Professional Documents
Culture Documents
12-Mta-Failures After Vital Pulp Therapy
12-Mta-Failures After Vital Pulp Therapy
5 th
Year
Lec. 12
-MTA
- FAILURES
FAILURES AFTER
AFTER VITAL
VITAL
PULP PULP THERAPY
THERAPY
Assistant
Assistant Professor
Professor
Aseel Haidar
Aseel Haidar
Lec.12 Pedodontics Fifth stage
Properties of MTA
It is biocompatible material and its sealing ability is better than that of amalgam or
ZOE.
Initial pH is 10.2 and set pH is 12.5
Antimicrobial activity.
The setting time of cement is 4 hours
The ability to set in the presence of moisture and blood.
Low cytotoxicity
It presents with minimal inflammation if extended beyond the apex.
MECHANISM OF ACTION
The successful usage of MTA in endodontic applications can be
attributed to its biocompatibility, bioactivity and mechanism of action. The four actions
of MTA after direct placement in contact with living tissues are:
(i) Creation of an unfavorable environment for growth of bacteria due to its alkaline pH.
(ii) Formation of hydroxyapatite like mineral structure on its surface and provide the
biological seal.
(iii) Formation of calcium hydroxide, which dissociates to release Ca ions, to promotes
cellular attachment and proliferation.
(iv) Modulation of cytokine production and encouragement of hard tissue forming cells to
differentiate and migrate.
INTERNAL RESORPTION
One of the most frequently seen evidence of an abnormal response in primary
teeth within the pulp canal several months after the pulpotomy procedure is the
radiographic evidence of internal resorption.
Internal resorption is a destructive process
generally caused by odontoclastic activity, and it
may progress slowly or rapidly. Occasionally,
secondary repair of the resorbed dentinal area
occurs. No satisfactory explanation for the post
pulpotomy type of internal resorption has been
given. However, that with a true carious exposure of
the pulp, an inflammatory process will be present to
some degree. The inflammation may be limited to
the exposure site, or it may be diffused throughout
the coronal portion of the pulp. Amputation of all
pulp showing the inflammatory change may be difficult or impossible, and abnormal
pulp tissue may be allowed to remain. If the inflammation extended to the entrance
of the pulp canal, odontoclasts may have been attracted to the area; if it were possible
to examine the tooth histologically; small bays of resorption would be evident. This
condition may exist at the time of pulp therapy, although there is no way to detect it.
The only indication would be the clinical evidence of a hyperemic pulp.
Inflammatory cells drawn to the area because of the placement of an irritating
capping material might well attract odontoclastic cells and initiate internal resorption.
This may explain the occurrence of internal resorption even though the pulp is
normal at the time of treatment. Because the roots of primary teeth are undergoing
normal physiologic resorption, vascularity of the apical region is increased. When an
irritant in the form of a pulp-capping material is placed on the pulp, odontoclastic
activity present in the area and may predispose the tooth to internal resorption.
ALVEOLAR ABSCESS
Some months after pulp therapy has been
completed, an alveolar abscess occasionally
develops. The tooth usually remains asymptomatic,
and the child is unaware of the infection, which may
be present in the bone surrounding the root apices or
in the area of the root bifurcation.
A fistulous opening may be present,
which indicates the chronic condition of the infection.
Primary teeth that show evidence of an alveolar abscess should be removed.
Endodontic treatment may be considered for permanent teeth that have previously
been treated by pulp capping or by pulpotomy and later show evidence of pulpal
necrosis and apical infection.