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References 1. Curth HO: Pseudo-acanthosis nigricans. Ann Dermatol Syphil 78:417, 1951 2. Curth HO: Acanthosis n&cans and its association with cancer. Arch Dermatol Syphil 57: 158, I948 3. Curth HO: Significance of acanthosis nigricans. Arch Dermatol Syphil 66:80, 1952 4. Fladung G, Heite HJ: Haufigkeitsanalytische Untersuchungen zur Frage der symptomatologischen Abgrenzung verschiedener Former der Acanthosis nigricans. Arch Klin Exp Dermatol 2051282, 1957 5. Curth HO: Classification of acanthosis nigricans. Int J Dermatol l5:592, 1976 6. Mostofi RS, Hayden NP, Soltani K: Oral malignant acanthosis niaricans. Oral Sure Oral Med Oral Path01 56:372. 1983 7. Pindborg JJ, Gorlin kr: Oral changes in acanthosis nigricans (juvenile type): Survey of the literature and report of a case. Acta Dermatovener 42:63, 1962 8. Bang G: Acanthosis nigricans maligna. Oral Surg Oral Med Oral Pathol 29:370, 1970 9. Gorlin RJ, Pindborg JJ: Syndromes of the Head and Neck. New York, NY, McGraw-Hill, 1964, p I 10. Andreev VC. Raichev RD. Stoianov A: Acanthosis nigricans of oral mucdsa. Dermatologica 126:25, 1963 I 1. Cobenour W, Gamble JW: Acanthosis nigricans: review of literature and report of case. J Oral Surg 29:48, I97 1

12. Jakhi SA, Parekh BK: Acanthosis nigricans: a case report. J Oral Medicine 37:18, 1982 13. Andreev VC, Boyanov L, Tsankov N: Generalized acanthosis nigricans. Dermatologica 163:19, 198I 14. Hall JM, Moreland A, Cox GJ, et al: Oral acanthosis nigricans: Report of a case and comparison of oral and cutaneous pathology. Am J Dermatopathol lO:68, 1988 15. Nomachi K, Mori M, Matsuda N: Improvement of oral lesions associated with malignant acanthosis nigricans after treatment of lung cancer. Oral Surg Oral Med Oral Pathol 68:74, 1989 16. Brown J, Winkelmann RK: Acanthosis nigricans: A study of 90 cases. Medicine 47:33, 1968 17. Misch KJ, Griffiths WAD, Eady RAJ: Warts as a presenting sign in acanthosis n&cans. Clin Exp Dermatol 8:65 1, 1983 18. Walton S, Krause L, Marks J: A case of acanthosis nigricansAn investigative approach. Clin Exp Dermatol 9:58, 1984 19. Rigel DS, Jacobs MI: Malignant acanthosis nigricans: A review. J Dermatol Surg Oncol6:923, 1980 20. Sedan0 HO, Gorlin RJ: Acanthosis nigricans. bra1 Surg Oral Med Oral Path01 63:462, 1987 21. Curth HO: Dermatoses and malignant internal tumors. Arch Dermatol Syphilol 71:95, 1955 22. Lerner AB: On the cause of acanthosis nigricans. N Engl J Med 281:106, 1969 23. MSller H, Eriksson S, Holen 0, et al: Complete reversibility of paraneoplastic acanthosis nigticans after operation. Acta Med Stand 203:245, 1978

J OralMaxillofacSurg 50:172-178.1992

Odontogenic Infection of the Orbit: Report of a Case CHARLES

H. HENRY, DDS,* CHRISTOPHER V. HUGHES, AND DAVID C. LARNED, MD+

The extension of an orofacial infection to the orbit can result in significant morbidity and mortality. The spread of an odontogenic infection to the orbit has been previously reported.‘-9 Infection of the orbit may also occur as a result of the direct extension of acute paranasal sinusitis, periorbital trauma, septic thrombophlebitis, orbital reconstruction, upper respiratory

* Former Chief Resident, Section of Oral and Maxihofacial Surgery, Department of Dentistry, Medical Center of Delaware, Wilmington; currently, in private practice, Keene, NH. t Assistant Professor of Pediatric Dentistrv and Oral Microbiology, _. Indiana University School of Dentistry, Indianapolis, IN. $ Attending Oculoplastics, Section of Ophthalmology, Department of Surgery, Medical Center of Delaware, Wilmington, DE; in private practice, Wilmington. Address correspondence and reprint requests to Dr Henry: 650 Court St, Keene, NH 0343 I.

