ISSN: 2643-3907

Ortiz and Espinoza. Res Rep Oral Maxillofac Surg 2021, 5:055
DOI: 10.23937/2643-3907/1710055
Volume 5 | Issue 2
Open Access

Research Reports in Oral and Maxillofacial Surgery

Literature Review

Odontogenic Infection. Review of the Pathogenesis, Diagnosis,

Complications and Treatment
Roberto Ortiz1* and Vanessa Espinoza2 Check for
updates
General Dentist, Private Practice, Guayaquil, Ecuador
1

Chief, Oral and Maxillofacial Surgery Department, Hospital General Guasmo Sur, and Private Practice, Guayaquil, Ecuador
2

*Corresponding author: Dr. Roberto Ortiz, General Dentist, Private Practice, Los Ceibos, Guayaquil, Ecuador, Tel: +593-
99-749-0300

Abstract Ocassionally, symptoms and clinical manifestations

may become severe, requiring in-hospital management.
Odontogenic infections are frequently seen in the dental
Dissemination of OI can compromise the airway, putting
practice, being dental caries its main etiology; therefore,
dentists should be familiarized with its presentation and life at risk [4].
management as it can spread rapidly and have serious
The principle of treatment dates back to the time of
consequences. The purpose of this article is to provide
essential knowledge on the pathogenesis, diagnosis, Hippocrates when it was established that the elimination
possible complications and treatment of odontogenic of the infectious agent along with incision and drainage
infections. (ID) are key to the resolution of an OI [5]. In addition, it
Keywords has to be accompanied by antibiotic therapy [6].
Odontogenic infections, Dental infection, Odontogenic The purpose of this article is to provide essential
infection complications, Odontogenic infection management knowledge on the pathogenesis, diagnosis, possible
Abbreviations complications and management of odontogenic
infections allowing the establishment of a treatment
OI: Odontogenic Infection; ID: Incision and Drainage; CT:
Computed Tomography; MRI: Magnetic Resonance Imaging that contains the infection localized, avoiding its
dissemination towards deep anatomical spaces; thus,
ensuring the patient's safety.
Introduction
Odontogenic infection (OI) is defined as those Pathogenesis
infections that originate from pulpal or periodontal Host response to infection
pathology that affect the alveolar bone and can spread
through the bone marrow, cortical bone and periosteum Immune response is mediated by the immune
to structures distant from the oral cavity [1]. system, which is a complex of specialized cells that
function as a protective barrier and is composed of an
OI is one of the most common diseases, accounting innate system and an acquired system [7].
for 60% of reason for dental consultation with the
dentist [1,2]. The main etiology is dental caries, but it can The innate system is a non-specific defense
also develop from pericoronitis, periodontal pockets or mechanism that activates upon contact with an antigen.
exodontia [3]. The severity of the infection depends on The acquired system, on the other hand, is an antigen-
multiple factors, such as the virulence of the bacteria, specific defense mechanism which has the capacity
the systemic state of the patient and the anatomical to recognize the antigen that is facing. Thus, creating
spaces affected. memory cells that identify and act quickly against an

Citation: Ortiz R, Espinoza V (2021) Odontogenic Infection. Review of the Pathogenesis, Diagnosis,
Complications and Treatment. Res Rep Oral Maxillofac Surg 5:055. doi.org/10.23937/2643-
3907/1710055
Accepted: August 10, 2020; Published: August 12, 2021
Copyright: © 2021 Roberto OB, et al. This is an open-access article distributed under the terms of the
Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction
in any medium, provided the original author and source are credited.

Ortiz and Espinoza. Res Rep Oral Maxillofac Surg 2021, 5:055 • Page 1 of 10 •
DOI: 10.23937/2643-3907/1710055 ISSN: 2643-3907

