The Maxillary Sinus: What the General Dental Team Need to Know Part 1: Paranasal Sinus Physiology, Infective Disease and Diagnosis of Pain

Paranasal sinus development

The paranasal sinuses are named after the bones within which they lie develop as epithelial outgrowths from the nasal cavity. Named after the maxillary, ethmoid, sphenoid and frontal bones, the location and three-dimensional anatomy of the paranasal sinuses in the adult are best viewed in a colour atlas of cross-sectional anatomy.

In the young child, the paranasal sinuses are minimally developed. The maxillary and ethmoid sinuses begin development around the third month of intra-uterine life, are present at birth, and have reached almost full adult size by puberty, although continue to pneumatize the bones within which they lie throughout life. The sphenoid sinuses develop after birth, becoming pneumatized by the age of five and, although they also reach adult size by puberty, they continue to enlarge through life. The frontal sinuses are the last to develop as an out-budding from the epithelium of the anterior ethmoid air cells, only reaching full size by the late teenage period.²

All of the sinuses drain into the nasal cavity through epithelized channels called ostia. The drainage of the maxillary sinus is complicated in that the ostium that opens into the nasal cavity is high up on the medial wall, close to the orbit, such that drainage has to occur against gravity. The ethmoid and maxillary sinuses drain into the middle meatus, below the middle turbinate. The location of this is often termed the osteo-meatal unit (Figure 1).

Paranasal sinus physiology

Historically, the paranasal sinuses were thought to drain by gravity, and it was for this reason that early treatment for infection of the maxillary sinus in the pre-antibiotic era often involved creating an antrostomy as inferiorly as possible on the medial wall of the sinus, on the lateral wall of the nose below either the inferior or middle turbinates.^3,4 Surgical drainage of maxillary sinus infection into the mouth through an extraction site was also performed.⁵ The development of electron microscopy increased understanding of cell function and immunology changed that concept.

All paranasal sinuses, including the nasal cavity, are lined with pseudo-columnar ciliated epithelium, among which is interspersed goblet cells and a few sero-mucous salivary gland cells.^6,7 It is the interactive role of the cilia and the secretions of the goblet cells that contributes to the special physiological environment within the paranasal sinuses⁸ (Figure 2)

The goblet cells secrete a complex blend of diverse glycoproteins (mucins), lysozymes and lactoferrins, alongside many other immune-modulating factors, including cytokines.^6,7,8,9 The mucin layer sits on top of the liquid phase layer which has a specific acid-base balance in health for optimal function.¹⁰

Within the liquid phase layer lie the cilia. The cilia, approximately 6μm in length, have a unique internal structure of dynein fibrils that enable controlled movement.¹¹ The cilia of the respiratory epithelium beat in a synchronized motion, usually at a rate of 10–20 times per second in health, reducing to 5 or less in the presence of infection or irritants.¹¹

It is the combined action of the cilia and the liquid/gel phase of the airway surface layer that traps microbial organisms and foreign bodies, propelling them to the maxillary ostia for removal via muco-ciliary clearance (Figure 1). The descriptive term gel on water, or gel on a brush, has been used to describe the interaction of the cilia with the mucin and liquid phases of the airway surface layer, which in health moves at a rate of 10 mm per minute, often against gravity and not in the most direct route to the ostium.¹¹ The rate is reduced in disease. Impaired muco-ciliary clearance contributes to stasis and infection, and may arise through ciliary dyskinesia or changes in mucous secretion.¹¹ Primary ciliary dyskinesia occurs through deranged protein coding in the formation of the dynein fibrils, usually as a result of genetic disease.¹¹ Secondary ciliary dyskinesia is caused by infection, or environmental influences.¹¹ Diseases, such as cystic fibrosis, will produce a mucous layer that becomes dehydrated, shrinks and impinges on the underlying serous layer, thereby impairing normal ciliary movement.^11,12 Excessive production of mucous with an increased viscosity in Chronic Obstructive Pulmonary Disease (COPD) and asthma, as a result of goblet cell metaplasia, also impedes normal ciliary movement.^10,11,13

From the perspective of the Dental Team, impaired muco-ciliary clearance, as a result of secondary ciliary dyskinesia, arises when oral micro-organisms move into the maxillary sinus, or when dental materials are introduced. The endotoxins produced by bacteria impair normal ciliary activity.¹⁴ The impaired muco-ciliary function, with or without oral microbial contamination, will result in stasis and lead to infection, usually bacterial or fungal.¹¹