0 1992 American

Association

027%2391/92/5002-0019$3.00/0

of Oral and Maxillofacial

Surgeons

DMD, PtiD,t

infection, and otitis media. 1o-‘5Orbital infections may result in the temporary loss of visual acuity and vision, optic neuritis, cavernous sinus thrombosis, epidural and subdural infection, meningitis, cerebritis, and brain Long-term ophthalmologic sequelae abscess. ‘~‘“~‘2~18~20 can include permanent loss in visual acuity, residual proptosis, diplopia, and blindness.2*338~9,‘0*‘3 As a consequence of orofacial infections involving the orbit and the central nervous system, hemiparesis, seizures, and death have been reported.3”0.““6-18 Classification of orbital infections has been described by Smith and Spenceti’ and modified by Chandler et al.22 It is important to differentiate between periorbital cellulitis, which is a commonly occurring infectious process limited to the eyelids, anterior to the orbital septum, from orbital cellulitis. Orbital cellulitis is a potentially lethal infectious process involving the contents of the orbit. Ethmoidal sinus disease in children is the most common source of orbital infection. In the

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adult, frontal, maxillary, and ethmoidal sinus disease are approximately equal as contributing factors to orbital infection.13 Computed tomography (CT) is the radiographic study of choice in the evaluation of orbital infection.” The presence of foreign bodies, and the location and extent of subperiosteal and intraorbital abscesses can be shown by CT. ‘* Contrast enhancement of orbital CT scans with intravenous iodinated contrast medium, meglumine iothalmate (Conray 60),can improve the evaluation and differentiation between diffuse inflammatory edema and cellulitis in the orbit.‘8,23Abnormal contrast enhancement occurs secondary to hyperemia. Orbital cellulitis is shown by CT as proptosis, nonlocalized retrobulbar contrast enhancement, and as an increase in the density and thickness of both the periorbital soft tissue and of the rim of the globe. The latter is also known as scleral enhancement. A localized mass with rim enhancement will be seen with orbital abscess.23The ability of CT to demonstrate minimal density differences in soft tissue in both the axial and coronal planes provides preoperative determination of the appropriate surgical approach. In acute cases, orbital ultrasound can also be used to determine the presence of an orbital abscess. Both contact B scan and quantitative A scan reflectivity can show the presence of such an abscess.‘0s’4 B scan has shown over 90% efficiency in detecting abscesses in the anterior orbit or of the medial wall.24 However, B scan is not used to follow posterior orbital space processes because of poor penetration. Periodic ultrasonography is an effective and convenient method to follow the clinical course of an orbital cellulitis to rule out abscess formation and to evaluate treatment.‘0,13 The typical odontogenic infection is now considered to be a mixed aerobic-anaerobic infection, with anaerobes outnumbering aerobes.25326Recognition of the contribution of anaerobic species relative to odontogenie infections has occurred with improvement in specimen collection and culture techniques that enhance preservation of anaerobic species.27 The concept of a mixed aerobic-anaerobic infection implies that an odontogenic infection occurs as a result of the interdependent and synergistic metabolism of various organisms.‘6 Bacteremia associated with acute orbital cellulitis, often with concomitant sinusitis, has been reported. ‘“~“~‘4~‘5~24~28 Nasal or conjunctival cultures have not been reliable in isolating the causative organisms in patients with orbital abscess.‘O When an orbital infection is suspected, early aggressive antibiotic therapy and surgical intervention, following appropriate consultations, should be initiated to prevent serious ocular complications and central nervous system involvement. The following case report describes the diagnosis and treatment of such a patient.

