IPC, DPC, APEXOGENESIS, APEXIFICATION, ALONG WITH THE MATERIALS COMMONLY USED FOR THEM NEWER MATERIALS AND THEIR APPLICATION

1. INDIRECT PULP CAPPING,
DIRECT PULP CAPPING, APEXIFICATION &
APEXOGENESIS
IN PEDIATRIC DENTISTRY
WITH RECENT TECHNIQUES & MATERIALS
PRESENTED BY:
DR. RUCHIKA BAGARIA
1ST YEAR POSTGRADUATE
PEDIATRIC & PREVENTIVE
DENTISTRY

2. INTRODUCTION
• Despite the modern advances in prevention of dental caries and an increased
understanding of the importance of maintaining the natural dentition, many
teeth are still lost prematurely.
• The primary objective of pulp treatment of an affected tooth is to maintain the
integrity and health of oral tissues.

3. • Additional reasons to preserve the integrity of the primary dentition are to :
1. Reduce the likelihood of mesial drift and the resultant malocclusion
2. Aids in mastication
3. Preserve a pulpally involved primary tooth in the absence of a succedaneous tooth
4. Prevent possible speech problems
5. Maintain esthetics
6. Prevent aberrant tongue habits
7. Maintain normal eruption time of the succedaneous teeth
8. Prevent the psychological effects associated with early tooth loss

4. VITAL PULP
THERAPY
PULP CAPPING
PULPOTOMY
APEXOGENESIS
NON-VITAL
PULP THERAPY
PULPECTOMY
APEXIFICATION
PULP THERAPY IN PEDIATRIC DENTISTRY

5. VITAL PULP THERAPY
 Defined as a treatment initiated to preserve and maintain pulp tissue in a healthy
state
 Stimulate the formation of reparative dentin to retain the tooth as a functional
unit
 Primary goal - Dentin bridge formation and continuation of root development

6. OBJECTIVES:
• The placement of a liner in a deep area of the preparation to preserve the
tooth’s vitality, promote pulp tissue healing and tertiary dentin formation, and
minimize bacterial micro leakage.
• Adverse post-treatment clinical signs or symptoms such as sensitivity, pain, or
swelling should not occur.

7. 1. Highly demineralized
2. Unremineralizable
3. Superficial layer
4. Lacking sensation
5. Stained by 0.5% fuschin or 1.0% acid red
solution
6. Ultrastructure- Intertubular dentin greatly
demineralized, with irregular scattered
crystals. Presence of deteriorated collagen
fibres that have only distinct cross bands
and no interbands.
7. Should be excavated
1. Intermediately demineralized
2. Remineralizable
3. Deeper layer
4. Sensitive
5. Does not stain
6. Ultrastructure: Intertubular dentin partially
demineralized, but apatite crystals bound like
fringes to the sound collagen fibres with
distinct cross bands and interbands.
7. Should be left to remineralize
INFECTED DENTIN AFFECTED DENTIN

8. Indirect Pulp Capping (IPC)
• Indirect pulp capping is defined as a procedure where in small amount of
carious dentin is retained in deep areas of cavity to avoid exposure of pulp,
followed by placement of a suitable medicament and restorative material
that seals off the carious dentin and encourages pulp recovery (Ingle).

9. Objectives of IPC (Eidelman in 1965)
1. Arresting the carious process
2. Promoting dentin sclerosis (reducing permeability)
3. Stimulating the formation of tertiary dentin
4. Remineralizing the carious dentin

10. INDICATIONS:
Tooth with minimal reversible
pulpitis
Signs/symptoms of tooth vitality
Deep caries, which if removed,
will cause pulp exposure
CONTRAINDICATIONS:
Tooth with irreversible pulpitis
Clinical and radiographic
signs/symptoms of non vitality
of pulp
Soft leathery dentin in a very
large area in a non restorable
tooth

