75TH ANNIVERSARY CONTRIBUTION
J Oral Maxillofac Surg
Management of Oral and Maxillofacial
Infections
Elie M. Ferneini, DMD, MD, MHS, MBA,* and Morton H. Goldberg, DMD, MDy
We discuss the history of the management of oral and
maxillofacial infections, with an emphasis on the
advances that have occurred during the past 100 years,
as a part of the journal’s celebration of the founding of
the American Association of Oral and Maxillofacial Sur-
geons and the 75 years since the launch of the Journal
of Oral and Maxillofacial Surgery.
As surgeons who treat infections daily, we still ask
ourselves the following questions: Is the pen truly
mightier than the sword? Or is the scalpel still more
useful than the prescription pad for the therapy of
oral and maxillofacial infections?
The triad of anesthesia, hemostasis, and asepsis is the
foundation of the contemporary glory and wonder that
is 21st century surgery and all its specialties and subspe-
cialties. Of this triad, only the prevention and control of
infection remains a persistent and occasionally contro-
versial issue, now some 75 years into the antibiotic era.
Since the chance discovery of the ‘‘wonder-drug’’
penicillin (1928) and its clinical introduction in
1940, the pathogens of infection have continued to
evolve, and therapy, rather than being simplified, has
become increasingly complex.1 Infection remains as
the common threat to all surgical procedures and the
bane of all surgeons. Although our knowledge of the
oropharyngeal biomass, the human immune system,
and bacterial genetics has increased exponentially in
the past 30 years, the problems of bacterial resistance,
antibiotic side effects, and drug–drug interactions
have proved to be insurmountable.
The defenses of the human immune system (and its
pharmaceutical allies) have been breached by the emer-
gence of resistant strains of staphylococci, oral strepto-
cocci, Escherichia coli, enterococci, Bacteroides,
*Private Practice, Beau Visage Med Spa; Greater Waterbury OMS;
Associate Clinical Professor, Division of Oral and Maxillofacial
Surgery, Department of Craniofacial Services, University of
Connecticut, Cheshire, CT.
yClinical Professor, University of Connecticut School of Dental
Medicine and Hartford Hospital, Hartford, CT.
Conflict of Interest Disclosures: None of the authors have any
relevant financial relationship(s) with a commercial interest.
Address correspondence and reprint requests to Dr Ferneini:
Beau Visage Med Spa, Greater Waterbury OMS, Division of Oral
469
76:469-473, 2017
Clostridium difficile, Klebsiella, Pseudomonas, Acine-
tobacter, and a host of others. From the human oral
cavity to the hospital intensive care unit (ICU), a rapid
evolution has occurred in the numbers, species,
virulence, and antibiotic resistance of bacteria, which
continue to challenge oral and maxillofacial surgeons.
Currently, man-eating tigers can still be found in India
(the Bengal), but if man-killing microbes are sought, a
stroll through the ICU will suffice.
The human oral cavity is a microbial swamp. Recent
investigational data gleaned from molecular genetic
studies, including gene sequencing for bacterial identifi-
cation, suggest that there might be as many as 400 spe-
cies of microorganisms in the microflora of the human
oropharynx. It has been estimated that during a long,
passionate (however, defined) kiss, up to 60 million
microorganisms could be exchanged during the kiss.
The development of this broader biological view of
the environment of oral and maxillofacial surgery
should have provided us with a more comprehensive,
science-based, and evidence-based rationale for
choosing between the pen and the sword and address-
ing the issue of using prophylactic antibiotics or not
and, if so, where and why (ie, orthopedic joint replace-
ment and endocarditis).
Although the antibiotic research ‘‘pipeline’’ has suf-
fered a severe drought during the past few decades,
a plethora of proven ‘‘oldies’’ remain, and only a few
are necessary in the therapy of odontogenic infections
in the non–immunocompromised host. Many of the
antibiotics developed in the past 50 years are not the
drugs of choice for oral and maxillofacial infections.