Report

of Case

A 27-year-old woman presented to the Oral and Maxillofacial Surgery Clinic at the Medical Center of Delaware with marked right periorbital edema, ecchymosis, chemosis, and pain in the upper right maxiliofacial region. The patient had noticed increased pain associated with the maxillary right first molar for 2 days. On the day of admission, she was unable to open her right eye. The patient had been seen 2 months previously by a general dentist who had recommended extraction of the maxillary right first molar due to a p&apical abscess. The patient had been in good health except for occasional urinary tract infections. The past medical history was otherwise unremarkable, with no known drug allergies and no current use of medications. Vital signs were blood pressure, 100/50 mm Hg; pulse, 72 beats per minute; respirations, 16; and axillary temperature, 37.4’C. A pkriapical radiograph of the involved tooth showed extensive caries and a periapical radiolucency. Clinical examination revealed gross caries and sensitivity to percussion. With the patient under intravenous sedation, the maxillary right first molar was extracted. A copious amount of purulent drainage from the right maxillary sinus was obtained through the extraction socket. The exudate was Gram-stained and specimens for culture of both anaerobic and aerobic organisms were collected. The patient was admitted and blood cultures were obtained prior to the initiation of antibiotic therapy. Admission laboratory studies included a white blood count (WBC) of 18.8/nL, neutrophils 49%, and bands 39%. Clindamycin 600 mg was administered intravenously every 6 hours. Immediate ophthalmology consultation was obtained even though the patient had noted no change in her vision. The bedside examination revealed near vision without correction of 53 in the right eye versus J 1 in the left eye (53 corresponds to 20/30 visual acuity on a Snellen chart). She had marked periorbital edema on the right side, with limitation of all extraocular motility, especially elevation and depression. She manifested 5 mm of proptosis. Most importantly, the pupils were round, reactive, equal in size, and without afferent pupillary defects. She had normal sensation over the first and second divisions of the right fifth cranial nerve. The anterior segments were grossly clear. The right funduscopic examination revealed disc, vessels, and macula to be normal in appearance. There was no evidence of cavernous sinus thrombosis, as there were normal pupillary responses as well as intact cranial nerves 4, 5, and 6. It was concluded that the motility disturbance was secondary to edema of the orbit. The clinical impression was right orbital cellulitis, presumably due to an odontogenic infection. The examination of the left orbit was unremarkable. The ophthalmologic plan was to rule out orbital abscess by a CT scan of the orbits and to intervene surgically to establish drainage, if necessary. An unenhanced CT scan of the paranasal sinuses and orbit revealed extensive opacification of the right maxillary sinus, right ethmoid air-cell complex, and right frontal sinus (Fig 1A,B). A small amount of gas immediately lateral to the right lamina papyracea, and in the roof of the right orbit, suggested extension of the infectious process from the right ethmoid air-cell complex into the medial right orbit, which was extraconal. Possible extension of the right frontal sinusitis to the right orbit was also suggested. A gas pocket in the roof of the orbit and possible air-fluid level were demonstrated (Fig IC). An air-fluid level was also demonstrated in the sphenoid sinus. No definite intracranial extension was noted. Consultation with otorhinolaryngology (ENT) was re-

ODONTOGENIC

INFECTION OF THE ORBIT

FIGURE 1. Axial CT scans of the paranasal sinuses. A, Extensive opacification of the right maxillary sinus and right ethmoid air-cell

complex are seen. B. Small amount of gas is seen lateral to the right lamina papyracea.C, Extension of right frontal sinusitis to right orbit. with a gas pocket in the superior aspect of the right orbit, possible air-fluid level.

