DOI: 10.1148/radiol.2391041243
(Radiology 2006;239:187-194.)
© RSNA, 2006
Odontogenic Orbital Inflammation: Clinical and CT Findings—Initial Observations1
Paul A. Caruso, MD,
Lynnette M. Watkins, MD,
Pantip Suwansaard, MD,
Mika Yamamoto, DDS,
Marlene L. Durand, MD,
Laura Vitale Romo, MD,
Sandra P. Rincon, MD and
Hugh D. Curtin, MD
1 From the Departments of Radiology (P.A.C., M.Y., L.V.R., S.P.R., H.D.C.) and Ophthalmology (L.M.W.), Massachusetts Eye and Ear Infirmary, Harvard Medical School, 243 Charles St, Boston, MA 02114; Department of Radiology, Phramongkutklao Hospital and Phramongkutklao Medical School, Bangkok, Thailand (P.S.); and Division of Infectious Disease, Massachusetts General Hospital, Harvard Medical School, Boston, Mass (M.L.D.). Received July 15, 2004; revision requested September 27; revision received February 23, 2005; accepted March 15; final version accepted June 17.
Address correspondence to: P.A.C. (e-mail: paul_caruso{at}meei.harvard.edu).
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ABSTRACT
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Purpose: To retrospectively review computed tomographic (CT) and clinical findings in patients with odontogenic orbital infection.
Materials and Methods: Approval from the institutional review board was obtained for chart and scan review, and informed consent was waived for this HIPAA-compliant study. Five patients, two male and three female (median age, 37 years; age range, 13–55 years), who had odontogenic orbital cellulitis underwent clinical evaluation, CT scanning, and treatment. CT findings, including periapical lucency suggesting abscess, sinus opacification, and the route of spread of infection, were analyzed in each patient. Imaging, clinical, and surgical findings, including the initial clinical diagnosis and the presence of a periapical abscess at surgery and at pathologic examination, were compared.
Results: Periapical lucency and sinus opacification were seen in all patients. The route of infection spread was through either the premalar soft tissues or the maxillary sinuses. The odontogenic origin of the orbital infection was not clinically suspected in any patients. Correct diagnosis was later made at CT in all patients. Four patients had periapical abscesses at pathologic analysis, and the fifth patient had apical periodontitis at clinical analysis and granuloma at pathologic analysis. Dental surgery was required in each of the five patients for resolution of infection; four patients underwent extraction of the infected tooth, and one patient underwent incision and drainage of a periapical abscess.
Conclusion: Abnormal periapical lucency, widening of the periodontal ligament space, and the presence of a subperiosteal abscess suggested an odontogenic origin of orbital infection.
© RSNA, 2006
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INTRODUCTION
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Orbital cellulitis is a serious infection that, depending on its extent, may result in permanent morbidity, including blindness. Identification of the source of infection facilitates effective management. In most patients, orbital cellulitis is caused by cutaneous or sinonasal infections. Some patients may develop orbital cellulitis as a result of dental infection and may require root canal therapy, apicoectomy, or extraction of the infected tooth. Computed tomography (CT) is typically used to evaluate orbital cellulitis and, if appropriately performed, can reveal odontogenic sources of infection that are not clinically suspected. There are few reported cases of imaging for odontogenic orbital cellulitis, and these cases are limited to imaging of the orbit (1–3). Thus, the purpose of our study was to retrospectively review CT and clinical findings in patients with odontogenic orbital infection.
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MATERIALS AND METHODS
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Patients and Clinical Record Review
Clinical and CT findings in five patients, two male and three female (four adults, one adolescent; median age, 37 years; age range, 13–55 years), were evaluated between November 2001 and June 2002; odontogenic orbital cellulitis was eventually diagnosed, and all patients were included for retrospective review. Approval from the institutional review board of the Massachusetts Eye and Ear Infirmary was obtained for chart and scan review, and informed consent was waived for this Health Insurance Portability and Accountability Act–compliant study. Patient history and physical examination records, surgical notes, and CT scans were available in all five patients. The results of sinus cultures were available in one patient with an orbital abscess, and the results of blood and facial bacterial cultures were available in another patient with an orbital abscess.
