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Azerbaycan Saytlari

 »  Home  »  Endodontic Articles 2  »  Endodontic implications of the maxillary sinus: a review
Endodontic implications of the maxillary sinus: a review
Differential diagnosis - Periapical infections.

Differential diagnosis.
Sinusitis can clinically be divided into acute, subacute and chronic. Symptoms associated with acute or subacute maxillary sinusitis can be mistaken for those of pulpal origin (Schwartz & Cohen 1992). A comprehensive review of the patient’s medical and dental history will frequently alert the clinician to a recent upper respiratory tract infection, chronic rhinitis or a painful episode associated with an aeroplane flight. Although it is not known whether ‘allergic sinusitis’ can be distinguished as a specific entity, the relationship between allergy and sinusitis has been discussed for many years (Demoly et al . 1994). The chief complaint associated with maxillary sinusitis is dull pain, generally unilateral and during mastication, or a feeling of ‘fullness’ around the first molar-second premolar area. The patient may report that the pain is exacerbated when lying down or bending over owing to increased intracranial pressure from blood flow.
Clinical examination of the patient with suspected maxillary sinus disease should include extra-oral tapping of the anterior and lateral walls of the sinus over the prominence of the cheekbones and/or palpation intraorally on the lateral surface of the maxilla between the canine fossa and the zygomatic buttress. Some authorities recommend palpation of the posterior wall of the maxillary sinus as a very useful diagnostic test but this is not featured in the literature. The affected sinus may be markedly tender to tapping or palpation (Schow 1993). The teeth affected by sinusitis will be moderately or extremely sensitive to palpation and/or percussion, but will respond within normal limits to conventional pulp sensibility tests. Pain typically radiates to all the posterior teeth in the quadrant so that all the teeth usually become tender to percussion. The nasal passage on the affected side may be partially or completely blocked. Nasal discharge is considered to be a significant sign of sinus infection. Without a discharge, it is unlikely that a significant sinusitis exists. Severe acute or subacute sinusitis rarely produces a fever, but a severe fulminating sinusitis will produce a high temperature and some degree of malaise. If only one tooth demonstrates tenderness to percussion, one should suspect this as the source of trouble and discount sinusitis. It is often helpful to use transillumination of the sinus (Schow 1993). This is done by placing a bright flashlight or fibre-optic light against the mucosa on the palatal or facial surfaces of the sinus and observing the transmission of light through the sinus in a darkened room. Decreased transmission of light would suggest congestion of the sinus, usually with swelling or thickening of the mucosa. Fluid or pus might also be present (Schow 1993). Decreased transillumination may also be owing to a hypoplastic or even a contracted sinus (Pinheiro et al . 1998). Radman (1983) suggested the placement of a cotton swab saturated with 5% lidocaine (lignocaine) in the nostril of the affected side as a differential diagnostic test. The swab is placed posteriorly to the area of the middle meatus and left in place for 20– 30 s. If the pain is of sinus origin it will be modified or eliminated within 1–2 min and thus lead to the presumptive diagnosis of maxillary sinusitis. Similarly, the use of a topical nasal decongestant may help in differentiating pain from sinusitis vs. pain of dental origin, the assumption being that the pain is as a result of the pressure from the inflamed sinus tissue. Possible radiographic changes that may be seen in sinusitis are thickened sinus mucosal membrane, an air-fluid level or complete opacification (Pinheiro et al . 1998).
In contrast to pain of sinus origin, pain of dental origin is much more variable and ranges from thermal sensitivities to spontaneous episodes of sharp pain and unrelenting severe pain and may be associated with regional swelling and cellulitis. In advanced dental disease, radiographic evidence is usually apparent. Negative responses to routine pulp tests are helpful in finding a dental source of disease, whereas normal responses might aid in eliminating possible dental foci and in establishing a diagnosis of sinusitis.