11. TREATMENT PROCEDURE
Toothshowingdeepcariouslesionadjacentto pulp
FIRST APPOINTMENT
Isolationwith
rubberdam
Establish
cavity outline
usinga high
speedhand
piece
Remove
superficial
debris andsoft
necrotic dentin
witha slow
speedhand
pieceusing
large round
burs-Do not
exposethe
pulp.
Local
Anesthesia

12. Placementof Ca(OH)2andZOEafterexcavationof
soft caries
Peripheral carious
dentin removed
using spoon
excavator
Flush cavity
withsalineand
drywithcotton
pellets
Siteiscovered
witha
commercialhard
setCa(OH)2
preparationand
cavity isfilled
withfast
setting ZOE
cement.

13. Between the appointment, history should be negative and temporary restoration
should be intact.
Treated tooth is
re-entered after
6-8 weeks
Rate of reparative
dentin deposition is
an average of
1.4 microns/day
which decrease
markedly after 48
days.
Take bitewing radio
graph & observe for
reparative dentin.
Then care fully
remove all
temporary filling
material
On re-entering
caries will appear
arrested, flaky,
dried out.
SECOND VISIT (6-8 WEEKS LATER)

14. Color will change from
deep red rose to light
grey to light brown.
Texture will change from
spongy & wet to hard.
Cavity is washed out &
dried gently
Cover the entire floor
with Ca(OH)2
Base is built up with GIC
Final restoration is
placed.
Afterplacementof final restoration

15. Sequelae/Outcome of IPC
Three distinct types of new dentin formation take place:
1. Cellular fibrillar dentin—first 2 months
2. Globular dentin—3 months
3. Tubular dentin (uniform mineralized dentin): One-fifth of reparative dentin formation
begins in less than 30 days. After 3 months, 0.1 mm is formed

16. Direct Pulp Capping (DPC)
• It is the placement of a medicament or non-medicated material on a pulp that has
been exposed in course of excavating the last portions of deep dentinal caries or as a
result of trauma – Kopel (1992)
• It is the procedure in which there is small pin point exposure of the pulp which is
caused due to:
Traumatic injury
Cavity preparation or
Caries
which is surrounded by sound dentin & covered with a biocompatible radiopaque base in
contact with exposed pulp tissue prior to restoration .

17. Objectives of DPC
To create new dentin in the area of the exposure and subsequent healing of the pulp
To achieve a biologic closure of the exposure site by deposition of hard tissue barrier
(dentin bridge) between pulp tissue and capping material thus walling off the exposure
site.
Rationale of DPC

18. INDICATIONS:
Small mechanical exposure that are
surrounded with sound dentin
Exposed pulp should have slight red
hemorrhage that is easily controlled.
Traumatic exposures in a dry & clean
field.
CONTRAINDICATIONS:
Severe tooth aches at night
Spontaneous pain
Tooth mobility
Thickening of periodontal ligament
Radiographic evidence of pulp or
periradicular degeneration
Excess of hemorrhage at the time of
exposure
Purulent or serous exudate from the
exposure

19. PROCEDURE
Tooth should be isolated with a rubber dam and disinfected with sodium
hypochlorite (NaOCl)
Cavity preparation with high-speed burs and caries removal with slow-
speed bur. Cavity is rinsed with NaOCl (every 3 to 4 minutes), which
disinfects the cavity and removes the blood clot
If the bleeding cannot be stopped within 1 to 10 minutes, it suggests
that the pulp inflammation has progressed deeper into the tissue, and
the treatment procedure should be modified
Pulp capping agent placed directly over the exposed pulp tissue
(1.5 to 2 mm thick)
The material should then be covered with a glass ionomer liner followed
by a permanent restoration.

