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BDS4 Endodontics > 1 - Resorption > Flashcards

1 - Resorption Flashcards

1
Q

Define root resorption.

A

Non-bacterial destruction of dental hard and soft tissue due to the interaction of clastic cells

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2
Q

What cells initiate root resorption?

A
  • osteoclast by definition, although referred to as dentinoclast when on dentine
  • originate from multinucleated giant cells
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3
Q

What are the features of dentinoclasts?

A
  • motile (can move from bone to dentine root surface when PDL is not present)
  • ruffled border that releases proteolytic enzymes
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4
Q

What stimulates dentinoclasts?

A

RANKL

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5
Q

What up-regulates RANKL?

A

Unknown although below answers are thought possible
- parathyroid hormone
- bacterial lipopolysaccharides
- trauma
- chronic inflammation

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6
Q

Give an examples of a RANKL inhibitor.

A

Denosumab

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7
Q

What trauma are most likely to result in root resorption?

A
  • avulsion
  • lateral luxation
  • intrusion
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8
Q

What surfaces protect against root resorption?

A
  • PDL
  • cementum (non mineralised layer)
  • predentine (non-collagenous component)
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9
Q

How is root resorption classified?

A
  • internal
  • external
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10
Q

What are the types of internal root resorption?

A
  • inflammatory
  • replacement
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11
Q

What are the types of external root resorption?

A
  • inflammatory
  • replacement
  • cervical
  • surface
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12
Q

How do you differentiate between external and internal resorption on a radiograph?

A
  • external, tramlines are still visible, parallax applies
  • internal, bulbous deformity in tramlines, parallax does not apply
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13
Q

Describe the clinical findings in internal inflammatory resorption.

A
  • no pocketing unless root surface perforated
  • no sinus unless periradicular disease
  • no TTP
  • no mobility
  • positive response to sensibility
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14
Q

Describe the radiographic findings in internal inflammatory resorption.

A
  • centred in canal, tramlines move with bulbosity
  • does not move with beam shift
  • usually no PA radiolucency
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15
Q

Describe the pathogenesis of internal inflammatory resorption.

A
  • coronal pulp is necrotic, apical pulp is vital
  • lesion includes inflammatory and vascular tissue and will communicate with PDL if perforation present
  • lesion progresses until apical pulp becomes necrotic and blood supply is lost
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16
Q

How do you manage internal inflammatory resorption?

A
  • orthograde endodontics only
  • CaOH used as intervisit medicament due to caustic properties that chemically disinfect areas that are unable to be instrumented due to morphology of resorption
17
Q

Describe the radiographic findings in internal replacement resorption.

A
  • incidental finding
  • pulp is replaced by bone/PDL/cementum and appears radiopaque with trabecular pattern
17
Q

Describe the clinical findings in internal replacement resorption.

A

No abnormal clinical findings

18
Q

How do you manage internal replacement resorption?

A
  • no treatment until symptomatic
  • if symptomatic or fractures, requires tooth replacement option
  • RCT very unpredictable
19
Q

Describe the clinical findings in external surface resorption.

A
  • increased physiological mobility
  • positive response to sensibility
20
Q

Describe the radiographic findings in external surface resorption.

A
  • roots appear short
  • PDL intact
  • pulp normal
  • root can appear with trabecular pattern after healing of previous surface resorption
21
Q

How do you manage external surface resorption?

A
  • remove source of resorption
  • endodontics ineffective
  • splint teeth if mobile
  • DWP risk associated with perio, as less supporting root structure and tooth loss more likely
22
Q

Describe the pathogenesis of external surface resorption.

A
  • orthodontics, as teeth move through bone the root is resorbed away, teeth used for anchorage are worst affected
  • ectopic teeth
  • cysts
  • idiopathic
23
Q

What is the percentage of teeth experience external surface resorption?

A
  • 90% experience
  • 2-5% have severe
24
Q

Describe the clinical findings in external inflammatory resorption.

A
  • usually previously restored teeth
  • may have increased mobility
  • negative to sensibility testing (pulp necrotic)
  • possible sinus, swelling, TTP or apical tenderness
25
Q

Describe the radiographic findings in external inflammatory resorption.

A
  • restoration can be close to pulp horn
  • apical area associated with resorption
26
Q

Describe the pathogenesis of external inflammatory resorption.

A
  • inflammatory reaction
  • necrotic pulp drives resorptive process
  • bacterial or dental trauma origin
  • PA inflammatory lesion precipitates resorption process
27
Q

How do you manage external inflammatory resorption?

A
  • remove cause of inflammation
  • orthograde endodontics (or re-RCT)
  • XLA
  • if lack of apical stop, refer
28
Q

Describe the clinical findings in external replacement resorption.

A
  • infraoccluded
  • no TTP, but high pitch percussion note
  • NO physiological mobility
  • positive to sensibility
29
Q

Describe the radiographic findings in external replacement resorption.

A
  • no PA radiolucency
  • no PDL
  • pulp normal
30
Q

Describe the pathogenesis of external replacement resorption.

A
  • trauma in which significant injury to PDL and allows osteoclasts to contact root dentine
  • most commonly avulsion and lateral luxation
31
Q

How do you manage external replacement resorption?

A
  • decoronate if infraocclusion >1mm in growing patient
  • remove crown to alveolar level and allow root to resorb to preserve bone volume and tooth replacement with denture or RBB
  • camouflage with composite if smile line suitable
32
Q

Describe the clinical findings in external cervical resorption.

A
  • if extensive, pocketing and +++ BOP
  • gingiva can be inflamed
  • pink spot lesion
  • normal mobility
  • positive to sensibility
33
Q

Describe the radiographic findings in external cervical resorption.

A
  • radiolucent area on root surface
  • tramlines intact
  • parallax applies with cone shift
  • CBCT shows pulp spared
34
Q

Describe the spread of external cervical resorption.

A
  • regular invasive pattern
  • predentine protects pulp
35
Q

How do you manage external cervical resorption?

A
  • can monitor although likely resorption will continue
  • decoronate with hypochlorite to disinfect and destroy resorptive cells
  • XLA and prosthetic replacement
  • internal repair and orthograde endodontics (specialist)
36
Q

How is external cervical resorption classified?

A

Apico-coronal
1 - crestal
2 - coronal 1/3
3 - middle 1/3
4 - apical 1/3
Circumferential
1/4
1/2
3/4
>3/4

37
Q

What are the risk factors for external cervical resorption?

A
  • orthodontics
  • trauma (avulsion/luxation)
  • historical non-vital whitening with heat
  • wind instruments
  • viral infection
  • systemic disturbance eg thyroid

BDS4 Endodontics (1 decks)

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