Dental Infections

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Continuing Education Activity

This activity is designed to provide healthcare professionals with essential knowledge and skills to effectively evaluate and manage dental infections, a common presentation in the medical setting, particularly in emergency departments. Dental infections, with dental abscesses being the most frequent culprits, can pose significant challenges for medical practitioners. This course will cover the origins of dental infections, often from necrotic pulp, periodontal pockets, or pericoronitis, and how they can spread to affect facial structures. Historical context will also be provided, shedding light on the gravity of dental infections in the past and highlighting the remarkable improvements in dental hygiene, modern dentistry, and antibiotic use that have made them rarely life-threatening today.

The course will address the various reasons patients seek medical attention for dental infections, such as financial constraints, limited access to dental care, dental anxiety, and misconceptions about antibiotic therapy. In such cases, medical practitioners play a pivotal role in managing dental infections, even though their knowledge in this area may be limited. By the end of this CME, participants will be equipped to identify early-stage dental infections, offer crucial oral health education, and make informed referrals to dental practitioners, ultimately improving patient outcomes. This educational program will empower medical professionals to confidently navigate the evaluation and management of dental infections and highlight their indispensable role in addressing this common medical concern.

Objectives:

  • Identify the etiology of dental infections.

  • Assess the presentation of a patient with a dental infection.

  • Compare the treatment options available for dental infections.

  • Compare interprofessional team strategies for improving coordination and communication to advance care for patients with dental infection and improve outcomes.

Introduction

Dental infections originate in the tooth or its supporting structures and can spread to the surrounding tissues. When facial structures are compromised, the infection originates from necrotic pulp, periodontal pockets, or pericoronitis. Dental infections have always been common and were one of the leading causes of death hundreds of years ago. The London, England Bills of Mortality in the 1600s reported teeth infections as the 5th or 6th leading cause of death.[1] In 1908, it was believed that dental infections were associated with 10% to 40% mortality.[2] Fortunately, due to improved dental hygiene, modern dentistry, and antibiotics, dental infections are rarely life-threatening today.

Dental infections are not an uncommon presentation in the medical setting, mainly in emergency departments. Of all dental-related visits, dental abscesses account for the majority of cases.[3] Patients may present to a medical hospital instead of a dental practice due to a variety of reasons, including financial constraints, lack of access to dental attention, dental anxiety, and the disbelief that antibiotics alone can solve the problem.[3] As a consequence, medical practitioners may have to manage dental infections. Medical practitioners often have limited knowledge regarding dental infections, making these conditions challenging to manage.[3] Furthermore, medical practitioners in the primary care setting have a unique opportunity to identify the early stages of dental infections, provide oral education, and make the appropriate referral to dental practitioners.

Etiology

Dental Caries

Dental caries result from the interaction between the tooth structure, the dental plaque on the tooth surface, and fermentable carbohydrates. Salivary and genetic factors also influence the development of dental caries.[4]

The biofilm bacteria metabolize fermentable carbohydrates (glucose, fructose, sucrose, and maltose) from the diet, producing organic acids, mainly lactic acid. These end products of bacterial metabolism decrease the pH and demineralize the dental structure's outer layer. After the sugars are cleared by swallowing and saliva dissolution, the acids are neutralized by the buffer capacity of the saliva, and the biofilm pH returns to neutrality. The biofilm is now saturated by calcium, phosphate, and fluoride ions, stopping demineralization and favoring the remineralization of the dental surface.[4] This process happens every time sugars are ingested, explaining why individuals with a reduced salivary flow are at increased risk of dental caries. However, if acidic conditions prevail due to frequent sugar consumption, there is a shift in the biofilm microorganisms to more acidogenic and cariogenic bacteria. The rate of mineral loss is higher than the deposition of minerals, resulting in the first clinical sign of the disease, the 'white spot,' also known as an incipient lesion.[4]

It is worth noting that white spots are reversible carious lesions that can be remineralized by non-invasive procedures like fluoride application and behavioral changes, such as improving dental hygiene and decreasing sugar intake. Hence, early referral to a dentist is vital if these lesions are discovered during a clinical examination. By contrast, if incipient lesions are not managed, they will gradually progress to microcavities in the enamel, collapsing and leaving a macroscopic cavity.[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, like cold drinks, but without spontaneous pain. This is known as reversible pulpitis, and treatment involves the removal of the carious tissue and placing a restoration.