20. MATERIALS USED FOR PULP CAPPING
• CALCIUM HYDROXIDE
• MINERAL TRIOXIDE AGGREGATE
• ANTIBIOTICS
• COLLAGEN
• CORTICOSTEROIDS
• ISOBUTYLCYANOACRYLATES
• TRICALCIUM PHOSPHATE
• BONE MORPHOGENIC PROTEIN
• DENATURED ALBUMIN
• LASER

21. CALCIUM HYDROXIDE
 Calcium hydroxide forms a dentin bridge when placed in contact with pulpal tissues.
 Initially, a necrotic zone is formed adjacent to the material, and, depending on the pH of the
calcium hydroxide material, a dentin bridge is formed directly against the necrotic zone.
 It has antimicrobial action. Release of Hydroxyl ions from calcium hydroxide damages the
cellular component of bacteria.
 High pH- induce formation of a hard tissue barrier

22. A. Twenty-fourhoursafter
applicationof calcium
hydroxide.
B. After2or3weeks.
C. After4or5weeks.
D. After8weeks
CELLULAR CHANGES WITH CALCIUM HYDROXIDE

23. MINERAL TRIOXIDE AGGREGATE
 Excellent sealing ability and biocompatibility.
 pH (12.5) similar to calcium hydroxide- antimicrobial action
 When compared with Ca(OH)2 , MTA produced significantly more dentinal bridging in a
shorter period of time with significantly less inflammation.
 Dentin deposition begins earlier with MTA.
 Less solubility and greater radiopacity.
 Hardens in the presence of moisture.
 Formation of hard tissue barrier at the root apex.

24. Corticosteroids and
antibiotics: Brosch JW
introduced in 1966. These
agents include neomycin
and hydrocortisone;
ledermix [Ca(OH)2 and
prednisolone], penicillin or
vancomycin with Ca(OH)2 .
Inert materials: Isobutyl
cyanoacrylate and
tricalcium phosphate
ceramic.
Collagen fibres: They
influence mineralization
and are less irritant
than Ca(OH)2 with
dentin bridge formation
in 8 weeks
4-META adhesive: It
can soak into the pulp,
polymerize there and
form a hybrid layer with
the pulp thereby
providing adequate
sealing.
Direct bonding: A
polygenic film can be
layered over an exposure
site without displacing
pulp tissue and onto
surrounding dentin where
it penetrates the tubules.

25. Isobutyl cyanoacrylate:
Berkman in 1971 used it and
aproved it to be an excellent
hemostatic agent as well as a
reparative dentin bridge
stimulator . It is cytotoxic
when freshly polymerized
Denatured albumin:
Has calcium-binding
properties. If a pulp exposure
is capped with a protein, the
protein may become a matrix
for calcification, thereby
increasing the chances of
biologic obliteration
Laser: Andreas Meritz in
1998 evaluated the effect of
laser on direct pulp capping
and reported a success rate
of 89%
Bone morphogenic protein:
Urist discovered bone
morphogenic protein (BMP)
in 1965

29. Qureshi A, Soujanya E. Recent advances in pulp capping materials: an overview. Journal of clinical
and diagnostic research: JCDR. 2014 Jan;8(1):316.

30. Shabahang S. Treatment options: apexogenesis and apexification. Pediatric dentistry. 2013 Apr 15;35(2):125-8.

31. APEXOGENESIS & APEXIFICATION

32. Open Apex
• At the time of tooth eruption- Root development is only two-third.
• Complete root development and apex closure occurs three years after eruption.
• If due to trauma or caries, exposure of the pulp occurs and it undergoes necrosis, dentin
formation ceases and root growth is arrested.
• Destruction of Hertwig’s epithelial root sheath results in cessation of normal root
development.
• No further differentiation of odontoblasts.
• The resultant immature root will have an open apex which is also called as blunderbuss apex.

33. TWO TYPES-
• Blunderbuss Apex
o DONDERBUS' which means 'thunder gun'.
o Canal walls diverge, flare, more especially in the
buccolingual direction
o The apex is funnel shaped and typically wider than the
coronal aspect
• Non Blunderbuss Apex
o Canal wall may be parallel to slightly convergent as it
exits the root
o The apex, therefore can be broad (cylinder shaped) or
tapered
• In both types, conventional root canal treatment
cannot be performed.

