Classification and histopathology of pulp disease Flashcards

1
Q

What does enamel organ develop from?

A

Dental lamina

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2
Q

Cells found in pulp

A

Fibroblasts and stem cells and some macrophages, lymphocytes (& lymphatics)

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3
Q

Post-eruption dentine

A

Secondary and tertiary

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4
Q

Secondary dentine

A

Physiological: laid down at relatively constant rate throughout life
Regular structure
Pulp gets smaller

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5
Q

Tertiary dentine

A

Reactionary: laid down in response to insult to pulp
-structure varies
Reparative: occurs through differentiation of new odontblasts after odontoblasts have been killed
-poor structure

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6
Q

Pulp stones

A

True: composed of dentine
False: amorphous calcifications
-increase in number and size with age

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7
Q

Classification of pulp pathology

A
Inflammatory (pulpitis)
Degenerative
-fibrosis
-calcifications
-internal resorption
-may be age changes or 'idiopathic'
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8
Q

Pulpitis

A

Most important disease to affect pulp
Inflammation of pulp
Most common aetiology: dental caries
Defence reactions of dentine (dentine sclerosis, reactionary dentine formation)

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9
Q

Classification of pulpitis

A

Pulpitis –> acute or chronic
Acute –> open (i.e. pulp chamber open to oral cavity) or closed
Chronic –> open or closed
Acute open due to exposure, tooth fracture
Acute closed due to trauma
Chronic open due to open caries
Chronic closed due to caries

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10
Q

Causes of pulpitis

A

Infection (bacterial)
Trauma
Secondary to attrition, abrasion, erosion

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11
Q

Causes of pulpitis: infection (bacterial)

A
Dental caries (main cause)
Secondary to
-crack/ fracture
-lateral root canals
-canals in furcation
-invaginated odontome
Bacteraemia
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12
Q

Causes of pulpitis: trauma

A
Physical
-direct blow
-heat
-dessication
Chemical
-filling materials/ liners
Mechanical
-cavity preparation
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13
Q

Clinical features of pulpitis

A

Often poorly localised pain
May radiate to adjacent jaw, neck, face
Continuous or intermittent
Reversible, symptomatic irreversible or asymptomatic irreversible

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14
Q

Correlation clinical and histological

A

Little to none

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15
Q

Pulpitis

A

Occurs within closed environment i.e. limited by dentine
Little/ no collateral blood supply
Closed vs open apex (open better prognosis)

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16
Q

Patterns of pulpitis

A

Starts as localised lesion directly related to proximity of caries e..g pulp horn
Inflammation will spread throughout pulp if caries untreated
Rate of progression and character of pulpitis will vary between teeth and individuals

17
Q

Protective responses

A

Tertiary dentine

  • forms in response to caries
  • > distance of pulp from irritant
  • this reduces and may halt pulpitis
18
Q

Response to early dentine caries

A

Wheat sheaving indicated oedema in odontoblast layer
Tertiary (reactionary) dentine formation
> blood flow
Lymphocytes, plasma cells and macrophages
-At this stage it is possible pulpitis may resolve if caries removed or ceases to progress

19
Q

Response to late dentine caries

A
Acute inflammation
> vascularity
inflammatory exudate
accumulation of neutrophils
death of odontoblasts
20
Q

Natural history

A

Closed environment

  • rapid rise in tissue pressure
  • collapse of venous circulation
  • leads to tissue hypoxia
21
Q

Natural history: pulp necrosis

A

Hypoxia leads to

  • local tissue necrosis
  • release of inflammatory mediators
  • further inflammation and neutrophil accumulation
  • formation of pus: pulp abscess
22
Q

Natural history: pulp abscess

A

May be:
localised to pulp horn
surrounded by granulation tissue

23
Q

Natural history: spread

A

Pulpitis may spread to involve whole pulp

  • pus may drain into oral cavity if there is pulp exposure (‘open’ pulpitis)
  • bacteria destroyed by neutrophils
24
Q

Following spread

A

Total necrosis may follow

One root may be affected first with spread of infection to apex in multi-rooted teeth

25
Q

What does untreated pulpitis lead to

A

Necrosis and periapical pathology

26
Q

Chronic hyperplastic pulpitis

A

‘pulp polyp’
Usually first permanent molars
-open apices - good blood suply
-open carious cavity with pulp exposure
Granulation tissue in pulp chamber
Surface ulcerated and covered by fibrin and neutrophils
May become covered by epithellium
-source of epithelium uncertain: either saliva or gingival crevice
Clinically appears red and bleeds easily (less so if epithelialsed), often painless

27
Q

Healing of pulp

A

Use of calcium hydroxide may stimulate dentine formation
Need contact with pulp for it to be effective
Clinically need to decide whether to ‘pulp cap’ or to extirpate pulp following exposure

28
Q

Pathological resorption

A

Internal
-secondary to pulpitis
-idiopathic (‘pink spot’)
External - many causes