Paranasal sinus infection

Paranasal sinus infection is classified as either acute or chronic and may arise as a result of viruses, bacteria and fungi. The paranasal sinuses are self-cleansing air-filled, humidified spaces, that in health have a limited and balanced microbial flora.^15,16

Acute paranasal sinusitis, usually of viral aetiology, characteristically arises a few days after the patient is recovering from an acute upper respiratory tract infection, most often, the common cold. The characteristic biphasic presentation is that of an individual who has just started to feel better after 4–5 days of acute upper respiratory symptoms, to relapse with acute intense pain in the mid-face or frontal area.¹⁷ When the maxillary sinus is involved, patients may also complain of toothache.¹⁷

The acute sinusitis will usually settle in one week, with or without treatment. Guidelines recommend symptom control with nasal decongestants, topical steroids sprays and analgesia.^17,18 Nasal decongestants should not be used regularly for prolonged periods as rebound mucosal oedema occurs when they are stopped.¹⁹ Nasal douching with saline can ease symptoms.²⁰

Most cases of acute paranasal sinus infection are of viral origin.¹⁷ Approximately 2% are of bacterial origin.¹⁷ The acute viral sinusitis should resolve in 10 days. If not, consideration should then be given to the possibility of bacterial acute sinusitis as a secondary infection.¹⁷ If there is bacterial rhinosinal disease, the clinician would expect the patient to report nasal obstruction and purulent nasal discharge. Systemic antibiotics are rarely required unless the patient is pyrexic, or there are other signs of spreading infection.¹⁷ Clinical guidelines provide evidence-based recommendations relating to antibiotic prescription.^17,18,21,22 The antibiotic of choice is co-amoxiclav. Second line antibiotics are macrolides and tetracyclines.^21,22 Radiological investigation is not indicated unless there are signs of spreading infection.^17,23

Acute bacterial rhinosinal disease in severe cases can present with orbital and intracranial extension and the clinical signs outlined in Table 1 would alert the practitioner to this.^24,25 Patients presenting with infective complications, as outlined above, will be clinically very unwell and more inclined to contact their medical rather than dental practitioner. However, peri-orbital oedema from acute bacterial infections of the ethmoids and maxillary sinus can be similar to that arising from a maxillary canine or lateral incisor tooth, and for that reason patients may occasionally contact their dental rather than medical practitioner.

Chronic sinusitis is defined as a symptom of nasal obstruction, facial pressure or full purulent nasal discharge, and hyposmia and occasionally anosmia lasting for 12 or more weeks.¹⁷ It is usually of bacterial or fungal aetiology, although can also occur as a result of the immune system response to fungal spores (fungal allergy). Chronic rhinosinal disease is classified by either the absence or presence of polypoid tissue and there are specific treatment guidelines for each.¹⁷ Polypoid tissue arises because of the immunological response of the nasal mucosa to irritants. Most polyps arise in the ethmoid sinuses, with a smaller proportion, usually antro-choanal, arising in the maxillary sinus.²⁶

Orofacial pain, including odontogenic pain and headache, is rarely a feature of chronic sinusitis except during rare acute exacerbations of chronic sinus infection.²⁷

Recurrent acute rhinosinal disease

Recurrent acute rhinosinal disease is classified as four or more episodes of nasal obstruction, purulent nasal discharge, with facial pain or pressure-like symptoms per year.¹⁷ Recurrent acute sinusitis is generally regarded as being an exacerbation of chronic rhinosinal disease.

Recurrent acute rhinosinal infection can occur in the presence of disease-modifying factors, such as asthma, cystic fibrosis, ciliary dyskinesia, or immune deficiency states. A patient presenting with recurrent infection without an obvious predisposing cause should be investigated further.¹⁷

Recurrent acute rhinosinal disease presents as a significant healthcare burden in developed countries with multiple work days lost and repeat prescriptions of antibiotics given,²⁸ hence multiple guidelines have been developed to assist the practitioner in making an accurate diagnosis.^17,18,22,29 There is now increasing doubt as to the real prevalence of recurrent infective acute rhinosinal disease, as there is considerable overlap of symptoms with primary headache syndromes and orofacial pain.^30,31,32 In addition, there is an increased prevalence of self-reported rhinosinal symptoms in patients presenting with generalized fatigue, chronic pain syndromes, non-specific gastrointestinal symptoms, and musculo-skeletal pain, suggestive that some cases of recurrent rhinosinal symptoms are of a functional rather than organic nature.^{33,34,35,36,37}

