ENDODONTICS  REVIEW    
TopRank  Review  Academy  
#DMDMAY2020  
 
 
PULP-­‐DENTIN  COMPLEX  
§ Function  closely  together  as  a  unit  
§ Embryologically  derived  from  ectomesenchyme  
§ Odontoblasts  (found  in  the  pulp)  produce  dentin    
§ Pulp  is  composed  of  cells,  extracellular  matrix  and  connective  tissue  fibers.    
 
PULP  
DISTINCT  ZONES  OF  THE  PULP  (Outermost  to  innermost  layer)  
 
1. Odontoblast  Layer  
 
2. Cell-­‐poor  Zone  of  Weil    
§ Contains  capillaries  and  myelinated  nerve  fibers  
 
3. Cell-­‐rich  Zone  
§ Contains  fibroblasts,  macrophages  and  dendritic  cells,  mesenchymal  
stem  cells  (migrate  to  the  DEJ  and  replace  odontoblasts)  
 
4. Pulp  proper  (innermost  pulp)  
§ Central  part  of  the  pulp  
§ Made  up  of  loose  connective  tissue,  larger  blood  vessels  (arterioles  and  
venules)  and  nerves  
§ Cells  in  the  pulp  proper:  Fibroblasts  (most  numerous),  macrophages,  
dendritic  cells,  lymphocytes,  mast  cells  (found  in  cases  of  inflammation)  
 
CELLS  IN  THE  PULP:  
1. Fibroblasts  (Most  Numerous  Cell  Type)  
§ Synthesizes  Types  I  and  III  collagen  
§ Produced  extracellular  matrix  
§ Produces  inflammatory  cytokines  (A  General  name  of  
signaling  molecules  that  mediate  and  regulate  immunity,  
inflammation  and  hematopoiesis)  
 
2. Macrophages  
§ These  are  Monocytes  (when  inside  the  vessels)  that  have  left  
the  blood  stream    
§ Functions:  Phagocytosis,  Antigen-­‐processing,  production  of  
pro-­‐inflammatory  cytokines  
 
3. Dendritic  cells  (Most  Numerous  Immune  Cells)  
§ Antigen-­‐presenting  cells  (Phagocytose  bacterial  antigens  and  
present  them  to  T-­‐Lymphocytes  to  activate  them)  
 
  

 
4. Lymphocytes  
§ T-­‐Lymphocytes:  Play  a  role  in  immunity  with  macrophages  
and  dendritic  cells    
§ B-­‐Lymphocytes:  Only  seen  in  inflamed  pulp  (Chronic)  
 
5. Mast  cells    
§ Mainly  found  in  chronically  inflamed  pulp  around  blood  
vessels  
§ Release  Heparin  &  Histamine  which  play  a  role  in  
inflammation    
 
Normal-­‐  Dendritic  Cells  (Most  common),  Macrophages,  Some  T-­‐Cells  
Inflamed  Pulp-­‐  Acute:  Neutrophils;  Chronic:  B-­‐cells  and  Mast  Cells  
 
Extracellular  Matrix  of  the  Pulp  
Ø Amorphous  (No  specific  shape)  
Ø Gel-­‐like  consistency  
Ø Made  up  of:  
• Glycoproteins  
• Proteoglycans  
• Glycosaminoglycans  (Hyaluronin)  
 
Connective  Tissue  Fibers  of  the  Pulp  
Ø Collagen  Type  I  (55%)  &  Type  III  (45%)  
 
Innervation  of  the  Pulp  
Ø Pulp  is  innervated  by:  
1. Afferent  Neurons:  Conduct  sensory  impulses  
2. Autonomic  (Efferent)  Neurons:  Modulate  circulation  in  the  pulp  
Ø Sensory  innervation  to  the  pulp  is  composed  of  mainly  two  types  of  neurons:  
1. A-­‐delta  fibers  (Myelinated)  
2. C  fibers  (Unmyelinated)  
-­‐Make  up  most  of  the  neurons  in  the  pulp  (80%)  
Ø Sensory  fibers  first  appear  in  the  pulp  during  the  Bells  Stage.  
1. First:  Unmyelinated  C  Fibers    
2. Last:  Myelinated  A-­‐delta  fibers  
Ø Pulp  only  has  Nociceptive  fibers  (Pain  is  the  only  sensation  the  pulp  can  feel  )  
§ Pain  is  POORLY  LOCALIZED  because  it  does  not  have  proprioceptors  
§ A  single  neuron  may  innervate  more  than  one  tooth  
 
