S2 - Intro to endo

Question 1

What type of tissue is the pulp classified as?

Answer 1

soft connective tissue

Question 2

2 main cells that compose the pulp? And others

Answer 2

odontoblasts
fibroblasts (most prevalent)

others: pericytes (close to endothelial, mesenchymal cells), macrophages (aka histiocytes)

Question 3

What does the pulp contain?

Answer 3

vessels, nerves, intracellular ground matrix

Question 4

What do odontoblasts do? (2) Lifespan? Location? Type of cell?

Answer 4

• secrete dentin and form dentinal tubules
• lifespan is same as vital tooth - once formed, cannot undergo mitotic division
• aligned along predentin
• odontoblast processes (Tome’s fibre) is housed within dentinal tubule and extend only to 1/3-1/2 of dentinal tubule
• considered terminal cells (like nerves)

Question 5

What do fibroblasts do?

Answer 5

• form and maintain pulp extracellular matrix which consists of collagens (type I and II mainly, higher density around blood vessels and nerves) and non-collagenous proteins

Question 6

Sensory innervation of the pulp

Answer 6

A-Beta, A-Delta (15%) - myelinated, very fast conduction speed and low excitability threshold -> sharp, transient pain typical of dentin senstivity
(e.g. cold test, vital tooth)

C Fibres - unmyelinated, slow conduction speed and high excitability threshold -> dull, aching, excruciating and sometimes diffuse pain, typical of symptomatic irreversible pulpitis

Question 7

What are the pathways of root infection?

Answer 7

• once exposed, dentin may present a route for bacteria to reach the pulp via tubules, however as long as pulp is vital, dentinal exposure does not represent a signficant risk of pulp infection except when dentin thickness is considerably reduced and dentine permeability is signficantly increased
• in situations where the vitality of the pulp is compromised and defence mechanisms are impaired, even very few bacteria may initiate infection
• exposed pulps will undergo inflammation, necrosis and become infected

(pathways = caries, iatrogenic damage from restorative tx, trauma, perio pocket reaching accessory foramen (lost cementum, bacteria can go through dentinal tubules into pulp), aggressive perio reaching apical foramen)

Question 8

T/F Goal of endo is to completely eliminate bacteria?

Answer 8

no, aim = microbial reduction, we cannot get rid of all

Question 9

In terms of microbiology, when do clinical signs and symptoms become evident? How can tx affect it?

bacterial load

Answer 9

1. bacteria have to reach a quorum of cells sufficient to cause disease (bacterial load), before threshold is reached no clinical signs/symptoms evident
2. after bacterial levels and reach that threshold, the infectious disease (apical perio) is established
3. if tx procedures do not succeed in reducing bacterial levels below the threshold, disease will persist
4. successful tx does not necessarily sterilise the canal but reduces bacteria to subcritical levels that are compatible to healing

Question 10

Can you do single session endo for apical perio?

Answer 10

no

Question 11

Explain this formula

Answer 11

pathogenicity = number of microbial cells, virulence, interactions
resistant = host immune system

Question 11

Explain this formula. What role does the dentist play?

Answer 11

pathogenicity = number of microbial cells, virulence, interactions
resistant = host immune system

we can only reduce N