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Received Date : 27-Sep-2013 Revised Date : 23-Oct-2013 Accepted Date : 24-Oct-2013 Article type : Review Article (non-solicited)

Running title: Rhinosinusitis in oral medicine and dentistry

Rhinosinusitis in oral medicine and dentistry M Ferguson* *Private Practice, London, United Kingdom.

ABSTRACT Rhinosinusitis is a very common condition which is normally readily recognizable. Given the intimate anatomic relationship between the antrum and the posterior maxillary teeth, maxillary sinusitis can present as odontalgia. Distinguishing between odontogenic orofacial pain and pain associated with maxillary sinusitis is important to prevent unnecessary dental intervention and to direct patients to medical colleagues. Conversely, odontogenic infection can spread to involve the antrum, termed odontogenic sinusitis, or maxillary sinusitis of dental origin. Odontogenic sinusitis accounts for about 10–40% of all cases of sinusitis, and usually requires combined dental and medical treatment. Maxillary sinusitis can also be a complication of exodontia, resulting from tuberosity fractures, displaced teeth or root fragments and the creation of oroantral communications and fistulae. Dental implants and endodontic materials can also impinge on the maxillary sinus, and are rare causes of sinusitis. Often it is stated that rhinosinusitis may contribute to a halitosis complaint, and widely used diagnostic protocols for rhinosinusitis sometimes list halitosis as a minor criterion. However, gold standards in halitotosis research such

This is an Accepted Article that has been peer-reviewed and approved for publication in the Australian Dental Journal, but has yet to undergo copy-editing and proof correction. Please cite this article as an “Accepted Article”; doi: 10.1111/adj.12193 This article is protected by copyright. All rights reserved.

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as organoleptic assessment or gas chromatography have not been use to validate a correlation between objective (genuine) halitosis and sinusitis. The pathophysiology of this mechanism is unclear, and the relative importance of this alongside other causes of extraoral halitosis is debated. Keywords: Halitosis, maxillary sinusitis, odontogenic sinusitis, oronantral communication,

rhinosinusitis, sinusitis. Abbreviations and acronyms: ARS = acute rhinosinusitis; CRS = chronic rhinosinusitis; FESS = functional endoscopic sinus surgery; OAC = oroantral communication; OAF = oroantral fistula;

URTI = upper respiratory tract infection; VSC = volatile sulfur compound. (Accepted for publication 24 October 2013.)

INTRODUCTION The maxillary antrum is often described as a four-sided pyramid, the base orientated vertically, lateral to the nasal cavity, and the apex extending into the zygomatic bone (the zygomatic recess). Relatively thin bony walls divide the sinus from the orbit superiorly and the oral cavity inferiorly. The medial wall is cartilaginous, dividing the antrum from the nasal cavity. Beyond the posterior wall lies the pterygomaxillary fossa medially and the infratemporal fossa laterally. The maxillary alveolar process forms the antral floor (alveolar recess), which often lies at a more inferior position relative to the nasal cavity floor in adults. The antral floor is intimately related to the roots of the maxillary teeth, particularly the first molar and second premolar. The morphology and degree of pneumatization is subject to significant interpersonal variation. The antral floor may extend as far anteriorly as the canine, or as posteriorly as the third molar. Bony irregularities, such as conical processes or dehiscences, are fairly commonly associated with the

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periapex of maxillary teeth in the antral floor.1 Whilst pneumatization of the sinus generally halts with eruption of the permanent teeth, the roots of maxillary teeth may disrupt the contours of the antral floor. This may be seen in healthy individuals, indicating that pneumatization has continued to some degree around the teeth. Edentulism triggers resorption of the alveolar ridge but also increased pneumatization of the sinus. The posterior, middle and anterior superior alveolar nerves are all associated with the walls of the antrum, and they may all be involved in its innervation.2 The mucoperiosteal lining of the antrum (the Schneiderian membrane) is a respiratory epithelium. A mucocillary clearance mechanism keeps mucous secretions slowly moving, at about 6 mm/min, towards the ostium.3 As a result of this, in health the microbiota is largely controlled, although the sinus is not sterile as was once believed. The osteomeatal complex or unit is a collective term for the final common route of drainage of the maxillary, frontal and anterior and middle ethmoid sinuses into the middle meatus, between the middle and inferior nasal conchae. The ostium of the maxillary sinus is situated superomedially. This is significant because the drainage of secretions is against gravity, meaning that there is no redundancy mechanism if dysfunction of mucocillary clearance occurs.1 The function of the paranasal air sinuses is open to debate, but generally speaking the

sinonasal apparatus as a whole is adapted to warming and adding moisture to inspired air, as well as filtering any particulate suspension.

