Odontogenic orbital cellulitis (OOC) represents only 3–5% of all orbital cellulitis cases but is generally associated with a poor prognosis pertaining to worse visual outcomes and increased risk of serious complications such as vision loss and cavernous sinus thrombosis [1]. This series demonstrates that patients with OOC more frequently present with an acute orbital compartment syndrome with vision loss and optic neuropathy, and the organism most commonly implicated is Streptococcus milleri. While the patients in this series did not experience any intracranial complications, repeated surgical interventions were necessary and visual prognosis was generally poor in cases secondary to Streptococcus milleri.
The spread of odontogenic infection to the orbit occurs via several pathways [1]. The most common mode of spread occurs via the maxillary sinus. The buccal plate is a thin layer of bone separating the maxillary premolars and molars from the maxillary sinus and dehiscence can facilitate rapid spread into the orbit via the orbital floor. Odontogenic orbital cellulitis is typically preceded by a periapical infection of carious maxillary molars and premolars [26]. Root proximity of these dentition to the maxillary sinus floor mucosa, serves as a conduit for the passage of bacterial organisms. Spread can also occur via the retromaxillary soft tissue and extend into the infratemporal fossa, inferior orbital fissure and finally into the orbit. In particular, the proximity of this portion of the inferior orbital fissure to the orbital apex can place patients at greater risk of visual impairment. The spread of odontogenic orbital cellulitis to the surgical orbital apex, defined as the posterior 3/5 of the retrobulbar orbital space, makes for a vision-threatening condition [27]. Infectious spread to this region presents higher risk of optic nerve decompression due to the most significant decrease in volume, attesting to the important of early recognition of clinical and radiological signs. Thrombophlebitic extension to the valveless pterygoid venous plexus can result in septic emboli and cavernous sinus thrombosis.
Clinical characteristicsOdontogenic orbital cellulitis can cause rapid vision loss with a poor prognosis for recovery. Youssef et al. reported 24 combined cases of odontogenic orbital cellulitis from the literature in 2008, of which 11 (45.8%) of which recorded a final vision of light perception/no light perception [18]. Similarly, of the 4 cases presented in our series, 1 (25%) recorded a final visual acuity of no light perception and one patient underwent an exenteration.
The thin nature of the buccal plate which sits atop the maxillary alveolar bone promotes the rapid spread of odontogenic infections via the maxillary sinus [1]. There is great variability in time to presentation with OOC – Bullock et al., from reported ranges from 48 h to 13 days [1]. In our series, the duration from dental infection to orbital cellulitis ranged from 24 h to 2 weeks. The delayed presentation may be due to partial treatment with oral antibiotics soon after a dental extraction.
Microbiological profile and virulence factorsThe microbiological profile of OOC consists of a mix of anaerobic and aerobic bacteria [28]. In Umeshappa et al.’s series of 100 patients with infection of the odontogenic space, Staphylococcus aureus, Streptococcus viridans and Streptococcus milleri were amongst the most common causative anaerobic bacteria [29]. The trends over time have remained consistent, with a review of the current literature revealing that 68% of cases are due to gram-positive and non-motile Streptoccoccus bacteria [1, 4,5,6,7,8,9,10,11,12,13,14,15,16,17,18, 20,21,22, 24, 30,31,32,33,34,35,36,37,38,39]. Importantly, much of these infections are polymicrobial and a combination of anaerobic and aerobic bacteria comprise 60% of odontogenic infectious flora [40] (Supplementary Table 1).
Despite residing as commensal flora within the oral cavity, the Streptococcus milleri species is virulent and a prominent cause of abscess formation [41]. Virulence factors specific to S. Milleri include adherence, invasion, spreading factors, cell wall proteins and component histadine kinases [42]. Unlike other mucosal streptococcal species, S. milleri, is more frequently associated with men [41]. In fact, male gender has been positively correlated with vision loss [18].
Radiological characteristicsA hallmark radiological finding of dental infection is the presence of lucency surrounding the root apex as well as a widening of the periodontal ligament (PDL). The presence of a dental subperiosteal abscess can appear radiologically similar to periapical lucency [2]. Widening of the PDL space occurs due to the presence or spread of periodontal pathogens [43]. Additionally, carious tooth damage, which serves as an inlet of bacteria, presents as a hypoattenuation within the crown.
Inflammation of the maxillary sinus can create a conduit for the spread of infection through the midface. Orbital inflammatory signs are apparent in the context of cellulitis, including extraocular muscle enlargement and retrobulbar fat stranding [44], which was present in all patients within our series. Orbital emphysema is another radiological sign of anaerobic infection due to a path of communication between the infected maxillary sinus and orbit, allowing the spread of anaerobic bacteria such as the streptococcal species. When considering all causes of orbital cellulitis, the medial rectus is the most commonly affected muscle likely due to adjacent involvement of the ethmoid sinuses [45] (Supplementary Table 1). In contrast, half of the patients in our series presented with lateral rectus enlargement, which would be more consistent with an inferolateral pathway of pathogenic spread from the maxillary soft tissue, infratemporal fossa and inferior orbital fissure in OOC.
Most Streptococcus species are facultative anaerobes and therefore can present with evidence of gas within the orbit on CT scans. Gas may be an indication of sinogenic spread of infection into the orbit, or it may be due to gas-producing organisms. Two cases (50%) in this study demonstrated orbital emphysema secondary to Streptococci milleri. In addition to anaerobic Streptococcus, other organisms implicated include Clostridium, Proteus, Klebsiella species and Escherichia coli [33, 46, 47]. Gas within the orbit has significant potential for vision loss via raised intraorbital pressure leading to tissue ischaemia and optic neuropathy [47]. Therefore, orbital emphysema is an ominous radiographic sign that should warrant concern for an aggressive organism.
Magnetic resonance imaging (MRI) is superior for its delineation and monitoring of soft tissue changes and abscess formation in the brain and orbit. However, in the acute setting, access can be limited and thus CT imaging predominated as the initial imaging of choice in our series. All patients in this study eventually had an MRI scan, which showed T2 hyperintensity in the regions of involvement, which is consistent with oedema and inflammation.
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