The dental pulp can be irreversibly damaged due to persistent inflammation, leading to constant, spontaneous, acute dental pain, which is poorly localized. Irreversible pulpitis is one of the main reasons for patients presenting 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 are not indicated in managing irreversible pulpitis as signs of infection, such as swelling of the adjacent mucosa, do not normally accompany it.[7] There is limited evidence that antibiotics reduce symptoms of dental pain or the number of analgesics used in untreated teeth with irreversible pulpitis.[8] Hence, antimicrobials are not prescribed before referral. Ultimately, irreversible pulpitis may lead to ischemia and pulp necrosis, where the tooth is asymptomatic.

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] Two forms of periapical abscess can develop: acute or chronic.

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 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 is usually a localized infection that does not require antimicrobials before referral to the dentist.[5] Antibiotics are only indicated when there are signs of systemic spread of the infection, eg, fever or cellulitis.[5] A broad-spectrum antibiotic is most commonly prescribed, usually amoxicillin/clavulanate.[11] Treatment of acute apical abscess includes drainage of the tooth, endodontic treatment to remove the necrotic pulp, and restoration of the affected tooth. Alternatively, the offending tooth is extracted.

Periodontal Disease

Periodontal infections first involve the gingival tissues, causing gingivitis, which may evolve into periodontitis in susceptible individuals. Periodontal disease results from poor dental hygiene, accumulating plaque and calculus, and subsequent inflammation of tissues surrounding and supporting the teeth: gingivae, 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 seems regulated by environmental and genetic factors specific to each patient.[12]

Epidemiology

It is estimated that 13% of adults seek dental care for dental infection or toothache within four years and that 1 per 2600 heads of the population in the United States is hospitalized due to dental infections.[13][14] More than 1 in 5 people have untreated dental caries, and 3 in 4 had at least one dental restoration. Periodontitis is also common, with estimations that 35% of all Americans aged 30 to 90 are afflicted.[15]

More than 1 in 5 people have untreated dental caries, and 3 in 4 had at least one dental restoration. Periodontal disease is also common, with estimations that 35% of Americans aged 30 to 90 are afflicted.[15]

Furthermore, the prevalence of dental caries varies significantly by socioeconomic factors. Untreated dental caries were more than 2.5 times as common in those living 100% below the poverty level (41.9%) relative to those living 200% above the federal poverty level or higher (16.6%). The prevalence of dental caries is also dynamic during the patient's lifetime. Dental caries are present in 90% of adults and 42% of children ages 6 to 19.[16] Dental caries did not appear to vary much with age, except that adolescents aged 12 to 19 were found to have a lower rate of untreated dental caries even when compared to children aged 5 to 11.

History and Physical

Dental Caries and Dental Pulp State

Caries can be acute or chronic, brown-yellow, and 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. They are white and opaque irregular spots that may appear on any tooth surface and are more prevalent in plaque stagnation areas, such as the union of the gingival tissue and the tooth surface.

Patients with reversible pulpitis present with toothache induced by stimuli like 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 serious complaints such as 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.[17]

Periodontal Disease

Patients with gingivitis and periodontitis will often present with a history of halitosis and bleeding after brushing their teeth. It is noteworthy that pain is not associated with periodontal diseases, except necrotizing periodontal disease.