Rhinosinusitis: background Sinusitis is inflammation of the mucosal lining of one or more of the paranasal sinuses,4 and it is a very common trigger to seek health care advice. It is estimated that about 50 patients with sinusitis will be seen by the average primary care physician annually,5 making it one of the top

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10 diagnoses made in ambulatory patients.6 ‘Rhinosinusitis’ is becoming an increasingly preferred term,7 since it is argued that there is mucosal continuity between the paranasal sinuses

and the nasal cavity proper, and that inflammation is generalized over these arbitrary anatomic boundaries. The ICD-10 describes a dichotomy between acute rhinosinusitis (ARS) if the condition lasts for less than 12 weeks, and chronic rhinosinusitis (CRS) if it lasts for more. However, many define ARS as lasting less than four weeks, and use the term subacute rhinosinusitis if the condition lasts between 4 and 12 weeks.8 Some also distinguish between

recurrent acute rhinosinusitis and CRS, in which the latter lacks any symptoms of CRS between acute symptomatic episodes.7

Most ARS represents extension of a viral upper respiratory tract infection (URTI) into the sinuses,7 usually caused by rhinoviruses. Viral URTI or allergic rhinitis may lead to secondary bacterial infection of the sinuses. This only occurs in a small percentage of all viral URTI cases;9 about 0.5–2% (or 6–13% in children).4,8 In bacterial sinusits, Streptococcus pneumoniae,

Haemophilus influenzae, and/or Moraxella catarrhalis are common causative organisms.8 CRS is a multifactorial chronic inflammatory disorder in which allergy, bacterial and fungal infection may be involved.10 Polypoid and non-polypoid forms of CRS are recognized.11 Obstruction of the osteomateal unit is thought to be pivotal in the development and persistence of sinusitis.1

The cardinal features of ARS are purulent nasal discharge (anterior and/or posterior); nasal obstruction/congestion; facial pain/pressure/fullness in the anterior face, periorbital region or headache.7 The cardinal features of CRS include those described for ARS in addition to olfactory chemosensory dysfunction (dysosmia or total anosmia). Minor diagnostic criteria for CRS are said to be headache, halitosis, fatigue, dental pain, cough and ear pressure/fullness.12 Although as

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described above the concept of isolated and localized inflammation is oversimplification, by tradition the signs and symptoms of maxillary sinusitis (antritis) are often listed slightly differently to ethmoid sinusitis (ethmoiditis), frontal sinusitis, etc. Since the focus of this article is maxillary sinusitis, the typical signs and symptoms maxillary sinusitis are discussed below in the context of how to distinguish this from dental pain. Viral URTI tends to be self-limiting, and the treatment is symptomatic (e.g. analgesics, antipyretics and/or decongestants).7 There is widespread over-prescription of antibiotics in ARS,9 which are usually ineffective since most cases represent viral URTI. One evidence based protocol advocated that clinicians assume that the aetiology of rhinosinusitis is viral if symptoms have been present for less than 10 days and are not worsening. If symptoms are present for more than 10 days, or there is double worsening (worsening after an initial improvement), then acute bacterial rhinosinusitis is presumed.7 CRS tends to be managed with nasal irrigation and topical

and systemic pharmacotherapies including corticosteroids, decongestants, antihistamines, antibiotics and antifungals.13 Functional endoscopic sinus surgery (FESS) is used in cases

recalcitrant to non-surgical treatment. This technique aims to restore sinus ventilation and drainage.12

Maxillary sinusitis masquerading as odontalgia Maxillary sinusitis is not uncommonly perceived as pain originating in the maxillary molar and premolar teeth, which may trigger patients to seek dental care. This is an example of so called non-odontogenic toothache.14 In one report, 11% of patients with sinusitis reported maxillary

toothache.15 In maxillary sinusitis, the posterior maxillary teeth may be tender to percussion,16 and hypersensitive to cold stimuli. This is secondary hyperalgesia (i.e. concentric spread of pain