Clinical records were reviewed separately, and conclusions were arrived at by the consensus of a neuroradiologist (P.A.C., with more than 5 years of subspecialty experience in head, neck, and orbital imaging), a board-certified staff ophthalmologist (L.M.W., with more than 5 years of experience in general and emergency ophthalmology), and an infectious disease physician (M.L.D., with more than 10 years of experience in orbital infections). Records were reviewed with regard to the initial clinical diagnosis and course of therapy, history of prior dental disease, and signs and symptoms of orbital inflammation, including fever, orbital pain, tenderness, erythema, proptosis, loss in visual acuity, decreased ocular motility, and subperiosteal abscess. The same three authors also evaluated the records for signs and symptoms of sinus inflammation, including facial pain, sinonasal congestion, and discharge, and determined the time interval between initial diagnosis at clinical examination and the diagnosis at CT. Culture results were reviewed by the infectious disease physician (M.L.D.).
Imaging Technique, Review, and Comparisons
All five patients underwent contrast material–enhanced multi–detector row CT (four detector rows), which was performed preoperatively in the transverse plane. CT scans were obtained from the frontal sinuses through the occlusal plane (the plane between the maxillary and mandibular dentition) to include the maxillary dentition. Scanning parameters included 1-mm collimation, 140 kV, 120 mAs, and a 165–193-mm display field of view. A total of 75 mL of low-osmolar iodinated contrast material (Omnipaque 300; Nycomed, Princeton, NJ) was administered by using a power injector at a rate of 1.5 mL/sec, with a delay of 30 seconds. The images were reconstructed at 2–3-mm intervals in the trensverse plane along a line parallel to the hard palate. Coronal reformatted images measuring 2–3 mm were then obtained along an axis perpendicular to the hard palate. The transverse and coronal reformatted images were then reviewed with a soft-tissue algorithm and soft-tissue window (window width, 352 HU; window level, 40 HU) and with a bone algorithm and bone window (window width, 3500 HU; window level, 500 HU).
CT images were reviewed by two radiologists (H.D.C., with more than 20 years of experience in head, neck, and orbital imaging, and P.A.C.) and a dental radiologist (M.Y., with 5 years of experience). Images were reviewed separately, and conclusions were reached by consensus.
Three authors (P.A.C., H.D.C., and M.Y.) reviewed the images with regard to evidence of (a) periapical disease such as periapical abscesses, which manifest as abnormal periapical lucency, (b) widening of the periodontal ligament (PDL) space, (c) erosion of the lamina dura, (d) subperiosteal abscesses, which manifest as subperiosteal lucency and enhancement, and (e) caries, which manifest as abnormal coronal lucency. The same authors also reviewed images with regard to the tooth of origin of the orbital infection, the presence of other diseased teeth, and the route of spread of infection from the diseased tooth to the orbit, including involvement of the premalar soft tissues.
Two authors (P.A.C. and H.D.C.) evaluated the images for findings of orbital inflammation, such as reticulation of the periorbital and orbital soft tissues, involvement of the extraocular muscles, presence of an orbital abscess, and involvement of the cavernous sinus and intracranial extension. The same two authors also evaluated the images for evidence of paranasal sinus inflammation, including the severity of sinus opacification and the site and laterality of sinus involvement. The site of sinus involvement was correlated with the dental findings.
Surgical Records
Surgical reports and follow-up records were reviewed separately, and conclusions were reached by the consensus of two authors (P.A.C. and L.M.W.) with regard to the surgical confirmation of dental abscess, surgical course, presence of orbital abscess, and postoperative course.
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RESULTS
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Clinical Findings
An odontogenic origin of the orbital cellulitis was not initially suspected at clinical analysis in any of the five patients. Orbital inflammation resulting from primary facial cellulitis (orbitofacial cellulitis) was initially diagnosed in two patients. In the remaining three patients, sinogenic orbital cellulitis was initially diagnosed (Table 1). Four patients were given antibiotics, but after 2–4 days of therapy these patients experienced unimproved, persistent, or worsening orbital pain, tenderness, and erythema and subsequently underwent CT scanning. One patient was scanned on the day of presentation. The diagnosis of odontogenic orbital cellulitis was made at CT in all five patients.
One patient had a history of endodontic treatment of the right maxillary canine (American Dental Association tooth 6) several years prior to presentation. A second patient had a history of dental surgery (not otherwise specified) 8 years prior to the onset of orbital symptoms. A third patient had a history of molar tooth pain 3 weeks prior to the onset of orbital symptoms for which he had seen a dentist and had undergone removal of material lodged between the teeth.
