Oral Facial Infection of Dental Origin: A Guide for the Medical Practitioner

Etiology

Dental Caries

Dental caries develop through the interaction of tooth structure, dental plaque on the tooth surface, and fermentable carbohydrates. Salivary composition and genetic predisposition further influence susceptibility to caries formation.[4]

Bacteria within the dental biofilm metabolize fermentable carbohydrates, eg, glucose, fructose, sucrose, and maltose, derived from the diet. This metabolic activity produces organic acids, primarily lactic acid, which lower the pH and initiate demineralization of the outer layer of the dental structure. Once dietary sugars are cleared through swallowing and dilution by saliva, the acids become neutralized by the saliva's buffering capacity. As the pH returns to neutral, the biofilm becomes saturated with calcium, phosphate, and fluoride ions, which arrest demineralization and support remineralization of the enamel surface.[4] This demineralization-remineralization cycle occurs with each exposure to fermentable sugars. Individuals with diminished salivary flow experience impaired buffering and clearance, heightening their risk for dental caries. Frequent sugar intake promotes persistent acidic conditions, which shift the microbial composition of the biofilm toward more acidogenic and cariogenic species. When mineral loss outpaces replacement, the earliest clinical sign appears as a "white spot" lesion, also referred to as an incipient carious lesion.[4]

White spot lesions represent a reversible stage of dental caries and may undergo remineralization with noninvasive strategies, including topical fluoride and behavioral modifications, eg, improved oral hygiene and reduced sugar consumption. Prompt dental referral following identification of such lesions during clinical evaluation supports timely intervention. Without appropriate management, incipient lesions may progress to enamel microcavities, which eventually collapse to form visible macroscopic cavities.[4]

Pulp Involvement

Pulpitis is the inflammation of the dental pulp, which can be caused by bacterial by-products reaching the pulp from dental caries, bacteria entering the pulp through the apical foramen from a periodontal infection, or through a tooth fracture.[5] Furthermore, traumatic and chemical insults can also result in pulpal inflammation.[6] The early stage of pulpitis elicits mild, intermittent dental pain, typically triggered by thermal stimuli, eg, cold drinks, but without spontaneous pain. This is known as reversible pulpitis, and treatment involves the removal of the carious tissue and the placement of a restoration.

The dental pulp can be irreversibly damaged due to persistent inflammation, leading to constant, spontaneous, and acute dental pain that is poorly localized. Irreversible pulpitis is a primary reason patients present to the emergency department.[7] Irreversible pulpitis must be referred to a dentist, as the standard of care is partial or complete pulp removal.[6]

Antibiotics do not play a role in the management of irreversible pulpitis, as clinical signs of infection, eg, swelling of the adjacent mucosa, typically do not accompany this condition.[7] Current evidence provides limited support for the effectiveness of antibiotics in reducing dental pain or decreasing the need for analgesics in patients with untreated teeth affected by irreversible pulpitis.[8] Consequently, antimicrobial therapy is not initiated before referral for definitive dental treatment. Over time, irreversible pulpitis may progress to ischemia and necrosis of the dental pulp, often leaving the affected tooth asymptomatic despite underlying pathology.

An apical abscess can further complicate pulp necrosis. Apical abscess, dentoalveolar abscess, and odontogenic abscess are usually used interchangeably to describe the localized collection of pus around the periapex due to the spread of infection of the root canal.[9] Acute or chronic forms of periapical abscess can develop.

Patients with an acute apical abscess report mild to severe pain and swelling. The tooth is usually extremely sensitive when touched or tapped with an instrument (percussion). In most cases, the swelling develops intraorally. Systemic symptoms may develop, including fever, fatigue, and lymph node enlargement (lymphadenopathy). In the maxilla, acute apical abscesses drain through the buccal or palatal bone plates into the buccal cavity. In the mandible, they may drain buccally or lingually into the oral cavity or spread into the fascial spaces of the neck, leading to cellulitis and potentially severe complications.[9] Apical abscesses in the mandibular molars can extend to the sublingual, submandibular, and submental spaces. This condition is known as Ludwig angina, a life-threatening condition that obstructs the airways if not managed in time.[10]

An apical abscess generally presents as a localized infection that does not warrant antimicrobial therapy before referral to a dental practitioner.[5] Antibiotic treatment becomes necessary only when clinical signs indicate systemic dissemination of the infection, eg, the presence of fever or cellulitis.[5] In such cases, broad-spectrum antibiotics are preferred, with amoxicillin/clavulanate serving as the most frequently prescribed agent.[11]

Management of an acute apical abscess involves drainage of the affected tooth, followed by endodontic therapy to eliminate necrotic pulp tissue and restore the tooth's structural integrity. In cases where the tooth cannot be preserved, extraction serves as an appropriate alternative to eliminate the source of infection.