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beyond the area of tissue injury), rather than true referred pain. There may also be mucosal tenderness, oedema and erythema in the area over the sinus intraorally.14 This clinical presentation may prompt consideration of dental pathoses. If dental radiographs are carried out to aid the diagnosis, artifactual widening of the periodontal ligament space may occur where the apices are superimposed on the sinus. Not unreasonably, and particularly in heavily restored

quadrants which may provide multiple apparent causes of dental pain, busy dentists may be motivated to carry out dental treatment in such a scenario. Differentiation between odontalgia from maxillary sinusitis and dental causes of odontalgia (e.g. pulpitis or a dentoalveolar abscess) is achieved mainly through a careful history and examination. The cardinal signs and symptoms of rhinosinusitis have been described above, including purulent nasal discharge and nasal obstruction/congestion. Classically, sinusitis pain increases during head movements (particularly when the head is placed below the level of the heart), or during valsalva manoeuvre. The pain is worse when the head is held upright compared to when lying supine.17 The explanation for this feature is related to local increases in blood

pressure which accompany postural changes. However, pain intensity modulation secondary to postural changes may also accompany an acute dentoalveolar abscess. In sinusitis, there may be tenderness to palpatation in the infraorbital region.14 Potentially useful diagnostic aids are

provided by the fact that local anesthetic given intraorally will not relieve sinusitis pain, whereas topical nasal anesthetic will.14 Intraoral transillumination of the sinuses in a darkened room may

show reduced transillumination of the involved side, caused by the presence of fluid and thickening of the Schneiderian membrane.3 With the patient's head held upright, a fluid level may even be demonstrable.16 Several teeth tend to be tender to percussion rather than a single tooth, which may help to rule out a dental cause, although generalized tenderness to percussion can also

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be seen in other conditions such as bruxism. A dental panoramic radiograph may show obvious pathology such as mucosal thickening or a fluid level in the inferior part of the sinus,3 appearing

as radiopaque areas relative to the contralateral side. Since this view aims to present the structures within the focal trough of the dental arches in greatest detail, it is by no means an ideal diagnostic aid, and it is questionable whether it is indicated specifically to investigate the sinus. Other features of acute maxillary sinusitis are non-specific (e.g. pyrexia, elevated erythrocyte sedimentation rate and elevated C-reactive protein),18 and not particularly helpful in ruling out odontogenic infection. If a patient’s pain is suspected to originate from the sinus rather than a dental cause, referral to a medical colleague is indicated.

Odontogenic maxillary sinusitis By tradition, odontogenic infection is considered a rare cause of sinusitis, said to account for about 10–12% of cases.3,19 In 1986, a study of 200 patients with sinusitis reported that 40% were odontogenic in nature.20 More recently in 2010, a study of 411 patients with CRS reported that 25% were odontogenic.21 Thickening of the sinus mucosa is almost 10 times more commonly

demonstrated in individuals with periapical lesions.22 The cause of odontogenic maxillary

sinusitis is usually a periapical or periodontal infection of a maxillary posterior tooth, where the inflammatory exudate has eroded through the bone superiorly to drain into the maxillary sinus. Less commonly, dentoalveolar trauma or surgery involving the posterior maxillary teeth result in infection which spreads to the sinus. The displacement of tooth apices or other foreign bodies into the sinus can cause sinusitis. Dental implants which penetrate the sinus membrane are sometimes cited as a potential cause of sinusitis. However, in a longitudinal study of 70 patients with implants perforating the sinus,

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none had evidence of sinusitis after an average review period of 10 years.23 Dental implants can be entirely lost into the sinus during their placement and act as a foreign body.24 Endodontic materials can also be extruded into the sinus. Aspergillosis sinusitis is a recognized complication of zinc oxide eugenol materials (e.g. obturation paste) being left in the antrum.25-27 (See Fig. 3.)