quested to evaluate the right pansinusitis. They agreed with the diagnosis of a right pansinusitis and right orbital subperiosteal abscess as a result of right ethmoid sinusitis. Gram stain of the exudate from the maxillary sinus after extraction of the maxillary right first molar revealed numerous grampositive cocci in pairs and many gram-negative pleomorphic rods. On the second hospital day, the patient’s temperature was 39S”C. Visual acuity decreased to 20170 in the right eye. The patient was taken to the operating room by ENT for a right external ethmoidectomy, right nasal antrostomy, and right maxillary sinus endoscopic surgery. A right external ethmoidectomy was performed through a Lynch incision. Minimal pus was noted in the right ethmoid air-cell complex; however, necrotic debris was present. A nasoantral window was made easily into the right maxillary sinus with a trochar due to the presence of necrotic bone. The natural ostium of the right maxillary sinus was enlarged. A drain was placed from the nose into the ethmoid sinus, and from the nose into the maxillary sinus. Gram stain of ethmoid sinus exudate demonstrated many pleomorphic gram-positive rods, grampositive cocci in pairs, and gram-negative pleomorphic rods. Gram stain of the maxillary sinus demonstrated numerous gram-positive cocci in pairs and many gram-negative pleomorphic rods. The organisms cultured were coagulase-neg-

ative and sensitive to cephalothin, clindamycin, erythromycin, oxacillin, and vancomycin. The patient became afebrile on the third day of hospitalization, with a decreasing leukocytosis, WBC of 11.4/r& and a marked shift of neutophils to 7 I %. Ceftriaxone 1 g intravenously every 12 hours was given in addition to the clindamycin regimen. The patient reported right supraorbital hypoesthesia on the third day. On the fourth hospital day, the patient appeared to have slight improvement in her general condition; however, increased right upper lid edema and fluctuance were evident. There was a decrease in visual acuity to 20/200 in the right eye. Computed tomography scan of the orbits was repeated to localize possible areas of abscess formation (Fig 2A,B). The right globe was proptotic and displaced inferiorly and laterally. A loculated abscess was present supranasal to the globe, with inflammatory extension along the roof of the right orbit and posteriorly along the medial wall. The patient was taken to the operating room for incision and drainage of the right orbital abscess. An orbitomy was performed through a 25mm incision made over the right upper lid down through the orbital septum and a large amount of yellow, mucopurulent material was evacuated. The orbital fat appeared to be highly inflamed and edematous. The abscess cavity was followed more nasally towards the ethmoids.

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coyqq abscess penetration, and activity at low pH. Imipenuti was added to provide coverage against staphylococci and gram-negative rods, with adequate cerebral spinal fluid penetration. As the patient did not show any sign of men-

I

I I I

ingismus, a lumbar puncture was not performed. On the seventh hospital day, the patient reported feeling less pressure about the right orbit. Visual acuity in the right eye improved to 20150, and there was decreased proptosis. The upper right lid continued to appear dusky and edematous; however, it was not tense. The drain from the upper lid was removed (Fig 3). Results of cultures taken from the maxillary sinus after extraction of the maxillary right first molar on the first day of admission, and from the right ethmoidectomy and maxillary sinus debris, showed moderate mixed anaerobic flora. On the 10th day, the antibiotic regimen was changed to ampicillin/sulbactam (Unasyn, Roerig, New York, NY) 3 g intravenously every 6 hours. Metronidazole and imipenum were discontinued. The patient appeared to have increased right lid edema on the 11th day of hospitalization. A repeated coronal CT scan showed new abscess formation in the anterior soft tissues overlying the globe and in the preseptal space. An incision and drainage was performed at the bedside. Copius pus exited from the preseptal space, and a drain was placed. Gram stain of the preseptal exudate showed the presence of many polymorphonuclear leukocytes, but no organisms. No aerobic or anaerobic growth occurred after 72 hours. Rapid resolution of the lid edema, with enhanced motility of the eye, occurred following this procedure. The patient underwent insertion of a Hickman catheter by the General Surgery service on the 18th day to allow 3

