INDBE this is what you need too pass your examn. I PASSED in 2023

NBDE Part II – Endodontics
31 QUESTIONS

,CLINICAL DIAGNOSIS, CASE SELECTION, TREATMENT PLANNING, AND PATIENT
MANAGEMENT (19 questions)

PULP BIOLOGY
 Contains loose fibrous connective tissue with nerves, blood vessels, and
lymphatics
 Contains fibroblasts that secrete fibrous connective tissue
 Contains odontoblasts that secrete primary dentin before root formation is
complete and secondary dentin after root formation is complete
 Contains undifferentiated mesenchymal cells that can differentiate into
secondary odontoblasts to form tertiary dentin to protect the pulp from
injury
 Surrounded by hard dentin which limits its ability to expand
 Lacks collateral circulation which limits its ability to cope with infection

DENTIN AND PULP DEFENSE
 Sclerotic dentin= calcification of tubules in response to slowly advancing caries or aging
 Reactionary dentin= secondary dentin, reaction to minor damage
 Reparative dentin= tertiary dentin, repair for major damage
 Pulpal necrosis= response to rapidly advancing caries or other severe damage
 Bacteria (0.5-1µm) from dental caries are the main cause of serious pulpal injury, and can
penetrate beyond the obvious caries through dentinal tubules (diameter of 1-2.5µm).

HISTOLOGIC ZONES OF PULP
 From outside to inside:
 Predentin
 Odontoblastic layer
 Cell-free zone of Weil= contains nerve bundles
 Cell-rich zone
 Pulp core

DENTINAL PAIN  Aδ fibers
 Large myelinated afferent nerve
 Course coronally through pulp
 Sharp transient “first pain”
 Cold
 Pulpodentinal complex refers to intimate association of A δ fibers with odontoblastic cell
layer and dentin, hence why it is called dentinal pain

PULPITIS PAIN  C fibers
 Small unmyelinated afferent nerve
 Course centrally in the pulp stroma

,  NOT associated with pulpodentinal complex and NOT as easily provoked
 Dull throbbing “second pain”
 Heat

Progression of pulpal inflammation can change pain response from first pain (A δ) to second pain (C).
PAIN SENSITIZATION
 Hyperalgesia= heighted response to pain, inflammatory mediators in pulp can increase the
pain from a stimulus
 Allodynia= reduced pain threshold, pain due to stimulus that does not normally provoke
pain sunburnt skin is an example of aloe-dynia

REFERRED PAIN
 Preauricular pain often refers from mandibular molars since both share V3 innervation

CLINICAL CLASSIFICATION OF PULP
Normal Pulp
 Asymptomatic
 Mild to moderate transient (subsides when removed, momentary) response to thermal and
electrical stimuli
 No pain on percussion or palpation

Reversible Pulpitis
 Symptomatic
 Thermal (usually cold) stimulus causes quick, sharp, hypersensitive, transient response
 No complaints of spontaneous pain
 Caused by an irritant that affects the pulp—caries, SRP, deep restorations without a base
 Symptom, not a disease—if irritant is removed, the pulp reverts to uninflamed state; if
irritant remains, the symptoms may lead to irreversible pulpitis
 Frank penetration of bacteria into the pulp frequently is the crossover point to irreversible
pulpitis

Symptomatic Irreversible Pulpitis
 Pulp has been irreversibly damaged beyond repair; even with removal of the irritant it will
not fully heal
 Microscopic findings include microabscesses, tiny zones of necrosis within dense acute
inflammatory cells and intact nerves in areas with dense inflammation and cellular
degeneration
 Characterized by spontaneous (unprovoked) intermittent or continuous pain
 Thermal (often cold) stimulus causes lingering (prolonged pain even after stimulus is
removed) pain
 Postural changes like bending over or lying down increases blood pressure to the head and
may exacerbate dental pain