Root resorption Flashcards

1
Q

Definition of root resoption

A
  • Non bacterial destruction of dental hard and soft tissue due to interaction of osteoclastic cells
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2
Q

What are osteoclasts , why do they contribute to root resoprtion?

A
  • Large multinucleated cells found within Howships lacunae on hard tissue
  • Highly motile
  • have ruffled border in contact with dentine
  • Integrins hold the ruffled border to dentine
  • Intracellular vesicles release proteolytic enzymes and hydrogen ions = acidic environment
    = dissolution calcified hard tissue
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3
Q

Give reasons for why RANKL stimulation causes osteoclasts to become activated?

A
  • Parathyroid hormone, B3, IL-1B
  • Bacterial lipopolysaccharides
  • Trauma (physical or chemical)
  • Chronic inflammation
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4
Q

What surfaces on the root act to prevent resorption?

A
  • Periodontal ligament
  • Cementum (in partic non mineralised layer)
  • Predentine ( non collagenous component)

all prevent osteoclasts adhering or reabsorbing unmineralized matrix

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5
Q

Give the types of Internal and External root resoprtion

A

Internal
- Inflammatory
- Replacement

External
- Inflammatory
- replacement
- Cervical
- Surface

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6
Q

What radiographic examination can be helped for root resorption diagnosis?

A
  • 2 angles (ideally 30degress mesial or distal beam shift)
  • CBCT
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7
Q

What are the clinical of internal inflammatory root resorption?

A
  • The coronal integrity can be unrestored
  • Colour normal
  • Mobility normal
  • +ve response to sensibility testing
  • Usually no sinus, swelling, apical tenderness
  • No perio pocketing unless lesion has perforated root surface
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8
Q

What type of root resorption is this? Give the radiographic findings

A
  • Internal inflammatory
  • The widening of pulp canal is centred in the canal and doesn’t move with beam shift
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9
Q

Give the pathogenesis of internal inflammatory root resroption

A
  • Coronal pulp necrotic
  • Lesion includes inflammatory and vascular tissue (if perforated then communicates with PDL)
  • Apical pulp vital
  • Lesion will progress until apical pulp is completely necrotic
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10
Q

Txt of internal inflammatory RR

A

Orthograde endo only
- May has poss haemorrhage
- Active irrigation sodium hypo
- Intervist medicament of Ledermix (anti inflam properties)
- Thermal obturation

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11
Q

Give the radiographic and clinical findings of internal replacement resorption

A
  • Asymm and irregular enlagrment of pulp canal with distortion of canal anatomy
  • Canal/pulp may appear obliterated or replaced with mixed radio-opaque area with loss of root canal walls
  • May appear as pink area on crown of tooth
  • +ve vitality test unless crown or root perforation
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12
Q

Txt of Internal replacement RR

A
  • Identify cause and holt osteoclastic actvity
  • orthograde endo
  • Stop ortho
  • XLA
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13
Q

What is the aetiology of external surface resoprtion?

A

Mainly ortho
- 90% 1mm expected 2yrs
- 1-5% severe (more than a 1/3 orig root)
- 15% mod
- Usually teeth used for anchorage worst affected

  • Ectopic teeth (pressure form erupting tooth)
  • Pathological lesions (P from adjacent pathological lesion)
  • idiopathic
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14
Q

What is this type of resorption?

A
  • External surface resorption
  • PDL remains intact
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15
Q

TXT of external surface resorption

A
  • Pulp is healthy therefore endo will have no effect
  • Remove source to stop resoprtion (stop endo) and splint if mobile teeth
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16
Q

What is the main difference between external inflammatory and external surface resorption?

A
  • External inflamm will have -ve response to sensitivity as the pulp is necrotic
17
Q

What type of RR is this? Pulp is negative to sensibility testing

A
  • External inflammatory
18
Q

What is the aetiology of external inflammatory resorption? What is the txt?

A
  • Pulp is necrotic so bacterial or dental trauma origin
  • PA inflam lesion precipitates the resorption process

TXT
- Remove cause of inflammation
- endo txt or XLA

19
Q

What are the clinical and radio findings of external replacement resorption?

A
  • May be infra occluded
  • May be erythematous gingivae
  • No tenderness but high pitched note
  • No mobility
  • Positive to sensitivty
20
Q

TXT options for external replacement resorption

A
  1. Accept pos and restore incisal level with comp and monitor
  2. Autotransplantation of premolar
  3. Surgical respositioning
  4. Extraction (time this with pubertal growth if in children) and ortho space closure
  5. Decoronation (if >1mm infraoccluded) to preseve bone vol and implant later on
21
Q

Aetiology of external replacement resorption?

A

Trauma
- Avulsion or lateral luxation
- Sig injuries to periodontium so osteoclasts in contact with external root dentine to begin RR

22
Q

Clinical and radiographic findings of external cervical resorption

A
  • Extensive perio pocketing and profuse BOP into soft granulation at CEJ
  • Pink spot colour
  • Normal or no mob
  • +ve sensitivty
23
Q

Describe this classification of external cervical resorption

A

Classified into apico-coronal direction and circumferential

Apico-coronal direction
1. Crestal
2. Coronal 1/3
3. Middle 1/3
4. Apical 1/3

Circumferential
1. 1/4
2. 1/2
3. 3/4
4. More than 3/4

24
Q

What are the risks ass with external cervical resorption?

A
  • Ortho
  • Trauma (avulsion and luxation)
  • Wind instruments
  • Internal bleaching
  • viral infections
  • Systemic disturbance like thyroid issues

Max canine > max incisor > mand molar

25
Q

TXT options external cervical resoprtion

A
  1. Monitor (likely will continue)
  2. XLA and prosthetic replacement
  3. Internal repair (MTA) and orthograde endo
26
Q

How are osteoclasts stimulated ?

A
  • RANKL stimulation
  • RANKL liverated from osteoclasts and stromal cells found on surface of monocytes and macrophages
  • Stimulation leads to fusion of mononuclear cells and macrophages to become osteoclasts
  • OPG inhbits RANKL so inhibts osteoclastic activity
  • Careful balance of OPG and RANKL needed for bone remodelling in ortho
27
Q

How does MTA work?

A
  • Mineral trioxide aggregate
  • release calcium ions for cell proliferation
  • Creates antibacterial envrion with alkaline pH regulating cytokine production
  • useful for perforation of root
28
Q
A