Gingivitis is the localized inflammation of the gums mainly caused by the accumulation of dental plaque on teeth. Clinically, it is characterized by swollen, erythematous gums, which tend to bleed.[18] In gingivitis, there are no periodontal pockets (pathological deepening of the gingival sulcus).[19]

Periodontitis involves the apical migration of the junctional epithelium and the development of periodontal pockets. According to the degree of destruction, clinical findings of periodontitis may include gingival recession, dental papilla detachment, loss of alveolar bone (visible on radiographs), tooth mobility, or fremitus.[20]

Evaluation

Depending on severity, dental infections can be further evaluated using dental radiographs, orthopantomography, CT scans, and MRIs. Imaging studies play an essential role in recognizing the source of infection and the proportions of the disease spread and also can detect any complications. The most common x-rays used in dentistry are orthopantomography and intraoral x-rays, including periapical and bitewings. These are usually sufficient to assess the extent of a dental infection. Cone-beam CT (CBCT) is useful in determining periapical disease, pericoronitis, and osteomyelitis. CT with contrast can help evaluate the extent and severity of fascial space infections. However, the first step in managing patients presenting with signs of fascial space infections, like breathing difficulty, is securing the airways via flexible nasotracheal intubation or tracheotomy. After the airways are secured, further imaging examination may be done.

Laboratory studies, including complete blood count, may be helpful in patients with more severe presentations. Patients with facial or deep space infections may present with sepsis and warrant the addition of blood cultures and lactic acid levels.[21]

Treatment / Management

Management of Patients Presenting with Dental Pain

Patients with odontogenic infections often present to the emergency department due to dental pain, usually caused by pulpitis or acute periapical abscess. Patients must be evaluated for signs of spread of infection beyond the oral cavity and systemic compromise to rule out the need for emergency management. If there is any suspicion of airway compromise, patients must be transferred to an emergency department where the airway can be managed, and the oral and maxillofacial unit must be informed.[22] Red flag symptoms suggesting that a worsening swelling may require emergency management include significant trismus (difficulty to open the mouth), swallowing difficulty, drooling, restricted tongue mobility, firm or swollen floor of the mouth, and a 'hot potato' voice.[23] Patients with Ludwig angina require hospital admission, airway management, and intravenous antibiotics.[23]

Patients should be referred to a dental practitioner for further management if emergency treatment is not indicated.[22] The standard of care for dental infections is surgically controlling the infection source.[22] Definitive treatment can only be administered by a dental practitioner. If the pain is caused by irreversible pulpitis, the treatment is root canal therapy. When the pain results from an acute periapical abscess, the initial management is done by draining through the swelling or the affected tooth by creating an opening on the occlusal surface and then either eliminating the pulp and infection of the root canal with a root canal treatment or extracting the tooth if it is deemed unrestorable.

When to Prescribe Antibiotics

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

Dental infections are polymicrobial, caused by a mixture of anaerobic and aerobic bacteria.[22] The selected antimicrobial must target these bacteria. For outpatients, combining penicillin, usually amoxicillin, with a beta-lactamase inhibitor provides appropriate coverage.[1][22] An alternate antimicrobial is metronidazole, which has improved pharmacokinetics and is better tolerated than erythromycin. Metronidazole is indicated as a first-line treatment when patients are allergic to penicillin, received penicillin recently for another infection, or if the infection is caused by predominantly anaerobic bacteria, which is confirmed with culture. Metronidazole is also used in combination with penicillin in severe spreading infections.

A macrolide, like a clarithromycin, can also be prescribed as a second-line treatment. Due to allergy or drug interactions, clindamycin may be the only alternative for some patients. The clinical outcomes with clindamycin are similar to those with penicillin in treating acute dental abscesses.[24] However, clindamycin treatment is associated with higher gastrointestinal adverse effects rates and increased risk of Clostridium difficile infections.[25] Such risks must be considered when prescribing clindamycin and included in the consent form.

Analgesics

Nonsteroidal anti-inflammatory drugs (NSAIDs) are more effective in controlling dental pain than opioids and are the first-choice treatment for managing acute dental pain.[26] Combining ibuprofen with paracetamol has also been recommended as they are more efficient together than either drug acting alone.[27] If NSAIDs are contraindicated, paracetamol can be prescribed alone or in combination with oxycodone.[26]

Differential Diagnosis

The differential diagnosis of dental infections is variable and based on presenting symptoms. Localized dental infections can be mistaken for salivary gland pathologies such as 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 significant mortality rate. Deep neck infections have a mortality rate of 1% to 25%, and mediastinitis can carry a mortality rate of 40%.[28][29]