FIGURE 2. A, Axial CT scan. There is a loculated abscess medial to the globe ofthe right eye, with the inflammatory process extending along the medial wall of the right orbit. B. Coronal CT scan. The right globe is proptotic, and displaced inferiorly and laterally. A large amount of pus was also evacuated from the more nasal loculation. Purulent material was also present posteriorly over the roof of the orbit for approximately 30 mm. A Penrose drain was inserted deep into the wound. The pupil was dilated to allow funduscopic examination. An increase

in the caliber of the vascular tree consistent with orbital engorgement due to decreased venous outflow from the eye was observed. Gram stain of the exudate from the right orbit revealed no organisms, and the rare presence of a WBC. No aerobic or anaerobic growth occurred after 72 hours. Following the surgery, the clinical course was marked by progressive proptosis, duskiness of the right eyelid, and difficulty in opening the eye for ophthalmologic examination. The pupils, however, remained equally reactive. Blood cultures taken on the first day of admission were reported positive for presumptive anaerobic gram-positive cocci in chains, presumptive anaerobic gram-negative rods, and gram-positive cocci in pairs. Consultation with Infectious Disease was requested. They agreed with the diagnosis of a right orbital abscess, ipsilateral pansinusitis, and anaerobic bacteremia of odontogenic origin, and recommended a change in antibiotic therapy. The patient received metronidazole (Flagyl, Schiapparelli Searle, Chicago, IL) 500 mg intravenously every 6 hours after a 1 g loading dose, and imipenum/cilastatin sodium (Primaxin, Merck Sharpe & Dohme, West Point, PA) 1 g intravenously every 6 hours. Ceftriaxone and clindamycin were discontinued. Metronidazole was selected for anaerobic

FIGURE 3. Facial photograph on seventh hospital day. There is marked right orbital edema, ecchymosis, and chemosis. The drains have been removed from the upper eyelid orbitomy and Lynch incisions.

176

ODONTOGENIC

weeks of home intravenous antibiotic therapy. Long-term

intravenous antibiotic therapy was suggested by Infectious Disease because of the evident bony destruction in the maxilla. The patient was to receive Unasyn 3 g intravenously four times daily. She was discharged after 20 days, with 20120 vision in each eye. However, there was still marked ptosis of the right upper eyelid, presumably due to the inflammatory distention of the orbital tissues, including the levator muscle complex. On follow-up she showed rapid resolution of the edema, proptosis, and motility disturbance. Within a period of 1 month, the upper lid had returned to a normal height, motility was full, and the eye was normal. At the 1S-month follow-up, the patient has a completely normal eye examination and no cosmetic deformity (Fig 4). The organisms in the blood cultures taken on the day of admission, which initially showed a moderate mixed anaerobic flora, were identified. Bacteroides loescheii, Peptostreptococcus anaerobius, and Propionibacterium acnes were isolated.

Discussion In the preantibiotic era, orbital cellulitis resulted in death from meningitis in 17% of cases and blindness in 20%.” The spread of an odontogenic infection to the orbit requires prompt recognition and aggressive medical and surgical intervention to prevent serious ocular complications and central nervous system involvement. Progression of an orbital infection posteriorly may involve the superior orbital fissure and spread to the cavernous sinus via the superior

FIGURE 4. Eighteenth-month follow-up facial photograph. There is normal height of the right upper eyelid, and no residual cosmetx deformity.

