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 »  Home  »  Endodontic Articles 2  »  Endodontic implications of the maxillary sinus: a review
Endodontic implications of the maxillary sinus: a review
Conventional endodontic treatment.



The maxillary sinus poses a special challenge when root canal treatment is performed on teeth with roots in close proximity to the maxillary sinus. Although it is well established that all endodontic instruments and materials should be restricted to the confines of the root canal system during treatment, procedural errors are common and part of every day practice. It frequently happens that instruments and medicaments are introduced beyond the apical foramen (Dodd et al . 1984, Fava 1993, Kaplowitz 1985, Kobayashi 1995). In addition, some degree of inflammatory response normally occurs after root canal preparation even when all instrumentation is kept within the canal. If the root apices are in close proximity to the maxillary sinus, then the inflammatory response may involve the sinus mucosa.
Results from several studies (Engström & Spångberg 1967, Seltzer et al . 1968, Seltzer et al . 1969) showed that for optimal repair in cases of vital pulp extirpation, instrumentation should be confined to the root canal. An inflammatory reaction normally occurs in the periapical tissues after pulp extirpation (Seltzer 1988). Despite strict control of working length during root canal preparation, extrusion of debris into the periapical tissues may occur, causing periapical inflammation, postoperative pain and possibly delayed healing (Fairbourn et al . 1987, McKendry 1990). When the periapical tissues are severely damaged by overzealous reaming or filing, the consequent inflammatory response is more severe (Seltzer et al . 1968). Mechanical injury to the periapical tissues is likely to initiate the release of non-specific mediators of inflammation. In addition, the continued release of antigens from an inflamed pulp or infected root canal into the periapical tissues (Engström et al . 1964) can result in various types of immunologic reactions. This is especially true for pulpless teeth with associated periradicular lesions (Baumgartner & Falkler 1991, Fukushima et al . 1990, Sundqvist et al . 1989, Yoshida et al . 1987). It is speculated that inadvertent inoculation of the infectious contents from the root canal predisposes the pulpless tooth to peripical exacerbation (Fukushima et al . 1990, Harrington & Natkin 1992). Additional periapical injury may be induced by the use of certain medicaments and still further irritation by root canal fillings, especially when they impinge on the periapical tissues (Bergenholtz et al . 1979). Thus, a compounding of irritation may occur during the sequence of normal endodontic procedures (Seltzer 1988). The irritation may be so severe that the defence resources of the periapical tissues cannot overcome it. A granuloma may thus persist in the periapical tissues after completion of root canal treatment. Should epithelial cell rests begin to proliferate, a cyst may form.
The inadvertent injection of sodium hypochlorite (NaOCl) into the periapical tissues may impact on the maxillary sinus (Ehrich et al . 1993, Kavanagh & Taylor 1998). Pashley et al . (1985) found that NaOCl elicited severe inflammatory reactions and was extremely toxic to all cells except heavily keratinized epithelia. Sodium hypochlorite solution is a commonly employed root canal irrigant, and there have been numerous reports of soft tissue complications as a result of its inadvertent injection beyond the confines of the tooth (Becker et al . 1974, Becking 1991, Cymbler & Ardakani 1994, Ehrich et al . 1993, Gatot et al . 1991, Harris 1971, Herrmann & Heicht 1979, Kavanagh & Taylor 1998, Reeh & Messer 1989, Sabala & Powell 1989). The immediate sequelae of these accidents include severe pain, oedema and profuse haemorrhage both interstitially and through the tooth. Several days of increasing oedema and ecchymosis occur, accompanied by tissue necrosis, paraesthesia and sometimes, secondary infection. The majority of cases showed complete resolution within a couple of weeks whilst a few have been marked by long-term paraesthesia or scarring (Gatot et al . 1991, Reeh & Messer 1989). Two cases of inadvertent injection of NaOCl into the maxillary sinus have been reported (Ehrich et al . 1993, Kavanagh & Taylor 1998). Ehrich et al . (1993) reported a case of endodontic therapy of a maxillary right first molar. Shortly after irrigation of the palatal canal with 5.25% NaOCl the patient complained about a taste in his throat despite the presence of an effective rubber dam. On irrigation of the canal with sterile water it was found that the water passed through the palatal canal into the maxillary sinus, into the nasal cavity via the ostium and thence into the pharynx. Apart from an initial congestion and mild burning sensation in the right maxilla the patient experienced no severe consequences and was asymptomatic 4 days after the incident. The second case (Kavanagh & Taylor 1998) involved a maxillary right second premolar. The patient experienced acute severe facial pain and swelling during irrigation with NaOCl solution. An attempt to drain the sinus through reopening the access cavity was unsuccessful and it was surgically drained by a Caldwell–Luc approach. Despite an apparent healing of the sinusitis, the tooth remained painful and was extracted 3 months after the initial presentation.