Complications

Serious complications can arise from dental infections as they spread to potential head and neck fascial planes. There are different paths for the dissemination of the infection. They can spread contiguously to the jaw, causing osteomyelitis. Lower second and third molars infections can migrate to the sublingual, submandibular, and submental spaces, causing Ludwig angina. In children, dental infections may spread to the retropharyngeal or the parapharyngeal space, causing retropharyngeal or parapharyngeal abscesses, respectively. Descending necrotizing mediastinitis is a severe life-threatening infection caused by the descent of dental infection through deep and superficial fascial planes. There have been reports of dental infections spreading and causing cavernous sinus thrombosis.[30] Very rarely, dental infections result in meningitis and subdural empyema.[31] Dental infections and tooth extractions can cause the hematogenous spread of bacteria (bacteremia), which may result in endocarditis, especially in patients with valvular prostheses.[17]

Deterrence and Patient Education

Patients should receive counseling on proper dental hygiene to prevent dental infections. Educating patients and the public on daily toothbrushing, flossing, and reducing sugar-containing foods can reduce dental cavities.

Pearls and Other Issues

Key considerations are as follows:

  • Dental infections originate in the tooth or its supporting structures and can spread to the surrounding tissues.
  • Dental infections most commonly occur when bacteria invade the pulp and spread to surrounding tissues. Infections can also affect the gums, causing gingivitis, which can later cause periodontal disease.
  • More serious complaints such as fever, facial edema, trismus, dysphagia, or dysphonia can be symptoms of a more serious dental infection that has spread into deep neck spaces.
  • CT with contrast can help evaluate the extent and severity of fascial space infection.
  • Drainage and removing the source of infection are the most important steps in treating dental infections.
  • Severe complications from dental infections are rare. They include osteomyelitis, Ludwig angina, retropharyngeal abscess, parapharyngeal abscess, necrotizing mediastinitis, cavernous sinus thrombosis, meningitis, and subdural empyema.

Enhancing Healthcare Team Outcomes

Medical practitioners likely to treat patients presenting with dental infections must be familiar with their etiology, pathogenesis, and management. The most common causes of dental pain are pulpitis and periapical abscesses. It is essential to understand that such conditions are treated by removing the source of the infection via drainage, pulp treatment, or extracting the offending tooth and that antibiotics alone are insufficient to control dental infections. It would be beneficial if dental education were more emphasized in the curriculum of medical schools. 


Details

Author

David Erazo

Updated:

11/13/2023 12:38:54 AM

References


[1]

Robertson D, Smith AJ. The microbiology of the acute dental abscess. Journal of medical microbiology. 2009 Feb:58(Pt 2):155-162. doi: 10.1099/jmm.0.003517-0. Epub     [PubMed PMID: 19141730]


[2]

Thomas TT. III. Ludwig's Angina (Part II): An Anatomical, Clinical and Statistical Study. Annals of surgery. 1908 Mar:47(3):335-73     [PubMed PMID: 17862124]


[3]

Vytla S, Gebauer D. Clinical guideline for the management of odontogenic infections in the tertiary setting. Australian dental journal. 2017 Dec:62(4):464-470. doi: 10.1111/adj.12538. Epub 2017 Jul 24     [PubMed PMID: 28621799]


[4]

Pitts NB, Zero DT, Marsh PD, Ekstrand K, Weintraub JA, Ramos-Gomez F, Tagami J, Twetman S, Tsakos G, Ismail A. Dental caries. Nature reviews. Disease primers. 2017 May 25:3():17030. doi: 10.1038/nrdp.2017.30. Epub 2017 May 25     [PubMed PMID: 28540937]


[5]

Nguyen DH, Martin JT. Common dental infections in the primary care setting. American family physician. 2008 Mar 15:77(6):797-802     [PubMed PMID: 18386594]


[6]

Ricucci D, Loghin S, Siqueira JF Jr. Correlation between clinical and histologic pulp diagnoses. Journal of endodontics. 2014 Dec:40(12):1932-9. doi: 10.1016/j.joen.2014.08.010. Epub 2014 Oct 12     [PubMed PMID: 25312886]


