Microbiologia Del Liquido Crevicular

Periodontology 2000, Vol. 50, 2009, 39–51
Printed in Singapore. All rights reserved

Ó 2009 John Wiley & Sons A/S

PERIODONTOLOGY 2000

One-stage, full-mouth
disinfection: fiction or reality?
WIM TEUGHELS, CHRISTEL DEKEYSER, MARK VAN ESSCHE & MARC QUIRYNEN

Periodontal breakdown develops when the microbial
load within a periodontal pocket overwhelms the
local and systemic host defensemechanisms. Such
an imbalance can occur in different situations, for
example, following a specific increase in the total
amount of bacteria, when an outgrowth ⁄ overgrowth
of pathogenic species (above a certain threshold
level) occurs and ⁄ or because of a change in the
efficiency of the host response (hyper-responsiveness
or hyporesponsiveness). Changes in the host response can be explainedby hereditary factors (30)
and by environmental factors such as poor oral hygiene and smoking. Immunosuppressive medications, stress, etc., can further impair the host defense
mechanisms.
Aggregatibacter actinomycetemcomitans, Tannerella forsythia and Porphyromonas gingivalis are
considered to be key periodontopathogens, but
Prevotella intermedia, Campylobacter rectus, Peptostreptococcusmicros, Fusobacterium nucleatum,
Eubacterium nodatum, Streptococcus intermedius
and spirochetes are also linked to periodontal
destruction (4, 64, 65, 81). Most of these species are
not only members of the subgingival flora, but also
colonize the oral mucosa, the tongue and the tonsils,
and are commonly found in saliva (8, 17, 18, 50, 75).
Because the susceptibility of the host cannot bemodulated at a clinical level (with the possible
exception of anti-inflammatory medications), periodontal therapy is primarily focused on the reduction ⁄ elimination of periodontal pathogens, in
combination with the re-establishment (often by
surgical pocket elimination) of a more suitable
environment (less anaerobic) for beneficial microbiota. Several studies indicate that the presence ofperiodontal pathogens (persisting or re-established
after treatment) is associated with a negative clinical outcome of periodontal treatment (14, 26, 58,
59, 68).

After mechanical debridement, the subgingival
microbial load (colony-forming units ⁄ ml) decreases
to 0.1% of pretreatment levels (23, 39). However, only
1 week later, the periodontal pocket has become
recolonized by a similar number ofbacteria, fortunately of a less pathogenic nature (27, 76). The origin
of these bacteria is still a matter of debate. The
multiplication of the remaining bacteria within the
pocket (49), or within either the junctional or pocket
epithelium (34) and ⁄ or within the dentinal tubules
(1, 22), is considered to be the major cause of this
subgingival recolonization.
The impact of thesupragingival environment on
this early subgingival recolonization process is
unclear. Oral implants, however, have facilitated the
investigation of the initial colonization of a pristine
pocket (created by a sterile abutment to the gingiva)
in an established ecosystem, with the supragingival
area as the sole bacterial source. Recent studies have
revealed that after only 1 week these ÔpristineÕpockets harbor a mature microbiota with a composition nearly identical to that of the neighboring
¨
periodontal pockets (56). Furst et al. (21) and Salvi
et al. (61) even observed periodontopathogens such
as A. actinomycetemcomitans and P. gingivalis in the
sulci of one-stage implants, within 30 min after
implant insertion. These observations indicate that
supragingival plaque also plays asignificant role in
the subgingival recolonization of periodontal pockets. As such, bacteria in the saliva or on the tongue,
tonsils or oral mucosa can have an impact on the
subgingival recolonization of pockets after periodontal therapy.
With this perspective, a one-stage, full-mouth disinfection procedure, was proposed by the research
group at the Catholic University at Leuven, Belgium,
as a...