Intracanal medicaments placed between visits may inadvertently be extruded into the sinus. The use of calcium hydroxide (Ca(OH) 2 ) paste as an interappointment dressing is common (Byström et al . 1985, Fava 1992, Heithersay 1975). Ca(OH) 2 is irritating to tissue and has an immediate degenerative effect upon cells (Kawahara et al . 1968), before the material is removed by macrophages or foreign body giant cells. Until such removal is complete, total repair with an absence of inflammation does not occur. Haanæs et al . (1987) injected Ca(OH) 2 into the maxillary sinus cavity of monkeys to evaluate its clinical, radiological and histological effect on the sinus mucosa. Results from this study clearly show that sinusitis can occur when Ca(OH) 2 is deposited into the sinus. The authors ascribed the inflammatory response of the sinus mucosa to the material initially acting as a chemical irritant and later as a foreign body. They also considered the amount deposited into the sinus as important to the inflammatory response. A few cases of Ca(OH) 2 extrusion into the maxillary sinus have been reported in the literature (Engström & Ericson 1964, Fava 1993, Marais 1996). Despite the reported effects of Ca(OH) 2 on the tissues, these cases have showed spontaneous healing.
During obturation, the sinus may be invaded by either sealer or by solid materials such as gutta percha or silver cones. Mechanical irritation results from overfilling the root canal, thereby impinging foreign materials on the vital tissues. The material produces an inflammatory reaction with an area of rarefaction in the periapical tissues. Such inflammation is likely to persist until the foreign object is removed. Many sealers have been reported to cause paraesthesia if extruded into the mandibular canal or the mental foramen (Fava 1993). Amongst the sealers that cause paraesthesia when in direct contact with the inferior alveolar nerve are: N2 (Grossman 1978, Orlay 1966), AH26 (Tamse et al . 1982), Endomethasone (Forman & Rood 1977, Kaufman & Rosenberg 1980, Ørstavik et al . 1983), Spad (Foreman 1982) and Hydron (Pyner 1980). Brodin et al . (1982) and Brodin & Ørstavik (1983) have documented the particularly strong and irreversible neurotoxic activity of the root filling materials N2 and Endomethasone, but indicated that other materials, including formulations like Kloroperka N-Ø, zinc oxide-eugenol and AH26 also displayed some neurotoxicity. The paraesthesia may be caused by direct pressure of the material over the neurovascular bundle or by a neurotoxic affect on the nerve trunk (Rowe 1983). There have been very few reports concerning sealer extrusion into the maxillary sinus. Orlay (1966) reported a case where N2 had been extruded into the maxillary sinus. The patient complained about severe pain radiating across the trigeminal region. After removal of part of the lateral wall of the sinus and irrigation of the sinus to remove a ball of N2, the area healed and the pain did not return. Block et al . (1980) found 14 C-labelled paraformaldehyde in blood, regional lymph nodes, kidney and liver after insertion of N2 paste into the root canals of dogs’ teeth after instrumentation of the canals 1–1.5 mm short of the radiographic apex. They concluded that paraformaldehyde should not be incorporated in any root canal sealer. The same concern was reflected in the guidelines for root canal treatment of the British Endodontic Society (1983), which stated that cements containing paraformaldehyde, with or without corticosteroids, were unacceptable. The use of these sealers in teeth with roots in close proximity to the sinus is thus strongly contraindicated.