[7]

Agnihotry A, Fedorowicz Z, van Zuuren EJ, Farman AG, Al-Langawi JH. Antibiotic use for irreversible pulpitis. The Cochrane database of systematic reviews. 2016 Feb 17:2():CD004969. doi: 10.1002/14651858.CD004969.pub4. Epub 2016 Feb 17     [PubMed PMID: 26886473]

Level 1 (high-level) evidence

[8]

Nagle D, Reader A, Beck M, Weaver J. Effect of systemic penicillin on pain in untreated irreversible pulpitis. Oral surgery, oral medicine, oral pathology, oral radiology, and endodontics. 2000 Nov:90(5):636-40     [PubMed PMID: 11077389]


[9]

Siqueira JF Jr, Rôças IN. Microbiology and treatment of acute apical abscesses. Clinical microbiology reviews. 2013 Apr:26(2):255-73. doi: 10.1128/CMR.00082-12. Epub     [PubMed PMID: 23554416]


[10]

Candamourty R, Venkatachalam S, Babu MR, Kumar GS. Ludwig's Angina - An emergency: A case report with literature review. Journal of natural science, biology, and medicine. 2012 Jul:3(2):206-8. doi: 10.4103/0976-9668.101932. Epub     [PubMed PMID: 23225990]

Level 3 (low-level) evidence

[11]

Bascones Martínez A, Aguirre Urízar JM, Bermejo Fenoll A, Blanco Carrión A, Gay-Escoda C, González-Moles MA, Gutiérrez Pérez JL, Jiménez Soriano Y, Liébana Ureña J, López Marcos JF, Maestre Vera JR, Perea Pérez EJ, Prieto Prieto J, de Vicente Rodríguez JC. Consensus statement on antimicrobial treatment of odontogenic bacterial infections. Medicina oral, patologia oral y cirugia bucal. 2004 Nov-Dec:9(5):369-76; 363-9     [PubMed PMID: 15580113]

Level 3 (low-level) evidence

[12]

Bartold PM. Lifestyle and periodontitis: The emergence of personalized periodontics. Periodontology 2000. 2018 Oct:78(1):7-11. doi: 10.1111/prd.12237. Epub     [PubMed PMID: 30198129]


[13]

Boykin MJ, Gilbert GH, Tilashalski KR, Shelton BJ. Incidence of endodontic treatment: a 48-month prospective study. Journal of endodontics. 2003 Dec:29(12):806-9     [PubMed PMID: 14686810]


[14]

Wang J, Ahani A, Pogrel MA. A five-year retrospective study of odontogenic maxillofacial infections in a large urban public hospital. International journal of oral and maxillofacial surgery. 2005 Sep:34(6):646-9     [PubMed PMID: 15955663]

Level 2 (mid-level) evidence

[15]

Dye BA, Li X, Beltran-Aguilar ED. Selected oral health indicators in the United States, 2005-2008. NCHS data brief. 2012 May:(96):1-8     [PubMed PMID: 23050519]


[16]

Beltrán-Aguilar ED, Barker LK, Canto MT, Dye BA, Gooch BF, Griffin SO, Hyman J, Jaramillo F, Kingman A, Nowjack-Raymer R, Selwitz RH, Wu T, Centers for Disease Control and Prevention (CDC). Surveillance for dental caries, dental sealants, tooth retention, edentulism, and enamel fluorosis--United States, 1988-1994 and 1999-2002. Morbidity and mortality weekly report. Surveillance summaries (Washington, D.C. : 2002). 2005 Aug 26:54(3):1-43     [PubMed PMID: 16121123]


[17]

Jevon P, Abdelrahman A, Pigadas N. Management of odontogenic infections and sepsis: an update. British dental journal. 2020 Sep:229(6):363-370. doi: 10.1038/s41415-020-2114-5. Epub 2020 Sep 25     [PubMed PMID: 32978579]


[18]