Periodontal Disease

Periodontal infections initially affect the gingival tissues, leading to gingivitis, which can progress to periodontitis in susceptible individuals. Periodontal disease results from poor dental hygiene, the accumulation of plaque and calculus, and subsequent inflammation of the tissues surrounding and supporting the teeth, including the gingiva, periodontal ligament, and alveolar bone. The etiology of periodontitis is multifactorial. While bacteria initiate it, the clinical presentation and outcome of the different forms of the disease are determined by the inflammatory response and modifying and predisposing factors. The main risk factors for periodontal disease include tobacco smoking and diabetes mellitus. The disease progression appears to be regulated by environmental and genetic factors specific to each patient.[12][13]

Epidemiology

Approximately 13% of adults seek dental care for dental infections or toothaches within 4 years, and an estimated 1 in 2,600 individuals in the United States require hospitalization due to dental infections.[14][15] Over 20% of the population lives with untreated dental caries, while nearly 75% have received at least 1 dental restoration. Periodontitis affects a significant portion of the adult population, with an estimated prevalence of 35% among Americans aged 30 to 90.[16]

Socioeconomic status plays a critical role in the distribution of dental caries. Individuals living at or below 100% of the federal poverty level experience untreated dental caries at a rate exceeding 41.9%, more than 2.5 times higher than the 16.6% observed in those living at or above 200% of the poverty threshold. Dental caries affect 90% of adults and 42% of children aged 6 to 19, with the prevalence remaining relatively stable across age groups.[17] However, adolescents aged 12 to 19 exhibit lower rates of untreated caries compared to children aged 5 to 11.

Certain populations are at a heightened risk of developing dental abscesses. Individuals with type 1 or 2 diabetes demonstrate a significantly greater prevalence and severity of odontogenic abscesses compared to nondiabetic counterparts, even after controlling for comorbid conditions, eg, periodontal and cardiovascular disease. Patients with periodontal disease also face elevated risk, with data indicating a markedly higher odds ratio for acute periapical abscesses, independent of diabetes status and tobacco use.[18][19][20]

Obese individuals have a higher prevalence of periapical abscesses compared to average-weight individuals, with risk remaining significant after adjustment for diabetes, smoking, and periodontal disease. Older adults are at increased risk due to higher rates of periodontal disease, comorbidities, medication-induced xerostomia, and barriers to dental care. Individuals with poor oral hygiene, low socioeconomic status, tobacco use, unhealthy alcohol use, or limited access to dental care are also at elevated risk, as these factors contribute to the development and progression of dental caries and periodontal disease.[21][22]

Populations at increased risk for developing dental abscesses specifically due to socioeconomic factors include individuals living in poverty, those without dental insurance or with public insurance, people experiencing homelessness, residents of rural or urban underserved areas, and those living in communities with dental professional shortages. Additional at-risk groups are racial and ethnic minorities, including Asian, Black, Hispanic/Latino, Native American/Alaska Native, and Native Hawaiian/Pacific Islander populations, adults with disabilities, and individuals living in institutional settings. These populations face barriers, eg, limited affordability and accessibility of dental care, which contribute to higher rates of untreated dental caries and periodontal disease, the primary precursors to dental abscesses.

The United States Preventive Services Task Force highlights that these disparities are driven by social determinants of health, including low income, lack of insurance, and geographic isolation, all of which limit access to preventive and restorative dental services and increase the risk of severe oral infections.[23] Furthermore, cost-of-living crises and food insecurity can exacerbate risk by limiting the ability to purchase oral hygiene products and increasing reliance on high-sugar diets, further elevating the risk of dental disease and subsequent abscess formation. Socioeconomic gradients in dental health are consistently observed, with lower education, income, and occupational status associated with higher prevalence of dental problems and reduced utilization of dental care, even after adjusting for behavioral and psychosocial factors.[24][25][26]

Additional populations at increased risk for dental abscesses include individuals with a history of dental trauma, failed endodontic procedures, or underlying immunocompromising conditions. Certain demographic factors, eg, female sex and African American race, have also been linked to higher prevalence rates in specific populations. The highest-risk groups encompass individuals with diabetes mellitus, periodontal disease, obesity, and advanced age. Poor oral hygiene practices further elevate the risk, particularly when combined with social determinants that restrict access to preventive and restorative dental care. These intersecting factors contribute to a greater burden of disease, underscoring the importance of early identification and targeted interventions within vulnerable populations.