Nerve  Supply  to  the  Pulp  
Ø Nerve  fibers  (w/  blood  vessels)  -­‐-­‐-­‐enter-­‐-­‐-­‐  root  (through  apical  foramen  and  
accessory  foramina)  -­‐-­‐-­‐travel  upwards-­‐-­‐-­‐  crown      
Ø Nerve  Plexus  of  Raschkow:  network  of  nerves  beneath  the  Cell-­‐Rich  Zone  (3rd  
layer  from  the  outside  and  the  layer  before  the  pulp  proper)  

 
  

§ A-­‐Delta  fibers  exit  this  plexus  and  the  nerve  endings  of  these  fibers  are  
unmyelinated  nerve  endings  
Ø Dentin  above  the  pulp  horns:  most  nerve  fibers  
Ø Radicular  dentin:  has  the  least  nerve  fibers    
 
Blood  Flow  to  the  Pulp  
Ø Arterioles  enter  the  pulp  through  the  apical  foramen  and  the  accessory  
foramina  
Ø Plexus  of  capillaries:  supplies  the  odontoblasts  with  nutrients  
Ø Lymphatic  drainage:  submental,  submandibular,  cervical  lymph  nodes  
 
Circulation  in  the  Inflamed  Pulp  
Ø Causes  vasodilation  and  increased  permeability  of  capillaries  
Ø Since  dentin  is  a  hard  structure,  it  cannot  expand  to  accommodate  this  
inflammation  causing  increase  in  intrapulpal  pressure  
 
DENTIN  
§ 70%  inorganic  material:  Calcium  hydroxyapatite    
§ 20%  organic  material:  Proteins  most  commonly,  Type  I  collagen  
:  Minor  components,  Type  III  and  V  
§ 10%  water  
 
Dentinal  Tubules    
§ From  dentin  to  predentin  
§ Increase  dentin  permeability  and  sensitivity  to  bacteria  and  restorative  
procedures  
§ Contain  Odontoblastic  Processes  and  Nerve  Endings  
Peritubular  Dentin  
§ Highly  mineralized  than  intertubular  dentin  
§ Less  collagen  than  intertubular  dentin  
Intertubular  Dentin  
§ Dentin  between  the  dentinal  tubules    
§ Tightly  interwoven  network  of  collagen  fibers  and  hydroxyapatite  crystals  
 
Predentin  
Ø Dentin  first  deposited  as  a  layer  of  unmineralized  matrix  (10  to  μm)  
Ø Principally  contains  collagen  similar  to  osteoid  in  bone  
Ø Gradually  mineralizes  into  dentin  which  can  either  be  globular  or  linear  
 
Mineralization  of  Dentin:  
a) Globular  Calcification  Pattern  (seen  in  mantle  dentin)  
b) Linear  Calcification  Pattern  
§ Dentin  is  formed  at  a  slow  rate  
   
Primary  Dentin  
Ø Formed  before  the  root  has  been  completed  
Ø Makes  up  most  of  the  dentin  of  the  tooth  
 
  

Ø Surrounds  the  pulp  chamber  (Circumpulpal  dentin)  

Ø Mantle  dentin    
 
Secondary  Dentin  
Ø Dentin  formed  after  root  completion  and  throughout  life  
Ø Found  between  the  predentin  and  the  primary  (circumpulpal)  dentin  
 
Tertiary  Dentin  
Ø Produced  in  reaction  to  attrition,  caries,  restorative  procedures  
Ø Produced  only  in  the  areas  affected  by  stimulus  
Ø Function:  Protects  the  pulp  from  further  injury  
Ø Further  classified  into:  
a. Reactionary  Dentin:  deposited  by  preexisting  odontoblasts  
b. Reparative  Dentin:  Formed  by  new  odontoblasts  from  stem  cells  after  
odontoblastic  death  
 
Sclerotic  Dentin  
Ø Dentin  in  which  the  dentinal  tubules  have  been  completely  occluded  
 
Lines  in  Dentin  (seen  histologically)  
1. Line  of  Owen    
2. Incremental  Line  of  Von  Ebner    
3. Enamel  Spindles  (Parang  ligaw  na  dentin)  
4. Enamel  Tufts  (Structural  defects  in  enamel)  
 