Establishing an accurate diagnosis

With the aim of improving diagnosis, guidelines recommend that, in addition to the recognized descriptive criteria for rhinosinal disease outlined in Table 2, for a diagnosis of rhinosinal disease there should also be:

These specialist examinations should only be undertaken in a specialist setting by an Ear Nose and Throat (ENT) surgeon. Cross-sectional imaging, even in the specialist setting, is generally reserved for cases of unilateral chronic pain, or when there are symptoms or signs suggestive of a sinister disease process.^17,38

Detailed description of clinical findings upon anterior rhinoscopy is beyond the scope of this paper, but is well outlined in ENT texts.³⁹ Computed tomography of the paranasal sinuses is performed to determine the presence or absence of any signs of disease, including inflammation within the paranasal sinuses or adjacent tissues. Computed tomography is also used to determine the patency of the osteo-meatal complex, where both the ethmoid and maxillary sinuses drain into the nasal cavity⁴⁰ (Figure 1).

The surgical management of chronic rhinosinal disease is also beyond the scope of this paper but interested readers are directed to ENT texts.⁴¹

Non rhinosinal causes for facial pain, headache and dental pain

Patients with acute or chronic rhinosinal disease do not necessarily have headache or orofacial pain. This is demonstrated by the following observations:

Therefore, even if criteria for a diagnosis of rhinosinal disease are fulfilled, it does not necessarily follow that their pain is solely attributable to paranasal sinus infection. It has been suggested that removing the symptom of pain or pressure-like symptoms from the diagnostic criteria allows for greater specificity and sensitivity when making a diagnosis of chronic rhinosinal disease.⁴⁶

At this stage, the criteria on which a diagnosis of headache or orofacial pain was based needs to be re-considered, which in turn takes the clinician back to the history of patient symptoms and the wider differential diagnosis of orofacial pain and headaches.

Primary headaches: migraine with autonomic symptoms

The International Classification of Headache Disorders recognizes that rhinosinal disease and primary headaches can co-exist in the same patient and have variable contribution to patient symptoms.⁴⁷ The International Headache Society also recognizes that secondary headaches as a result of acute rhinosinal disease are relatively rare.⁴⁷

It is now acknowledged that many patients with unilateral facial pain or a headache that present in the area of the paranasal sinuses have migrainous type headaches which can occur with or without an aura.^32,47,48 Migraine can occur as mid-facial pressure without headache, termed a typical aura without headache.^32,47 The clinical picture is blurred even further when it is recognized that some migraine-type headaches can be bilateral.⁴⁹ Parasympathetic stimulus to the sino-nasal mucosa during a migraine may cause oedema of nasal soft tissue, and increase nasal secretions, although the secretions would not be purulent.⁵⁰ The parasympathetic stimulus will therefore mimic the symptoms stated by clinical guidelines as being indicative of rhinosinal disease. It would only be upon examination by an ENT surgeon that polypoid disease or purulent discharge in the middle meatus could be excluded.

There is therefore a risk that patients complaining of chronic or recurrent facial pain and headaches, with nasal discharge or congestion, may fulfil the criteria outlined for diagnosis of chronic or recurrent rhinosinal disease and be started on an incorrect treatment pathway when they have a primary headache disorder.

There is evidence that patients with facial pain or a headache without purulent nasal discharge respond well to triptan medication.⁵¹ However, the clinical picture is further blurred when it is recognized that some patients can also experience migraines at the same time as having symptoms related to chronic rhinosinal disease.^47,52

Primary headaches: trigeminal autonomic cephalgias

The trigeminal autonomic cephalgias, recognized as primary headache syndromes by the International Headache Society, produce pain but, because of parasympathetic activity, also cause nasal congestion and nasal discharge, in addition to lacrimation, flushing of skin, conjunctival injection, eyelid oedema and ptosis.⁴⁷ Recurrent attacks of facial pain and headaches, caused by any of the trigeminal autonomic cephalgias outlined in Table 3, can be mistakenly diagnosed as recurrent acute rhinosinal disease. It is not possible to discuss trigeminal autonomic cephalgias in detail in this paper but interested readers are referred to a further text.⁵³

Trigeminal neuralgia

Although it would be unusual for trigeminal neuralgia to be mistakenly diagnosed as recurrent rhinosinal disease, it has been reported.⁴² Trigeminal neuralgia has, on most occasions, a very characteristic unilateral presentation and is not usually associated with any autonomic symptoms that may cause nasal obstruction or discharge. However, the careful clinician would consider this as part of a broader possible diagnosis in cases where the clinical picture is not clear.⁵⁴

Temporomandibular disorders: confusion with rhinosinal disease

The clinician may experience diagnostic difficulties when the patient describes unilateral or bilateral facial pain, with zygomatic/temporal or retro-orbital radiation, especially when the patient may describe many years of facial pain and headache attributable to sinus disease. The problem is even more challenging when other primary care practitioners have reinforced the incorrect diagnosis of rhinosinal disease by multiple antibiotic prescriptions.