The causative organisms in odontogenic sinusitis tend to differ from non-odontogenic sinusitis. In the latter, normal nasal cavity commensals are frequently implicated, whereas in the former, the infection may involve oral commensals and is most commonly a predominantly anaerobic, polymicrobial infection of anaerobic streptococci spp., gram-negative bacilli, and Enterobacteriaceae.29 Once odontogenic infection involves the maxilary sinus, if untreated or inadequately treated, it may progress to pansinusitis. Rare complications include osteomyelitis, orbital celulitis, cavernous sinus thrombosis, meningitis, subdural empyema, or intracranial abscess. There have been reported cases of blindness, paralysis or death resulting from complications of odontogenic sinusitis.3,30,31

In a review of 33 cases of odontogenic sinusitis, the clinical features commonly found were sinus pain, postnasal drip, congestion and maxillary toothache. Over half the cases demonstrated a periapical abscess on CT, but in 12 cases there was no obvious dental pathology. Odontogenic sinusitis and non- odontogenic sinusitis present with similar clinical features, but the former is

usually unilateral and may be present in the absence of obstruction to the drainage of the sinus.19,32 Odontogenic maxillary sinusitis may be resistant to conventional sinusitis therapy.29 Rather,

management of both the sinusitis and the dental cause is required to resolve the condition. Dental management is by extraction or endodontic treatment of the causative tooth. Antibiotics are

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usually required, and cover for both oral and sinus flora should be prescribed.34 In the case of foreign bodies, their location should be confirmed radiographically and then removed by either a Caldwell-Luc or endoscopic approach.

Maxillary sinusitis secondary to oroantral communications and fistulae Sinusitis can occur secondary to an oroantral communication (OAC) created during exodontia. Fractures of the maxillary tuberosity may create OAC, especially if the tuberosity is completely removed. OAC are more commonly created than is generally realized, although most small defects tend to close spontaneously without any intervention. If a patent communication persists, mucosal epithelia proliferate from the sinus lining and the oral mucosa, taking about a week to fully line the defect, which is then termed an oroantral fistula (OAF). Classically, OAC/OAF present with a complaint of beverages entering the nose when drinking, a bad, salty taste or the inability to draw on a cigarette or to inflate the cheeks.33 These features are mixed on a

background of the usual sinonasal symptoms if acute sinusitis develops. On examination, a prolapse of antral lining may be visible in the tooth socket. Immediately following extraction, it has been suggested that asking the patient to blow through their nose while occluding their nares, and observing the socket for escaping bubbles can confirm the presence of an OAC. However, this risks creation of an OAC where it did not exist before and is an inadvisable diagnostic test.

Depending upon the experience of the clinician, management of this complication may warrant referral to a specialist in oral surgery. However, measures to prevent OAC/OAF should be common knowledge to all clinicians carrying out exodontia. Firstly, the risk assessment on all maxillary posterior teeth for extraction should include consideration of the possibility or creating an OAF. Example factors which predispose to OAC/OAF are listed in Table 1. About 50% of

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reported OAF are associated with the maxillary first molar, most commonly in middle aged males.28 The maxillary first molar region often corresponds to the most inferior position of the antral floor and hence the closest part of the antrum to the oral cavity. Also, the maxillary first molar is a large tooth, leaving a large socket after extraction, and making it less likely that a thrombus will be retained and organize. Teeth which are deemed to be at high risk may be more appropriately extracted by a specialist in oral surgery, or the surgical plan amended to reduce the risk. For example, sectioning of the tooth carries less risk of OAF creation than extraction with forceps and elevators. Similarly, curettage of lesions such as periapical granulomata risks creation of an OAC if in close proximity to the antrum. Following the extraction, postoperative advice (e.g. avoid blowing the nose, drinking through a straw or sucking at or otherwise disturbing the extraction site, which risks loss of the thrombus), should be given to the patient. Sinusitis secondary to OAF tends not to resolve until the defect is closed. Detailed descriptions

of the surgical management of OAF are outside the scope of this review. The treatment options for established defects are flap closure (buccal or palatal mucoperiosteal flap, or buccal fat pad), or minimally invasive techniques utilizing bioresorbable root analogues or haemostatic gauze. A systematic review held these to have comparable reliability.35 The buccal advancement flap

technique may result in loss of sulcus depth, but is favoured by some. Other sources also state that excision of the epithelial lining of the tract is indicated to prevent inclusion of epithelia which may later proliferate and cause the OAF to persist. Immediately following closure of an OAF, an antral regime is indicated, aiming to avoid increased pressure in the sinus. A typical antral regime consists of nasal decongestants (e.g. ephedrine), implicit instructions not to blow the nose, antibiotics and antiseptic mouthwash (e.g. chlorhexidine).