Pathophysiology

The pathophysiology of dental infections involves a complex interaction among microbial invasion, tissue destruction, the host inflammatory response, and anatomical pathways of spread. Many infections remain localized and self-limiting when managed appropriately; however, delayed recognition or inadequate treatment can result in extensive tissue involvement and serious systemic complications.

An accurate understanding of these underlying mechanisms supports early diagnosis, facilitates informed clinical decision-making, and enables prompt referral to dental or surgical specialists when necessary. Timely intervention remains essential to prevent progression to life-threatening sequelae, eg, deep neck space infections, airway compromise, or sepsis.

History and Physical

Dental Caries and Dental Pulp State

Caries can be acute or chronic, and may appear as brown-yellow, soft, or black and hard cavities. Pulp exposure may be seen. Incipient caries are more challenging to identify and represent the first clinical manifestation of caries. Incipient caries are white, opaque, irregular spots that may appear on any tooth surface and are more prevalent in areas of plaque stagnation, eg, the junction of the gingival tissue and the tooth surface.

Patients with reversible pulpitis typically present with a toothache triggered by stimuli, eg, hot or cold drinks or foods. Irreversible pulpitis presents as unprovoked tooth pain that usually exacerbates overnight. A periapical abscess may present as a palpable swelling. A dental abscess can originate from the pulp, periodontal structures, or both. More severe complaints, including fever, facial edema, trismus, dysphagia, or dysphonia, can be symptoms of a more serious dental infection that has extended into deep neck spaces. Patients may be in respiratory distress or hemodynamically unstable with sepsis.[27]

Periodontal Disease

Patients with gingivitis and periodontitis often report a history of halitosis and bleeding during toothbrushing. Pain generally does not accompany periodontal diseases, except in cases of necrotizing periodontal disease, where discomfort becomes a prominent feature.

Gingivitis refers to localized inflammation of the gingival tissues, primarily resulting from the accumulation of dental plaque on the tooth surfaces. Clinically, gingivitis is characterized by swollen, erythematous gums that bleed easily.[28] The condition does not involve periodontal pocket formation, as the gingival sulcus remains within normal depth.[29]

Periodontitis involves the apical migration of the junctional epithelium and the formation of periodontal pockets. As the disease progresses, clinical signs may include gingival recession, detachment of the dental papilla, alveolar bone loss visible on radiographic imaging, tooth mobility, and fremitus.[30] The degree of destruction varies depending on individual risk factors and the severity of the disease.

Pericoronitis represents a specific form of odontogenic infection characterized by inflammation of the soft tissues surrounding the crown of a partially erupted tooth, most often the mandibular third molars. This condition frequently initiates localized dental infections and, in more severe presentations, can serve as a source of deeper fascial space infections with systemic consequences.

Clinical History

A detailed and focused history provides critical insight into the nature of the infection and helps identify potential red flags.

History of present illness

Chief complaint and symptom analysis should include characterization of pain, including its location, onset, duration, nature, radiation, and factors that aggravate or relieve it. Assessment of swelling should determine its progression, precise location, and whether fluctuation is present. Systemic symptoms, including fever, malaise, and chills, may signal the spread of infection. Additional symptoms, eg, difficulty chewing, dysphagia, impaired speech, trismus, halitosis, or a bad taste in the mouth may also suggest underlying purulence or advanced disease.

The dental and medical history should document the following:

• Recent dental procedures or trauma (eg, extraction, root canal, fillings)

• History of recurrent infections or untreated caries

• Presence of partially erupted teeth (eg, third molars)

• Underlying systemic conditions:

  • Diabetes mellitus

  • Immunosuppression (HIV/AIDS, steroids, chemotherapy)

  • Previous episodes of cellulitis or abscess

Physical Examination

Extraoral findings

Findings on extraoral examination associated with oral dental infection include:

• Facial asymmetry, swelling, or erythema

• Fluctuance or tenderness on palpation

• Lymphadenopathy (especially submandibular, cervical)

• Signs of fascial space involvement (eg, fullness of the submandibular or buccal regions)

• Evaluate the airway:

  • Voice changes (“hot potato” voice)

  • Drooling or inability to manage secretions

  • Stridor or respiratory distress (indicates potential airway compromise)

Intraoral findings

Clinicians should assess the dentition for carious lesions, fractures, or mobility, and evaluate the gingival tissues for inflammation, recession, or abscesses. Additional findings may include:

• Pus, sinus tracts, or draining fistulae
• Swelling of the vestibule, floor of the mouth, or palate
• Pericoronal flap (operculum) in pericoronitis

Additionally, trismus should be measured by interincisal distance, and clinicians must differentiate cellulitis (induration) from abscess (fluctuation).

