A

Tetracycline and corticosteroid

556
Q

What is odontopaste composed of?

A
  • Corticosteroid
  • Clindamycin
  • CaOH
  • ZnO
557
Q

What is metamerism?

A

2 colours appear same colour under same lighting but not under different lighting

558
Q

What is the difference between chroma and hue?

A

Chroma is the amount of colour (it can appear faded)

Hue is the shade of colour (dominant wavelength)

559
Q

What has the CIE/Lab system been changed to for enhanced readability?

A

Lch

(lightness, chroma, hue)

560
Q

What are the hues of shade A, B, C and D?

A
  • A: reddish-brown
  • B: reddish-yellow
  • C: grey
  • D: reddish-grey
561
Q

What is the problem with vitapan classical?

A

Colours aren’t evenly distributed

Lightness plays no role

562
Q

What colour qualities does enamel produce?

A

Opalescence

Translucency, Lightness (comes from prismatic structure)

563
Q

What does opalescence do?

A

Reduces show through effect

564
Q

Describe the smooth transition of the dentine core from marginal to incisal.

A

Marginal: dark, high chroma, opaque

Incisal: light, low chroma, translucent

565
Q

What are the 3 levels of translucency?

A

Incisal: 55%

Opaque: 30%

Universal: 51%

566
Q

What is the purpose of the silicone index?

A

To keep incremental layering under control

567
Q

What are the steps of the layering sequence for aesthetic restorations?

A

Opalescent layer first

Place opaque layer along fracture line

Place first dentine layer as core

Place second dentine layer, creating mamelons at this stage

Place first enamel layer

Place second enamel layer just short of incisal edge

Place clear layer on incisal edge.

568
Q

How does a spectrophotometer determine tooth colour + problem with it?

A

Device measures spectrum of lights reflected by and coming from tooth and coverts it into shade

  • Measures LCh
  • Calculates distance to all tooth colours
  • Table and sort colours
  • Find smallest distance and report connected tooth colour

Teeth colour positions can be very close so measurements can vary greatly

569
Q

What is the classification of composite materials according to translucency?

A
  • Opaque and characterising colours
  • Dentine
  • Enamel
  • Enamel opalescent
  • Translucency
570
Q

What is the biological width and how big is it?

A

Combined width of junctional epithelium and connective tissue attachment. Also known as SCAT.

2.04mm

571
Q

What procedures can be undertaken if there is not enough tooth structure for crown?

A

Crown lengthening

Ortho extrusion

572
Q

When should paracetamol instead of NSAIDs be given?

A

If pt has stomach ulcers, diabetic, taking warfarin

573
Q

What is an intrapulpal injection?

A

Once access cavity is drilled, you place needle into canal and deposit LA. Thin needle and high pressure

574
Q

What to do if vital extirpation is not possible (hot pulp)?

A

Expose pulp at small point and place ledermix or odontopaste.

Seal with cotton pellet and GIC

Reopen after 24hours and try to extirpate

575
Q

If pain persists after endo tx for tooth with pulpitis what is likely the reason? How should this be treated?

A

Pulp tissue remaining in canals

  • Redetermine working length and shape the canals
  • Disinfect (consider other disinfection routine)
  • Dress with CaOH
576
Q

Do antibiotics provide pain relief? Why/why not?

A

No, they just reduce bacterial count

577
Q

What is the difference between spread and radiation of pain?

A

Spread is across a jaw

Radiation is from mx to md or vice versa

578
Q

What can have similar appearance to calcified submandibular gland?

A

SCC

579
Q

What do lymphomas vs scc feel like upon palpation?

A

Lymphomas are rubbery hard

SCC are rock hard and non-movable

580
Q

What are the 4 vital signs?

A

Temperature

Heart rate

Respiratory rate

Blood pressure

581
Q

What is a normal temperature range?

A

35-37.5

582
Q

What are important components of the full blood count test?

A

WBC

Neutrophil

Platelets

Hb

583
Q

What is the haemoglobin normal range for males and females?

A
  • Males: 135-180
  • Females: 115-160
584
Q

What is the normal WBC range?

A

4-11

585
Q

What is the normal platelet range?

A

150-400

586
Q

What is the normal neutrophile range?

A

2-7.5

587
Q

What is systolic vs diastolic?

A

Systolic is BP when your heart is contraction

Diastolic is BP when you heart is resting

588
Q

What systolic pressure is considered hypertension?

A

140-160mmHg

589
Q

Is high diastolic or systolic pressure more concerning?