All five patients presented to the emergency room with common findings of orbital cellulitis, including fever (n = 3), orbital pain (n = 5), tenderness (n = 5), erythema (n = 5), proptosis (n = 3), loss in visual acuity (n = 2), and decreased ocular motility (n = 3).
All five patients had signs and symptoms of sinus inflammation of variable degree, including facial pain (n = 3), sinonasal congestion (n = 3), and sinus or nasal discharge (n = 4) (Table 1). The average time between the initial diagnosis at clinical examination and the diagnosis at CT was 2 days.
No cultures were obtained directly from the dental or orbital abscesses. In one patient with an orbital abscess, sinus cultures grew S milleri and oral anaerobes (peptostreptococci and Fusobacterium nucleatum). In a second patient with an orbital abscess, blood cultures grew oral anaerobes (peptostreptococci and anaerobic Gram-negative rod-shaped bacteria), and facial cultures grew S aureus (methicillin sensitive).
Imaging Findings
Findings of periapical disease were noted in all five patients (Table 2). All patients demonstrated evidence of a periapical abscess, which manifested as abnormal lucency surrounding the root apices, and showed widening of the PDL space and erosion of the lamina dura, which manifested as a loss in definition of the hyperattenuating line normally seen along the margin of the PDL space (Figs 1–4). A dental subperiosteal abscess, which manifested as an abnormal rim-enhancing area of hypoattentation located adjacent to the affected root, was seen in two patients (Fig 2). Caries, which manifested as abnormal lucency in the tooth crown, were seen in another patient (Fig 3). Dental fillings obscured the crowns of the teeth in three patients. The canines were the source of orbital infection in two patients in whom the route of spread was observed to be from the canines through the premaxillary soft tissues to the orbit (Figs 1, 2). The first molar teeth were the source of infection for the remaining three patients in whom the route of spread was observed to be from the teeth through the maxillary sinuses into the orbits (Figs 3, 4). In all instances, the inflammation was continuous from the dental abscess to the orbit.
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Figure 1a: Odontogenic facial and orbital cellulitis in 55-year-old woman with route of spread via the premalar soft tissues. (a, b) Coronal CT scans demonstrate (a) apical abscess (arrow) of the left maxillary canine and (b) reticulation (arrows) of the premalar soft tissues extending from the alveolus of the canine to the inferior orbital rim, resulting in bulging (arrowheads) of fat and skin. (c, d) Transverse CT scans demonstrate (c) involvement of the levator labii superioris (short arrow) and bulging (long arrow) of the premalar soft tissues and (d) predominantly preseptal soft-tissue swelling (arrows). Note that only minimal left maxillary sinus opacification is seen in c.
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Figure 1b: Odontogenic facial and orbital cellulitis in 55-year-old woman with route of spread via the premalar soft tissues. (a, b) Coronal CT scans demonstrate (a) apical abscess (arrow) of the left maxillary canine and (b) reticulation (arrows) of the premalar soft tissues extending from the alveolus of the canine to the inferior orbital rim, resulting in bulging (arrowheads) of fat and skin. (c, d) Transverse CT scans demonstrate (c) involvement of the levator labii superioris (short arrow) and bulging (long arrow) of the premalar soft tissues and (d) predominantly preseptal soft-tissue swelling (arrows). Note that only minimal left maxillary sinus opacification is seen in c.
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Figure 1c: Odontogenic facial and orbital cellulitis in 55-year-old woman with route of spread via the premalar soft tissues. (a, b) Coronal CT scans demonstrate (a) apical abscess (arrow) of the left maxillary canine and (b) reticulation (arrows) of the premalar soft tissues extending from the alveolus of the canine to the inferior orbital rim, resulting in bulging (arrowheads) of fat and skin. (c, d) Transverse CT scans demonstrate (c) involvement of the levator labii superioris (short arrow) and bulging (long arrow) of the premalar soft tissues and (d) predominantly preseptal soft-tissue swelling (arrows). Note that only minimal left maxillary sinus opacification is seen in c.