Periapical infections (Endo–antral syndrome).
The direct extension of dental sepsis into the sinus was shown for the first time in a study by Bauer (1943). His study was performed on cadavers and showed examples of pulpally involved teeth with histologically evident extension of disease into the maxillary sinus. These examples ruled out generalized sinus disease and clearly implicated the infected teeth. Microscopically, the ‘diseased areas’ showed the destruction of the bone separating the sinus from the teeth, with particular loss of the cortical bone normally found on the sinus floor. In addition, the sinus mucosa was seriously altered in many ways such as swelling with inflammation, granulation tissue, hypertrophy, fibrous changes, hyalinization or complete necrosis. The pathological disruption of both periapical and adjacent sinus tissue resulting from endodontic infection has since been well documented (Selden & August 1970, Selden 1974, Selden 1977, Selden 1989). The reported frequency of sinusitis of dental origin varied considerably, between 4.6 and 47% (Mélen et al . 1986) of all sinusitis cases. The spread of pulpal disease beyond the confines of the dental supporting tissues into the maxillary sinus was termed Endo–antral syndrome (EAS) by Selden (1974), Selden (1989) and Selden (1999). It has been shown that the closer the apex of a pulpally involved tooth is to the floor of the sinus, the more likely and the greater the impact will be on the sinus tissues (Matilla 1965). According to Bauer (1943), periapical infection spreads through the bone marrow, following the path of blood vessels and lymphatics. If pulpal disease develops slowly, as in chronic inflammation with no significant infection, then the spread to the sinus can be slow with minimal impact. Acute infectious pulpal disease is much more destructive and rapidly spreading, capable of significantly involving the adjacent sinus within a short time. Reports in the literature of the rapid spread of dental infections through the maxillary sinus and subsequent periorbital cellulitis, blindness and even life-threatening cavernous sinus thrombosis (Albin et al . 1979, Gold & Sager 1974, Jarrett & Gutman 1969, Pellegrino 1980, Robbins & Tarshis 1981) exemplify the serious potential complications of EAS. The findings that characterize EAS are: (i) pulpal disease in a tooth whose apex approximates the floor of the maxillary sinus; (ii) periapical radiolucencies on pulpally involved teeth; (iii) radiographic loss of the lamina dura defining the inferior border of the maxillary sinus over the pulpally involved tooth; (iv) a faintly radiopaque mass bulging into the sinus space above the apex of the involved tooth, connected neither to the tooth nor the lamina dura of the tooth socket (representing a localized swelling and thickening of the sinus mucosa); and (v) varying degrees of radiopacity of the surrounding sinus space (comparison of the contralateral sinus is often helpful) (Selden 1999). The variable presentation of EAS can create diagnostic and therapeutic difficulties, because cases do not always show all five features.
Sinus mucosal hyperplasia is present in approximately 80% of teeth with periapical osteitis (Matilla 1965, Matilla & Altonen 1968). Microscopically, other changes in the sinus mucosa, such as swelling, cyst formation, hypertrophy and even transformation of the mucosa to granulation tissue can be seen (Bauer 1943). In the past these mucosal changes in the sinus led to the belief that the involved teeth should be extracted (Bauer 1943). The belief was reinforced by the study of Ericson & Welander (1966) who found that inflammatory reactions occur in the lateral wall of the sinus as a result of periapical osteititis and disappear after the extraction of the affected teeth. In 1967, Nenzen & Welander performed a study on 24 patients with periapical lesions of which 14 (58%) displayed local hyperplasia of the sinus mucosa. Seven of these 14 cases received conventional endodontic treatment and all seven showed regression of the mucosal hyperplasia. The control group (who did not receive endodontic treatment) showed regression in only one case. The results indicated that conservative root canal therapy could eliminate local hyperplasia of dental origin in the mucosa of the maxillary sinus. Selden & August (1970) also managed to retain teeth and attain resolution of sinusitis after treatment of a periodontal-endodontic lesion involving first and second premolars. These studies seem to indicate that most cases of EAS will respond satisfactorily to nonsurgical root canal treatment. For those cases refractory to routine conservative management, a surgical approach was recommended (Selden & August 1970, Selden 1989).