Root filling materials have also been reported as causative agents of maxillary sinus aspergillosis (Beck- Mannagetta & Necek 1986, De Foer et al . 1990, Krennmair & Lenglinger 1995). Kopp et al . (1985) and Stammberger et al . (1984) found that the typical radiopaque maxillary sinus concretions seen in more than 50% of the cases with diagnozed sinus aspergillosis were iatrogenically placed endodontic materials. These findings were confirmed in a study by Legent et al . (1989), who reported that 85% of 85 reported cases of aspergillosis of the maxillary sinus were related to overextended root canal sealer in maxillary teeth. Stammberger et al . (1984) and Kopp et al . (1985) described the influence of root-filling materials containing zinc oxide-eugenol on the pathogenesis of sinus aspergillosis, confirming the microbiological findings of Ross (1975) who demonstrated that Aspergillus fumigatus needs heavy metals such as zinc oxide for proliferation and metabolism. According to this ‘dental’ hypothesis, sinus aspergillosis is caused by overfilling of the root canal, with the zinc oxide in the root filling material inducing the infection. However, Odell & Pertl (1995) found that zinc oxide eugenol sealers showed antifungal activity against Aspergillus. In addition to the hypothesis of Aspergillus spore-induced zinc oxide metabolism, sinus aspergillosis may also be owing to nonremovable heavy   metal foreign bodies situated within an altered soft tissue and additional spore inhalation. By paralysing the cilia or by inducing soft tissue hypervascularization and oedema, these trace elements may cause an alteration of the respiratory epithelium (Hybbinette & Mercke 1982, Reinhold 1975), the heavy metal concretions thus becoming a hiding place for spores that cannot be removed by the respiratory epithelium. Therefore, it appears as though the dental origin of sinus concretions can be explained not only by the metabolic effect of zinc oxide but also by the ‘inorganic mass’ itself as it has a heavy texture and is difficult for the respiratory epithelium to remove. According to the findings of Krennmair & Lenglinger (1995), the use of zinc oxide-containing root canal filling materials can be considered a risk factor and may have a promoting effect on the pathogenesis of sinus aspergillosis. Kobayashi (1995) reported a case of a patient with asymptomatic sinus aspergillosis developing around a foreign body. Inductively coupled mass spectrometry (ICP) revealed that the foreign body corresponded to gutta-percha, with zinc, sulphur and calcium the principal elements present. Khongkhunthian & Reichart (2001) reported two cases of sinus aspergillomas related to overextended root canal material in maxillary first molars. They suggested that all overextended root canal filling materials in the maxillary sinus should be removed to prevent the development of aspergillosis infection. Aspergillosis can be divided into noninvasive, invasive and allergic variants (Khongkhunthian & Reichart 2001). The invasive form is usually associated with immunocompromised patients. The noninvasive and allergic forms result in obstruction and a chronic sinusitis. These forms do not respond to conventional medical management and the suggested treatment is surgical removal of the fungal masses. In vitro and in vivo data showed that zinc oxide eugenol containing sealers, especially those which release paraformaldehyde, should not be applied for the filling of root canals of upper posterior teeth (Geurtsen 2001).
Sjögren et al . (1995) showed in their study that gutta percha evoked two distinct types of tissue response and that the size and surface character of the material determined the type of tissue reaction. Large pieces were well encapsulated and the surrounding tissue was free of inflammation, whilst fine particles of gutta-percha evoked an intense, localized tissue response, characterized by the presence of macrophages and multinucleated giant cells. In a further study by Sjögren et al . (1998) it was found that mouse peritoneal macrophages, when exposed to gutta percha particles, released factors which have bone resorbing activity. Kaplowitz (1985) reported two cases with penetration of the maxillary sinus by gutta percha cones extending through the palatal root of maxillary first molars. In one case this caused a chronic maxillary sinusitis, which persisted for 1 year. The condition was finally resolved by the extraction of the tooth and the administration of an antihistamine. In the other case, no complications were noted.
Dodd et al . (1984) reported a case in which a maxillary first molar was overfilled with silver cones, resulting in chronic sinusitis. The aetiology was initially undiagnozed and the patient was subjected to unnecessary surgery of the sinus. Endodontic retreatment of the case eliminated the patient’s symptoms and returned the tooth to a state of health and function. Corrosion is a well known property of silver points and can also be a potential hazard in cases where the silver point is overextended. Seltzer et al . (1972) found that silver points contacting tissue fluids became corroded with the formation of silver sulphide, silver sulphate and silver carbonate. These corrosion products are known to be cytotoxic and silver cones pushed beyond the apex of the tooth are severely toxic to the periapical tissue (Seltzer et al . 1972).