34. • Due to large apical diameter and smaller coronal canal diameter debridement
is difficult.
• Lack of apical stop makes obturation difficult.
• The thin root canal wall becomes prone to fracture.
Problems faced with Open Apex

35. APEXOGENESIS OR APEXIFICATION???
Proper assessment of
the affected tooth
Assessment of pulp
vitality
If vital and not irreversibly
inflamed, maintenance of
its vitality will allow natural
continued root
development
Assessment of the tooth in
question is made by using
radiographic evaluation to
determine the maturity of the
developing root and clinical
evaluation that is based on
history and clinical testing.
If pulpal necrosis occurs in
immature teeth, an
alternative treatment
approach must be used
because of the presence of an
open apex
Shabahang S. Treatment options: apexogenesis and apexification. Pediatric dentistry. 2013 Apr 15;35(2):125-8.

36. APEXOGENESIS
 It is defined as physiologic root end development and formation.
 This is achieved by:
o Indirect pulp capping
o Direct pulp capping
o Pulpotomy
 Materials used:
o Calcium hydroxide
o MTA
o Bone Morphogenic Protein

37. • Goals of Apexogenesis, as stated by Webber-
1. Supporting a Hertwig sheath, it so allows a continued development of a root length for a
more favorable crown-root ratio
2. Maintaining pulp vitality, allowing the remaining odontoblasts to deposit dentin,
producing a thicker root and decreasing the chance of fracture
3. Closing the root end, thus creating a natural apical constriction for the following
obturation of the root canal .
4. The formation of a dentine bridge at the pulpotomy site.
Webber RT.Apexogenesis versus apexification. Dent Clin N Am 1984;28:669–97.

38. Clinical and Radiographic Examination as well as follow-up is mandatory
Clinical Evaluation of Apexogenesis
• No clinical symptoms.
• No radiographic changes in pulp or
periapex area.
• Continued root development.
• Radiographically observed hard tissue
barrier at the site of procedure.
Re-evaluate after every 3 months for 1 year , after that every 6 months for 2-4 years

39. (A) Mandibular premolar with
incomplete root development due to
partial pulp necrosis. Apexogenesis
with calcium hydroxide was
instituted.
(B) Two years later, apical closure was
evident in the radiograph. Root canal
treatment was completed using gutta-
percha with a root canal sealant

41. Dubey B, Rathore M. Mineral Trioxide Aggregate as an Apexogenesis Agent for Complicated Crown Fractures in
Young Permanent Incisor. Case Reports in Dentistry. 2023 Jul 3;2023.

42. APEXIFICATION
 It is the method of inducing the development of root apex in an immature pulp
less tooth by formation of osteocementum or other bone like tissue (Cohen)
 Apexification is a method of inducing apical closure through the formation of
mineralized tissue in the apical pulp region of a nonvital tooth with an
incompletely formed root and an open apex (Morse et al. 1990)

43. Objectives of Apexification:
• The aim of the apexification procedure is to induce root end closure with
no canal wall thickening or continuous root lengthening.
• It can be achieved in two ways:
(1) as a long-term procedure using calcium hydroxide dressing to allow the
formation of a biologic hard tissue barrier, or
(2) as a short-term (more recent) procedure, creating an artificial apical
plug of MTA or other bio ceramic material

44. Restorable immature
permanent tooth with
pulp necrosis.
- Resorptions
- Short roots
- Periodontally
broken down
tooth
- Vital pulp
INDICATIONS
CONTRAINDICATIONS

45. MATERIALS USED:
 Calcium Hydroxide
o Ca(OH)2 powder with saline
 Tricalcium Phosphate
 Collagen – Calcium Phosphate Gel
 Mineral Trioxide Aggregate (MTA)