antigen in case of new exposure [7]. The cells that In uncontrolled diabetes hyperglycemia occurs,
comprise the immune system are leukocytes consisting affecting the defense cells, favoring the persistence
of T, B and killer lymphocytes, granulocytes such as of an infectious process due to the following factors
neutrophils, basophils, eosinophils and mast cells, [7,13,14]:
and antigen-presenting cells such as macrophages,
1. Decreased chemotaxis, adhesion, migration and
Langerhans cells and dendritic cells [8].
phagocytosis of leukocytes. They present less
Bacterial invasion induces a series of immunological defensive capacity against bacteria and prolong
events to fight infection. The first defense cell of the inflammatory state.
the organism is the macrophage, which fulfills a
2. Decreased proliferation of fibroblasts, endothelial
dual function by releasing chemotactic factors that
cells and collagen. Impairs tissue repair.
attract neutrophils to the site of the lesion and as an
antigen-presenting cell to the neutrophils, responsible 3. Macrophages and monocytes evade apoptosis,
for bacterial phagocytosis. The release of chemical thus increasing cytokine production and
mediators such as histamines, bradykinins, cytokines prolonging the inflammatory process. Chronic
and prostaglandins, causes vasodilatation and opening inflammation increases insulin resistance.
of spaces between endothelial cells allowing the 4. Microangiopathy decreases blood flow and
extravasation of plasma into the interstitial spaces consequently decreases oxygen and nutrients to
where it accumulates, followed by the formation of defensive and reparative cells. Also, it hinders the
fibrin. During an infectious process the classic signs of arrival of antibiotics to the site of infection.
inflammation such as swelling, erythema, pain, edema
and loss of function are observed [9]. This process is 5. Decreased proliferative capacity of keratinocytes
summarized as: 1) Hyperemia due to vasodilatation; which delays re-epithelialization of wounds.
2) Plasma and leukocyte extravasation; 3) Increased Microbiology
permeability and neutrophil diapedesis; 4) Fibrin wall
formation; 5) Bacterial phagocytosis; 6) Deposition of The normal oral flora is mixed, composed of aerobic/
necrotic material by macrophages [2]. facultative anaerobic and strict anaerobic bacteria
[15]. Aerobic bacteria have the ability to survive and
Immunocompromised patient grow in an oxygenated environment. They prepare
There are multiple conditions that lead to a the environment for the proliferation and invasion
depression of the immune system such as long-term of anaerobic bacteria which survive and develop in
use of corticosteroids, transplants, HIV, alcoholism, liver a hypoxic environment. Strict anaerobic bacteria are
disease, diabetes, among others [10]. responsable for greater invasion and destruction of
tissues due to their high virulence [4].
The presence of immunosuppressive medical
conditions is very important in the development of OI is polymicrobial with a higher prevalence of
OI. Systemic diseases, even more than the location gram-positive cocci and gram-negative rod, being the
of infection, have been shown to influence in longer streptococci the most prevalent Table 1 [16,17]. There
hospitalization and recovery time [11]. is a 3:1 ratio of anaerobic to aerobic bacteria. Anaerobic
bacteria are found in 75% while aerobic bacteria are
The most common systemic condition is diabetes, found in 25% [2]. Although the virulence of the bacteria
which when uncontrolled, increases the severity of is a feature that can determine the severity of the
infection and hospital stay due to decreased immune infection, on many occasions the bacterial load will be
system function [12].
Table 1: Frequent bacterias in odontogenic infections. Adapted from Brook I, et al. [17].

Gram stain Type of bacteria Aerobes or facultative anaerobes Strict anaerobios

Streptococcus spp Peptococcus spp
Cocci
Staphylococcus spp Peptostreptoccus spp
Gram-positive
Eubacterium
Rods Lactobacillus spp
Actinomyces
Cocci Veilonella
Porphyromonas spp
Capnocytophaga spp Bacteroides spp
Gram-negative
Rods Actinobacilo spp Prevotella spp
Eikenella spp Fusobacterium spp
Selenomonas sputigena

Ortiz and Espinoza. Res Rep Oral Maxillofac Surg 2021, 5:055 • Page 2 of 10 •
DOI: 10.23937/2643-3907/1710055 ISSN: 2643-3907

Table 2: Anatomic spaces of the oral and maxillofacial region. Adapted from Hupp JR, et al. [20].

Localization Spaces
Maxillary Buccal, palatal, vestibular
Primary
Mandibule Vestibular
Maxillary Canine/infraorbital, orbital
Secondary Sublingual, submandibular, parotid, pterigomandibular, superficial temporal,
Mandibule
submental, deep temporal, peritonsillar masseteric
Advanced Deep neck Lateral pharyngeal, retro pharyngeal, carotid, pretracheal, visceral, mediastinum

Table 3: Severity scale of the compromised anatomic spaces. Adapted from Flynn T, et al. [21].

Severity Scale Anatomic space

1 : Mild risk Canine, vestibular maxillary and mandibular, palatal
2: Moderate risk Submandibular, sublingual, submental, pterigomandibular, submasseteric, temporal,
3: Severe risk Retropharyngeal, pterigopalatal, pretracheal, pterigopharyngeal
4: Extreme risk Mediastinum, intracranial, prevertebral