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Figure 1d: Odontogenic facial and orbital cellulitis in 55-year-old woman with route of spread via the premalar soft tissues. (a, b) Coronal CT scans demonstrate (a) apical abscess (arrow) of the left maxillary canine and (b) reticulation (arrows) of the premalar soft tissues extending from the alveolus of the canine to the inferior orbital rim, resulting in bulging (arrowheads) of fat and skin. (c, d) Transverse CT scans demonstrate (c) involvement of the levator labii superioris (short arrow) and bulging (long arrow) of the premalar soft tissues and (d) predominantly preseptal soft-tissue swelling (arrows). Note that only minimal left maxillary sinus opacification is seen in c.
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Figure 2a: Odontogenic orbital cellulitis in 43-year-old woman with route of spread via the premaxillary soft tissues and sinuses. (a) Transverse CT scan demonstrates abnormal lucency (arrow) in the root of the right maxillary canine, with erosion of the buccal margin of the alveolus. Bilateral maxillary sinus opacification (*) is noted. (b, c) Transverse CT scans demonstrate (b) small area of lucency (arrow) at the tip of the right canine that is consistent with an apical abscess and (c) rim-enhancing subperiosteal abscess (arrowhead), with spread of infection via the premalar soft tissues (short arrows) to the periorbital region and inferior palpebra (long arrows). Note that the canine has undergone prior endodontic treatment in b. (d) Transverse CT scan demonstrates marked periorbital inflammation (arrows).
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Figure 2b: Odontogenic orbital cellulitis in 43-year-old woman with route of spread via the premaxillary soft tissues and sinuses. (a) Transverse CT scan demonstrates abnormal lucency (arrow) in the root of the right maxillary canine, with erosion of the buccal margin of the alveolus. Bilateral maxillary sinus opacification (*) is noted. (b, c) Transverse CT scans demonstrate (b) small area of lucency (arrow) at the tip of the right canine that is consistent with an apical abscess and (c) rim-enhancing subperiosteal abscess (arrowhead), with spread of infection via the premalar soft tissues (short arrows) to the periorbital region and inferior palpebra (long arrows). Note that the canine has undergone prior endodontic treatment in b. (d) Transverse CT scan demonstrates marked periorbital inflammation (arrows).
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Figure 2c: Odontogenic orbital cellulitis in 43-year-old woman with route of spread via the premaxillary soft tissues and sinuses. (a) Transverse CT scan demonstrates abnormal lucency (arrow) in the root of the right maxillary canine, with erosion of the buccal margin of the alveolus. Bilateral maxillary sinus opacification (*) is noted. (b, c) Transverse CT scans demonstrate (b) small area of lucency (arrow) at the tip of the right canine that is consistent with an apical abscess and (c) rim-enhancing subperiosteal abscess (arrowhead), with spread of infection via the premalar soft tissues (short arrows) to the periorbital region and inferior palpebra (long arrows). Note that the canine has undergone prior endodontic treatment in b. (d) Transverse CT scan demonstrates marked periorbital inflammation (arrows).
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Figure 2d: Odontogenic orbital cellulitis in 43-year-old woman with route of spread via the premaxillary soft tissues and sinuses. (a) Transverse CT scan demonstrates abnormal lucency (arrow) in the root of the right maxillary canine, with erosion of the buccal margin of the alveolus. Bilateral maxillary sinus opacification (*) is noted. (b, c) Transverse CT scans demonstrate (b) small area of lucency (arrow) at the tip of the right canine that is consistent with an apical abscess and (c) rim-enhancing subperiosteal abscess (arrowhead), with spread of infection via the premalar soft tissues (short arrows) to the periorbital region and inferior palpebra (long arrows). Note that the canine has undergone prior endodontic treatment in b. (d) Transverse CT scan demonstrates marked periorbital inflammation (arrows).
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Figure 3a: Odontogenic orbital cellulitis in 29-year-old woman with route of spread via the sinuses. (a) Coronal CT scan in soft-tissue window demonstrates maxillary and ethmoid sinus opacification (*), with secondary orbital phlegmon resulting from spread of infection across the orbital process of the maxilla (arrowhead) and lamina papyracea (white arrow). The inferior (i) and medial (m) recti and superior oblique muscle (s) appear enlarged and inflamed. Spread of infection into the lateral orbit (black arrows) is noted. (b) Coronal CT scan in bone window demonstrates periapical disease, with bilateral carious molars (long arrows), periapical abscess of the lingual root (arrowhead), and abnormal lucency along the buccal root (short arrow). Odontogenic sinusitis, with right maxillary and ethmoid sinus opacification (*), is noted. (c) Transverse CT scan demonstrates pre- and postseptal orbital phlegmon (arrowheads) with proptosis, stretching of the optic nerve, and resultant deformity of the posterior aspect of the globe (arrow).