Numerous studies in the late 20th and early 21st cen-
turies have revealed and reinforced that penicillin
and Maxillofacial Surgery, University of Connecticut, 435 Highland
Avenue, Suite 100, Cheshire, CT 06410; e-mail: eferneini@yahoo.
com
Received November 17 2017
Accepted November 27 2017
Ó 2017 American Association of Oral and Maxillofacial Surgeons
0278-2391/17/31452-0
https://doi.org/10.1016/j.joms.2017.11.032
470
(amoxicillin) remains the drug of choice for mild to
moderate odontogenic infections in the otherwise
healthy patient but not necessarily so for those with
serious comorbid diseases or those who are, or have
recently been, inhabitants of an ICU.
Before the 1980s, the decision to hospitalize pa-
tients with odontogenic infections was an amalgam
of guess work, experience (always the great teacher),
and surgical judgment. Large data-based studies during
recent decades have culminated in generally accepted
criteria for hospitalization and offer some predictabil-
ity regarding the length of stay and the need for inci-
sion and drainage:
1 Airway obstruction—present or impending
(pharyngeal space infections, severe trismus)
2 Dehydration or electrolyte imbalance
3 Profound immunosuppression (which can cam-
ouflage inflammation)
4 Temperature greater than 101 F
5 Elevated white blood cell count, sedimentation
rate, C-reactive protein
6 Ludwig’s angina, necrotizing fasciitis, generalized
sepsis
This seemingly endless conflict between virulent
microorganisms and human defenses has resulted in
the worldwide phenomenon and risks of returning
to the pre-antibiotic era. In 1940, before the availabil-
ity of penicillin, the father of one of us experienced
an infected finger laceration, lymphangitis, and subse-
quent generalized sepsis—his wife was warned that if
sulfanilamides were ineffectual, she ‘‘would be a
widow,’’ like so many others in that pre-antibiotic era.
Before the advent of antibiotic therapy, odontogenic
infections, both mild and severe, were managed by
exodontia, curettage, irrigation, and incision and
drainage. Such infections, often secondary to rampant
caries, were commonplace in an era in which, gener-
ally, adequate caries control and fluoride were not
available. Airway impingement, pharyngeal spaces,
and Ludwig’s angina were known to be life-
threatening but were misdiagnosed (and therapy de-
layed) all too often. In fact, Ludwig’s angina was
described as a severe infection affecting the ‘‘mouth,
throat, neck, submandibular and parotid regions’’
and ‘‘a gangrenous odor develops, the lungs become
affected and death ensues’’ (Fig 1).2 As a first-year gen-
eral surgery resident in the early 1960s, the senior
author was taught the airway safety maxim: ‘‘the
time to perform a tracheostomy is when you first think
that a tracheostomy might be necessary.’’
Before the antibiotic era, facial fractures, especially
those of the mandible, were subject to a high inci-
dence of local or deep infections, including osteomye-
litis caused by both oral microflora and/or facial
cutaneous bacteria. Osteomyelitis and nonunion
MANAGEMENT OF ORAL AND MAXILLOFACIAL INFECTIONS
FIGURE 1. Patient with Ludwig’s angina.
Ferneini and Goldberg. Management of Oral and Maxillofacial In-
fections. J Oral Maxillofac Surg 2018.
were all too frequently the results, inasmuch as even
lower border wires and dental arch bars did not always
prevent micro-movements of osseous fragments and
secondary bacterial invasion. In that era, oral and
maxillofacial surgeons (OMSs) could not enjoy the
genius and luxury of rigid titanium fixation (Fig 2).
In the 1960s, at Bellevue Hospital, an intramuscular
‘‘cocktail’’ of penicillin and an aminoglycoside (strepto-
mycin) was used without any hard data proving any
efficacious effect in preventing infection in fractured
mandibles. A few years later, Zallen and Curry3 re-
ported a controlled study proving that antibiotics are
very efficacious in preventing post-fracture infection.
By 1945, Fleming noted (in the NY Times)4 that the
great gift (penicillin) was at risk because of bacterial
(staphylococcal) resistance and suggested that overus-
age and underdosing were possibly responsible. Phar-
maceutical research then altered the chemistry of
penicillin, attempting to stay ahead of the rapidly devel-
oping resistance, and begat ampicillin, which then
begat amoxicillin, which begat Augmentin, and so forth.
