Diagnosis and Management of Odontogenic Oral and Facial Infections

by William L. Frydman, DDS, MS, FRCD(C); Keyvan Abbaszadeh, DMD, FRCD(C)

Substantial public and private resources are spent on the prevention and management of infections. Public health campaigns around the world have made considerable gains in the improvement of hygiene practices and disease prevention. Specific strategies have been employed, including water fluoridation that have significantly reduced dental decay. Significant efforts are directed at reducing the incidence and severity of periodontal infections, especially due to its established links with systemic health issues. The discoveries of penicillin and subsequent advances in antimicrobial therapy have significantly improved outcomes of infection treatment.

Despite this, oral infections remain among the top reasons for seeking healthcare in the world. Dentists, regardless of their focus of practice, remain the frontline practitioners for diagnosis and management of oral and facial infections.

In this article, we will outline the basic pathophysiology of infections. A systematic approach to evaluation and treatment of odontogenic infection will be outlined including surgery and pharmacotherapy as well as a discussion of potential complications.

The prerequisites for any infection include a susceptible host, virulent organism(s) and the appropriate circumstances. This is usually represented as the altered balance between disease and health or


Odontogenic infections are invariably caused by bacteria. Despite the predominance of one or two species, these infections are caused by a complex interplay of microflora that may normally inhabit the oral cavity.

Bacteria are classified based on shape, Gram stain characteristics, as well as their oxygen use and/or demand. This classification will help clinicians to arrive at the correct treatment.

Three main shapes are mentioned when discussing bacterial morphology. These are Bacilli (rods), Cocci (spheres), and Spirochetes (spirals) (Fig. 1a).


Gram Stain
Developed by Hans Christian Gram in 1884, this technique stains the peptidoglycans of the cell walls of bacteria. It divides bacteria into the two main categories of Gram positive and negative, staining deep purple and pink respectively. It is usually, the first step in identification of bacteria (Fig. 1b).

FIGURE 1B. Gram positive (purple) and Gram negative (pink) organisms seen in this photomicrograph.

Oxygen Use/Demand
Bacteria can also be divided into aerobes which need oxygen for growth or anaerobes, which find oxygen harmful. Facultative anaerobic bacteria are those that can survive oxygen rich environment, but prefer anaerobic conditions for optimal growth. Table 1 shows classification of some of the more commonly encountered oral bacteria.


Bacterial Virulence Pathobiology

For an infection to occur, bacteria need;

• a portal of entry into the body

• protection from host defenses, and

• to cause tissue damage.

Typically, this means that the infection may be initiated by the aerobic bacteria gaining entry into the body through a break in the natural barriers of the body (skin, mucosa, tears, saliva, enamel). This causes inflammation, which reduces the oxygen content of the environment, thus making it more anaerobic. This environment becomes more conducive to support anaerobic organisms. It is this synergy that causes serious infections.

If untreated or unresolved, mild infection and inflammation will progress into cellulitis, which is usually caused by aerobic bacteria. If it progresses further without resolution and/or treatment, an abscess, which is a pus-filled cavity, (typically caused by anaerobic organisms) forms. Pus is a collection of necrotic debris (usually of white blood cells and microorganism byproducts). As we see in Figure 2, chronic or long-standing abscesses, will usually lead to formation of a continually draining sinus tract, which is the body’s way of relieving pressure of infection.

FIGURE 2. Sinus tract noted on the skin as a result of a long-standing periapical infection. Note that the gutta percha traces to the apex of the lateral incisor tooth.

Spread of infection
Infections spread along the path of least resistance. Anatomical structures in the body will limit and direct the spread of infection in a known pattern. These structures include fascial layers, ligaments, tendons, muscles and bony architecture.

Fascial Spaces
Muscles are surrounded by dense layers of connective tissue called fascia, which allow for easy movement or sliding of different layers. These fascial layers create boundaries to limit the spread of infections. The spread of liquids and gases produced by infections follows a known pattern that will dissect between different fascial layers to create the typical infected fascial spaces (Fig. 3).


Muscular Attachment
The muscles of facial expression and mastication, along with others in the head and neck, originate and insert into various parts of the skeleton and soft tissues. Depending on this muscular insertion, the spread of infection can be diverted or blocked. The spread of odontogenic infection, is dependent upon the relationship of the teeth apices to the muscle attachments as this will dictate whic
h potential spaces will become involved (Fig. 4).

FIGURE 4. Effect of mylohyoid attachment (red line) of the spread of perapical infection.