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Figure 3b: Odontogenic orbital cellulitis in 29-year-old woman with route of spread via the sinuses. (a) Coronal CT scan in soft-tissue window demonstrates maxillary and ethmoid sinus opacification (*), with secondary orbital phlegmon resulting from spread of infection across the orbital process of the maxilla (arrowhead) and lamina papyracea (white arrow). The inferior (i) and medial (m) recti and superior oblique muscle (s) appear enlarged and inflamed. Spread of infection into the lateral orbit (black arrows) is noted. (b) Coronal CT scan in bone window demonstrates periapical disease, with bilateral carious molars (long arrows), periapical abscess of the lingual root (arrowhead), and abnormal lucency along the buccal root (short arrow). Odontogenic sinusitis, with right maxillary and ethmoid sinus opacification (*), is noted. (c) Transverse CT scan demonstrates pre- and postseptal orbital phlegmon (arrowheads) with proptosis, stretching of the optic nerve, and resultant deformity of the posterior aspect of the globe (arrow).
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Figure 3c: Odontogenic orbital cellulitis in 29-year-old woman with route of spread via the sinuses. (a) Coronal CT scan in soft-tissue window demonstrates maxillary and ethmoid sinus opacification (*), with secondary orbital phlegmon resulting from spread of infection across the orbital process of the maxilla (arrowhead) and lamina papyracea (white arrow). The inferior (i) and medial (m) recti and superior oblique muscle (s) appear enlarged and inflamed. Spread of infection into the lateral orbit (black arrows) is noted. (b) Coronal CT scan in bone window demonstrates periapical disease, with bilateral carious molars (long arrows), periapical abscess of the lingual root (arrowhead), and abnormal lucency along the buccal root (short arrow). Odontogenic sinusitis, with right maxillary and ethmoid sinus opacification (*), is noted. (c) Transverse CT scan demonstrates pre- and postseptal orbital phlegmon (arrowheads) with proptosis, stretching of the optic nerve, and resultant deformity of the posterior aspect of the globe (arrow).
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Figure 4a: Odontogenic orbital cellulitis in 13-year-old boy with route of spread via the sinuses. (a) Transverse CT scan demonstrates abnormal lucency consistent with periapical infection involving the mesiobuccal (m), distal buccal (d), and lingual (arrow) roots of the left first maxillary molar. Alveolar cortex appears intact. (b, c) Coronal CT scans show (b) apical tooth abscess (arrow) and opacification of the left maxillary sinus, ethmoid sinus, and nasal cavity (*) and (c) diffuse opacification of the left maxillary and ethmoid sinuses (*), with prominence of superior oblique (s) and medial rectus (m) from secondary spread of infection to the orbit. (d) Transverse CT scan demonstrates ethmoid opacification (e), with spread of infection across the lamina papyracea into the medial orbit (*), inflammation of the left medial rectus (m), and involvement of the periorbital soft tissues (arrows).
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Figure 4b: Odontogenic orbital cellulitis in 13-year-old boy with route of spread via the sinuses. (a) Transverse CT scan demonstrates abnormal lucency consistent with periapical infection involving the mesiobuccal (m), distal buccal (d), and lingual (arrow) roots of the left first maxillary molar. Alveolar cortex appears intact. (b, c) Coronal CT scans show (b) apical tooth abscess (arrow) and opacification of the left maxillary sinus, ethmoid sinus, and nasal cavity (*) and (c) diffuse opacification of the left maxillary and ethmoid sinuses (*), with prominence of superior oblique (s) and medial rectus (m) from secondary spread of infection to the orbit. (d) Transverse CT scan demonstrates ethmoid opacification (e), with spread of infection across the lamina papyracea into the medial orbit (*), inflammation of the left medial rectus (m), and involvement of the periorbital soft tissues (arrows).