The diagnostic criteria for acute or chronic rhinosinal disease do not overlap with the diagnostic criteria for temporomandibular disorder (TMD).⁵⁵

Careful history-taking from a patient will determine whether or not there is a history of nasal congestion, nasal discharge, loss or reduction of smell. Careful examination, as outlined in the diagnostic criteria for the most common pain-related temporomandibular disorders, should guide the clinician towards an accurate diagnosis.⁵⁵

Atypical facial pain or tension type headache

In the absence of any specific patient symptoms or clinical signs that would suggest a specific disease process, the diagnosis of atypical facial pain or tension type headache should be considered. Research has demonstrated that non-specific, mid-facial pain was caused by atypical facial pain, TMD and tension type headaches as frequently as migraines or trigeminal autonomic cephalgias.⁴²

Contact point headaches

There are multiple contributions to the literature that aim to demonstrate that various points of contact between the medial and lateral nasal walls, including contact of some of the turbinates with either the medial or lateral nasal walls, will contribute to areas of mucosal pressure and cause headaches.⁵⁶ Such contact points are observed on CT scanning.

While this topic has been explored with vigour in the literature, there is a paucity of reliable evidence to support this concept. Mucosal contact points have been demonstrated in patients with and without symptoms of pain.⁵⁷ The concept risks exposing patients to unnecessary radiation, and also unnecessary surgery that will not provide long-term control of symptoms.

Acute maxillary sinus pain or odontogenic pain

The dental surgeon can be presented with a patient complaining of acute onset unilateral maxillary pain. As for chronic or recurrent facial pain and headache, the importance of a comprehensive history of symptoms cannot be under-estimated.

Clinical and radiological examination as outlined in Table 4 will guide the dental surgeon through the diagnostic process of symptoms and signs that are specific to acute infection of the maxillary sinus or specific to odontogenic disease. Some symptoms and signs will be shared. Accurate diagnosis will not be made on one sign or symptom but rather a combination of both.²⁷

A periapical radiograph is the image of choice for diagnosis. A sectional dental panoramic tomogram (DPT) may be used if the patient cannot cope with a film holder. Radiological signs suggestive of apical periodontitis are; widening of periodontal ligament space, loss of lamina dura around apices, apical radioluency. Condensing apical periodontitis is a sign rarely observed in the posterior maxilla. Gross or extensive secondary caries are obvious signs suggestive of pulpal necrosis.

There is no role for the use of Cone Beam Computed Tomography as a first line radiographic investigation in the diagnosis of acute or chronic orofacial pain.^17,27,58

In the same context that guidelines exist to enable accurate diagnosis of chronic or recurrent rhinosinal disease, in an effort to avoid unnecessary antibiotic prescription or surgery, an accurate diagnosis of unilateral maxillary alveolar or facial pain will hopefully avoid unnecessary dental treatment.

Summary

This paper has discussed the diagnostic criteria required for a diagnosis of either acute or chronic rhinosinal disease, to give the dental surgeon greater confidence in making a diagnosis. The potential for misdiagnosis of recurrent or chronic orofacial, mid-facial pain, with or without headaches, has been emphasized.

It is recommended that the dental surgeon who is unable to provide a reliable diagnosis for mid-facial pain or headache should refer to the patient's medical practitioner, or a secondary care oral medicine/oral surgery/maxillofacial surgery service.

The practice of prescribing antibiotics in the presence of pain but absence of specific signs of spreading infection or pyrexia is discouraged.

It has not been possible for this paper to provide an outline of all paranasal sinus disease with a broad pathogenic basis. This is covered in more detail in other texts.^{1,7,9,27,39,40}

The following three papers will outline how dental care may impact on the health, function and ultimately disease of the maxillary sinus. In the next paper the removal of teeth that are closely related to the maxillary sinus, and the possible complications that may arise, will be discussed.