more important in overcoming the host defense system Diagnosis

[4]. The increment in bacterial load increases the
diversity of microorganisms. When interacting among Clinical presentation
them there is a synergism that increases their virulence The diagnosis of an OI is made from the patient's
[18]. clinical history and symptoms. Establishing the onset
of symptoms and propagation speed of the infection
Dissemination of odontogenic infection
clarifies the severity [20].
OI initiate in dental and/or periodontal tissues which
Physical examination of the patient plays an
they spread through to deep anatomical structures
important role during diagnosis. In advanced stages
[19]. When bacteria reaches the dental pulp, it causes
of OI an alteration of vital signs along with leukopenia
necrosis and induces the formation of an abscess. Once
are manifested as a Systemic Inflammatory Response
the infection is established in the periapical tissue, it
Syndrome. Temperature is < 36° or > 38°, heart rate >
crosses cortical bone periosteum and goes through the
90/min, respiratory rate > 20/min, and neutrophils >
path of least resistance determined by [20]:
12,000 mm3 [25].
1. Muscle attachments that mark the direction and
During the examination, swelling with redness of
location of infection.
the affected area are observed Figure 1. The dental,
2. Position of the dental apex. periodontal and perioral status of the patient should be
3. Thickness of the bone surrounding the tooth. assess [9]. Three stages can be determined during the
examination of the patient with OI: Inoculation, cellulitis
The dissemination of OI occurs by three routes: or abscess [20] Table 4.
1) By continuity through anatomical spaces which,
by being virtual spaces and not having real physical The classic signs and symptoms of inflammation
limits, facilitate the spread of the infection between are evidenced: pain, redness, heat, edema and loss of
them Table 2. 2) By hematic route when entering the function. Depending on the severity of the infection
circulatory system. 3) By lymphatic route when entering thermal elevation, diaphoresis, general malaise,
the lymphatic system of the head and neck it can spread odynophagia, dyspnea, dysphagia and trismus are
through the lymph from the primary nodule, close to present; some of these signs and symptoms are
the infectious focus, to a secondary nodule in a distant indicators of an infection that requires in-hospital
site [4]. management by a specialist [3,9,20].

Flynn, et al. classify the severity of infection Imaging

according to the anatomical spaces invaded [21] There is a wide variety of options such as panoramic
Table 3. It has been reported that the most frequently radiography, computed tomography (CT), magnetic
involved aponeurotic space is the vestibular space (50%) resonance imaging (MRI) and ultrasound [16,26].
[1]; while other studies concluded it was the buccal
space (60%) [4] and the submandibular space (35%) Panoramic radiography is the imaging study of first
[22]. Beyond these differences, it was concluded that choice in the protocol for the OI management since it
odontogenic infections are responsible for 43%-60% of shows signs of bone and dental destruction that guides
deep neck space infections [23,24]. the clinician to the origin of the infection [27] Figure 2.

Ortiz and Espinoza. Res Rep Oral Maxillofac Surg 2021, 5:055 • Page 3 of 10 •
DOI: 10.23937/2643-3907/1710055 ISSN: 2643-3907

Table 4: Stages of infection. Adapted from Hupp JR, et al. [20].

Stages of infection
Edema Cellulitis Abscess

Spread of bacteria into Breakdown of liquefactive

Interstitial fluid from neighboring
Definition space along with interstitial necrosis to form purulence
inflammation or infection
accumulation within the soft tissue
Duration 0-3 days 3-7 days > 5 days
Pain Mild-moderate Severe Severe

Location Diffuse Diffuse Well-circumscribed

Palpation Soft Tender Fluctuant

Skin Normal to firm Firm Firm to hard

Loss of function None to minimal Moderate to severe Moderate to severe
Tissue fluid Edema Serosanguineous or purulence Collection of purulence
Severity Mild Moderate to severe Severe
Bacteria profile Aerobic Mixed Anaerobic

A B

Figure 1: A) Swelling of the buccal space, Loss of nasolabial fold; B) Remission of infection.

Figure 2: Panoramic X-ray, Periapical osseous destruction of the second left lower molar. Roots remains of the second
right lower molar.

Ortiz and Espinoza. Res Rep Oral Maxillofac Surg 2021, 5:055 • Page 4 of 10 •
DOI: 10.23937/2643-3907/1710055 ISSN: 2643-3907

Figure 3: Image ordering guidelines for odontogenic infection. Adapted from Weyh AM, et al. [28].