James P, Worthington HV, Parnell C, Harding M, Lamont T, Cheung A, Whelton H, Riley P. Chlorhexidine mouthrinse as an adjunctive treatment for gingival health. The Cochrane database of systematic reviews. 2017 Mar 31:3(3):CD008676. doi: 10.1002/14651858.CD008676.pub2. Epub 2017 Mar 31     [PubMed PMID: 28362061]

Level 1 (high-level) evidence

[19]

Bosshardt DD. The periodontal pocket: pathogenesis, histopathology and consequences. Periodontology 2000. 2018 Feb:76(1):43-50. doi: 10.1111/prd.12153. Epub 2017 Nov 30     [PubMed PMID: 29194796]


[20]

Trombelli L, Farina R, Silva CO, Tatakis DN. Plaque-induced gingivitis: Case definition and diagnostic considerations. Journal of periodontology. 2018 Jun:89 Suppl 1():S46-S73. doi: 10.1002/JPER.17-0576. Epub     [PubMed PMID: 29926936]

Level 3 (low-level) evidence

[21]

Mardini S, Gohel A. Imaging of Odontogenic Infections. Radiologic clinics of North America. 2018 Jan:56(1):31-44. doi: 10.1016/j.rcl.2017.08.003. Epub 2017 Oct 21     [PubMed PMID: 29157547]


[22]

Beech N, Goh R, Lynham A. Management of dental infections by medical practitioners. Australian family physician. 2014 May:43(5):289-91     [PubMed PMID: 24791770]


[23]

Miah MR, Ali AS. Ludwig's angina. British dental journal. 2020 Sep:229(5):268. doi: 10.1038/s41415-020-2132-3. Epub     [PubMed PMID: 32917993]


[24]

Gilmore WC, Jacobus NV, Gorbach SL, Doku HC, Tally FP. A prospective double-blind evaluation of penicillin versus clindamycin in the treatment of odontogenic infections. Journal of oral and maxillofacial surgery : official journal of the American Association of Oral and Maxillofacial Surgeons. 1988 Dec:46(12):1065-70     [PubMed PMID: 3142979]

Level 1 (high-level) evidence

[25]

von Konow L, Köndell PA, Nord CE, Heimdahl A. Clindamycin versus phenoxymethylpenicillin in the treatment of acute orofacial infections. European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology. 1992 Dec:11(12):1129-35     [PubMed PMID: 1291309]


[26]

Timmerman A, Parashos P. Management of dental pain in primary care. Australian prescriber. 2020 Apr:43(2):39-44. doi: 10.18773/austprescr.2020.010. Epub 2020 Apr 1     [PubMed PMID: 32346209]


[27]

Moore PA, Ziegler KM, Lipman RD, Aminoshariae A, Carrasco-Labra A, Mariotti A. Benefits and harms associated with analgesic medications used in the management of acute dental pain: An overview of systematic reviews. Journal of the American Dental Association (1939). 2018 Apr:149(4):256-265.e3. doi: 10.1016/j.adaj.2018.02.012. Epub     [PubMed PMID: 29599019]

Level 1 (high-level) evidence

[28]

Almuqamam M, Gonzalez FJ, Kondamudi NP. Deep Neck Infections. StatPearls. 2023 Jan:():     [PubMed PMID: 30020634]


[29]

Sanders JL, Houck RC. Dental Abscess. StatPearls. 2023 Jan:():     [PubMed PMID: 29630201]


[30]

Yeo GS, Kim HY, Kwak EJ, Jung YS, Park HS, Jung HD. Cavernous sinus thrombosis caused by a dental infection: a case report. Journal of the Korean Association of Oral and Maxillofacial Surgeons. 2014 Aug:40(4):195-8. doi: 10.5125/jkaoms.2014.40.4.195. Epub 2014 Aug 26     [PubMed PMID: 25247150]

Level 3 (low-level) evidence

[31]

Cariati P, Cabello-Serrano A, Monsalve-Iglesias F, Roman-Ramos M, Garcia-Medina B. Meningitis and subdural empyema as complication of pterygomandibular space abscess upon tooth extraction. Journal of clinical and experimental dentistry. 2016 Oct:8(4):e469-e472     [PubMed PMID: 27703619]