Bony Architecture
Similar to muscular attachment, the relationship of the tooth apex to adjacent bone as well as bone composition, determines the path of spread of the infection. For example, the labial plate of the maxilla is generally much thinner than the palatal cortex. The roots also tend to be more labially positioned in most, but not all, cases (Fig. 5) Therefore periapical infections tend the perforate through the thinner labial plate most commonly into the vestibular space (Fig. 6). The roots of some maxillary incisors are known to have a posterior inclination. Therefore, a periapical infection of these teeth may erode through the palatal bone (Fig. 7).

FIGURE 5. The labial bone overlying the root apecies is usually thin and may be perforated to allow for spread of infection.

FIGURE 6. (above) Left mandibular vestibular swelling secondary to the extension of the gingival swelling from an infected molar.

FIGURE 7. (right) Palatal infection secondary to an infected maxillary incisor.

Other anatomic considerations
The veins of the head are unique in that they do not have valves and as such do not prevent backflow of blood. As such, this creates a potential path of spread of odontogenic or other superficial infections to the deeper structures such as the orbits, sinuses and even the brain (Fig. 8).


It must be stressed that the fascial spaces in the body are contiguous. It is quite likely that infection in a particular fascial space will spread to adjacent ones. For example, Ludwig’s angina constitutes an infection that has spread to involve the submental and bilateral submandibular and sublingual spaces) which could cause impingement and embarrassment of the airway (Figs. 9 & 10). Therefore, a seemingly ‘simple’ odontogenic infection, under the right circumstances, may have fatal complications.

FIGURES 9 & 10.

FIGURE 9A. Clincal images of Patient with Ludwig’s Angina. Note the elevation of the floor of mouth (left image) and submandibular swelling (right).


FIGURE 10. Axial (left) and sagittal CT scans of a patient with Ludwig’s Angina. Note the loculations of infection (arrows).

Patient Evaluation
The approach to evaluation and management of the infected patient is no different than any other dental patient. Patient’s chief complaint and history of illness will provide invaluable clues leading to the proper diagnosis. A patient’s medical history including any systemic disease which may cause immune compromise will impact the management of the patient, as these patients will need more aggressive management. See Table 2 for a list of some of these conditions.


The above will guide the clinician’s investigation for identifying the cause of the infection. As part of the examination of the patient, vital signs, including temperature, need to be obtained since this will help to determine the severity of the infection or possible systemic involvement of the patient such as sepsis. Any sign of trismus points to involvement of the muscles of mastication, while any changes in patient’s voice, or dysphagia (difficulty in swallowing), usually means involvement of the deeper structures of the hypopharynx and possible impending airway compromise.

The presence of fever, trismus, dysphagia (difficulty swallowing), dysphonia (altered speech) or difficulty breathing herald a more serious infection that would need to be dealt with urgently and aggressively.

It is only after a thorough clinical that imaging and appropriate laboratory studies are obtained to help guide the treatment.

Clinical Presentation
Infection invariably is accompanied with inflammation. Hallmarks of inflammation are rubor (redness), tumor (swelling), calor (warmth), dolor (pain), and functio laesa (reduced function) (Fig. 11). This is the body’s way of trying to mobilize its local and systemic immunity apparatus against the offending source(s).

FIGURE 11. Showing submandibular infection with hallmarks of inflammation.


Principles of Treatment
The most important tenets of treatment of infections are removal of the offending source and proving path of drainage. Therefore, infection is often a surgical disease requiring the “tincture of cold steel” for a cure.

Ancillary measures such as pharmacotherapy are aimed as supportive measures for the host, especially in cases of immune compromise. They are not meant to replace surgical intervention unless the infection is very early in its stages of development

Infections should be treated as soon as possible. No benefit is gained by “waiting for an abscess to form”, as this delay may carry grave consequences and may be potentially fatal.

Surgical Management
As with any other surgical procedure, the primary requirements for surgical treatment of an infection are good access to the involved site, profound anaesthesia, and sound knowledge of anatomy.

Adequate access is necessary to ensure the offending source (such as necrotic tooth) can be removed in its entirety. It should also allow for proper drainage of the infection. Timely and proper access will mitigate future issues such as scarring, deformity or functional deficits.

Due to the typical acidic pH of infected tissue, injected local anesthetics, which are more alkaline, become ionized and therefore would not be able to cross the nerve membrane and provide profound anaesthesia. Despite this, the clinician is obligated to ensure patient comfort throughout the peri-operative period, by employing alternate pain management strategies. The use of nerve blocks as well as adjunctive sedation may be beneficial in management of the apprehensive patient.

Sound knowledge of the anatomy of the affected area, will ensure that the infection is treated appropriately, efficiently, while morbidity and complications are minimized. This will allow for optimal drainage of infection and avoidance of vital structures such as nerves and blood vessels.