The overuse of CT as diagnostic imaging in cases of treatment are sufficient for the remission of the
OI has been discussed on several occasions. Weyh, et al. infection. Most are localized and can be treated on
published a guideline for CT request that considers signs the outpatient basis; therefore, culture is not justified
and symptoms as "red flags" that suggest an increased risk [28,30].
of dissemination of the infection to deep anatomic spaces
Culture and bacterial sensitivity testing are ordered
increasing the risk of complications [28] Figure 3. Some
when infections progress rapidly to spaces of moderate or
of them are trismus, dyspnea, dysphagia, non-palpable
severe risk, recurrent infections, immunocompromised
lower jaw border, tachycardia, among others [28,29].
patients, infections that don’t improve after 48 hours of
The use of MRI, despite being superior in the antibiotic therapy [20,30].
diagnosis of bone and soft tissue alterations, has great
The technique of sample collection for culture and
disadvantages such as the time and money needed to
antibiogram is of great importance. Contamination of
perform it. On the other hand, the ultrasound can be a
the sample by bacteria belonging to the normal flora of
great tool in cases where a CT scanner is not available,
the skin or oral cavity should be avoided at all times, so
allowing the evaluation and differentiation of purulent
the area should be previously sterilized [4].
collections and vascularized areas [16].
The best method for taking a sample is by aspiration
Laboratory studies of at least 2 ml of purulent content. However, if incision
Laboratory studies are not usually solicited during the and drainage are required, “culturettes” tubes, which
treatment of an odontogenic infection. However, they are sterile tubes containing conveyance for aerobic and
can be useful when the infection occupies deep spaces anaerobic bacteria, should be prepared [20].
that complicate the clinical examination. The study to
Complications
request is a complete blood count; in which the white cells
are evaluated with greater emphasis on the differential In normal systemic circumstances the immune system
count. During the development of the bacterial infection, manages to contain the dissemination of the infection,
neutrophils are elevated above 12,000 mm3 as a sign so the vast majority of OI are localized. Patients with
that the immune system is fighting the infection; while systemic diseases in which their defense mechanisms
after treatment, as a sign of resolution of the infection, are affected, present a greater risk of developing
neutrophils return to normal levels [19]. complications, which can be local, by establishing
themselves in adjacent tissues of the face and neck, or
Culture systemic, by spreading towards the circulation causing
Regularly the elimination of the infectious focus, septicemia or infection distant from its source [22]. Due
incision and drainage, and empirical pharmacological to the proximity of structures such as the airway, brain

Ortiz and Espinoza. Res Rep Oral Maxillofac Surg 2021, 5:055 • Page 5 of 10 •
DOI: 10.23937/2643-3907/1710055 ISSN: 2643-3907

Osteomyelitis
Osteomyelitis is a rare infection and inflammation of
the medullary zone of the bone due to bacterial invasion
originating from different factors such as mandibular
trauma, odontogenic or non-odontogenic infections
that spread by blood. The extensive bone destruction
that is usually seen implies risk of fracture of the affected
bone [35]. Is more frequent in the mandible since the
blood vessels of the periosteum do not penetrate the
cortical bone [20].
Among the characteristics of osteomyelitis are
pain, tenderness, sinuous tracts, suppuration, bone
sequestration. Radiographically, no signs of infection
are observed during the first weeks. In chronic stages,
bone sequestrum is observed as a radiolucent image
that represents necrosis and bone destruction. A halo
of greater density around the sequestrum, called
involucrum, suggests bone regeneration as a response
to inflammation [25]. The indicated treatment are
Figure 4: Abscess of the temporal space. broad-spectrum antibiotic therapy and profuse
surgical curettage; also, bone resection for large bone
and heart, early diagnosis and treatment should be destruction [2].
carried out to prevent danger to the patient's life. The
OI has a mortality rate of 10-40% [25].
Cavernous sinus thrombosis
Is an infection that affects the cerebral sinuses.
Multiple complications have been reported as
Because veins don't contain valves, blood flow arrives
a consequence of odontogenic infection such as:
from several directions, connecting the cavernous sinus
Necrotizing mediastinitis [31], Ludwig's angina [32],
to the face through the angular vein which connects
infratemporal and temporoparietal fossa abscesses
with the superior ophthalmic vein and to the palate
[33] Figure 4, deep neck infections [23,24], meningitis
through the pterygoid plexus via the inferior ophthalmic
[34], osteomyelitis [35], intracranial abscesses [36,37],
vein [25]. When infection reaches the cavernous sinus,
cavernous sinus thrombosis [38], necrotizing fasciitis
regardless of the route, thrombosis occurs [9]. However,
[25], airway obstruction [25], and death [31,39].
infections from the canine region via the angular vein
Ludwig's angina are more frequent [38].
Is the most common complication of OI [2]. It refers The cavernous sinus contains cranial nerves III, IV,
to a diffuse cellulitis that occupies the submental, VI, V1 and V2. Ophtalmoplegia, loss of infraorbital and
submandibular and sublingual space bilaterally. Is supraorbital sensitivity, mydriasis, palpebral ptosis and
considered as an emergency because of its rapid amaurosis can be observed [38].
onset [6]. Ludwig’s angina from odontogenic source,
Surgery and intravenous broad-spectrum antibiotics
usually, originates from second and/or third lower
are indicated. If treatment has not been initiated within
molar due to the proximity of the dental apices with
the first 4 to 7 days, death usually occurs [25,38]. Along
the submandibular and sublingual spaces which
the years the mortality rate has decreased to less than
communicate intimately with the submental space,
30% [38].
and can spread to pharyngeal spaces until reaching the
mediastinum [40]. Orbital abscesses
Some classic signs of Ludwig's angina are lingual Orbital abscesses are classified according to their
proptosis and elevation of the floor of the mouth which location as pre-septal or post-septal. Post-septal
obstructs the airway causing dyspnea, dysphagia, abscesses, due to their proximity to the brain, have the
dysphonia and cyanosis [4]. potential to evolve into severe complications [41]. Its
clinical characteristics are periorbital edema, chemosis,
Treatment consists primarily on securing the airway
proptosis, ophthalmoplegia and loss of visual acuity
either by endotracheal intubation or tracheostomy
[42].
[6]. Elimination of the source of infection, incision and
drainage of all infected spaces, and antibiotic therapy Deep neck infections
[41].
Occurs when the infection spreads through anatomical

