Article Options


Advanced Search

This service is provided on D[e]nt Publishing standard Terms and Conditions. Please read our Privacy Policy. To enquire about a licence to reproduce material from and/or JofER, click here.
This website is published by D[e]nt Publishing Ltd, Phoenix AZ, US.
D[e]nt Publishing is part of the specialist publishing group Oral Science & Business Media Inc.

Creative Commons License

Recent Articles RSS:
Subscribe to recent articles RSS
or Subscribe to Email.

Blog RSS:
Subscribe to blog RSS
or Subscribe to Email.

Azerbaycan Saytlari

 »  Home  »  Endodontic Articles 7  »  Hemisection for treatment of an advanced endodontic-periodontal lesion
Hemisection for treatment of an advanced endodontic-periodontal lesion

H. Haueisen & D. Heidemann
Department of Restorative Dentistry, University of Dentistry ZZMK (Carolinum), Johann Wolfgang Goethe University, Frankfurt, Germany.

There is a close ontogenetic relationship between endodontic- and periodontal tissue structures, which is anatomically reflected in the apical foramen and accessory and lateral canals (Pineda & Kuttler 1972, Burch & Hulen 1974, Gutmann 1978, Harndt 1979, Schroeder 1987).
Clinically, this relationship promotes the spread of infection, potentially resulting in typical manifestations of endo–perio osseous lesions (Nolden 1986, Konig et al. 1994, Simon & Worksman 1994, Bergenholtz & Hasselgren 1997).
These lesions often remain free of symptoms for long periods, as they are rarely diagnosed until the disease starts manifesting itself in the form of acute symptoms of inflammation and/or increased pain. Sometimes, the lesions are detected accidentally during a general check-up (Simon & Worksman 1994, Bergenholtz & Hasselgren 1997, Trope 1998, Haueisen et al. 1999). Once symptoms occur, they tend to be so severe, and the periodontal aspect can seem so dominant, that dentists tend to settle for strictly symptomatic periodontal therapy whilst overlooking the endodontic aspect. The cumulative effects of carious and iatrogenic irritation acting on the tooth/pulp often do not get the attention they deserve in the diagnostic workup, and are not recognized as a potential cause of chronic pulpitis, frequently associated by sclerosed root canals (Simon & Worksman 1994, Kim & Trowbridge 1998, Haueisen et al. 2000). Teeth with endo–perio lesions typically have a history of deep caries treated and subsequently covered with a full or partial crown.
Endo–perio lesions are difficult to classify, because they lack the characteristic manifestations of strictly endodontic or strictly periodontal lesions (Kresic 1994, Lo¨ st 1994, Kocher 1997, Haueisen et al. 1999, Ratka-Kru¨ ger et al. 2000). Long-term preservation of the tooth seems an unlikely prospect in the presence of clinical and radiographic findings such as acute inflammation, isolated deep pockets and circumradicular/interradicular radiopacities. It is difficult to distinguish by hindsight which parts of the lesion are endodontic and which parts are periodontal in origin.
The classification by Mutschelknauss (1975), Guldener (1975) or Simon et al. (1972) is based on a etiology and describes the development of endo–perio lesions, whilst the classification by Geurtsen et al. (1985) focuses on therapeutic and prognostic aspects (Tables 1 and 2).

Table 1. Classification according to Mutschelknauss (1975) and Guldener (1975).

Classification according to Mutschelknauss and Guldener

Table 2. Classification according to Geurtsen et al. (1985).

Classification according to Geurtsen et al. (1985)

For the treatment of endo–perio lesions to be successful, it is helpful to understand the pathogenesis as well as the clinical and radiographic manifestations of endodontic and periodontal lesions.
Endo–perio lesions that are primarily endodontic in origin characteristically expand to the periodontal structures via the apical foramen, resulting in an osseous defect that progresses relatively fast along the periodontal ligament from apical to coronal, or forms a sinus tract. The probing depths of the tooth remain normal until a closely circumscribed location reveals significant probing depths of 10–12 mm. Radiographs show a normal-shaped alveolar ridge in the proximal area and osteolysis spreading from an apical/interradicular focus to the periapical area (Konig et al. 1994, Kresic 1994).
Periodontal structures such as the attachment of Sharpey’s fibres in the (still healthy) root cementum initially remain intact. This means that the bony defect may fully regenerate after the inflammatory focus is removed by endodontic treatment. Only if the lesion has persisted for an extended period will the epithelial tissue migrate into the periodontal pocket and result in a combined lesion that, much like premature scaling of the root surface, reduces the potential for complete healing (Nolden 1986, Ko¨ nig et al. 1994, Lost 1994, Simon & Worksman 1994).
The periodontal aspect of combined lesions develops over an extended period of time, starting at the marginal periodontal tissue. Radiographs reveal a coronally wide vertical bony defect. Closed or open surgical periodontal procedures will usually only achieve healing by repair; in some indications, guided tissue regeneration (GTR) yields better results (Cortellini et al. 1996).
To structure the complex treatment of endo–perio lesions, a treatment concept was developed by Haueisen et al. (1999) that combines endodontic and periodontal measures in a special sequence and at defined intervals (Fig. 1). The different progression of lesions of endodontic versus periodontal origin (relatively fast/slow development of bony defects), as well as the different levels of healing (regeneration/repair), were taken into account.
Following initial treatment, priority is given to the endodontic aspect to allow healing by regeneration—unless the patient presents with acute periodontal symptoms. Any decision in favour of periodontal measures or even surgical endodontics will be based on the clinical and radiographic findings 6 months after root-canal therapy. An additional 6 months later, the regeneration of the endodontically induced part of the bony defect should be more or less complete; any residual periodontal defects should subsequently be treated by regenerative periodontal techniques. In most cases, it takes 18 months after the completion of root-canal treatment before it can be definitively determined whether or not the treatment as a whole was successful.
The objective of the following case report is to present both the characteristic diagnostic features of an endo–perio lesion and a treatment concept that can be applied even in complex cases.
During the course of successful treatment, the patient reported improvement in her general state of well-being, including the disappearance of a long-standing unilateral headache.

Figure 1. Treatment concept for combined endodontic-periodontal lesions.

Treatment concept for combined endodontic-periodontal lesions