Microbiology and treatment of
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Microbiology and treatment of

DisciplinaOdontologia Morfofuncional do Ecossistema Bucal154 materiais1.381 seguidores
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Periodontology 2000, Vol. 28, 2002, 206\u2013239 Copyright C Munksgaard 2002
Printed in Denmark ¡ All rights reserved
ISSN 0906-6713
Microbiology and treatment of
dental abscesses and
periodontal-endodontic lesions
Dental or dentoalveolar abscesses are infections of
dental origin, the majority with an endodontic or a
periodontal pocket origin. Dental abscesses also in-
clude pericoronitis and abscesses caused by trauma
and surgical infections. The incidence of serious
odontogenic infections has decreased dramatically
over the last half century due to preventive dental
care and the availability of more effective antibiotics.
However, dental abscesses still occur, and they may
lead to serious consequences by spreading, involving
the bone or various spatia, which might result in life-
threatening conditions. Periapical and periodontal
abscesses may advance into combined periodontal-
endodontic lesions. Most dental abscesses are
caused by the resident oral microflora that enters
normally sterile tissues. Mechanical removal of ne-
crotic infected tissues and surgical drainage are the
most important treatment steps. Antibiotics are indi-
cated in case of systemic symptoms and to limit the
spread of the infection. This chapter reviews present
knowledge of the dental abscess in respect to pathol-
ogy, microbiology and treatment.
Definition and clinical
characterization of dental abscesses
and periodontal-endodontic lesions
An abscess is a localized collection of pus in a cavity
formed by the disintegration of tissues. The forma-
tion of pus is termed suppuration. To emphasize the
presence of pus in abscesses, the term purulent ab-
scess is often used. Abscesses of odontogenic origin
are dental abscesses formed in or around the tooth
and dentoalveolar abscesses that also involve the al-
veolar bone, but the two terms are often used syn-
onymously. Dentoalveolar abscesses consist of two
main types: the endodontic (periapical) abscess
formed after necrosis of the dental pulp and sub-
sequent infection of the root canal, and the peri-
odontal abscess formed after infection of the peri-
odontal tissues by bacteria of the subgingival micro-
biota. A special variant of the periodontal abscess is
pericoronitis, which may develop as an infection of
the pericoronal soft tissue overlying the crown of the
tooth. Inflamed pockets normally drain continu-
ously, but microorganisms and debris may become
entrapped in the pocket, leading to an acute infec-
Abscess formation is readily identified clinically
due to concurrent signs and symptoms such as pain,
redness and swelling of the abscess area, regional
lymph node enlargement, spasm of the muscles and
trismus (57). The expanding lesion can spread con-
siderably through soft tissue. An abscess that only in-
volves soft tissue is termed cellulitis. The spreading
may also involve bone (osteitis) or the bone marrow
(osteomyelitis), which both constitute serious com-
plications (147). Destruction of bony tissue may not
occur immediately, and radiographic signs of bone
destruction are not always detectable. Dental ab-
scesses and abscesses in general expand through
tissue providing least resistance by forming a sinus
tract (fistula). In case of the periodontal abscess,
drainage is most likely to take place through the peri-
odontal pocket since this is usually the path of least
resistance. In case of a periapical abscess, the spread
is primarily dictated by the thickness of the overlying
bone and the location of the abscess in relation to
muscle attachments. In the maxilla, periapical ab-
scesses drain through the palatal bone into the oral
cavity or rarely into sinus maxillaris or the nasal cavity.
The mandibular periapical abscess drains commonly
through the buccal bone into the oral cavity. Infection
may occasionally spread along facial spaces or by the
Microbiology and treatment of dental abscesses and periodontal-endodontic lesions
Fig. 1. Equation of infection
lymphatics to regional lymph nodes (18). Spread via
the bloodstream is rare; however, in patients under-
going surgical incision and drainage of the dentoalve-
olar abscess, bacterial spreading by blood is quite
common (56, 140). The mandibular periapical ab-
scess may expand below musculus myohyoideus and
reach facial spaces. If the sublingual and submandib-
ular (Ludwig\u2019s angina) or pterygomandibular space
are involved, respiratory obstruction or other life-
threatening conditions may occur (20). Mediastinitis,
orbital infections and brain involvement are rare
complications of dental abscesses (58, 132, 190).
In periodontal health, the fistula drains rarely
from a periapical abscess along the root surface into
the gingival pocket. On the other hand, in peri-
odontally diseased sites, it is plausible that the peri-
apical infection drains through the deep periodontal
pocket to form a periodontal-endodontic lesion.
Even after drainage of the abscess, the causative
bacteria may not be completely eliminated but may
reside in the tissues, such as in the apical part of the
root canal or in the root-cement layer of the tooth.
If so, the abscess may transform into a chronic state.
Pathology of dental abscess
Anaerobic infection
The vast majority of dental abscesses are polymicrob-
ial anaerobic infections (54). Anaerobic infections are
opportunistic in the sense that they develop under
certain general and/or local predisposing conditions
(54). Diabetes mellitus, corticosteroids, neutropenia,
hypogammaglobulinemia, malignancy, immunosup-
pression and cytotoxic drugs are well-known systemic
conditions that favor the bacteria in the delicate bal-
ance (microbial homeostasis) between the host and
the parasites (140). Local factors that may disrupt the
microbial homeostasis and facilitate the tissue in-
vasion of microorganisms are related to decreased
redox potential (216). Obstruction, stasis, necrosis,
tissue destruction, vascular insufficiency and foreign-
body presence are local factors commonly involved in
dental abscess development.
Acute and chronic infection
Infection can be defined as the \u2018\u2018invasion of the body
by pathogenic microorganisms and reaction of the
tissues to their presence or to the toxins generated
by them\u2019\u2019 (42). The acute infection is characterized
by invading and multiplying bacteria. Host tissues
respond with vascular dilatation and increased
blood flow, accumulation of liquid (edema) and in-
flux of phagocytic leukocytes, in particular polymor-
phonuclear leukocytes, possibly resulting in abscess
formation. The tissue reaction is a rapid and primar-
ily unspecific inflammatory response to foreign ma-
terials, bacteria and bacterial products entering the
tissues. If bacteria and their products are acciden-
tally forced into the tissue, such as by pocket probing
or endodontic instrumentation beyond the apex, the
host response may be efficient enough to phagocyt-
ize entering microorganisms with no clinically de-
tectable consequences. The critical stage arises when
bacteria survive and start multiplying within the
tissues (185). The anaerobic infection is usually poly-
microbial and thus different from infections caused
by many facultative pathogens. The frequently low
virulence of single anaerobic species and the need
for cooperation and synergism between bacteria to
form pathogenic combinations are characteristics of
anaerobic infections (159). It is also probable that
in a locally or systemically compromised host, the
presence of certain virulent microorganisms or an
increased number of microorganisms or combi-
nations of certain microorganisms may invade host
cells or tissue and induce clinical infection (Fig. 1).
Evidence for the occurrence of bacterial invasion in
oral tissues is given in Table 1. Depending on the
Table 1. Evidence for tissue invasion