Dokumentation 41

In diesem Grundsatzartikel aus der November-Ausgabe 2003 der Zeitschrift Endodontic Topics, beschreiben die Autoren, dass:

a) apikale Aufhellung und Granlulom entgegen der verbreiteten Lehrmeinung sehr wohl bakteriell besiedelt sind, dass also die endodontische Infektion nicht per Definition auf den Wurzelkanal beschränkt ist

b) es sich um das selbe Keimspektrum handelt, wie es auch in aktiven Parodontaltaschen nachzuweisen ist

c) dass zumindest die Hälfte der bei der Endodontitis beteiligten Keime nicht kulturell, wohl aber molekularbiologisch nachzuweisen sind

d) dass Biofilmbildung nicht nur auf der Wurzeloberfläche und im Wurzelkanal, sondern auch auf von den Bakterien produzierten Granula in den Granulomen nachzuweisen ist

Vollständiger Text als .pdf-Datei 


The evolving new understanding of endodontic infections

Leif Tronstad, Pia Titterud Sunde

The science of oral microbiology is in a period of change from the era of
bacterial cultivation to an era of molecular
genetic methods and techniques. Already a significant body of new knowledge
exists with regard to the oral flora in
health and disease. Inevitably, this new knowledge has led to a better
understanding of many oral diseases. In
endodontics, the prevailing concepts are still to a great extent based on
the results of the classical cultivation studies.
However, a few groups have started to use molecular methods, and a new
understanding of endodontic infections is
presently evolving. Thus, the root canal infection clearly is more complex
than revealed by cultivation methods
alone, and both previously unidentified and uncultivable microorganisms
have been detected by molecular
methods. A reasonable estimate at present is that the infected root canal
contains, not less than 10, but rather
between 10 and 50 bacterial species which coincide well with the number of
bacterial species normally found in a
dental plaque sample and at different sites in the oral cavity. A further
interesting finding in the studies using
molecular techniques is that the microbiota of the infected root canal
appears to be very similar to the flora of the
periodontal pocket in patients with active periodontal disease. With regard
to infection of periapical lesions in
patients with asymptomatic apical periodontitis, electron microscopic and
molecular methods have confirmed our
cultivation findings that this is a common occurrence. Mature biofilms have
been demonstrated on the external
surfaces of root tips and in the form of sulfur granules within periapical
granulomas. As in dental plaque,
Actinomyces species appear to have a special role as scaffold builders in
the development of sulfur granules. Other
bacteria are then attracted to the site and a multibacterial granule
(biofilm) develops. In addition, in situ
hybridization studies show a variety of different bacteria and bacterial
morphotypes in periapical lesions. With
DNADNA hybridization between 11and 39 bacterial species have been
recognized in the lesions, again
confirming that in patients with active disease, the microbiotas of
endodontic and periodontal infections are very
similar. Thus, the recent findings demonstrate and confirm that the
periapical endodontic lesion is not as hostile to
microorganisms as many have thought. As clinicians we have to understand
and accept that an infection might not
be limited to the root of the tooth, but include the periapical lesion as well.


More than 700 different bacterial species, of which over
50% have not yet been cultivated, have been detected in
the oral cavity. The breadth and diversity of the oral
flora in health and disease are continuously being
investigated, and with the molecular methods that have
become available in recent years, great progress has
been made in understanding the nature of oral
infections and assessing the organisms associated with
disease. With regard to endodontic infections, to a
great extent we are still in the era of bacterial
cultivation, although a few groups have taken up
molecular methods in their work. Thus, a new understanding
of endodontic infections is slowly evolving
due to the results of molecular and electron microscopic
studies. Many more bacteria are found with
hybridization studies than with cultivation, and interestingly,
the flora of endodontic infections appears to
be very similar to the flora of the periodontal pocket in
patients with active periodontal disease. Even the

numbers of infecting organisms in mature periodontal
and endodontic biofilms are similar in that about the
same number of bacterial species is found in infected
root canals and in periapical lesions as in plaque samples
from patients with active periodontal disease.
Extraradicular infection is a common occurrence in
asymptomatic teeth with apical periodontitis. This has
now been verified with bacterial cultivation, checkerboard
DNADNA hybridization, FISH and electron
microscopic demonstration of mature bacterial biofilm
at the surfaces of root tips and in the form of granules
inside the lesions. It has been difficult to gain
acceptance for these new findings in that the periapical
granuloma has been regarded as a very hostile
environment for bacterial growth and survival (49,
90, 91). This has been an unfortunate misunderstanding.
Most of the microorganisms recovered from the
periapical lesions are known to adapt over time to live in
many different environments, and their numbers, rapid
fluctuations and amenability to genetic change give
them effective tools for adaptation (92). Also, bacteria
have a variety of strategies to avoid engulfment and
degradation by phagocytes, facilitating proliferation
and spread in host tissues (93). Moreover, they have a
number of strategies for overcoming host innate and
adaptive immune responses (53), and in fact can
establish life-long chronic infections in their hosts
(94, 95). Also, evidence that recently has become
available suggests the involvement of herpes viruses in
the etiopathogenesis of apical periodontitis (96, 97).
The viruses may cause the release of tissue destructive
cytokines and the initiation of cytotoxic and immunopathologic
events. The immune impairment and tissue
changes resulting from the herpes virus infection may
then aid bacteria in invading and surviving in the
periapical lesion. Thus, the periapical lesion may not be
as hostile to bacteria as many have thought (98), and as
clinicians we have to understand and accept that an
infection might not be limited to the root canal, but
include the radiolucent periapical lesion as well.

direkt zurück zu "Die Wissenschaft"