Ortiz and Espinoza. Res Rep Oral Maxillofac Surg 2021, 5:055 • Page 6 of 10 •
DOI: 10.23937/2643-3907/1710055 ISSN: 2643-3907

planes to posterior regions of the neck such as the lateral The treatment of OI depends on the stage of the
pharyngeal and retropharyngeal spaces [23]. disease and is composed of local management, antibiotic
therapy and surgical management [19].
Deep neck infections from odontogenic source
account for 43% of cases [23] with amortality rate of 10- Local management
40% [43]. The airway can be compromised manifesting
The initial treatment should consist of analgesics for
as dyspnea, dysphagia and dysphonia [23]. Because
pain control, glycemic balance in diabetic patients and
signs may appear in late stages, CT is recommended
control of temperature and electrolyte balance, since for
to observe the extent and location of the infection
each degree of fever there is a fluid loss of 250 ml through
[44]. Surgical drainage and intravenous antibiotics are
perspiration [10,19]. The use of steroids is controversial,
indicated [23].
but some authors recommend the administration of a
Necrotizing fasciitis single dose of 2-3 mg/kg of methylprednisolone or 4-8
mg of dexamethasone over 24 hours to reduce swelling,
Is an infection of the skin and subcutaneous tissue
pain and trismus [6,16]. In the authors experience it has
characterized by extensive and rapid dissemination
been observed that warm physical means in the area
associated to a mortality rate of 20-40%. Aggressive
of infection accelerates the formation of an abscess
and extensive surgical debridement, fasciotomy and
allowing early incision and drainage.
ventilatory and circulatory support are mandatory [25].
Cervicofacial actinomycosis Antibiotic therapy
To choose the appropriate antibiotic, the stage
An infection of the soft tissues of the maxillofacial
of infection, causative microorganisms, route of
region, but may involve osseous tissue [20]. Its etiologic
administration, immunological status of the patient,
agent is Actinomyces israelii, an anaerobic gram-positive
and the spectrum and effect of action of the drug should
rod. It can develop within days, weeks, months or years
be analyzed [2].
[45].
The spectrum of the antibiotic to be administered
Clinically observed as a reddish-brown discoloration
should be in accordance with the stage of infection,
of the mandibular skin and sometimes as a suppurative
avoiding the excessive elimination of microorganisms
irregular masses on the skin [45]. Unlike other infections,
of the normal flora that induces the overgrowth of
it does not spread through anatomic planes; rather,
resistant bacteria. During inoculation, there is only a
breaks through the soft tissues forming a sinuous tract gram-positive aerobic flora, so that reduced-spectrum
that drains into the skin [20]. antibiotics such as penicillin V can be administered.
Diagnosis depends exclusively on culture results. As In cellulitis stage the flora is mixed and in abscess
an anaerobic bacteria, maximum caution must be taken stage is strictly anaerobic with a greater prevalence of
during sample collection, which should be by aspiration gram-negative bacilli. Wide-spectrum antibiotics such
preferably [45]. as amoxicillin/clavulanic acid, ampicillin/sulbactam,
cephalosporins, azithromycin, clindamycin, moxifloxacin
Elimination of the infection source, extensive
and metronidazole must be prescribed [2,19]. The
debridement, excision of the fistulous tract and
length of treatment will depend on the clinician and the
placement of a drain are necessary for resolution of the evolution of the infection; however, it is recommended
infection [20]. It should be accompanied by antibiotics as between 2 and 7 days [46].
penicillin G, penicillin V, erythromycin, cephalosporins
or clindamycin [45]. Selection between bactericidal and bacteriostatic
antibiotic is of great importance. Bacteriostatic
Airway obstruction such as macrolides and tetracycline inhibit bacterial
When the airway is compromised, the use of growth and multiplication, allowing the immune
accessory muscles such as the platysma and intercostal system cells to reach the site of infection and carry
will be observed during respiration [46], stridor and out phagocytosis. Bactericidal such as penicillin and
sibilance will be heard, and to improve ventilation, clindamycin kill bacteria without relying on the immune
the patient will present a head posture tilted forward system; therefore, are the antibiotics of choice in
or to the opposite side from the infection to align the immunocompromised patients [2,20].
upper airway with the trachea. Oxygenation less than If the infection progresses rapidly, there is no
94% along with clinical signs of airway obstruction are response to the first drug or increased coverage and
indicative for establishing a safe airway by endotracheal bactericidal effect are required, the use of a double
intubation, tracheostomy or cricothyroidotomy [10]. antibiotic regimen is indicated. Likewise, when the
The presence of trismus requires conscious intubation infection begins to spread from primary spaces,
by fiberscope [47-49]. intravenous administration of antibiotics is ideal [2].
Treatment Surgical management