Sensitivity  of  Dentin  
1. Hydrodynamic  Theory  (Most  accepted)  
§ When  dentin  is  stimulated,  the  fluid  in  the  tubules  will  move  and  will  
stimulate  the  free  nerve  endings  (A-­‐Delta)  
2. Transduction  Theory  
§ Membrane  of  odontoblast  process  conducts  an  impulse  to  the  nerve  endings  in  
the  predentin,  odontoblast  zone,  and  pulp.  
3. Direct  Conduction  Theory  
§ Stimuli  directly  affect  the  nerve  endings  in  the  tubules  
 
Pulp  Stones  
Ø Discrete  calcified  masses  found  within  the  pulp  
Ø Mineralized  by  Carbonated  hydroxyapatite  
Ø Most  frequently  found  at  the  orifice  or  within  the  root  canal  
 
Age  Changes  of  the  Pulp-­‐Dentin  Complex  
Ø Decrease  in:  
a. Size  of  pulp  chamber  and  root  canals  due  to  secondary  dentin  formation  
b. Cellularity  of  the  pulp  
c. Number  of  nerves  and  blood  vessels  
d. Dentin  permeability  (less  injury=less  sensitive)  
e. Sensitivity  
 
  

Ø Increase  in:  
a. Number  and  thickness  of  collagen  fibers  
b. Deposition  of  Peritubular  dentin  (Dentinal  Sclerosis)  
 
 
DIAGNOSTIC  TESTS  
Control  Teeth  
§ Should  be  tested  first  before  testing  the  endodontic  tooth  
§ Should  be  the  adjacent  or  contralateral  teeth    
§ Patient  must  NOT  be  told  that  it  is  a  control  tooth  that  is  being  tested  to  
provide  a  BASELINE  
 
1. Percussion  
2. Palpation  
3. Mobility  
§ Increase  in  tooth  mobility  is  not  an  indication  of  tooth  vitality  
§ It  is  merely  an  indication  of  a  compromised  periodontal  attachment  
 
Normal  Mobility    
0.2  mm:  Horizontally  
0.02  mm:  Verticallu  
 
Grading  of  Mobility  
Grade  I:  movement  greater  than  normal  
Grade  II:  1  mm  in  any  direction  
Grade  III:  >  1mm  in  any  direction,  vertical  depression  or  rotation  of  the  
crown  in  its  socket  
 
4. Probing  
5. Pulp  Vitality  Tests  
A. Cold  Test  
B. Heat  Test  
C. Electric  Pulp  Test    
D. Blood  Flow  Determination  
E. Test  Cavity  
 
 
ENDODONTIC  DIAGNOSIS  
Pulpal  Diagnosis  
1. Normal  Pulp  
§ Pulp  is  symptom-­‐free  
§ Responds  normally  to  pulp  vitality  tests:  
o Mild/transient  response  on  cold  test  (1-­‐2  seconds)  
 
2. Reversible  Pulpitis  
§ Exaggerated  response  when  a  stimulus  is  applied  to  the  tooth  
§ No  lingering  discomfort  after  removal  of  stimulus  
 
  

 
3. Symptomatic  Irreversible  Pulpitis  
§ Sharp,  spontaneous,  lingering  pain  (sometimes  more  than  30  seconds)  
even  after  removal  of  thermal  stimulus  
§ Referred  pain  (ear,  forehead,  back  of  the  mouth)  
 
 
Tooth/ Teeth Involved Site of Pain Referral
Maxillary Incisors Forehead Region
Maxillary Canines and Premolars Nasolabial Region and Orbit
Maxillary Second Premolars Temporal Region
Mandibular Molars Ear, Angle of the Jaw, or Posterior
Regions of the Neck
Mandibular Incisors, Canines and Mental Region of the Mandible
Premolars
Maxillary Molars Zygomatic, Parietal, and Occipital
Regions of the Head
Maxillary and Mandibular Molars Opposing quadrant or to other teeth in
the same quadrant
 
 
4. Asymptomatic  Irreversible  Pulpitis  
§ No  symptoms  and  teeth  respond  normally  to  thermal  testing    
§ Etiology:  Trauma,  Deep  Caries  
 
5. Pulp  Necrosis  
§ Pulp  tissues  are  dead  
§ Heat  test:  Painful  due  to  remaining  gases  and  fluids  that  expand  and  
extrude  into  the  periapical  tissues  
 
6. Previously  Treated    
§ Diagnostic  term  indicating  that  a  tooth  has  been  endodontically  treated  
and  the  pulp  canals  have  been  obturated  with  root  cana  filling  (gutta  
percha  or  silver  points),  not  with  medicaments  
§ No  response  to  thermal  test  or  EPT  
 