Risk Stratification

Clinicians must determine the severity of the infection and identify high-risk features necessitating urgent intervention or hospitalization.

Mild to Moderate Infections

Mild dental infections typically involve localized pain or swelling without systemic symptoms and do not impair oral intake or airway function.

Severe Infections and Red Flag Signs

Severe dental infections associated with red flag signs include systemic toxicity (eg, fever above 38.5 °C, tachycardia, or hypotension)alongside deep space involvement (eg, submandibular, parapharyngeal, or masticator spaces), trismus, dysphagia, rapidly spreading cellulitis, airway compromise, or immunocompromised status.

Evaluation

Evaluating a patient with a dental infection demands a systematic, thorough, and timely approach to distinguish localized conditions from potentially life-threatening complications. Dental infections possess the capacity to spread rapidly through fascial planes, leading to airway compromise or sepsis. Clinicians, especially those working in emergency or primary care settings, must assess both local and systemic manifestations of the infection. A comprehensive evaluation involves a structured combination of patient history, physical examination, risk stratification, and, when indicated, diagnostic imaging and laboratory testing.[31]

Diagnostic Imaging

Imaging becomes necessary when deep-space infection, abscess formation, or unusual progression is suspected. A panoramic radiograph (orthopantomogram) helps identify periapical lesions, impacted teeth, or osseous involvement. Periapical radiographs allow for detailed assessment of individual teeth. Contrast-enhanced computed tomography imaging serves as the gold standard for evaluating deep-space involvement and distinguishing cellulitis from abscess. Ultrasound offers a noninvasive method for detecting superficial abscesses, especially in the submandibular or buccal regions.

Laboratory Investigations

In moderate to severe or systemic presentations, laboratory testing provides valuable diagnostic support. A complete blood count (CBC) may reveal leukocytosis, while C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) indicate inflammatory activity. Blood cultures are recommended when sepsis or unexplained fever is suspected. Blood glucose measurement assists in identifying undiagnosed diabetes or evaluating glycemic control in patients with known diabetes, given the strong association between hyperglycemia and poor infection outcomes.

Treatment / Management

Oral Facial Infection Management

Patients with odontogenic infections frequently seek care in emergency departments due to acute dental pain, most often resulting from pulpitis or an acute periapical abscess. Clinicians must evaluate these individuals for signs indicating that the infection has extended beyond the oral cavity or caused systemic involvement, which may necessitate emergency intervention. Any indication of potential airway compromise warrants immediate transfer to a facility equipped to manage the airway, with prompt notification of the oral and maxillofacial surgical team.[32] 

Red flag symptoms suggesting advanced or rapidly progressing infection include marked trismus, difficulty swallowing, drooling, limited tongue mobility, a swollen or firm floor of the mouth, and the characteristic "hot potato" voice.[33] Patients presenting with Ludwig angina require urgent hospital admission, airway stabilization, and intravenous antibiotic therapy.[33]

When emergency intervention is not required, referral to a dental practitioner remains essential for definitive care.[32] The standard of care for dental infections focuses on surgically removing the source of infection.[32] Only dental professionals are qualified to perform this definitive treatment. In cases of irreversible pulpitis, root canal therapy serves as the primary intervention. For acute periapical abscesses, initial management involves draining the swelling or accessing the pulp chamber through the occlusal surface of the tooth. This procedure is followed by either root canal therapy to eliminate the infection or extraction of the tooth when it cannot be restored.

Antibiotic Therapy

Antibiotics play a secondary role in managing dental infections. They are only prescribed as adjuvants to surgical treatment when patients exhibit signs of local or systemic infection spread, including cellulitis, fever, lymphadenopathy, or fatigue. In this case, antibiotics can be prescribed before referral.

The American Dental Association recommends that amoxicillin is the preferred first-line antibiotic for most dental infections due to its efficacy against oral pathogens and favorable adverse effect profile. The typical adult dose is 500 mg every 8 hours or 875 mg every 12 hours. Penicillin VK is an alternative first-line agent; however, amoxicillin is generally preferred due to its broader coverage and better gastrointestinal tolerability. Antibiotics should be discontinued 24 hours after symptom resolution, and patients should be reevaluated within 3 days of starting therapy.[34](A1)

For patients with a true penicillin allergy, the American Dental Association recommends alternatives, eg, clindamycin 300 mg every 8 hours, cephalexin 500 mg every 6 hours, or azithromycin 500 mg on day 1, followed by 250 mg daily for 4 days. However, clindamycin carries a significant risk of Clostridioides difficile infection, and azithromycin has higher resistance rates among oral pathogens; thus, these agents should be used with caution, and patients should be monitored for adverse effects.[34](A1)