Currently, numerous generations of cephalosporins are
available, and lincomycin (discovered in a soil sample
from Lincoln, Nebraska) begat clindamycin, and multi-
ple choices of macrolides and fluoroquinolones
are available.
Fortunately, some new antimicrobial agents are in the
dehydrated and shriveled pipeline; however, the profit
motive remains primary, and pharmaceutical research
dollars have been invested in drugs that are useful in
long-term therapy (years) rather than short-term treat-
ment (antibiotics). Research dollars have been shunted
to tranquilizers, antipsychotics, mood stabilizers, anti-
depressants, antihypertensive agents, and cholesterol
controllers. More efficacious types of quinolones, tetra-
cyclines, and b-lactamase inhibitors are among those
somewhere in the pharmaceutical future. However, if
they are too costly or are denied by health insurance
FERNEINI AND GOLDBERG
FIGURE 2. Rigid internal fixation with an early plating system.
Ferneini and Goldberg. Management of Oral and Maxillofacial In-
fections. J Oral Maxillofac Surg 2018.
industry payers, or, like their predecessors, are overused
and misused, their addition to the pharmacopeia of
infection therapy will be of little or short avail.
In 1992, J. B. Levy,5 a career researcher on the hazards
of antibiotic misuse, prophetically authored The Anti-
biotic Paradox—How Miracle Drugs Are Destroying
the Miracle. He clearly described the consequences of
antibiotic resistance at the individual, regional, and in-
ternational levels and the critical roles of physicians,
dentists, and veterinarians, as well as livestock pro-
ducers, in the persistence of antibiotic resistance.5
Simply put, we—all of us—do not own our bacteria.
We are constantly (24/7) shedding them into the envi-
ronment by exhaling, coughing, sneezing, spitting,
excreting, shedding (skin and hair), touching, and,
yes, kissing (and so forth)—all universal human biolog-
ical activities but all potentially dangerous. If a patient
receives antibiotic therapy or prophylaxis and
develops resistant microflora in the skin, saliva, and/
or gut, these can be and will be shed onto and into
others, thus creating a virtual micro- or macro-local
or diffuse (by travel) epidemic or pandemic of anti-
biotic resistance.
471
As OMSs, we have been trained to treat or prevent
local orofacial infections and to consider the possible
systemic consequences (ie, ‘‘my patient is allergic to
penicillin, may I safely prescribe a cephalosporin?’’).
However, as the past few decades have proved, we
also need to consider the present and future global
implications of prescribing or administering an anti-
biotic if it is not necessary. Presciently, Levy5 dedi-
cated The Antibiotic Paradox to ‘‘. all future
generations.’’
Ideally, cost should not be a primary consideration in
the therapy for orofacial infections, but thus it has so
evolved. For 30 years, computed tomography (Fig 3)
and magnetic resonance imaging have become indis-
pensable in the diagnosis of deep fascial space infec-
tions, abscess formation and location, airway
compromise or displacement, and, even, lost drains.
However, the question remains, should not an initial
clinical examination suffice in the emergency room
(ER), rather than routine expensive imaging studies
of patients with garden-variety buccal and submandib-
ular infections? The research of McCormick et al6 has
revealed that as many as 2 to 3% of ER patient visits
could be for orofacial problems, most commonly
dental pain or infection, a seemingly small number.
However, if extrapolated nationally, it represents
many thousands of hours and mindboggling millions
of dollars for our beleaguered healthcare system. A
relatively inexpensive periapical or panoramic film
and midnight bupivacaine will often suffice. ER
personnel can be educated to use the sword for the
non–life-threatening superficial intra- or extraoral pre-
sentation of infection, as well as their more familiar
penicillin drugs.
