Biomedical Engineering Reference
In-Depth Information
communities from infected implants and healthy residual teeth were also similar.
This leaves the question open why there is only infection on one implant and none
on the others although the microbial communities are more or less the same. One
interpretation could be that the barrier function of the gingival has been damaged and
bacteria are reaching now areas where they cause inflammation and severe immune
responses. A similar scenario has been proposed as the cause for inflammatory bowel
disease [
24
].
3 Are Asymptomatic Biofilm Communities the Beginning
of an Infection?
Our findings indicate that the notion that implants are essential sterile seems not be
always the case. However, the presence of biofilm communities on implants does
not cause
per se
a problem because most implants did not show any clinical signs of
infection and the microbial communities did not harbour any human pathogens. But,
what is the role of these asymptomatic biofilm communities and—more important—
are they the entry port for any implant infection? Such a question is difficult to
answer, but some observations may indicate that asymptomatic biofilm communities
are not the beginning of an infection. No pathogenic bacteria were found among
them excluding the possibility that they are hideaways for pathogens waiting for
their time to come. Furthermore, the comparison between asymptomatic and infec-
tious biofilm communities shows fundamental changes in community composition
between these types which seems to indicate that pathogens have their own group
of accompanying bacteria different from those found in asymptomatic biofilms. On
rhythmic management devices we found few examples of biofilms which contained
pathogens but had not yet developed an infection (they all did, however, after the
replacement of the implants). These biofilm communities may be seen as somehow
transient to infectious one and they harboured non-pathogens which were similar
to the asymptomatic biofilm communities. This may point to an invasion of asymp-
tomatic biofilm communities by pathogens but there were too few samples to draw
any clear conclusion.
The focus in clinical microbiology is on the identification of the pathogen. This
makes absolutely sense because the agent causative for the disease has to be identified
as fast as possible and a remedy for its control has to be found to cure the patient.
But this approach ignores the non-pathogens and hampers our understanding of their
role in the infection process. Only in recent years it became obvious that bacteria
are present in many infectious biofilm communities which are not known as human
pathogens and which do not cause infections in humans. However, it is reasonable
to assume that they are no bystanders but influence, in one way or another, the
progress of the infection and its course. An impressive example how pathogens can
interact in biofilms is the occurrence of
Burkholderia cepacia
and
Pseudomonas
aeruginosa
in human cystic fibrosis lungs.
B. cepacia
always occurs together with
