classification and histopatholgy of pulpal disease

Question 1

What is the dental pulp developed from

Answer 1

dental mesenchyme

dental papilla enclosed by the tooth, then forms the dental pulp

Question 2

Normal pulp anatomy

Answer 2

Within cell rich zone

• contains nerve plexus
• individual nerves will go through odontoblast layers into the dentinal tubules

Pulp also contains inflammatory cells
‘Lymphatics’
-	macrophages 
-	lymphocytes
also has stem cells

Question 3

secondary dentine

Answer 3

• Physiological 2 dentine is laid down throughout life
• regular tubular structure
• pulp gets smaller over time

Question 4

types of tertiary dentien

Answer 4

reactionary

reparative

Question 5

reactionary detntine

Answer 5

• laid down in response to an insult to the pulp
• shrinks pulp away from the insult
• structure varies

Question 6

reparative dentine

Answer 6

• dentine which is laid down to repair a defect eg a resoption defect
• very unnormal structure, can sometimes look like bone

Question 7

pulp stones

Answer 7

stones composed of dentne

false ones are amorphous calcifications (increase with no and size with age)

Question 8

classifications of pulp pathology and what is included within them

Answer 8

1) Inflammatory
- pulpitis
2) Degenerative
- fibrosis
- calcifications
- internal resorption
- may be age changes or idiopathic

Question 9

pulpitis

Answer 9

inflammation of the pulp

Question 10

defecnce reactions to pulpitis

Answer 10

• dentine sclerosis (dentine tubules will close over)

- reactionary dentine formation

Question 11

classifications of pulpitis

Answer 11

acute/chronic

closed/opn

Question 12

acute open pulpitis

Answer 12

exposed tooth fractose

Question 13

chronic open pulpits

Answer 13

result of massive carious lesion

crown of tooth generally destroyed

Question 14

causes of pulpitis

Answer 14

Infection (bacterial)

• plaque bacteria
• extend to pulp
  1) Dental caries
  2) Secondary to:
• crack/fracture
• lateral root canals (open to oral environment)
• canals in furcation
• invaginated odontoma (crown infolds on itself, leading to a pouch in the crown, bacteria can get into the pulp)
  3) Bacteraemia

Question 15

trauma types

Answer 15

1) physical
- direct blow
- heat
- desiccation (over use of drying 3 in 1)
2) chemical
- filling materials/liners
3) mechanical
- cavity preparation

Question 16

pulpits clinical features and if it is reversible or not

Answer 16

1) often poorly localised pain
- patients unlikely to be able to pin it on one tooth
- due to differences in the nerves innervating the soft tissues and the nerves
2) may radiate to adjacent jaw, neck, face
3) continuous or intermittent

• Symptomatic irreversible
• asymptomatic irreversible

Question 17

responce to early dentine caries

Answer 17

• start of the acute inflammation
  This has a cellular component (neutrophil) and fluid component (oedema)
• a layer of fluid begins to build up in the odontoblast layer
  We can see the inflammatory effects and also the dentine responding in the start of tertiary dentine formation
• increased blood flow
• inflammatory cells can be seen

If caries removed pulpits could be resolved at this point in time

Question 18

responce to established dentine caries

Answer 18

Acute inflammation

• vasodilation
• inflammatory exudate (protein rich fluid which forms the oedema fluid)
• accumulation of neutrophils
• death of odontoblasts

Question 19

issue with pulpits and the pulp anatomy

Answer 19

Pulpitis occurs within a closed environment i.e. limited by dentine

• little/no collateral blood supply (i.e. one blood vessel in ad one vein out) – if there is compromise to that blood supply then you put the vitality of the pulp in danger)
• closed vs open apex. – if pulpitis occurs when you don’t have a closed apex yet, then there might not be as much of a problem)

Question 20

closed pulp blood supply

Answer 20

• inflammatory exudate causes rapid rise in tissue pressure
• eventually the tissue pressure will exceed the blood pressure in the veins, venous circulation collapses
• blood flow stops, leading to tissue hypoxia
• Then the pulp becomes necrotic
• This can occur to the entire pulp or part of the pulp

Question 21

hypoxia

Answer 21

Causes necrosis
-	leads to local tissue necrosis
-	release of inflammatory mediators
-	further inflammation and neutrophil accumulation
Eventually might form an abscess (an area of dead and dying neutrophils)
Pulp abscess maybe
-	localised to the pulp horn
-	surrounded by granulation tissue

Question 22

what does untreated pulpits lead to

Answer 22

pulp necrosis and periapical pathology

Question 23

chronic hyperplastic pulpitis

Answer 23

• open apices – good blood supply
• open carious cavity with pulp exposure
• the blood supply can cope with the increase in tissue pressure
  Mass of granulation tissue in the pulp chamber
  Surface ulcerated and covered by fibrin and neutrophils
• may become covered by epithelium
  source of epithelium uncertain (either saliva or gingival crevice)
  Clinically appears red and bleeds easily
• less so if epithelised
• often painless

Question 24

what can calcium hydroxide do

Answer 24

stimulate dentine formation

but needs to be in contact with with pulp to be effective

Question 25

internal pathological resopriton

Answer 25

- secondary to pulpitis (when inflamed can eat itself) - idiopathic (pink spot) - dentinoclasts start to eat the tooth from within