In severe or treatment-resistant cases, or when anaerobic infection is suspected, adjunctive metronidazole may be combined with amoxicillin to broaden antimicrobial coverage. Alternatively, amoxicillin/clavulanate may be selected to enhance efficacy against anaerobic organisms. Hospitalized patients with severe odontogenic infections often respond well to intravenous ampicillin/sulbactam or a cephalosporin. For individuals with beta-lactam allergies, moxifloxacin or cotrimoxazole may serve as effective alternatives.[34][35](A1)

Definitive dental treatment, eg, drainage, extraction, or root canal therapy, remains the cornerstone of managing odontogenic infections. Antibiotics serve only as adjunctive therapy and should not be used as a standalone treatment, except when systemic involvement or the spread of infection necessitates their use.[36] Timely surgical intervention by a dental professional ensures optimal resolution and prevents further complications.

Analgesics

Nonopioid analgesics are recommended as first-line therapy. The American Dental Association and the United States Centers for Disease Control and Prevention recommend NSAIDs, eg, ibuprofen 400 mg every 6 to 8 hours with a maximum total dosage of 2,400 mg/day or naproxen sodium 440 mg every 8 to 12 hours (maximum 1,100 mg/day) either alone or in combination with acetaminophen 500 to 1,000 mg every 6 hours with a maximum total dosage of 4,000 mg/day.[1][4][7][4] The combination of ibuprofen and acetaminophen provides superior analgesia and safety compared to opioids, and is associated with the highest proportion of patients achieving maximal pain relief.[37][38][39] (A1)

If NSAIDs are contraindicated (eg, due to gastrointestinal, renal, or cardiovascular comorbidities), acetaminophen alone at full therapeutic dose is recommended.[37] Opioids (eg, hydrocodone or oxycodone in combination with acetaminophen) are reserved for rare cases where pain control is inadequate with nonopioid regimens. When used, opioids should be prescribed at the lowest effective dose, for the shortest duration (rarely exceeding 3 days), and with informed consent and risk counseling, particularly in adolescents and young adults.[37][38][39] Acetaminophen-codeine combinations are effective but not superior to acetaminophen alone and carry opioid-related risks.[38][40] (A1)

Short-acting local anesthetics (eg, 2% lidocaine with 1:100,000 epinephrine or 4% articaine with 1:100,000 epinephrine) can provide immediate pain relief, while long-acting agents (eg, 0.5% bupivacaine with 1:200,000 epinephrine) may be used for extended effect.[37] Topical benzocaine (10% to 20%) may be considered for short-term relief.[37] In pediatric and special needs populations, nonopioid analgesics are preferred, with careful attention to dosing and potential drug interactions. Analgesic selection should always consider comorbidities, medication history, and contraindications.[37](A1)

Differential Diagnosis

The differential diagnosis of dental infections varies and is based on the presenting symptoms. Localized dental infections can be mistaken for salivary gland pathologies, including sialadenitis, sialolithiasis, and salivary gland tumors. Sialadenitis and sialolithiasis can present with localized facial edema, erythema, and tenderness. A salivary gland tumor can present as a unilateral facial mass. Patients with sinusitis can complain of warm, erythematous skin over the maxillary sinus.

Prognosis

The prognosis for uncomplicated dental infections is good. Dental infections that spread to deeper neck structures carry a worse prognosis and a significant mortality rate. Deep neck infections have a mortality rate ranging from 1% to 25%, and mediastinitis can carry a mortality rate of up to 40%.[41][42]

Complications

Serious complications can arise from dental infections as they spread to the potential head and neck fascial planes. Various paths for the dissemination of the infection are present. They can spread contiguously to the jaw, causing osteomyelitis. Furthermore, infections of the lower second and third molars can spread to the sublingual, submandibular, and submental spaces, leading to Ludwig angina.

In children, dental infections can spread to the retropharyngeal or parapharyngeal space, resulting in a retropharyngeal abscess or a parapharyngeal abscess, respectively. Descending necrotizing mediastinitis is a severe, life-threatening infection caused by the descent of dental infection through deep and superficial fascial planes. Dental infections spreading and causing cavernous sinus thrombosis have been reported.[43] Very rarely, dental infections result in meningitis and subdural empyema.[44] Dental infections and tooth extractions can lead to the hematogenous spread of bacteria (bacteremia), which may result in endocarditis, particularly in patients with valvular heart disease or prosthetic heart valves.[27]