Although prevention is always the best treatment,
our use of antibiotic prophylaxis in oral and maxillofa-
cial surgery has varied historically as more data and
experience have been acquired, but a definitive answer
remains elusive. Although many, perhaps most,
impacted third molars will, eventually, become symp-
tomatic and require extraction, can the routine use of
pre- and/or postoperative antibiotics be justified,
except in the presence of active infection? Although
recent studies have suggested that prophylaxis might
reduce the relatively small postoperative infection rate
somewhat, is it rational to administer prophylactic anti-
biotics to a large population of patients in the hope of
preventing postextraction infection in a few? Similarly,
is prophylaxis necessary with implant placement if
the site is healthy? Should antibiotics be de rigueur
with immediate implant placement? Has the ‘ high’’ suc-
cess rate of immediate implants in the presence of peri-
apical infection, despite curettage, resulted from the
use of 7 to 10 days of antibiotic therapy, a more than
adequate time to develop resistance in oral, gut, and
skin bacteria?
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FIGURE 3. Computed tomography scan of a right submandibular abscess.
Ferneini and Goldberg. Management of Oral and Maxillofacial Infections. J Oral Maxillofac Surg 2018.
We need not be nay-sayers nor even minimalists;
however, our uses and abuses of the ‘‘great gift’’
continue to haunt the future. Although we perform
procedures locally (ie, 1 patient), we must also think
globally and generationally. The changes in therapy
have been remarkable, but the risks remain high. We
must be a part of the solution to antibiotic resistance
rather than participate in the problem.
Endocarditis and Orthopedic
Prophylaxis
Endocarditis was first described by Sir William Osler,
the ‘ father of modern Medicine’’ (in the late 19th and
early 20th centuries) at Johns Hopkins Hospital.7 Inves-
tigators Okell and Elliot are given credit for establishing
the relationship between odontogenic infection and en-
docarditis. Although their observations have been
accepted by both medicine and dentistry for decades,
there has never been and perhaps never will be, for
ethical reasons, a carefully controlled study of a large
cohort of patients with susceptibility to endocarditis
who receive either prophylactic antibiotics or
a placebo.
Because the risks (death) and costs (surgery) of
endocarditis outweigh those of prophylaxis, the latter
has been recommended by the American Heart Associ-
ation (AHA) for well over half a century. These recom-
mendations have been changed frequently since the
1950s, with considerable variations in the drugs,
doses, and duration, directed primarily at oral strepto-
cocci. Amoxicillin is currently the drug of choice
because of its rapid bioavailability and slightly broader
MANAGEMENT OF ORAL AND MAXILLOFACIAL INFECTIONS
spectrum of activity. For a fortunately, short period,
pre-extraction intravenous vancomycin was the
AHA’s recommended drug of choice, without any
input from dentistry, with no dentist included in the
AHA’s guidelines committee.
The current (2007) AHA guidelines have limited and
changed the indications for endocarditis prophylaxis
to reduce the overuse and misuse of antibiotics in their
era of rapidly progressing bacterial resistance; this is
certainly a worthy goal.8 Those 2007 recommenda-
tions were also intended to reduce the serious side ef-
fects and complications of prophylactic antibiotic use,
namely anaphylaxis. However, true anaphylaxis is rare
if a thorough medical history is obtained and if peni-
cillin is ingested rather than injected.
Furthermore, the AHA guidelines have chronically
failed to consider the quantitative aspects of
odontogenic-induced endocarditis. Although the simple
acts of flossing, brushing, or extracting an uninfected
tooth will induce a transient bacteremia, the removal
(perhaps surgically) of multiple grossly periodontally
or periapically infected teeth would be expected to pro-
duce an exponentially greater bacterial load into the
vasculature. Perhaps in such cases, a larger prophylactic
antibiotic dose or longer duration should be considered.
This is not an apple versus orange issue, it is more of an
acorn versus oak tree concern.
Contemporarily, since the latest guidelines publica-
tion, the cause and effect issues have increased. In a
preliminary study reported in The Lancet in 2014, as
expected, a substantial decrease was reported for anti-
biotic prescriptions for endocarditis prophylaxis in
Great Britain.9 However, a significant and unpredicted
FERNEINI AND GOLDBERG
increase in cases of endocarditis also occurred.9
Perhaps it will soon be time for yet another review
and revision of the AHA’s recommendations.