7. Previously  Initiated  Therapy  
§ This  indicates  that  the  tooth  has  been  treated  by  partial  endodontic  
treatment  (Pulpectomy  and  Pulpotomy)  
 
Periapical  Diagnosis    
1. Normal  Periapical  Tissues  
§ Teeth  are  not  sensitive  to  percussion  and  palpation  test  
§ Radiograph:  Intact  lamina  dura,  uniform  periodontal  space  
2. Symptomatic  Apical  Periodontitis  
§ Inflammation  of  the  apical  periodontium  
 
 
  

3. Asymptomatic  Apical  Periodontitis  

§ Inflammation  and  destruction  of  the  apical  periodontium  after  the  tooth  
has  become  necrotic  
§ No  pain  to  percussion  and  palpation  
§ Though  the  tooth  does  not  produce  and  painful  symptoms,  patient  may  
feel  different  to  biting    
§ Histological  Appearance:  Lesion  may  either  be  a  granuloma  or  a  cyst    
 
 
4. Acute  Apical  Abscess  
§ Acute  inflammatory  reaction  caused  by  pulpal  necrosis  
§ Clinical  Appearance:  Pus  formation,  swelling  of  soft  tissues,  rapid  onset,  
spontaneous  pain,  extreme  tenderness  to  percussion,  tooth  may  be  
mobile,  patient  may  experience  malaise,  fever,  lymphadenopathy  
§ Management:  
Measure  body  temperature  
Evaluate  for  lymphadenopathy  
 
Cellulitis  
§ Spread  of  Acute  Apical  Abscess  into  fascial  spaces  
§ Diffuse  swelling  and  life-­‐threatening  
 
Incison  and  Drainage:  (Most  important  management)  
§ Relieves  pressure  and  pain  
§ Eliminates  source  of  infection  (bacteria  and  their  products)  
 
5. Chronic  Apical  Abscess  
§ Inflammatory  reaction  to  pulpal  necrosis  
§ Gradual  onset  with  mild  symptoms  (little  or  no  discomfort)  
§ SINUS  TRACT  is  associated  with  the  tooth  and  there  is  intermittent  
discharge  of  pus  from  the  sinus  tract  
§ Sinus  Tract:  usually  located  on  the  oral  mucosa    
 
6. Condensing  Osteitis  (Periapical  Sclerosing  Osteitis)  
§ Reaction  to  a  low-­‐grade,  chronic  inflammation  of  the  pulp  
§ Seen  at  apex  of  the  tooth  (Mandibular  1st  molars,  Very  Carious,  May  be  
vital,  Necrotic,  Usually  Asymptomatic  Teeth)  
 
SAMPLE PROBLEMS
1. Mandibular right first molar had been hypersensitive to cold and sweets over the
past few months but the symptoms have subsided. Now there is no response to
thermal testing and there is tenderness to biting and pain to percussion.
Radiographically: There are diffuse radiopacities around the root apices.
DIAGNOSIS:

 
  

2. Following the placement of a full gold crown on the maxillary right second molar,
the patient complained of sensitivity to both hot and cold liquids; now the
discomfort is spontaneous. Upon application of Endo-Ice on this tooth, the patient
experienced pain and upon removal of the stimulus, the discomfort lingered for 12
seconds. Responses to both percussion and palpation were normal;
Radiographically: There was no evidence of osseous changes.
DIAGNOSIS:

3. Maxillary left first molar has occlusal-mesial caries and the patient has been
complaining of sensitivity to sweets and to cold liquids. There is no discomfort to
biting or percussion. The tooth is hyper-responsive to Endo-Ice® with no lingering
pain.
DIAGNOSIS:

4. Mandibular right lateral incisor has an apical radiolucency that was discovered
during a routine examination. There was a history of trauma more than 10 years
ago and the tooth was slightly discolored.
The tooth did not respond to Endo-Ice® or to the EPT; the adjacent teeth
responded normally to pulp testing. There was no tenderness to percussion or
palpation in the region.
DIAGNOSIS:

5. Mandibular left first molar demonstrates a relatively large apical radiolucency

encompassing both the mesial and distal roots along with furcation involvement.
Periodontal probing depths were all within normal limits.
The tooth did not respond to thermal (cold) testing and both percussion and
palpation elicited normal responses. There was a draining sinus tract on the mid-
facial of the attached gingiva which was traced with a gutta-percha cone. There
was recurrent caries around the distal margin of the crown.
DIAGNOSIS:

6. Maxillary left first molar was endodontically treated more than 10 years ago.
The patient is complaining of pain to biting over the past three months.
There appear to be apical radiolucencies around all three roots. The tooth was
tender to both percussion and to the Tooth Slooth.
DIAGNOSIS:

7. Maxillary left lateral incisor exhibits an apical radiolucency. There is no history of

pain and the tooth is asymptomatic. There is no response to Endo-Ice or to the
EPT, whereas the adjacent teeth respond normally to both tests.
There is no tenderness to percussion or palpation.
 