Ortiz and Espinoza. Res Rep Oral Maxillofac Surg 2021, 5:055 • Page 7 of 10 •
DOI: 10.23937/2643-3907/1710055 ISSN: 2643-3907

and facilitating the irrigation of the site [46].

Follow-up
Mild OI should be evaluated at 48 hours to assess the
progress or resolution of the infection [10]. Severe OI in
which ID and drain placement was performed require
daily wound irrigation, as well as drain change every
72 hours. Between 48 and 72 hours postoperatively,
trismus, pain, inflammation and neutrophil count
should decrease [46].
If there is no favorable evolution of the patient
within 48 postoperative hours, laboratory tests, imaging
studies and rotation of antibiotic therapy should be
updated until adequate evolution is observed. The
patient can be discharged once there is remission of the
infectious process [46].
Conclusion
Figure 5: Incision and drainage of submandibular space.
Odontogenic infection is polymicrobial, being gram-
negative rods and gram-positive cocci the most frequently
Surgical management of OI is based on two found; complications derived from odontogenic
principles, which are elimination of the infection source infections can be lethal if not well controlled and the
and incision and drainage [20]. most important factor in the resolution of the infection
Elimination of the primary source of infection can is the elimination of the primary source along with
range from endodontic treatment to dental extraction. antibiotic therapy. Is a frequently consulted pathology;
However, is recommended to wait for the antibiotic to therefore, the clinician should know the basics on the
take effect for a few days in cases of trismus or acute management in order to prevent it from progressing
suppurative pericoronitis since the manipulation of and putting the patient's life at risk. This work provides
tissues in this state may cause the infection to spread information about odontogenic infection that allows to
[10]. asses its presentation and possible complications; as
well as, guidelines for diagnosis and management.
The purpose of ID is the debridement of necrotic
tissue and elimination of bacteria found in underlying Declarations
tissues. When an abscess is drained, the hydrostatic
pressure of the area decreases, improving blood flow, Acknowledgements
thus increasing the supply of defense cells and antibiotic Not applicable.
to the infected site [20] Figure 5.
Funding
The ideal time for an ID is a controversial topic. Some
clinicians advise it should be performed during the No funding was received.
cellulitis stage since it changes the environment in the Competing interests
infection, decreasing the risk of dissemination and tissue
necrosis. In deep neck infections it is almost impossible The authors declare they have no competing
to diagnose clinically or radiographically the formation interests.
of an abscess, therefore, waiting is not recommend References
[46]. On the contrary, those who advise waiting for the
1. Monasterio RB, Henriquez SG (2018) Prevalence and
formation of an abscess, based on the fact that cellulitis characterization of Odontogenic Infections in the Public
can remit with antibiotic therapy and the elimination Assistance Emergency Hospital between the Months of
of the infection source avoiding an invasive procedure July to September of the Year 2015: Prospective Study. 12.
[16]. 2. Topazian RG, Goldberg MH, Hupp JR (2002) Oral and
The incision is made under certain principles such Maxillofacial Infections. (4th edn), Philadelphia, London,
New York, St. Louis, Sydney, Toronto: W.B. Saunders
as avoiding neurovascular structures, at the lowest Company.
possible point in the tension zone, following the facial
3. Gonçalves L, Lauriti L, Yamamoto MK, Luz JGC (2013)
relaxation lines and must be supported by healthy skin Characteristics and Management of Patients Requiring
and subcutaneous tissue [46]. Intraorally, incisions are Hospitalization for Treatment of Odontogenic Infections.
made at the point of maximum swelling or through the Journal of Craniofacial Surgery 24: e458-e462.
gingival sulcus [9]. The use of a surgical drain may be 4. Ogle OE (2017) Odontogenic Infections. Dental Clinics of
necessary, allowing the exit of fluids through the wound North America 61: 235-252.