INFECTION

OF THE ORBIT

ophthalmic vein. Superior orbital fissure syndrome (SOFS), orbital apex syndrome, and cavernous sinus thrombosis may result.‘V’9’20,29~30 Superior orbital fissure syndrome includes anesthesia of the upper eyelid and forehead, ophthalmoplegia, ptosis, proptosis, and fixation and dilation of the pupil. In the case presented, the patient reported hypoesthesia over the area of distribution of the right frontal branch of the ophthalmic division of the trigeminal nerve and had both ptosis and proptosis. Pupillary response, however, was maintained. The decrease in ocular motility was felt to be a result of orbital edema, not secondary to nerve involvement. The hypoesthesia was most likely due to local inflammation along the superomedial orbital wall. Orbital apex syndrome includes the signs of SOFS and additionally optic neuropathy. The patient had decreased visual acuity, but pupillary responses were maintained. The decrease in visual acuity was most likely due to elevated intraorbital pressure. Elevated intraorbital pressure is the primary, and potentially reversible, mechanism of visual impairment produced by orbital cellulitis. I4 Infection within the fat of the central surgical space forces the globe anteriorly in axial proptosis, and produces chemosis.‘* Forward displacement of the globe is limited by the intraorbital optic nerve and extraocular muscles. The blood supply to the optic nerve and retina is compromised by such traction. Ischemia is compounded by the net decrease in perfusion pressure that occurs with increased intraorbital pressure. Decreased vision may also occur as a result of septic optic neuritis, embolic or thrombotic lesions in the vascular supply of the optic nerve, retina, or choroid.14 Cavernous sinus thrombosis was excluded by the absence of contralateral eye signs or signs of meningeal irritation. No ophthalmologic or neurologic deficits persisted after resolution of the orbital abscess. Computed tomography scan is indicated for patients with proptosis, ophthalmoplegia, decreased visual acuity, and if extreme eyelid edema prevents an adequate ophthalmologic examination. If a foreign body or orbital abscess is suspected, CT preoperatively will guide the surgical approach and allow monitoring of a resolving orbital abscess. I3 In addition, sinus disease and the intracranial extension of the infectious process can be shown with CT. In the case presented, repeated CT scans were performed as signs and symptoms warranted to follow the intraorbital infectious process. The case presented is interesting from the standpoint of the bacteriology of this potentially dangerous infection. Determination of the organisms involved in mixed odontogenic infections has changed dramatically over the last decade as techniques for the culture and identification of anaerobic organisms have been developed and become available for use in clinical laboratories. 27 Bacteroides spp are the anaerobes most commonly isolated from odontogenic infections.3’ The

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present case is one of the few in which clear identitication of the causative organisms of a mixed anaerobic infection of dental origin exists. The blood cultures obtained at the time of diagnosis identified Bacteroides loescheii, Peptostreptococcus anaerobius, and Propionibacterium acnes. These three species are pleomorphic gram-negative rods, gram-positive cocci, and gram-positive rods, respectively, which corresponds to the bacterial cell types identified in the exudates from both the maxillary and ethmoid sinuses. Each of these organisms has as its primary habitat the oral cavity, and thus the odontogenic origin of the orbital infection, ipsilateral pansinusitis, and anaerobic bacteremia is clear. Mixed microbial infections have been described in the bacteriologic literature for many years3” Bacteroides species have been particularly associated with these types of infections. 33-36The mechanisms by which mixed anaerobic infections are initiated are unclear. The possibility that each organism independently infects the host seems unlikely. More likely, these organisms represent a metabolic and pathologic consortium that uses virulence properties of each member to initiate and maintain the infection. Numerous animal studies have demonstrated that certain mixtures of bacteria are highly virulent, whereas the individual species that comprise them are avirulent.33-36 Bacteroides spp are able to participate in these mixed infections in the laboratory. This heightened virulence may arise from metabolic and other synergisms that may enable the participating organisms to avoid host defenses, The ability of many Bacteroides spp to form aggregates with other species may contribute to their ability to initiate mixed infection.37”9 In addition, nutritional relationships between different cell types appear to play a role in these infections.36l40 A clear nutritional relationship has been demonstrated between B assacharolyticus and Kpneumoniae in experimental subcutaneous infections in guinea pigs.36 The K pneumoniae strain used glucose for its metabolic needs and produced succinate as a metabolic product that was subsequently used for growth by a B assacharolyticus strain. It has been proposed that the vitamin K required by B melaninogenicus may be provided by other bacteria, whereas the B melaninogenicus may provide the mixed infection with its destructive potential because of its ability to produce collagenase and other proteolytic enzymes.4’ Presumably, these kinds of interactions are fundamental to the initiation and maintenance of mixed infections. The recent reclassification of Bacteroides loescheii, B meianinogenicus, and other Bacteroides spp into a novel genus, Prevotella, emphasizes the genetic diversity of microorganisms in mixed anaerobic infections.42 Antibiotic therapy for such mixed infections must necessarily take into account their complex nature. Moenning et al, in their review of odontogenic infec-

