Occurrence of external cervical resorption is a serious complication following internal bleaching procedures (MacIsaac & Hoen 1994, Friedman 1997). Cervical resorption is mostly asymptomatic and is usually detected only through routine radiographs (Trope 1997). Heithersay (1999) analysed 257 teeth in 222 patients with cervical resorptions and discovered that in24.1%of cases the resorption was caused by orthodontic treatment, 15.1% by dental trauma, 5.1% by surgery (e.g. transplantation or periodontal surgery) and 3.9% by intracoronal bleaching. A combination of internal bleaching procedures with one of the other causes is responsible for13.6% of cervical resorption cases.
Table 3. Occurrence of cervical resorption after internal bleaching procedures in clinical studies and case reports.
Table 3 provides an overview of clinical studies and case reports in which the occurrence of cervical resorption was observed, partly diagnosed many years after internal bleaching was applied (Harrington & Natkin 1979, Lado et al. 1983). However, experimental animal studies showed histological signs of resorptions only 3 months after internal thermocatalytic bleaching therapy with heated 30% H2O2 (Rotstein et al.1991a, Heller et al. 1992). One month after bleaching, no changes in the tooth substance could be detected. Cervical resorptions often proceed in an asymptomatic way, however, sometimes swelling of the papilla or percussion sensitivity of the bleached teeth can be observed (Harrington & Natki n 1979, Lado et al. 1983). Table 2 shows that teeth that were root-filled as a result of trauma often show cervical resorption. Furthermore, the studies and case reports indicate that application of heat (thermocatalytic method), lack of a cervical seal and the use of 30% H2O2 are associated with the occurrence of cervical resorption. In an experimental animal study, Madison & Walton (1990) showed that the thermocatalytic technique supported the development of external resorption. However, the walking bleach technique applied in that study with a sodium perborate-H2O2 solution did not cause cervical resorption even 1 year after bleaching. This observation may be explained by the fact that sodium perborate inhibits the function of macrophages, because macrophages stimulate both osteoclastic bone resorption and destruction of dentine and cementum induced by lytic processes in periodontal tissue (Jime. nez-Rubio & Segura1998).
The mechanisms responsible for resorption in bleached teeth have not yet been adequately explained. It has been proven that formulations using either 30% H2O2 alone or in combination with sodium perborate are more toxic for periodontal ligament cells as compared to a perborate-water suspension (Kinomoto et al. 2001). Lado et al. (1983) presumed that application of bleaching agents led to denaturation of dentine in the cervical region of tooth. According to the authors, this denatured dentine induces a foreign body reaction, although this could not be verified. Other authors claim that diffusion of H2O2 via dentine causes irritation in the periodontium, which later results in bacterial colonization of the open dentinal tubules (Cvek& Lindvall 1985). This could trigger inflammation of adjacent tissues and external resorption. Harrington & Natkin (1979) suspected that H2O2 diffuses into the periodontium via dentinal tubules and directly induces an inflammatory resorptive process. It is known that H2O2 can diffuse through dentine (Pashley & Livingston 1978, Wang & Hume 1988, Hanks et al.1994) and radicals and the low pH value of highly concentrated H2O2 can be considered as tissue damage inducing factors (Friedman et al.1988).Table 3 reveals that patients who had bleaching therapy at a young age often have external resorption. A possible explanation is that H2O2 can more easily penetrate into the periodontium because of wide dentinal tubules in young teeth (Schroder1992).Increasing permeability of dentine is associated with both decreasing dentine thickness and high surrounding temperature (Outhwaite et al.1976). Application of heat leads to widening of dentinal tubules and facilitates diffusion of molecules in the dentine (Pashley et al. 1983). This explains the increasing dissemination of H2O2 into dentine with rise in temperature (Rotstein et al. 1991c). Moreover, application of heat resulted in generation of hydroxyl radicals from H2O2 that are extremely reactive and have been shown to degrade components of connective tissue (Dahlstrom et al. 1997). Diffusion of H2O2 to cervical tissues is also increased after pretreatment of dentine in the pulp chamber with 5% NaOCl (Barbosa et al. 1994). In addition, the penetration of H2O2 into the cervical region can be facilitated by cervical defects or special morphological patterns at the enamel-cementum junction (Rotstein et al. 1991b, Koulaouzidou et al. 1996, Neuvald & Consolaro 2000). According to Rotstein (1991), lack of root cementum resulted in diffusion of up to 82% of the H2O2 (30% concentration) which was applied in the pulp chamber. However, dissemination of H2O2 into dentine cannot be totally prevented using mixtures of sodium perborate with 30% H2O2 or water. The amount of H2O2 diffusion is significantly lower when a mixture of sodium perborate-tetrahydrate and water is used, than in case of application of 30% H2O2 mixed with different sodium perborates (Weiger et al. 1994b). Even if there is low-H2O2 diffusion into adjacent tissues when sodium perborate solutions are applied, a sound cervical seal should be assured in order to prevent penetration of H2O2 through dentine (see above).
Tooth extraction is often inevitable in cases of severe external root resorption (Goon et al. 1986, Latcham 1986). Inflammatory osteolytic lesions have a low-pH value that is optimal for hard tissue resorption (McCormick et al.1983). Root-canal dressings consisting of calcium hydroxide are able to induce a higher pH in dentine (Tronstad et al. 1981, Webber 1983). Tronstad et al. (1981) assumed that reparative formations of hard tissue are supported by this treatment. Cases have shown that an intracoronal dressing with calcium hydroxide can sometimes prevent progression of external resorption (Montgomery 1984, Gimlin & Schindler 1990). However, on the radiograph, only osseous regeneration of the defect and no dental hard tissue regeneration could be detected.
Another possible therapy for external cervical resorption is orthodontic tooth extrusion, followed by restoration of the tooth with a post-retained crown (Latcham 1991, Emery1996). Cervical resorption can also be treated by direct restorations after gaining surgical access to the defect (Meister et al. 1986, Friedman 1989, Al-Nazhan1991).