Incision and Drainage
Incision and drainage (I&D) allows for decompression of infection loculation(s), which will provide significant relief for the patient. It will also provide a portal for irrigation and placement of the drain. Additionally, it allows for obtaining appropriate samples for culturing the offending microorganisms. More importantly, I&D will alter the chemical environment to one that is more aerobic, thus less optimal for the more virulent anaerobic bacteria.

In their 2011 article, Shanti and Aziz found no benefit in delaying the drainage of an infection until an abscess was formed. In fact, the majority of infections that were diagnosed as cellulitis were indeed abscesses. The delay in treatment will only lead to more complications and morbidity.

Typically, I&D is done at the same time as the removal of the offending source. However, there are times that due to the acuity of the infection, drainage is done first in conjunction with pharmacologic therapy while the definitive treatment is planned and carried out at a later time. This delay should be as minimal as possible as exacerbation of the infection will be likely.

The incision should be placed in such a way that it will avoid vital structures. It should also avoid any areas of mucosal or skin breakdown, such as a sinus tract as delayed healing or deformities may result (Fig. 12).

FIGURE 12. Avoid placing the incison or the drain in the opening of the spontaneous drainage.

Contrary to popular belief, the sharp incision need not be “carried to bone”. It only has to be deep enough to pass through the epithelium and underlying connective tissue. The subsequent blunt instrumentation will then explore all spaces including periosteal spaces. This method will prevent unnecessary injuries.

A patent drainage path is paramount in ensuring the resolution of an infection. In the case of a periapical odontogenic infection, the socket of the extracted tooth will provide such a path. However, if there is extension of the infection to contiguous spaces, and a mucosal incision is made, this osteum should remain patent. In these cases, a pliable material, such as a Penrose drain, needs to be secured for a few days to allow for proper drainage. This drain also provides a portal for irrigation of infection (Figs. 13-15).

FIGURE 13. Diagram showing incision and drainage of intra-oral vestibular infection.

a. Incision through the mucosa

b. Blunt exploration of infection loculation

c. Placement of Penrose drain

d. Drain secured with suture

FIGURE 14. Intra-oral incision and drainage of an oral vestibular abscess.

A. Mucosal incision.

B. Purulent drainage is expressed after blunt instrumentation.

C. Penrose drain place in the loculation of infection.

D. Drain is secured with a suture to healthy mucosa.

Extra-oral incision and drainage of submandibular abscess.

A. Sharp incision through the skin

B. Blunt exploration of infection loculation

C. Expression of purulence

D. Drain placed and secure with a suture to skin

Even though, infection is a surgical disease, antibiotics have changed the way clinicians manage infections. These drugs are a crucial adjunct in appropriate treatment of patients.

When treating an infection, the overriding consideration is if an antibiotic is indeed necessary. That is, are the symptoms those of an infection, and if so, are they related to a bacterial infection. A clear example of this would be a reversible pulpitis since bacterial involvement of the pulp has not been established.

The cost of the antibiotic, spectrum of coverage as well as toxicity, and side effects are all-important considerations in the choice of antibiotic use.

Antibiotics can be classified into two main categories; bacteriostatic, those that retard the growth of the microorganisms, thus allowing the host to eradicate them and bactericidal, those that kill bacteria. The former relies on a competent immune status and the latter is usually selected for more serious infection.

Each group of antibiotics, exert their effect on a different component of the bacterial cell structure (Fig. 16). Some antibiotics are considered narrow spectrum, affecting a small group of organisms, while others have a broader spectrum.

FIGURE 16. Cell wall structure showing sites of action of antibiotics.

Ideally, antibiotics are chosen after identification of the offending bacteria, and culture and sensitivity testing. This will allow the utilization of the most appropriate antibiotic for the target organism. However, since the majority of oral infections are of mixed flora, the goal of treatment, is to target the most likely culprit(s) and disrupt the bacterial synergy. This will usually lead to an empiric choice of antibiotics, i.e. based on our past experiences.

In general, antibiotics are indicated if the bacterial infection is rapidly progressing, of diffuse and systemic involvement, or if host immune compromise is suspected. However, if the infection is very mild and focal, and the source of infection is eradicated, antibiotics may not be needed.

Penicillin, is a bactericidal antibiotic with good oral absorption. It also has a good spectrum of coverage against the main oral virulent microflora. It is well tolerated by patients and has a low toxicity profile.

Amoxicillin, has a more broad spectrum of coverage than penicillin, but it is an acceptable alternative. Its dosing regimen (three times daily) may lead to better compliance.

Even though, some patients report a history of rash as a child with the use of penicillins, they have not undergone further testing to confirm the presence of a true allergy. In these cases, one may consider cephalexin, a first-generation cephalosporin. One has to be mindful that there is a potential risk of cross-allergenicity in up to 10 percent of cases.