tions, indicated that certain characteristics of mixed infections suggest approaches to clinical management. First, the anaerobic nature of these infections argues for vigorous surgical therapies, such as debridement and incision and drainage. In addition, the nature of these infections should influence the antibiotic selection. Clearly, the antibiotic selected should be etfective against the greatest range of participating organisms. However, because each participant is probably necessary for pathogenicity, agents effective against a more narrow range may still render the infectious complex nonpathogenic. Patients with signs and symptoms of postseptal orbital infections should be hospitalized. The patient’s temperature, visual acuity, visual fields, and proptosis should be monitored daily. In children, visual acuity and ocular motility should be monitored every 12 hours. Visual acuity is the most important sign in evaluating success of treatment, and in planning whether surgical intervention is or will be necessary. Laboratory studies should include a leukocyte count and blood cultures with proper anaerobic collection and culturing techniques. Ophthalmology consultation is indicated if fever persists despite adequate antibiotic therapy, the patient manifests decreased visual acuity, or impairment of ocular motility occurs. Incision and drainage are indicated if a subperiosteal or orbital abscess is identified.22 Acknowledgment The authors would like to thank Thomas P. Dougherty, DDS, of Wilmington, DE, for the material presented in this case report, and Jay Luft, MD, for ENT consultation and treatment.

References 1. Ogundiya DA, Keith DA, Mirowski J: Cavernous sinus thrombosis and blindness as complications of an odontogenic infection: Report of a case and review of the literature. J Oral Maxillofac Surg 47: 13 17, 1989 2. O’Ryan F, Diloreto D, Barber D, et al: Orbital infections: Clinical and radiographic diagnosis and surgical treatment. J Oral Maxillofac Surg 46:99 1, 1988 3. Bullock JD, Fleishman JA: The spread of odontogenic infections to the orbit: Diagnosis and management. J Oral Maxillofac Surg 43:749, 1985 4. Janakarajah N, Sukumaran K: Orbital cellulitis of dental origin: Case report and review of the literature. Br J Oral Maxillofac Surg 23:140, 1985 5. Pellegrino SV: Extension of dental abscess to the orbit. J Am Dent Assoc 100:873, 1980 6. Kaban LB, McGill T: Orbital cellulitis of dental origin:Differential diagnosis and the use of computed tomography as a diagnostic aid. J Oral Surg 38:682, 1980 7. Yates C, Monks A: Orbital cellulitis complicating the extraction of infected teeth. J Dent 6229, 1978 8. LimongeUi WA, Clark MS, Williams AC: Panfacial cellulitis with contralateral orbital cellulitis and blindness after tooth extraction. J Oral Surg 35:38, 1977 9. Gold RS, Sager E: Pansinusitis, orbital cellulitiq and blindness as sequelae of delayed treatment of dental abscess. J Oral Surg 32140, 1974 10. Krohel GB, Krauss HR, Winnick J: Orbital abscess: diagnosis, therapy, and squelae. Ophthalmology