Ortiz and Espinoza. Res Rep Oral Maxillofac Surg 2021, 5:055 • Page 8 of 10 •
DOI: 10.23937/2643-3907/1710055 ISSN: 2643-3907

5. Rastenienė R, Pūrienė A, Aleksejūnienė J, Pečiulienė V, 22. Seppänen L, Lauhio A, Lindqvist C, Suuronen R, Rautemaa
Zaleckas L (2015) Odontogenic Maxillofacial Infections: A R (2008) Analysis of systemic and local odontogenic
Ten-Year Retrospective Analysis. Surgical Infections 16: infection complications requiring hospital care. Journal of
305-312. Infection 57: 116-22.
6. DeAngelis AF, Barrowman RA, Harrod R, Nastri AL (2014) 23. Yılmaz S, Baş B, Özden B, Selçuk Ü, ÇengelKurnaz S
Review article: Maxillofacial emergencies: Oral pain (2015) Deep neck infection after thrid molar extraction. J
and odontogenic infections: Oral Pain and Odontogenic Istanbul Univ Fac Dent 49: 41-45.
Infections. Emerg Med Australas 26: 336-342.
24. da Silva Junior AF, de Magalhaes Rocha GS, da Silva
7. Gordon NC, Connelly S (2003) Management of head and Neves de Araujo CF, Franco A, Silva RF (2017) Deep neck
neck infections in the immunocompromised patient. Oral infection after third molar extraction: A case report. J Dent
and Maxillofacial Surgery Clinics of North America 15: 103- Res Dent Clin Dent Prospects 11: 166-169.
110.
25. Bali R, Sharma P, Gaba S, Kaur A, Ghanghas P (2015)
8. Rich R, Fleisher T, Schwartz B, et al. (2008) Clincial A review of complications of odontogenic infections. Natl J
immunology and practice.3rd ed. St. Louis: Mosby-Year MaxillofacSurg 6: 136-143.
Book Inc.
26. Mardini S, Gohel A (2018) Imaging of Odontogenic
9. Troeltzsch M, Lohse N, Moser N, Kauffman P, Cordesmeyer Infections. Radiologic Clinics of North America 56: 31-44.
R, et al. (2015) A review of pathogenesis, diagnosis,
27. Sklavos A, Beteramia D, Delpachitra SN, Kumar R (2019)
treatment options, and differential diagnosis of odontogenic
The panoramic dental radiograph for emergency physicians.
infections: A rather mundane pathology? Quintessence
Emerg Med J 36: 565-571.
International 46: 351-361.
28. Weyh AM, Dolan JM, Busby EM, Smith SE, Parsons
10. Velasco MI, Soto NR (2012) Principios para el tratamiento
ME, et al. (2021) Validated image ordering guidelines for
de infecciones odontogénicas con distintos niveles de
odontogenic infections. International J Oral Maxillofac Surg
complejidad. Rev Chil Cir 64: 586-598.
50: 627-634.
11. Peters S, Wormuth W, Sonis T (1996) Risk Factors Affecting
29. Christensen BJ, Park EP, Suau S, Beran D, King BJ (2019)
Hospital Length of Stay in Patients With Odontogenic
Evidence-Based Clinical Criteria for Computed Tomography
Maxillofacial Infections. J Oral Maxillofac Surg 54: 1386-
Imaging in Odontogenic Infections. J Oral Maxillofac Surg
1391.
77: 299-306.
12. Park J, Lee JY, Hwang DS, Kim YD, Shin SH, et al. (2019)
30. Miloro M, Ghali GE, Larsen PE, Waite PD (2011) Peterson’s
A retrospective analysis of risk factors of oromaxillofacial
Principles of Oral and Maxillofacial Surgery. (3rd edn),
infection in patients presenting to a hospital emergency
Shelton, Connecticut: People’s Medical Publishing House-
ward. Maxillofac Plast Reconstr Surg 41: 49.
USA, 841-859.
13. Castellanos Suárez JL, Díaz Guzmán LM, Lee Gomez
31. Moncada R, Warpeha R, Pickleman J, Spak M, Cardoso
EA (2015) Medicina en Odontología: manejo dental de
M, et al. (1978) Mediastinitis from odontogenic and deep
paceintes con enfermedades sistémicas. (3rd edn), México
cervical infection. Anatomic pathways of propagation.
DF, México: El Manual Moderno 186-216.
Chest 73: 497-500.
14. Berlanga-Acosta J (2010) Cellular and molecular
32. Miller CR, Von Crowns K, Willoughby V (2018) Fatal
insights into the wound healing mechanism in diabetes.
Ludwig’s Angina: Cases of Lethal Spread of Odontogenic
Biotecnologíaaplicada 27: 255-261.
Infection. Academic Forensic Pathology 8: 150-169.
15. Haug RH (2003) The changing microbiology of maxillofacial
33. Chatterji P, Goyal I (2018) Temporoparietal and
infections. Oral and Maxillofacial Surgery Clinics of North
Infratemporal fossa abscess as a complication of dental
America 15: 1-15.
extraction-a rare and potentially lethal condition. Asian J
16. Taub D, Yampolsky A, Diecidue R, Gold L (2017) Med Sci 9: 57-60.
Controversies in the Management of Oral and Maxillofacial
34. Cariati P, Cabello-Serrano A, Monsalve-Iglesias F,
Infections. Oral and Maxillofacial Surgery Clinics of North
Roman-Ramos M, Garcia-Medina B (2016) Meningitis and
America 29: 465-473.
subdural empyema as complication of pterygomandibular
17. Brook I, Sandor G, Jeffcoat M, Samaranayake L, Vera Rojas space abscess upon tooth extraction. J Clin Exp Dent 8:
J (2007) Clindamicina para el tratamiento de infecciones e469-e472.
dentales. Revista ADM 64: 230-237.
35. González-Navarro B, Arranz-Obispo C, Albuquerque R,
18. Peters BM, Jabra-Rizk MA, O’May GA, Costerton JW, Jané-Salas E, López-López J (2017) Osteomyelitis of the
Shirtliff ME (2012) Polymicrobial Interactions: Impact on jaw (with pathological fracture) following extraction of an
Pathogenesis and Human Disease. Clinical Microbiology impacted wisdom tooth. A case report. J Stomatol Oral and
Reviews 25: 193-213. Maxillofac Surg 118: 306-309.
19. Loredo SBE, Romo MSA, Frías MÁN, Vargas LOS (2020) 36. Maraki S, Papadakis IS, Chronakis E, Panagopoulos D,
Principios fundamentales para el diagnóstico, manejo y Vakis A (2016) Aggregatibacteraphrophilus brain abscess
tratamiento de las infecciones odontogénicas. Revisión de secondary to primary tooth extraction: Case report and
la literatura. Revista Odontológica Mexicana 24: 9-19. literature review. Journal of Microbiology, Immunology and
Infection 49: 119-122.
20. Hupp JR, Ellis EI, Tucker MR (2019) Contemporary Oral
and Maxillofacial Surgery. (7th edn), Philadelphia, PA: 37. Moazzam AA, Rajagopal SM, Sedghizadeh PP, Zada G,
Elsevier 318-363. Habibian M (2015) Intracranial bacterial infections of oral
origin. J Clin Neurosci 22: 800-806.
21. Flynn T, Wiltz M, Adamo A, Levy M, McKitnick J, et al. (1999)
Predicting lenght of hospital stay and penicilin failure in severe 38. Aggarwal K, Rastogi S, Joshi A, Kumar A, Chaurasia A,
odontogenic infections. Int J Oral Maxillofac Surg 28: 48. et al. (2017) Cavernous sinus thrombosis following dental