In the case of true anaphylactic penicillin allergies, clindamycin would be the appropriate substitute. It is also used for more serious infections as it has excellent coverage for anaerobes. Its absorption is equally good orally and parenterally.

A multitude of other antibiotics exist that may be of benefit. A prudent practitioner should however weigh the risks vs. benefits of any medication used.

Failure to respond to an antibiotic can be due to; poor compliance such as inconsistent use, inadequate dose (based on body weight) and organism resistance. In the case of organism resistance, the clinician should choose another antibiotic. Alternatively, combination therapy may be employed. Metronidazole may be used with penicillin or amoxicillin, as it would provide coverage against ß-lactamse producing organisms, which render penicillins ineffective. The combination of amoxillin and clavulonic acid (Clavulin®) is another example of an antibiotic that is effective against ß-lactamse producing organisms.

We hear a lot about patients who develop ‘upset stomachs’ due to the use of antibiotics. Antibiotic associated colitis (AAC) is an extension of the therapeutic effect of these drugs. It is usually seen with the use of broad-spectrum antibiotics, as they alter the balance of the normal bacterial inhabitants of the GI tract, and selecting more virulent ones, such as clostridium difficile. This could be seen with the use of any antibiotic, but the more common culprits are amoxicillin, cephalosprins and clindamycin. Prevention of AAC is prudent, starting with narrow spectrum antibiotic selection. Probiotics, such as those found in yogurt, are also thought to be helpful. Once developed, the AAC is best treated with the termination of the causative antibiotics, supportive therapy such as hydration, as well oral metronidazole or vancomycin. In suspected cases of AAC, help of the primary physician should be considered.

Dentists who are comfortable with surgical treatment quite capably treat infections on a daily basis with I&D, removal of the infection source and adjunctive antibiotic management in an outpatient or clinic setting. There are however, instances that the patient may need to have more extensive surgery and medical support as well as continued inpatient observation in a hospital. In these cases, enlisting the help of an oral and maxillofacial surgeon would be advisable. Some of these situations are listed in table 3.


Follow Up Care
Patients who undergo incision and drainage treatment along with antibiotic therapy should be followed closely to ensure the infection is resolving. Patients that have received intraoral procedures should be encourage to rinse frequently with warm water as well as chlorhexidine 0.12 percent, twice daily. Seeing a patient daily for the first few days is not unreasonable. Instructions should be provided that encourage the patient to contact the practitioner if they feel their symptoms are worsening. Remember that infection patients can decline rapidly for the many reasons discussed.

Infections continue to challenge clinicians daily. Even though most remain focal and quite limited, when left untreated, they may have significant systemic involvement with potentially morbid, and possibly fatal, consequences.

Proper antibiotic selection has made combatting infections more predictable and improved patient outcomes. However, infection remains a surgical disease. Early, thorough, and definitive treatment directed at removal of the source and providing path of drainage will ensure proper care of the patient.

Don’t let the sun set on an untreated infected patient! OH

Dr William Frydman is an Oral and Maxillofacial Surgeon at the Interface Centre in London Ontario. After completing his DDS at the University of Toronto, he completed an Internship at Mt. Sinai Hospital and a residency in OMFS at the University of Illinois in Chicago.

William is past Chief of Surgery at St Thomas Elgin General Hospital where he also held the position of VP Medical Staff. William is a Fellow and an examiner for the Royal College of Dentists of Canada and a Diplomate of the American Board of Oral and Maxillofacial Surgery. He is an Adjunct Clinical Professor at the University of Western Ontario

Dr. Keyvan Abbaszadeh is an Oral and Maxillofacial Surgeon at the Interface Centre, in London, Ontario. He completed his training at Tufts University in Boston followed by his residency at University of Illinois at Chicago.

Keyvan is a Fellow of, and an examiner for, the Royal College of Dentists of Canada. He is also a Diplomate of the American Board of Oral and Maxillofacial Surgery. Keyvan is an Adjunct Clinical Professor at the University of Western Ontario.


1.  Oral and Maxillofacial Infections, 3rd Edition. Topazian, RG, Goldberg, MH. WB Saunders Co. 1994.

2. Peterson’s Principles of Oral and Maxillofacial Surgery, 3rd Edition. Miloro, M, et. Al. People’s Medical Publishing House. 2012.

3. Anatomy for the Surgeons. The Head and Neck, 3rd Edition. Hollinshead, WH. Lippincott, Williams, and Wilkins, 1982.

4. Essential Microbiology for Dentistry, 4th Edition. Samaranayake, L. Churchill Livingston 2012.

5. Shanti R., Aziz S. Should We Wait for Development of an Abscess Before We Perform Incision and Drainage?

6. Oral Maxillofacial Surg Clin N Am 23 (2011) 513–518 William L Frydman DDS MS FRCD(C)