  

DIAGNOSIS:

 
RELATED  PATHOLOGICAL  CONDITIONS  
1. Root  Resorption  
Ø Loss  of  dental  hard  tissues  
Ø Odontoclasts:  cells  responsible  for  resorption  of  dental  hard  tissues  
 
External  Root  Resorption  (ERR)  
§ Resorption  of  the  external  root  surface  (Osteoclast)  
§ Etiologies:    
1. Inflammatory  lesions    
2. Reimplanted  Teeth  (Replacement  resorption  [ankylosis])  
3. Tumors,  cysts,  and  impacted  teeth  
4. Excessive  mechanical  and  occlusal  forces  
 
 
               Internal  Root  Resorption  (IRR)  
§ Resorption  of  the  internal  root  surface  (Odontoclast)  
§ Originates  in  the  canal  wall  
§ Cause  is  unknown  
§ Pulp  must  be  vital  in  order  for  it  to  produce  odontoclasts  and  cause  internal  
resorption  of  the  root  canal  wall  
§ Various  etiological  factors  have  been  associated  with  it:  
a. Trauma  (45%  of  all  cases)    
b. Caries  
c. Periodontal  infections  
d. Heat  generated  during  restorative  procedures  
e. Calcium  Hydroxide  
f. Orthodontic  treatment  
g. Cracked  teeth  
h. Idiopathic    
 
2. Periapical  Cemento-­‐osseous  Dysplasia  
§ Benign  fibro-­‐osseous  lesion  that  is  associated  with  apices  of  vital  
mandibular  incisors  
§ Periapical  lesions  of  pulpal  in  origin  are  non-­‐vital    
 
 
3. Periodontic-­‐Endodontic  Lesion  

 
  

§ Routes  of  communication  between  PDL  and  pulp:  

a. Apical  Foramen  
b. Lateral  Canals  
c. Exposed  Dentinal  Tubules  
§ May  be  classified  as:  
a. Primary  Endodontic  with  Secondary  Perio  Involvement  
-­‐Endodontic  disease  leads  to  Periodontal  Attachment  Loss  
b. Primary  Periodontal  with  Secondary  Endodontic  involvement  
-­‐Periodontal  Attachment  Loss  leads  to  Endodontic  Disease  
c. True  Combined  lesions  
-­‐Endodontic  Disease  +  Periodontal  Attachment  Loss  
 
 
1.  Primary  Endodontic  with  Secondary  Periodontal  Involvement  
Ø Etiology:  Pulp  Necrosis  (Chronic  Apical  Abscess  that  drains  through  the  
periodontium  and  gingival  sulcus.  This  causes  plaque  accumulation  in  the  
gingival  sulcus)  
 
2.  Primary  Periodontal  with  Secondary  Endodontic  involvement  
Ø Etiology:  Extensive  Periodontal  Destruction  
a. As  attachment  loss  occurs,  lateral  canals  will  become  exposed  
b. PDL  Inflammation  will  spread  from  the  PDL  to  the  pulp  via  the  lateral  
canals  
c. The  pulp  will  become  inflamed  and  necrotic  
 
3.  True  Combined  lesions  
Ø Etiology:  
a. Pulp  necrosis  causes  a  periapical  lesion.  At  the  same  time,  there  is  a  
periodontal  bone  loss  around  the  tooth.  
b. Separate  Endo  and  Perio  lesions  will  eventually  join  together  
 
PERIODONTIC-­‐ENDODONTIC  LESIONS  
1. In  all  cases,  Endodontic  therapy  is  completed  FIRST    
2. This  allows  healing  of  the  Endodontic  component  of  the  bone  loss  
3. The  Periodontal  component  of  the  bone  loss  is  then  more  easily  assessed  and  
then  treated  
 
 
ENDODONTIC  MICROBIOLOGY  
Ø Infections  develop  after  pulpal  necrosis  
Ø Microorganisms  associated:  Bacteria  (Major  cause),  Fungi,  Viruses  
Ø Initial  Species:  Facultative  species  
Ø After  a  few  days:  Anaerobic  species  (Pulp  lacks  collateral  circulation)  
 