Although viridans streptococci and other strepto-
cocci have been among the most commonly cultured
bacteria in endocarditis, other species have also
been implicated, including the culture-fastidious
HACEK group from the oropharynx.
Prosthetic Joint Prophylaxis
The use of prophylactic antibiotics for exodontia in
patients with total joint replacement has been contro-
versial since the mid to late 20th century when joint
replacement became available. Now more frequent in
an increasingly aging population, the fear of post-joint
replacement infection necessitating hospital readmis-
sion or loss of the prosthesis has resulted in a plethora
of various and sundry recommendations for antibiotic
selection by orthopedic surgeons and infectious disease
specialists.
The variations in dosage and duration and the up to a
lifetime necessity for prophylaxis can be confusing and
contradictory, ranging from amoxicillin to vancomycin.
Inasmuch as staphylococci are commonly the infecting
pathogens of joint prosthesis infection via tropism (ie,
their ability to colonize the surface of metal and other
foreign objects) and because staphylococci are more
predominately skin, rather than oral, residents, the cur-
rent empirical choice of antibiotics would seem to be ir-
rational and ineffective. Amoxicillin is not a first-line
anti-staphylococcal drug.
The American Dental Association (ADA) Council on
Scientific Affairs 2015 position has evolved after de-
cades of uncertainty: ‘‘there is no demonstrable associ-
ation between dental procedures and prosthetic joint
infection.’’ The Journal of the Canadian Dental Asso-
ciation (CDA) is of the opinion that ‘‘recommenda-
tions for antibiotics in patients with prosthetic joints
are irresponsible and indefensible.’’10 Thus, we can
only hope that the ADA and CDA will, together
with national orthopedic associations, formulate a
473
consensus opinion based on rational scientific data,
if those exist. More than 75 years into the ever-
evolving antibiotic era, glaring issues of overuse and
misuse of antibiotics surely need to be resolved.
Conclusion
Oral and maxillofacial infections are seen daily in our
clinical practice. OMSs need to use disciplined
approaches to prevent and appropriately manage these
infections. We must become part of the solution to anti-
biotic resistance and prescribe them when needed and
apply evidence-based clinical recommendations.
References
1. American Chemical Society: Discovery and development of
penicillin. Available at: https://www.acs.org/content/acs/en/
education/whatischemistry/landmarks/flemingpenicillin.
html. Accessed August 30, 2017
2. Davis GG: Acute septic infection of the throat and neck: Lud-
wig’s angina. Ann Surg 44:175, 1906
3. Zallen RD, Curry JT: A study of antibiotic usage in compound
mandibular fractures. J Oral Surg 33:431, 1975
4. Rosenblatt-Farrell N: The landscape of antibiotic resistance. En-
viron Health Perspect 117:A244, 2009. Available at: https://
www.ncbi.nlm.nih.gov/pmc/articles/PMC2702430/. Accessed
August 30, 2017
5. Levy B: The antibiotic Paradox: How Miracle drugs are Destroy-
ing the Miracle. New York, NY, Plenum, 1992
6. McCormick AP, Abubaker AO, Laskin DM, Gonzales MS,
Garland S: Reducing the burden of dental patients on the busy
hospital emergency department. J Oral Maxillofac Surg 71:475,
2013
7. Geller SA: Infective endocarditis: a history of the development of
its understanding. Autops Case Rep 3:5, 2013
8. American Heart Association: Infective endocarditis. Available
at: https://www.heart.org/HEARTORG/Conditions/Congenital
HeartDefects/TheImpactofCongenitalHeartDefects/Infective-
Endocarditis_UCM_307108_Article.jsp. Accessed August 30,
2017
9. Dayer M, Jones S, Prendergast B, et al: Incidence of infective en-
docarditis in England, 2000–13: A secular trend, interrupted
time-series analysis. Lancet 385:1219, 2014
10. Sollecito T, Abt E, Lockhart P, et al: The use of prophylactic anti-
biotics prior to dental procedures in patients with prosthetic
joints: Evidence-based clinical practice guideline for dental prac-
titioners—a report of the American Dental Association Council
on Scientific Affairs. J Am Dent Assoc 146:11, 2015