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Displacement of root into the antrum Most often, this occurs with the palatal root of the maxillary first molar, or an impacted maxillary third molar, and is due to excessive vertical force applied to the tooth with forceps or elevators, combined with predisposing anatomic factors such as a thin or otherwise structurally weakened floor of the antrum. As with the risk factors for OAC/OAF creation, periapical lesions are sometimes responsible. The sudden disappearance of a tooth or root during the extraction, combined with a routine check that the apices of extracted teeth are intact means that this complication is usually immediately detected by the dentist. Root fracture is a common occurrence in tooth extraction, but is generally preventable with due care. Most root fractures occur with premature attempts to deliver the tooth, before sufficient luxation has been carried out, or movements made without regard for the root morphology, e.g. rotational movements in a tooth with a sharp apical bend. However, there will always be some teeth which are impossible to extract whole. Some are of the opinion that if there is only a small fragment of root left in the socket and no periapical pathology present, then the root can be left as its retrieval would cause more harm than good. Such retained roots may spontaneously erupt or sequestrate in later years, where their removal will be much easier. However, if a fractured root from a maxillary posterior tooth is not visible in the socket, it cannot be left and it must be located. This commonly occurs in addition to the creation of an OAC, but the mucosal lining of the antrum may not necessarily be penetrated since the root can be pushed submucosally under the lining rather than being displaced to lie free in the antrum. Again, depending upon the setting and the clinician's experience, this complication may warrant referral to a specialist. The management involves initially locating the fragment radiographically,

ideally in two different views so the exact position can be determined via parallax. Attempts to

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remove the fragment can be exacted via the tooth socket if an OAC has been created, or via a Caldwell–Luc approach if no OAC exists. If these attempts fail, intranasal antrostomy may be required.

Rhinosinusitis as a cause of halitosis There is general agreement that about 10% of all objective (genuine) halitosis complaints are caused by extraoral processes; however, the relative importance of said processes is debated. One research group report that halitosis caused by the blood-borne mechanism is the most common,36-

38

whilst others state that tonsillar pathology is the most common.39 Sinusitis is sometimes cited

as a possible cause of halitosis.40-43 Indeed, the RSTF 1996 criteria lists halitosis as a minor

clinical feature of chronic sinustitis,44 and one source reported 50–70% of chronic sinusitis

patients will complain of halitosis,45 which may be present even when features such as nasal

obstruction, postnasal exudate, pain, sneezing and secretion are clinically absent.46 The many sources that list halitosis as a possible symptom of sinusitis must be interpreted with caution. Clinicians and researchers unfamiliar with gold standard techniques such as organoleptic assessment or analysis of breath gases with gas chromatography may utilize unreliable methods of halitosis detection, e.g. questionnaires and patient self reports. Subjective (non-genuine) halitosis complaints may account for between 5% and 71% of all patients who complain of

halitosis, and these are explained in the large part by psychologic factors, but also by retronasal olfaction or neurologic factors such as chemosensory dysfunction.36,47 A marked lack of

standardization of research methodologies has led to some authors calling for greater efforts in standardizing protocols in halitosis research.48 Many reported correlations between halitosis and various ailments may prove to be uncorroborated by studies with more reliable methodologies.

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For example, upon reviewing the literature one will find a several studies which report a correlation between halitosis and Heliobacter pylori infection, and yet when researchers who specialize in halitosis carried out a study using gas chromatography, no such association was demonstrated.49 Unfortunately, researchers who are unfamiliar with the complexity of the halitosis topic readily accept self reported halitosis as a reliable measure of objective halitosis. To the author's knowledge there is no available evidence of the exact pathophysiologic mechanism by which sinusitis may cause either an objective or subjective halitosis complaint. Therefore, several possible mechanisms are suggested here. Perhaps it would be more accurate to suggest that sinusitis is a possible cause of nasal fetor, but regardless this is usually considered within the halitosis topic. On a side note, some claim that halitosis secondary to sinonasal pathoses is more strongly detectable on the nose breath while the mouth is closed than on the mouth breath when the nares are occluded.50 Stasis and stagnation of secretions, the result of

