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

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. 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. In addition, it Keywords has to be accompanied by antibiotic therapy. 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. 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. 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. 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. 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. 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. 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. facultative anaerobic and strict anaerobic bacteria. 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. responsable for greater invasion and destruction of tissues due to their high virulence. 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. 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%. 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. Table 1: Frequent bacterias in odontogenic infections. Adapted from Brook I, et al.. 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.. 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.. 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. 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. clinical history and symptoms. Establishing the onset of symptoms and propagation speed of the infection Dissemination of odontogenic infection clarifies the severity. 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. 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 : 12,000 mm3. 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. 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 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. management by a specialist [3,9,20]. Flynn, et al. classify the severity of infection Imaging according to the anatomical spaces invaded 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]. ; while other studies concluded it was the buccal space (60%) and the submandibular space (35%) Panoramic radiography is the imaging study of first. 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 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.. 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.. 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 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. collections and vascularized areas. 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. 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. 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. 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. Is more frequent in the mandible since the blood vessels of the periosteum do not penetrate the cortical bone. 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. 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. carried out to prevent danger to the patient's life. The OI has a mortality rate of 10-40%. 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 , Ludwig's angina , to the face through the angular vein which connects infratemporal and temporoparietal fossa abscesses with the superior ophthalmic vein and to the palate Figure 4, deep neck infections [23,24], meningitis through the pterygoid plexus via the inferior ophthalmic , osteomyelitis , intracranial abscesses [36,37], vein. When infection reaches the cavernous sinus, cavernous sinus thrombosis , necrotizing fasciitis regardless of the route, thrombosis occurs. However, , airway obstruction , and death [31,39]. infections from the canine region via the angular vein Ludwig's angina are more frequent. Is the most common complication of OI. 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. onset. 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%. and can spread to pharyngeal spaces until reaching the mediastinum. 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. potential to evolve into severe complications. 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.. Elimination of the source of infection, incision and drainage of all infected spaces, and antibiotic therapy Deep neck infections. 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. disease and is composed of local management, antibiotic therapy and surgical management. Deep neck infections from odontogenic source account for 43% of cases with amortality rate of 10- Local management 40%. The airway can be compromised manifesting The initial treatment should consist of analgesics for as dyspnea, dysphagia and dysphonia. 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. Surgical drainage and intravenous antibiotics are perspiration [10,19]. The use of steroids is controversial, indicated. 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. 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. 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.. 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. 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. 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. 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. It should be accompanied by antibiotics as between 2 and 7 days. penicillin G, penicillin V, erythromycin, cephalosporins or clindamycin. 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 , 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. 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. 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. Follow-up Mild OI should be evaluated at 48 hours to assess the progress or resolution of the infection. 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. 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. 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. 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. 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 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. 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.. 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. 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. 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

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