Ø Endodontic  Infections  can  be  classified  into:  
1. Primary  Infections  

 
  

Caused  by  microorganisms  that  initially  invade  and  colonize  

§
necrotic  pulp  tissues  
§ Anaerobic  gram  negative  bacteria  are  the  most  dominant  
§ Most  commonly  found  bacteria:    
 
 
2. Persistent  Infections  
§ Caused  by  microorganisms  from  a  primary  infection  that  stayed  in  
the  root  canal  even  after  root  canal  treatment  
§ Ability  to  resist  intracanal  medicaments,  survive  for  long  periods  
without  adequate  nutrients,  invade  dentinal  tubules  and  escape  
cleaning  procedures  of  the  canal  
 
VITAL  PULP  THERAPY  
§ Aims  to  preserve  pulp  vitality  and  protect  it  from  further  damage  
§ Indications:  Vital  teeth  with  reversible  pulpitis  
§ Contraindications:  Irreversible  Pulpitis  and  Pulp  Necrosis  
§ Types:  
1. Indirect  Pulp  Capping  (Stepwise  Caries  Excavation)  
-­‐Removal  of  most  of  the  carious  lesion  and  leaving  the  deepest  part  in  order  
to  avoid  pulp  exposure  
 
2. Direct  Pulp  Capping  
-­‐Vital  Pulp  may  be  exposed  during  cavity  preparation  or  trauma.  A  material  
is  then  placed  directly  on  the  vital  pulp  exposure  
-­‐For  small  exposures  less  than  0.5  mm  
 
3. Pulpotomy  (done  in  an  immature  permanent  teeth)  
-­‐Accessing  the  pulp  and  removing  the  part  that  is  infamed.  The  healthy  pulp  
tissue  is  left  and  allowed  to  heal.    
                           4.  Partial  Pulpotomy  
           -­‐Involves  removing  only  a  part  of  the  coronal  pulp  and  not  all  of  it.  
 
Immature  teeth  with  Pulpal  disease  can  be  treated  by:  
1. Apexogenesis  
2. Apexification  
3. Regenerative  Endodontics      
 
ROOT  CANAL  TREATMENT  
Objectives:    
1. Elimination  of  diseased  tissue  and  pathogens  from  the  root  canal  system    
2. Total  Obturation  of  the  Root  Canal  Space  
3. Apical  and  Coronal  Seal  
 
Procedural  Steps  of  RCT:  
1. Access  Opening  and  Preparation  
2. Working  Length  (WL)  determination  
 
  

3. Cleaning  and  Shaping  

4. Obturation  
5. Coronal  Seal  
 
APICOECTOMY  
Steps:    
1. Radiograph  
2. Anesthesia  
3. Incision  and  Flap  Reflection  
4. Osteotomy  to  expose  root  end  
5. Curettage  of  the  periapical  lesion  
6. Root-­‐end  Resection  
7. Root-­‐end  preparation  
8. Placement  of  a  retrograde  filling  
9. Irrigate  Surgical  Site  
10. Suture    
 
 
 
 
PROCEDURAL  MISHAPS  
During  Access  Preparations:  
1. Lateral  Root  Peforation  
2. Furcation  Perforation  
 
During  Cleaning  and  Shaping:  
1. Aspiration  or  Ingestion  
2. Extrusion  of  Irrigant  Solution  
3. Ledge  Formation  
4. Zipping  
5. Root  Canal  Perforation    
6. Overinstrumentation  
7. Instrument  Separation  
During  Obturation:  
1. Underfilling  
2. Overextension  
3. Overfilling  
4. Vertical  Root  Fracture    
 
LONGITUDINAL  ROOT  FRACTURES  
1. Craze  Line  
2. Fractured  Cusp  
3. Cracked  Tooth  
4. Split  Tooth  
5. Vertical  Root  Fracture  
 
 
 
  

TRAUMA    
A. General  Recommendations  
B. Immature  Vs  Mature  Permanent  Teeth  
C. Canal  Obliteration  
D. Splinting  Type  and  Duration  
E. Use  of  antibiotics    
 
 
Prepared  by:    
Dr.  Chloe  Marianelli  M.  Hernando  
TopRank  Review  Academy  
#DMDMAY2020  
 
 
“Who  you  are  is  defined  by  what  you’re  willing  to  struggle  for.”  
                    -­‐Mark  Manson