mucosal inflammation which obstructs drainage, will likely be associated with increased bacterial load. Consequently, increased volatile sulfur compound (VSC) release may occur, along with other volatiles. In purulent sinusitis, the presence of pus may contribute to the malodour, particularly if anaerobic bacteria predominate in the infection. The so-called post-nasal drip syndrome is postulated to be caused by sinusitis among other things, and it is said to be a cause of halitosis in addition. In post-nasal drip, mucus drains onto the posterior dorsal tongue via the nasopharynx.51 However, it has been argued that nasal mucus dripping down the back of the

throat occurs in normal, healthy people, and furthermore there are no pathologic or biochemical tests for this condition.52 Also, the relationship between post-nasal drip and halitosis has not been formally investigated. Some have suggested that obstructive nasal pathology can cause mouth breathing, which results in oral malodor (intraoral halitosis) secondary to xerostomia.53,54

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Xerostomia reduces the mechanical cleansing and antimicrobial action of saliva and results in a sharp increase in bacterial growth in the mouth. The higher the bacterial load, the more VSC are released during bacterial putrefaction. The nasal congestion which accompanies sinusitis is readily imagined as a cause of nasal obstruction. However, to contradict this possible mechanism, others report that mouth breathing is not associated with halitosis.55 On the other hand, subjective halitosis (odour perceived only by the patient) could be explained by dysosmia, retronasal olfcation, or a foul taste caused by posterior nasal discharge.

CONCLUSIONS Rhinosinusitis may present as maxillary toothache and such patients may present to the dentist. In this scenario, differentiation between dental causes of odontalgia and maxillary sinusitis can be challenging, requiring a careful history and examination. Odontogenic maxillary sinusitis has a higher incidence than is traditionally recognized, and requires joint dental and medical management once established. Although rhinosinusitis is frequently described as causing halitosis, it is unclear if this constitutes an objective or subjective halitosis complaint since the evidence of a relationship is performed in the absence of gold standards for halitology research. Theoretically, both objective and subjective halitosis may be caused by several mechanisms in rhinosinusitis.

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2. Norton N. Netter's Head and Neck Anatomy for Dentistry. Philadelphia: Saunders Elsevier, 2007:402. 3. Hupp JR, Ellis E, Tucker MR. Contemporary Oral and Maxillofacial Surgery. 5th edn. St. Louis: Mosby Elsevier, 2008:383, 385, 388. 4. Shaikh N, Wald ER, Pi M. Decongestants, antihistamines and nasal irrigation for acute sinusitis in children. Cochrane Database Syst Rev CD007909. doi: 10.1002/14651858.CD007909.pub3. 5. Venekamp RP, Thompson MJ, Hayward G, et al. Systemic corticosteroids for acute sinusitis.

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Address for correspondence: Dr Matthew Ferguson Email: [email protected]

Legends Fig. 1 Anatomic relations of the maxillary sinus. Fig. 2 CT showing maxillary sinusitis (image courtesy of Murat Aydin DDS, PhD). Fig. 3 CT showing Aspergillosis sinusitis of right maxillary sinus (image courtesy of Murat Aydin DDS, PhD).

Table 1 Oroantral communication, predisposing factors Local factors • • • • • • •

Intimate relationship between tooth apices and antral floor Widely divergent root morphology – more likely to remove a section of bone Tooth size – large teeth more prone Tooth position – maxillary first molar most common Periapical lesions – lead to bony remodelling of the contour of the antral floor and weakness Hypercementosis Ankylosis

Systemic factors • • • •

Patient age – middle aged and elderly patients more predisposed Impaired wound healing – e.g. smoking Predisposition to infection – e.g. diabetes Systemic bone disorder – especially alterations in bone density

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Accepted Article This article is protected by copyright. All rights reserved.

Accepted Article This article is protected by copyright. All rights reserved.

Accepted Article This article is protected by copyright. All rights reserved.

Rhinosinusitis in oral medicine and dentistry.

Rhinosinusitis is a very common condition which is normally readily recognizable. Given the intimate anatomic relationship between the antrum and the ...
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