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11. Krohel GB, Krauss HR, Christensen RE, et al: Orbital abscess. Arch Ophthalmol98274, 1980 12. Jarrett WH, Gutman FA: Ocular complications of infection in the paranasal sinuses. Arch Ophthalmol 8 1:683,1969 13. Hornblass A, Herschom BJ, Stem K, et al: Orbital abscess. Surv Ophthalmol29: 169, 1984 14. Harris GJ: Suboeriosteal abscess of the orbit. Arch Oohthalmol 101:751, 1983 15. Jackson K, Baker SR: Periorbital cellulitis. Head Neck Surg 9: 227, 1987 16. Hollin SA, Gross SW, Hayashi H: Intracranial abscesses of odontogenic origin. Oral Surg Oral Med Oral Pathol23:277, 1967 17. Haymaker W: Fatal infections of the central nervous system and meninges after tooth extraction with analysis of 28 cases. Am J Orthod 31:117, 1945 18. Zimmerman RA, Bilaniuk LT: CT of orbital infection and its cerebral complications. AJR 134:45, 1980 19. Price DC, Hameroff SB, Richards RD: Cavernous sinus thrombosis and orbital cellulitis. South Med J 64: 1243, 197 1 20. Childs HG, Courville CB: Thrombosis of the cavernous sinus secondary to dental infection. Am J Orthod Oral Surg 28: 367, 1942 2 I. Smith AT, Spencer JT: Orbital complications resulting from lesions of the sinuses. Ann Otol Rhino1 Laryngol 57:5, 1948 22. Chandler JR, Langenbrunner DJ, Stevens ER: The pathogenesis of orbital complications in acute sinusitis. Laryngoscope 80: 1414, 1970 23. Leo JS, Halpem J, Sackler JP: Computed tomography in the evaluation of orbital infections. Computed Tomography 4: 133, 1980 24. Schramm VL, Myers EN, Kennerdell JS: Orbital complications of acute sinusitis: Evaluation, management, and outcome. Otolaryngology 86:22 1, 1978 25. Labriola JD, Mascaro J, Alpert B: The microbiologic flora of orofacial abscesses. J Oral Maxillofac Surg 4 I:7 11, 1983 26. Aderhold L, Knothe H, Frenkel G: The bacteriology of dentogenous pyogenic infections. Oral Surg 52:583, 1981 27. Moenning JE, Nelson CL, Kohler RB: The microbiology and chemotherapy of odontogenic infections. J Oral Maxillofac Surg 47~976, 1989

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28. Watters EC, Wallar PH, Hiles DA, et al: Acute orbital cellulitis. Arch Ophthalmol 94:785, 1976 29. Hedstrom J, Parsons J, Maloney PL, et al: Superior orbital fissure syndrome: Report of a case. J Oral Surg 32: 198, 1974 30. Kronschnabel EF: Orbital apex syndrome due to sinus infection. Iaryngoscope 84:353, 1974 3 1. Kannangara DW, Thadepalli H, McQuirter JL: Bacteriology and treatment of dental infections. Oral Surg Oral Med Oral Path01 50:103, 1980 32. Dack GM: Non-spore forming anaerobic bacteria of medical importance. Bact Rev 4:227, 1940 33. Hite KI, Locke M, He&tine HC: Synergism in experimental infections with nonsporulating anaerobic bacteria. J Inf Dis 84:1, 1949 34. MacDonald JB, Socransky SS, Gibbons RJ: Aspects of the pathogenesis of mixed anaerobic infections of mucous membranes. J Dent Res 42:529, 1963 35. Socransky SS, Gibbons RJ: Required role of Bacteroidesmelaninogenicus in mixed anaerobic infections. J Infect Dis 115: 247, 1965 36. Mayrand D, McBride BC: Ecological relationships of bacteria involved in a simple, mixed anaerobic infection. Infect Immun 27:44, 1980 37. Kolenbrander PE, Andersen RN: Cell-to-cell interactions of Capnocytophagaand Bacteroidesspecies with other oral bacteria and their potential role in development of plaque. J Periodontal Res 19:564, 1984 38. Kolenbrander PE, Andersen RN, Holdeman LV: Coaggregation of oral Bacteriodes species with other bacteria: Central role in coaggregation bridges and competitions. Infect Immun 48: 741, 1985 39. Grenier D, Mayrand D: Nutritional relationships between oral bacteria. Infect Immun 53:616, 1986 40. Gritfee MB. Patterson SS. Miller CH: Bacteroidesmelanino~enicus and dental infections: Some questions and some answers. Oral Surg Oral Med Oral Path01 54486, 1982 4 1. Holt SC, Bramanti TE: Factors in virulence expression and their role in periodontal disease pathogenesis. Crit Rev Oral Biol Med 2:177, 1991 42. Shah HN, Collins DM: Prevotella,a new genus to include Bacteroidesmelanogenicus and related species formerly classified in the genus Bacteroides. Int J Syst Bacterial 40:205, 1990