46. CALCIUM HYDROXIDE APEXIFICATION
Fill the canal with Calcium Hydroxide paste using a lentulospiral with low speed engine and seal with a
temporary restorative material.
Clean the canal, irrigate it with 0.5% to 2.5% NaOCl followed by saline without pressure and then dry it with
a paper point
Minimal instrumentation- To prevent damage to the thin dentinal walls
Use large reamers and files- To remove the debris from the canal
The length of the root canal should be determined radiographically using a large GP point. WL kept to be 1 mm
short of the radiographic root end
Isolate with rubber dam, and access is gained into the pulp chamber.
FIRSTAPPOINTMENT

47. SECONDAPPOINTMENT (2 weeks to 1 month later)
The goal in the second visit is to complete the debridement and remove the tissue remnants
denatured by the calcium hydroxide dressing that could not be removed mechanically in the
first appointment.
Remove the temporary restoration and disinfect the
canal
A thick paste of calcium hydroxide is packed in the root
canal to a level apical to the cemento-enamel junction
(CEJ) using endodontic pluggers
The coronal access should be restored with a filling that
will provide a long-term coronal seal

48. When a completed apical barrier can be traced, the canal is obturated with a permanent root canal filling
material (e.g., thermoplasticized GP) and sealer
If the barrier is incomplete then the apexification procedure is reestablished until a complete barrier is
formed.
On every 3 Month Recall, See Radiographic evidence of apical closure.
Obtain a Radiograph to check the accuracy of the root canal filling.

49. (A) Clinical photograph of a traumatized left central incisor with an acute apical abscess (notice the vestibular swelling). (B)
Radiograph of the same tooth showing an incompletely formed root, an open apex, and periapical bone destruction. (C)
Radiograph of the tooth filled with a calcium hydroxide paste to achieve apexification. (D) Radiograph showing the completeness
of the apical barrier checked with a gutta-percha point. (E) The tooth after root canal filling with gutta-percha and sealer

50. Limitations of Ca(OH)2 Apexification
• variability in treatment time
• unpredictability of formation of an apical seal
• difficulty in following up patients, and delayed treatment.
Long-term exposure to Ca(OH)2 may also have detrimental effects on dentin. Studies have shown that
long-term therapy that would expose root dentin to Ca(OH)2 for periods exceeding 1 month results in
structural changes in the dentin, with higher susceptibility to root fracture.
Longer exposures of dentin to Ca(OH)2 , its ability to resist fracture is significantly decreased

51. FOLLOW-UP & EVALUATION:
• The time taken for this processfor completion may range from 18– 24months.
• The final obturationof the canal shouldbe carried out when the there is:
 Absenceof any symptoms.
 Absenceof any fistula or sinus.
 Absenceor decrease in mobility.
 Evidence of firm apical stop both clinically as well asradiographically.

52. Frank has described four successful results of Apexification treatment's:
1. Apex is closed, through minimum recession of the canal
2. Apex is closed with no change in root space
3. Radiographically apparent calcific bridge at the apex
4. There is no radiographic evidence of apical closure, but upon clinical instrumentation,
there is definite stop at the apex, indicating calcific repair.
Dentistry for the Child and Adolescent- Ralph E. McDonald, David R. Avery, Jeffrey A. Dean.-8th ed.

53. Root-end
development
in normal
pattern
Apex closes ,
but is wider
at the apical
end
Development
of calcific
bridge just
coronal to
apex
Formation of
thin barrier
at or close to
the apex

54. Short-Term Apexification With
Mineral Trioxide Aggregate
(First visit)
Disinfection of the root
canal followed by Ca(OH)2
dressing
(Second visit)
After rubber dam
placement, the canal is
irrigated and dried.
MTA plug compacted into
apical 4 - 5 mm of the
canal, about 1 mm short of
the radiographic apex
Placement of a resorbable
material at the root end
(e.g., calcium sulfate;
CollaCote, Zimer Dental,
Carlsbad, CA) against which
the MTA can be compacted
Proper placement of
material verified by
radiograph
A wet cotton pellet/paper
point placed over the MTA,
providing moisture for its
setting, and the tooth is
sealed with a temporary
filling