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Figure 4c: Odontogenic orbital cellulitis in 13-year-old boy with route of spread via the sinuses. (a) Transverse CT scan demonstrates abnormal lucency consistent with periapical infection involving the mesiobuccal (m), distal buccal (d), and lingual (arrow) roots of the left first maxillary molar. Alveolar cortex appears intact. (b, c) Coronal CT scans show (b) apical tooth abscess (arrow) and opacification of the left maxillary sinus, ethmoid sinus, and nasal cavity (*) and (c) diffuse opacification of the left maxillary and ethmoid sinuses (*), with prominence of superior oblique (s) and medial rectus (m) from secondary spread of infection to the orbit. (d) Transverse CT scan demonstrates ethmoid opacification (e), with spread of infection across the lamina papyracea into the medial orbit (*), inflammation of the left medial rectus (m), and involvement of the periorbital soft tissues (arrows).
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Figure 4d: Odontogenic orbital cellulitis in 13-year-old boy with route of spread via the sinuses. (a) Transverse CT scan demonstrates abnormal lucency consistent with periapical infection involving the mesiobuccal (m), distal buccal (d), and lingual (arrow) roots of the left first maxillary molar. Alveolar cortex appears intact. (b, c) Coronal CT scans show (b) apical tooth abscess (arrow) and opacification of the left maxillary sinus, ethmoid sinus, and nasal cavity (*) and (c) diffuse opacification of the left maxillary and ethmoid sinuses (*), with prominence of superior oblique (s) and medial rectus (m) from secondary spread of infection to the orbit. (d) Transverse CT scan demonstrates ethmoid opacification (e), with spread of infection across the lamina papyracea into the medial orbit (*), inflammation of the left medial rectus (m), and involvement of the periorbital soft tissues (arrows).
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Additional actively diseased or previously diseased teeth were seen in four of five patients. The youngest patient in the series (a 13-year-old boy) had evidence of only a single diseased tooth (Fig 4).
All five patients demonstrated orbital or periorbital inflammation, with abnormal enhancement and reticulation of the pre- or postseptal soft tissues. Enlargement and abnormal enhancement of the extraocular muscles were noted in two patients (Figs 3, 4). Orbital abscesses were also noted in two patients. No patient had evidence of cavernous sinus involvement or of the intracranial spread of infection.
In two of the three patients in whom the infection originated in the molar teeth, there was severe and unilateral sinus opacification and reticulation of the premalar soft tissues that reached the orbit ipsilateral to the infected tooth (Figs 3, 4). In the third patient, there was severe sinus opacification, reticulation of the premalar soft tissues that reached the orbit ipsilateral to the infected tooth, and only mild contralateral sinus opacification. No obstructing lesions were seen at imaging nor were such lesions reported at surgery in these patients (Figs 3, 4).
In the two patients in whom the infection originated in the canines, sinus opacification was only mild. In one of these patients, the sinus opacification was mild, bilateral, and symmetric. In the second patient, sinus opacification was mild and unilateral. There was contiguous inflammation from the abscessed tooth, through the premaxillary soft tissues and levator labii musculature, to the orbit (Figs 1, 2).
Opacification of the maxillary sinuses was noted in all five patients, opacification of the ethmoid sinuses was noted in four patients, opacification of the frontal sinuses was noted in three patients, and opacification of the sphenoid sinus was noted in one patient.
Surgical Findings
All five patients underwent surgery for drainage of the radiographically defined periapical lesions. Four patients underwent tooth extraction, and one underwent incision and drainage. Four patients were found to have frank dental abscesses with purulent material noted both intraoperatively and pathologically. One patient was found to have apical odontitis at surgery and a periapical granuloma at pathologic analysis.
The three patients without orbital abscesses underwent dental procedures only. Two of them underwent extraction of the diseased tooth, and one underwent incision and drainage of a periapical abscess without extraction.
The two patients with orbital abscesses (patients 2 and 4) underwent orbital and sinus drainage in addition to the dental procedure. One underwent orbital abscess and sinus drainage and tooth extraction in the same sitting. However, this patient subsequently developed orbital fasciitis and required further orbital débridement. This patient presented with unilateral vision loss (no light perception) and did not recover vision in the affected eye. The second patient underwent orbital abscess drainage, canthotomy, cantholysis, sinus drainage, and tooth extraction in the same sitting but required further sinus drainage. This patient presented with decreased vision in the affected eye but recovered normal vision after treatment.
