Do brain abscesses have a higher incidence of odontogenic

origin than previously thought?

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frequency :
Although rare, brain abscesses are associated with significant morbidity and
mortality. Overall, the incidence has dramatically decreased over the last 50
years. Between 1935 and 1981, approximately 2.7 to 3.9 per 100,000 people
were diagnosed with brain abscesses, whereas more recent findings in 2015
have suggested that the rate has fallen to 0.3 to 0.4 per 100,000.1
Approximately 1500 to 2500 cases are reported annually in the United States,
and, with the advent of advanced imaging and broad-spectrum antibiotics,
mortality rates have declined to less than 15% over the last few decades.

E3
Although multiple etiologies have been cited, the most frequent ones include ENT (ear, nose. and
throat) infections (sinusitis and otitis) as well as invasive neurologic procedures. Less frequent
etiologies include dental infection, cardiac anomalies and associated endocarditis, and pulmonary
infections.4 A few case reports of brain abscesses have been attributed to an odontogenic origin,
and in most of those cases, the incidence has been reported to be less than 5%.5 Over the last 2
decades, however, an increasing proportion has been attributed to odontogenic sources.4 The
reasons for this are speculative and include heightened awareness of the predilection of oral
infections to spread in this manner, maintenance of a greater number of retained teeth in older
populations, and the increasing number of foreign bodies being implanted in the oral and
maxillofacial area (dental and zygomatic implants; hardware, including plates and screws, etc.).
Microbial resistance patterns to multiple antibiotics may also play a role. Approximately 30% of brain
abscesses have an unclear etiology.6-9 Determination of the definitive source can be problematic,
but variables, such as microbiology, may be suggestive of odontogenic infections. Ruling out the
more common etiologies, such as sinus infection or otitis, and identifying a definitive dental
pathology are imperative.

Proves for brain abcess from odontogenic origin

To prove that an abscess has truly developed from an odontogenic source, 3 criteria should be met:
(1) No alternative source of bacteremia is found; (2) the bacteria responsible for the abscess are
typically found in the oral microflora; and (3) clinical signs of active dental disease are present
.10 Given these conditions, validating an odontogenic source can be dif ficult. A few studies have
shown preliminary associations among the microbiology of the infection, the localization of the
abscess, and the routes of oral infection spread.10 However, better documentation is needed.

The purpose of this study was to answer the following clinical

question: “Among all patients admitted to a tertiary care hospital with a diagnosis of brain
abscess, how many appear to be of odontogenic origin?” The secondary aims were better
understanding of the clinical course of the infection and treatments received by patients and
addressing the following questions: (1) “Are the organisms cultured similar to those represented in
cultures from odontogenic infections, and are resistance patterns to antibiotics similar?” (2) “What
treatment and outcome information is available?” We hypothesized that the proportion of brain
abscesses of odontogenic etiology is higher than previously reported in the literature and needs to
be taken into account in all cases without a clear etiology

DISCUSSION:
medical history
dental history
signs and symptoms
Laboratory tests and radiologic examinations
Mechanism of infection and mode of spread
Microbiology
Treatment
Treatment outcomes

Brain Abscess
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PATHOPHYSIOLOGY
A brain abscess may occur as a single focus involving contiguous lobes, or as a contiguous,
multilobular process.3 The most common sites of brain abscesses are the frontal and temporal lobes
followed, in descending order of frequency, by the frontoparietal, parietal, cerebellar, and occipital
lobes. The microorganism enters the brain and produces an initial area of focal cerebritis, which
leads to a softening, edema, hyperemia, and petechial hemorrhage.12 The early lesion (first 1–2
weeks) is poorly demarcated with no evidence of tissue necrosis.2 After 2 to 3 weeks, fibroblasts
from the capillaries adjacent to the focal cerebritis deposit collagen fibers to contain and
encapsulate the purulent focus.2,12–14 The developed abscess consists of 3 layers: a center
polymorphonuclear leukocytes and necrosis, a collagenous capsule surrounding the central areas,
and peripheral gliosis.15 A brain abscess acts as an expanding mass lesion and causes edema in the
surrounding tissue. The edema may lead to life-threatening complications such as uncal or brainstem
herniation, ventricular rupture, ventriculitis, or meningitis.

PATHOGENESIS
Bacteria may invade the brain either by direct spread, which accounts for 20% to 60% of cases, or
through hematogenous seeding.16 The direct spread from a contiguous site usually causes a single
brain abscess. Primary infections that can directly spread to the cerebral cortex include subacute and
chronic otitis media and mastoiditis (inferior temporal lobe and cerebellum), frontal or ethmoid
sinuses (frontal lobe), and dental infection (frontal lobe). Developed countries have seen decreased
rates of brain abscess as the result of ear infections.17,18 Brain abscess arising from a sinus infection
remains an important consideration in both adults and children.19–22 Penetrating trauma to the
brain is another direct method of infection. This type of trauma may be the result of any invading
foreign body or retained fragments that can result in necrotic tissue and serve as a nidus for
infection.2 In addition, neurosurgical procedures can be a direct source of development of brain
abscess.23–25 The common organisms from direct sources are listed in Table 1. Hematogenous
spread via bacteremia is associated with multiple abscesses in the distribution of the middle cerebral
artery.26 Cerebral abscesses usually form at the gray–white matter junction where microinfarction
damages the blood-brain barrier.

Table 1

Do Dental Infections Really Cause Central Nervous System

Infections?

cavernous sinus blood network :

. It receives blood from the superior and inferior ophthalmic veins, as well as the sphenoparietal
sinus, superficial middle cerebral vein, and pterygoid plexus of veins.

abducens nerve palsy is usually the first cranial nerve injury seen in cavernous sinus thrombosis
(CST).
CFT CAUSES

The cause of CST is 2-fold: hematogenous spread of septic emboli to the cavernous sinus via the
blood supply of the head and neck or by direct extension of contiguous space infections. Most cases
of CST are secondary to infections of the paranasal sinuses (ethmoid, sphenoid, frontal), nasal cavity,
tonsils, middle ear, orbit, skin of the nose and face, or teeth.