55. After few days, tooth is
reentered and the
hardness of the MTA is
examined
If the MTA is not set, its
placement should be
repeated
After setting, the root
canal filling can be
completed using
thermoplasticized GP and
sealer.
Permanent restoration
done with a bonded
composite resin
extending into the canal
space in an attempt to
strengthen the root.
In short roots, composite
resin is directly placed in
contact with the MTA
plug

56. (A) Immature mandibular molar with
periapical pathologic radiolucent
areas.
(B) Apical plugs with mineral trioxide
aggregate (MTA).
(C) Warm gutta-percha filling over the
hardened MTA plugs.
(D) Successful follow-up after 15
months showing healing of the
periapical lesions.

57. ADVANTAGES OF MTA APICAL PLUG
(1) patient compliance is less crucial,
(2) cost and clinical time are reduced,
(3) the dentin will not lose its physical properties, and
(4) it allows for earlier restoration with bonded composite resin within the root canal, thus
minimizing the likelihood of root fracture.
DISADVANTAGE:
In case of retreatment, MTA cannot be removed after it sets. So, complete debridement
and disinfection of the root canals is mandatory.

58. LIMITATIONS
CALCIUM HYDROXIDE
• Variability in
treatment time
• Unpredictability in
formation of apical
plug
• Difficulty in following
up of patients
• Delayed treatment
APICAL PLUG
TECHNIQUE
• Only addresses the
apical opening &
does not account for
complete root
development along
the entire root length

59. MTA: SEALING PROPERTY & BOND STRENGTH
• a combination of MTA–dentine bond
• setting expansion
• friction with the dentinal surface
The release of calcium ions (Ca2+) which interact with Pi from the tissue fluid to form calcium
phosphate salts that undergo hydration to hydroxyapatite-like precipitates. The apatite-like crystals
precipitate at the MTA–dentine interface and within the dentine collagen fibrils, producing chemical
and mechanical bonds between MTA and dentine, and improving the push-out bond strength and
sealing ability

60. MTA : BIOLOGICAL PROPERTIES
• cement’s biocompatibility
• dentinogenic activity
• sealing ability
• After setting, MTA produces Portlandite (crystalline Ca[OH]2). Portland cement and MTA
are rich in CaO, and in the presence of water,
CaO + H20 = Ca(OH)2
• Alkaline pH levels and Ca2+ in the fluid surrounding MTA are conducive to hard-tissue
precipitation.
• The Ca2+ released by MTA enhances osteoblastic viability, proliferation, and
differentiation, and OH increases the alkalinity of the environment, which is unfavorable
for bacterial growth

61. MTA: LIMITATIONS
Long setting time
Poor handling properties and high cost.
Difficult retrieval from the treated area,
Post treatment tooth discoloration,
MTA shares with Ca(OH)2 the mechanism of inducing hard-tissue formation, which is known
to cause inflammatory and necrotic changes in the subjacent pulp tissue.
MTA releases low levels of arsenic, as it has a similar elemental composition to Portland
cement.
Retrieval of set MTA from within the root canal is difficult, as there is no known solvent.

62. BIODENTINE : BIOLOGICAL PROPERTIES
• highly-biocompatible,
• non-cytotoxic material
• increase in Ca2+ release stimulate hard-tissue formation
Pulp cell differentiation into odontoblast-like cells
There was no statistically-significant difference between the responses of human pulp
tissue to Biodentine and MTA used as pulp-capping materials to cover iatrogenic pulp
exposure sites in intact human molars scheduled for orthodontic extraction.