The three patients without orbital abscesses defervesced and showed clinical improvement after the dental procedure and antibiotic therapy; these patients required no other surgical intervention. The two patients with orbital abscesses required orbital and sinus abscess drainage in addition to the tooth extraction.
Postoperative follow-up ranged from 2 days to 4 weeks and averaged 17 days. Clinical findings, imaging diagnosis, and surgical results are summarized in Table 1.
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DISCUSSION
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Clinical Aspects
Orbital inflammation may result from primary infection of the sinuses, skin, or teeth. Primary sinus infection, which is the most common cause of orbital inflammation, underlies 64% of cases of orbital cellulitis, and most of these cases are of bacterial origin (4,5). Cutaneous lesions, such as eczema, furunculi, or facial cellulitis, may spread to the orbits and have been found to account for 16% of cases of orbital cellulitis (5). Odontogenic orbital cellulitis is a less frequent but important cause of orbital infection. In a series of 190 patients with orbital inflammation, Gans et al (5) found that 68% of cases occurred in patients who were 2 months to 14 years of age and that odontogenic sources of orbital infection represented 2% of cases. In our series, four (80%) of five patients were adults. These findings likely reflect the preponderance of periapical disease in the adult population.
The orbital manifestations of odontogenic orbital cellulitis are the same as those seen in orbital cellulitis secondary to sinus or facial infection (2). Thus, the dental nidus, as in our series, may be clinically unsuspected. A history of recent dental procedure may be the only clinical clue to the diagnosis (2,6). Our series, however, exemplifies cases of clinically unsuspected odontogenic orbital cellulitis. In all of the patients in our series, the dental nidus was not obvious at initial clinical examination and diagnosis was made at CT.
Preseptal cellulitis almost always responds to antibiotics alone. Orbital cellulitis often responds to antibiotics as well. Orbital or subperiosteal abscesses, however, nearly always require emergency drainage to protect vision (4,5).
Our series suggests that odontogenic orbital cellulitis does not respond to antibiotics alone and requires incision and drainage of the periapical abscess or tooth extraction. In our series, four patients received 2–4 days of oral or intravenous antibiotic therapy and failed to improve. In one patient, diagnosis was made more quickly at CT, and thus a preoperative course of antibiotics alone was not attempted. The three patients without orbital abscesses improved following incision and drainage of the periapical abscess (one patient) or tooth extraction (two patients). The two who had progressed to more severe involvement of the orbital abscess required tooth extraction and additional sinus and orbital abscess drainage.
Bacteria account for most cases of orbital and periorbital infection (7). S aureus, Streptococcus pyogenes, Streptococcus pneumoniae, and (in children) Hemophilus influenzae are the most commonly reported organisms (4,5). Organisms reported in odontogenic orbital cellulitis include S aureus (including methicillin-resistant strains) and 
-hemolytic streptococci (6,8,9). In our series, cultures were not obtained from the dental or orbital abscesses. Sinus cultures that were obtained in one patient with an orbital abscess were notable for growth of S milleri, which is an -hemolytic streptococcus that is found in the normal oral flora and is notorious for causing soft-tissue abscesses when it spreads beyond the oral mucosal barrier.
Imaging
Imaging often plays a key role in the diagnosis of odontogenic orbital cellulitis. Several authors have reported odontogenic orbital cellulitis but presented only the CT orbital imaging results without a description of the dental radiographic findings (4,5). Our series emphasizes the imaging findings and technical considerations that are key to the diagnosis of odontogenic orbital infection at CT.
The most common modality for the imaging of apical abscesses is periapical radiography; however, CT is commonly used for the imaging of orbital infection. Therefore, it is important to recognize the manifestations of dental infection on CT scans. The hallmark diagnostic findings of dental infection on CT scans include abnormal periapical lucency, loss in definition of the lamina dura, and widening of the PDL space (10). These findings may be considered in terms of the pathogenesis of periapical disease. Periapical disease begins with dental caries, which are demonstrated on dental radiographs or CT scans as an abnormal area of lucency or defect in the crown of the tooth (10). From there, infection may spread to the pulp chamber. The pulp may become necrotic, thereby facilitating the spread of infection through the devitalized pulp chamber. Once the infection reaches the root apex, a periapical abscess or granuloma may form; such infection may be demonstrated on CT scans as abnormal lucency at the root apex (10). In normal teeth, the alveolus or tooth socket is delineated by a hyperattenuating line—that is, the lamina dura (11). The lamina dura, in turn, is separated from the radiopaque tooth root by a thin area of lucency that represents the PDL space (11). In periapical disease, infection results in a loss of definition in the lamina dura and a widening of the PDL space. If there is further progression of the infection, the alveolus itself may thin or develop a defect, and a subperiosteal abscess, which manifests as a rim-enhancing area of hypoattenuation in the adjacent soft tissues, may form.