Ortiz and Espinoza. Res Rep Oral Maxillofac Surg 2021, 5:055 • Page 9 of 10 •
DOI: 10.23937/2643-3907/1710055 ISSN: 2643-3907

extraction: A rare case report and forgotten entity. J Korean 44. Zeitoun I, Dhanarajani P (1995) Cervical cellulitis and
Assoc Oral Maxillofac Surg 43: 351. mediastinitis caused by odontogenic infections: Report of
two cases and review of literature. J Oral Maxillofac Surg
39. Carter L, Lowis E (2007) Death from overwhelming
53: 203-208.
odontogenic sepsis: A case report. Br Dent J 203: 241-242.
45. Goldberg MH (2003) Diagnosis and treatment of
40. Jiménez Y, Bagán JV, Murillo J, Poveda R (2004)
cervicofacial actinomycosis. Oral and Maxillofacial Surgery
Infecciones odontogénicas.Complicaciones. Manifestacio-
Clinics of North America 15: 51-58.
nes sistémicas. Med Oral Patol Oral Cir Bucal 9: S139-S147.
46. Flynn RT (2000) Surgical management of orofacial
41. Bullock J, Fleishman J (1985) The spread of odontogenic
infections. Atlas of the Oral and Maxillofacial Surgery
infections to the orbit: Diagnosis and management. J Oral
Clinics of North America 8: 77-100.
Maxillofac Surg 43: 749-755.
47. Greenberg S, Huang J, Chang R, Ananda S (2007) Surgical
42. Youseff O, Stefanyszyn M, Bilky J (2008) Odontogenic
management of Ludwig’s angina. ANZ J Surg 77: 540-543.
orbital cellulitis. Ophtal Plast Reconstr Surg 24: 29-35.
48. Boscolo-Rizzo P, Da Mosto M (2009) Submandibular
43. Dolezalova H, Zemek J, Tuček L (2015) Deep Neck
space infection: a potentially lethal infection. Int Infect Dis
Infections of Odontogenic Origin and Their Clinical
13: 227-233.
Significance. A Retrospective Study from Hradec Králové,
Czech Republic. Acta Medica 58: 86-91. 49. Flavell E, Stacey M, Hall J (2009) The clinial management
of airway obstruction. Curr Anaesth Crit Care 20: 102-112.

Ortiz and Espinoza. Res Rep Oral Maxillofac Surg 2021, 5:055 • Page 10 of 10 •