63. BIOAGGREGATE
• A modified version of MTA.
• Bioaggregate was produced under controlled conditions to create a contamination- and aluminum-free
ceramic biomaterial.
• Differs from MTA due to the addition of tantalum oxide, instead of bismuth oxide in MTA, for radiopacity.
• INDICATIONS
 root perforation repair,
 root resorption repair,
 root-end filling,
 apexification, and
 pulp capping.
• Although Bioaggregate has comparable biocompatibility and sealing ability to MTA, along with hard tissue
forming potential expected to be greater than MTA because of the presence of Pi source in Bioaggregate, the
poorer mechanical properties and long setting time of Bioaggregate limit the situations where it could
replace MTA

64. ENDOSEQUENCE
• Premixed CSC :A ready-to-use syringeable paste or compactable putty with easier
handling and application compared to MTA.
• Perforation repair, apical surgery, apical plug, and pulp
• Ease of handling and application, strength and biological effect, similar to MTA.

65. CALCIUM-ENRICHED MIXTURE CEMENT
• A tooth-colored, water-based endodontic repair cement with similar applications to MTA, but with a
different chemical composition.
• INDICATIONS
 Internal and external root resorption,
 Apexification,
 Apexogenesis,
 Repair of furcation perforation,
 Root-end filling, direct pulp capping, and
 Pulpotomy in primary and permanent teeth
 Revascularization of necrotic immature permanent molars.

67. CONCLUSION
• Clarity on the biology of caries, comprehension of technological advances and conviction
about improved restorative materials has initiated a pulp preservation that indeed is a
boon to the clinician and the patient.
• The MTA barrier as a treatment of apexification is a technique that is applied as a
substitution to Ca(OH)2 apexification; this technique does not require several
appointments, and the conformation of the barrier does not need an external factor to
develop, as in the case of the apexification with Ca(OH)2 , as well as in the regeneration
of the pulp.

68. REFERENCES
• Pediatric Dentistry (Infancy through Adolescences) Jimmy R. Pinkham, Paul S.Casamassimo, DennisJ.
McTigue, Henry W.Fields, Arthur J. Nowak,.- 4th ed.
• Marwah N. Textbook of Pediatric Dentistry. 4th Ed. New Delhi: Jaypee Brothers Medical
Publishers; 2018. 646-683p.
• Tandon S. Textbook of Pedodontics. 2nd Ed. Hyderabad: Paras Medical Publisher; 2009. 265-292p.
• Hargreaves KM. Cohen S. Cohen’s Pathways of the Pulp. 11th Ed. United States. St. Louis, Mo. :
Mosby Elsevier ; c2011. 766-772p.
• McDonald RE, Avery DR. Dentistry for the child and adolescent. 8TH Edition, Lea & Febiger,
Elsivier, Mosby; 2004.
• Shabahang S. Treatment options: apexogenesis and apexification. Pediatric dentistry. 2013
Apr 15;35(2):125-8.

69. • Webber RT.Apexogenesis versus apexification. Dent Clin N Am 1984;28:669–97.
• Rafter M. Apexification: a review. Dent Traumatol 2005; 21: 1–8.
• Tuculina M, et al. Apexogenesis and Apexification - Review. J Dental Health Oral Res. 2023;4(1):1-9
• Dawood AE, Parashos P, Wong RH, Reynolds EC, Manton DJ. Calcium silicate‐based cements:
composition, properties, and clinical applications. Journal of investigative and clinical dentistry.
2017 May;8(2):e12195.
• Ageel BM, El Meligy OA, Quqandi SM. Mineral trioxide aggregate apexogenesis: A systematic
review. J Pharm Bioall Sci 2023;15:S11-7
• Dubey B, Rathore M. Mineral Trioxide Aggregate as an Apexogenesis Agent for Complicated Crown
Fractures in Young Permanent Incisor. Case Reports in Dentistry. 2023 Jul 3;2023.
• Qureshi A, Soujanya E. Recent advances in pulp capping materials: an overview. Journal of clinical
and diagnostic research: JCDR. 2014 Jan;8(1):316.