Our series emphasizes an important technical consideration: If severe sinus opacification is seen at imaging, the pitfall for the radiologist may be to conclude erroneously that the orbital infection is primarily sinogenic. In many such cases, however, the sinus and orbital inflammation are both truly odontogenic. Severe unilateral or asymmetrically severe sinus opacification ipsilateral to the infected orbit was seen in three patients in our series with infected molar teeth and may be a clue to the dental origin of the orbital infection. It is important to perform scanning through the occlusal plane and to scrutinize the maxillary dentition for a nidus of infection. We did not include the mandible in the scaning excursion because mandibular odontogenic orbital cellulitis is rare.
Pathogenesis of Odontogenic Orbital Cellulitis
Three basic routes of spread of infection have been described in odontogenic orbital cellulitis—that is, via the paranasal sinuses, via the premaxillary soft tissues, or posteriorly via the infratemporal fossa and inferior orbital fissure (2,6,12).
The most common route of spread of odontogenic orbital infection is via the paranasal sinuses (6). The apices of the maxillary molars and premolars lie in close proximity to the floor of the maxillary sinus. Dental infection may result in sinusitis that may, in turn, involve the orbit. In three of the five patients in our series, the infection arose from the first molar tooth, thereby demonstrating this route of spread.
Infection of the maxillary incisor, canine, or first premolar may spread through the premaxillary soft tissues to the orbit, thereby resulting in orbitofacial cellulitis. The results of previous reports have implicated valveless facial, angular, and ophthalmic veins as facilitating this route of spread (5). In our series, the two patients with periapical disease of the canines exemplified this route of infection.
Spread of infection to the orbit via the masticator space or infratemporal fossa has been described secondary to molar tooth infection and may involve facial cellulitis (6).
The PDL space is implicated in periapical disease. The PDL space, reported to measure normally between 0.15–0.38 mm, may widen at the site of infection (13). Several hypotheses have been advanced concerning the homeostatic maintenance and derangement of the PDL; these hypotheses involve a wide range of factors, including alkaline phosphatase and bone morphogenetic protein (13,14). In our series, the PDL space was widened in all five patients.
The limitations of our study include a small sample size and the fact that culture results were not available in all patients.
In conclusion, odontogenic orbital infection is an uncommon but serious disease with substantial risk of morbidity. Odontogenic orbital cellulitis requires drainage of the dental abscess for definitive cure. Because a history of recent dental procedures may be lacking and because the presenting signs and symptoms are often nonspecific, the dental focus may be unsuspected clinically. Familiarity with CT findings of dental infection may be crucial to the diagnosis and management of this condition. Our series exemplifies CT findings for periapical disease and highlights the routes of spread of dental infection to the orbit through the sinuses and premaxillary soft tissues. Abnormal periapical lucency, widening of the PDL space, subperiosteal dental abscess, unilateral or asymmetrically severe sinus opacification ipsilateral to the infected orbit, and premalar soft-tissue swelling may suggest the odontogenic origin of orbital infection.
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FOOTNOTES
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Abbreviations: PDL = periodontal ligament
Author contributions: Guarantors of integrity of entire study, P.A.C., H.D.C.; study concepts/study design or data acquisition or data analysis/interpretation, all authors; manuscript drafting or manuscript revision for important intellectual content, all authors; manuscript final version approval, all authors; literature research, P.A.C., L.M.W., P.S., M.Y.; clinical studies, P.A.C., L.M.W., M.L.D.; and manuscript editing, P.A.C., L.M.W., L.V.R., S.P.R., H.D.C.
Authors stated no financial relationship to disclose.
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ABSTRACT
INTRODUCTION
