L8 Pulpitis Flashcards

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1
Q

What is pulpitis?

A

The inflammatory response to tissue damage of pulp.

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2
Q

How is the pulp affected in caries?

A
  • Tooth surface cavitates
  • Bacteria enters cavity and dentinal tubules
  • Products of bacterial metabolism penetrate along tubules to reach pulp
  • These products damage cells of the pulp including odontoblasts
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3
Q

Pulp can be classified according to what 2 factors?

A

Clinical classification:

  • Acute
  • Chronic

Pathological classification:

  • Parital or total
  • Open or closed (open = coronal pulp is open to oral cavity)
  • Exudative (serum based) or suppurative (pus based)
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4
Q

Describe the clinical presentation of pulptitis.

A
  • Predominantly pain but some patients will present without pain
  • Pain will be difficult to localise to a specific tooth, pain may radiate to adjacent jaw and sometimes to the face, ear and neck
  • Pain may be continuous or intermittent
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5
Q

What are the clinical signs of acute pulptitis?

A

Severe, throbbing pain.
Made worse by hot or cold, and lying down.
May keep patient awake.

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6
Q

What are the clinical signs of chronic pulpitis?

A

Spontaneous attacks of dull, aching pain.

Lasts 1-2 hours.

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7
Q

What is the difference between reversible and irreversible pulpitis?

A
  • Reversible pulptitis: restorative treatment will cause pulpitis to resolve
  • Irreversible pulpitis: no matter what intervention, pulpal inflammation is likely to persist and ultimately cause total pulp necrosis
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8
Q

What does pulp management depend on?

A
  • Patient age
  • Size of carious lesion
  • Presence of symptoms
  • Vitality testing
  • Radiographic changes
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9
Q

Describe physical causes of pulpitis.

A

Physical trauma:

  • Tooth fracture
  • Cracked tooth
  • Iatrogenic (e.g. during cavity preparation)
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10
Q

Describe microbial causes of pulpitis.

A

Microbial:

  • Bacteria and bacterial products reach the plup as a result of caries
  • Pulp changes seen when bacteria are 1mm from pulp in adult teeth, 2mm from pulp in deciduous teeth
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11
Q

Describe chemical causes of pulpitis.

A

Chemical:

  • Irritant chemicals reach pulp by diffusing through dentinal tubules e.g. during restorative treatment
  • Iatrogenic: applied directly to exposed pulp during restorative treatment
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12
Q

Describe thermal causes of pulpitis.

A

Thermal:

  • Heat generated by friction in cavity preparation
  • Unlined large metallic fillings may transmit thermal changes to the pulp (e.g amalgam in contact with gold)
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13
Q

What factors may modify the inflammatory process?

A
  • Local anatomy of the pulp chamber
  • Nature of the damaging agent
  • Duration and severity of tissue damage
  • Pre-existing state of the pulp
  • Host defences
  • Apical blood flow: whether the apical foramen is already closed, or if tooth is still developing and apex still open
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14
Q

How can pulpitis lead to total pulp necrosis?

A
  • Increased vascular permeability causes inflammatory exudate to enter pulp chamber
  • Local rise in tissue pressure could cause local collapse of venous part of microcirculation
  • Local tissue hypoxia and anoxia produces further tissue damage, and further inflammation causes increase in pressure
  • Can lead to total pulp necrosis
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15
Q

What is the main host defence against pulpitis?

A

Reparative dentine formation:

  • Begins 20 days after initial damage
  • Produced at rate of 0.1mm over next 100 days
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16
Q

What tissue type may be seen in pulpitis?

A

Granulation tissue

17
Q

What immune cells may be present in pulpitis?

A

Lymphocytes (large dark nucleus), plasma cells (odd positioned nucleus) and macrophages (pale nucleus).

NB: loss of odontoblasts

18
Q

Pulpitis progression depends on what?

A
  • Severity and duration of tissue damage
  • Properties of the bacteria
  • Host resistance
19
Q

How do neutrophils reach the pulp tissue and what can neutrophil accumulation cause?

A
  • When bacteria reach the pulp there is vascular dilation
  • Neutrophils migrate from vessels
  • Majority of pulp entering the pulp is destroyed by neutrophils and other defence mechanisms
  • Local tissue necrosis and neutrophil accumulation leads to suppuration (pulp abscess)
20
Q

Describe the cellular composition of a pulp abscess.

A
  • Necrotic tissue with many neutrophils (multi-lobed nucleus)
  • Almost no viable tissue remaining
21
Q

What membrane may form around a pulp abscess?

A

A pyogenic membrane (made of granulation tissue)

22
Q

How can a pulp abscess cause pulp necrosis?

A

Abscess may extend through the pulp, causing necrosis.

23
Q

What is pulp necrosis?

A

Inflammation of the entire pulp, reaches the root apices. Pulp completely dead.

24
Q

What is a pulp polyp?

A
  • A pink soft tissue swelling attached to the dental pulp
  • Seen as bright red or pink soft tissue mass within large carious caivty
  • Seen in primary teeth or
    permanent teeth with wide
    open root apices thus pulp
    has good blood supply
  • Core of dense fibrous tissue, oftem with squamous epithelium on surface to protect from bacteria
  • Called chronic hyperplastic pulpitis
25
Q

Describe the formation and structure of a pulp polyp.

A
  • Large area of inflamed pulp
  • Causes granulation tissue to proliferate and produces a nodule of tissue (polyp)
  • Surface may epithelialise and can be keratinised (keratinised stratified squamous epithelium)
  • Underlying tissue is vascularised connective tissue
26
Q

What happens once the surface of a polyp epithelialises?

A

The core is largely protected from the oral environment, so inflammation will reduce and granulation tissue replaced by fibrous scar tissue.

27
Q

What are the theories regarding the origins of the epithelial layer on pulp polyps?

A
  • Said to be from desquamated epithelial cells but these are usually inactive cells incapable of division
  • May be some epithelial basal cells in saliva, possibly released by trauma