A

Diastolic

590
Q

What is the normal beats per minute?

A

50-80

591
Q

What is the normal breaths per minute?

A

12-18

592
Q

What are the 3 drug types than can lead to MRONJ + examples?

A

Bisphosphonates

RANKL inhibitors

Anti-angiogenic (most risky)

593
Q

What can a pt do to reduce risk of MRONJ?

A

Quit smoking

Healthy diet

Maintain OH

Limit alcohol intake

Get pt dentally fit

594
Q

How can you prepare the pt with risk of MRONJ?

A

Assess risk and inform them of the risk

Advise them to quit smoking, have healthy diet and maintain OH

Aim to get them as dentally fit as possible

595
Q

How can you manage pt with low risk of MRONJ?

A
  1. Inform patient of the risks and that they are low risk. Gain consent.
  2. Carry out the procedure normally. No AB prophylaxis is necessary.
  3. Recall in 8 weeks to see if socket has healed. If no signs of healing and you suspect MRONJ, refer to oral specialist
596
Q

How can you manage pt with high risk of MRONJ?

A
  1. Try to consider other alternatives to extraction. If it is the best option, continue with extraction. Inform pt of risks and gain consent
  2. Carry out procedure as normal
  3. Recall in 8 weeks to see if the socket has healing. If no signs of healing and you suspect MRONJ, refer to oral specialist.
597
Q

What are the components of haemostasis?

A

Platelet plug

Coagulation cascade

Fibrin clot

Vasoconstriction

Thrombin activation

598
Q

What is characteristic of patient with clotting disorder?

A

They will have normal bleeding while in the chair as vasoconstriction and platelet function are part of primary haemostasis. One their way home they will start bleeding excessively

599
Q

What are management considerations for pt with CV disease?

A
  • Sedative Pre-Medication (benzo)
  • Brief Treatment Visits
  • Careful Use of LA with Vasoconstrictor (last thing you want to do for cardiac disease pt who is anxious to is have inadequate LA so using vasoconstrictor is appropriate)
  • Consider Patient Positioning (don’t want to lie pt who has heart failure flat- accumulation of fluid within thoracic cavity and lungs, preventing them from breathing properly)
  • Monitor BP and Pulse Oximeter
  • Endocarditis Prophylaxis
600
Q

What is normal bleeding time?

A

7 minutes

601
Q

How long should pressure be kept to control bleeding?

A

10 minutes

602
Q

What is this + how to manage?

A

Liver clot

  • Gently remove clot
  • Apply haemostatic agent
  • Suture
603
Q

How to manage pt with diffuse facial ecchymosis after exo?

A

Reassure pt that it will start to improve within 1-2weeks

604
Q

How to manage pt with persisting immediate or recurrent aggressive bleeding?

A

Apply haemostatic agents

Suture

If inadequate to control bleeding, send to hospital

605
Q

What is the risk of G6PD deficiency & use of Aspirin?

A

Haemolysis- anaemia

606
Q

What conditions are characterised by pink puffer and blue bloater?

A

Blue bloater: chronic bronchitis

Pink puffer: emphysema

607
Q

What patients require supplementary steroid cover (what dose)?

A

Pts undergoing surgery and are on long term steroid therapy that is >7.5mg. Recommended to double dose before procedure.

608
Q

Why do some patients require steroid cover?

A

Because they will be unable to make enough natural steroid to deal with stress when they are taking long term steroid therapy. Can lead to Addisonian crisis if pt does not get steroid cover when needed

609
Q

What are causes of hypoglycaemia?

A

Excessive exercise

Not eating enough

Excessive insulin

Stress

Alcohol

Hypoglycaemics

610
Q

What are symptoms of hypoglycaemia?

A
  • Dizziness
  • Irritability
  • Sweating
  • Drowsiness
  • Tingling
611
Q

What are complications of diabetes?

A
  • Renal failure
  • Cataracts, retinopathy
  • Peripheral neuropathy
  • Arteriosclerosis- amputations more common
  • Depression more common
612
Q

What are functions of the liver?

A

Metabolism

Cholesterol and bile formation

Blood clot factor production

Detoxification

Glycogen storage

Immune function

613
Q

What are symptoms of liver disease?

A

Jaundice

Excessive bleeding

Dark urine

Oedema

Finger clubbing

Sialosis

614
Q

What is important for dental management and liver disease?

A

Pt may have excessive bleeding (important for exos)

Pt may not be able to metabolise drugs effectively

Transmission of viral hepatitis

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