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Azerbaycan Saytlari

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

Treatment procedure Successful treatment of endo–perio lesions depends upon their timely and accurate diagnosis. The patient had been treated for unspecific symptoms as far back as 1991. A chronic pulpitis developed to necrosis and 3 years later induced an endo–perio lesion that had not been recognized as such. Rather, the finding of significant probing depths and a radiographically visible bone loss were interpreted and treated as a periodontal defect, the treatment of which temporarily rendered the patient free of symptoms.
A thorough differential diagnosis would have made it apparent that the manifestations of the defect were atypical. The periodontal defect was confined to a single tooth. It extended in an arch-like fashion from the apical area along the distal root surface rather than being angular. Based on this finding, at least the possibility of a retrograde pulpitis should have been considered (Geurtsen et al. 1985, Ko¨ nig et al. 1994, Simon & Worksman 1994, Bergenholtz & Hasselgren 1997). The vitality test is not an absolute but a relative indicator of pulpal integrity. Especially in teeth with multiple roots, the situation may be misinterpreted by a variable degree of pulp degeneration in different tooth segments or root canals (Lost 1994).
The fact that the DPT of 1996 demonstrated progression of the bony defect would have been another indicator of an endodontic lesion. It is also known that cumulative carious and iatrogenic irritation can initiate pulp necrosis.
In early 2000, when the symptoms once again became acute and the clinical and radiographic findings had acquired significant dimensions, the patient received drug therapy and surgical periodontal treatment. Despite the fact that it would have been high time to refer the patient to a specialized unit, there was no reconsideration of the diagnosis, and the treatment once again failed.
When the patient first presented at our clinic, this treatment history called for a thorough diagnostic workup. Several factors played a determining role in evaluating the current status of the endo–perio lesion as the patient presented at our clinic, in order to determine the subsequent course of therapy. The patient’s dental history and the radiographs of 1994 showed that the endo–perio lesion of tooth 46 was primary endodontic in origin.
Lesions of a purely endodontic origin, like the endodontic aspects of combined lesions, have an excellent prognosis. This was demonstrated by a number of case reports (Simon & Worksman 1994, Bergenholtz & Hasselgren 1997, Trope 1998) and by a study of 10 lower molars conducted by Haueisen et al. (2000). Endodontic treatment alone results in complete reversion in many cases.
Our case was complicated by the fact that the lesion had existed for several years. An initially minor bony defect now showed a sizeable aperture coronally. There was a high probability that the junctional epithelium had proliferated downward, resulting in a combined endo–perio lesion with secondary periodontal involvement, typically associated with a less favourable prognosis.
From a clinical viewpoint, the attempt to preserve the mesial root was justified because probing depths in the mesial circumference of the tooth were only slightly increased. Radiographically it was justified by an intact gingival septum between teeth 46/45 and interradicular bony structures in the coronal-third of the mesial root. Also, the single-tooth radiograph showed fine bony structures mesially in tooth 47 at two-thirds of the root.
Depending on intraoperative findings, guided tissue regeneration could also be considered as an alternative. The intraoperative situation was such, however, that the procedure carried out appeared sufficient, a decision later confirmed by the favourable postoperative outcome.

Patient’s general health.
Another interesting aspect is the apparent improvement in the patient’s general health. The unilateral stress-independent headache attacks continuously decreased and finally vanished as the healing of the defect proceeded.
Focal infection theory was prominent during the early 20th century, but scientific evidence was lacking (Murray & Saunders 2000). In the present case, erythrocyte sedimentation rates returned to normal after treatment, which is plausible given the elimination of the chronic infection around tooth 46. What is more difficult to explain is why the unilateral headache disappeared. Pertinent publications are rare. There are only a few case reports, none of them too well documented. A systematic follow-up by Lunardon & Barolin (1997) showed that in one-quarter of the 785 headache patients odontogenic factors were implicated. Of these, 158 were systematically followed. Two-thirds of these showed improvement of the headache symptoms. Suitable treatment of oral foci is recommended, although improvement does not necessarily follow.

General health - local microbial findings.
The issue of intraoral pathological findings as a factor in systemic health problems is reopened as the development of improved microbiological techniques and evaluation methods continues. C-reactive protein serum levels are acknowledged to be clinical indicator of microbiological findings. Noack et al. (2001) proved the relevance of CRP serum levels following periodontitis treatment in a study that included 174 patients (65 healthy patients, 59 with mild periodontitis, 50 with chronic periodontitis). Ebersole et al. (1997) examined the course of C-reactive protein and haptoglobin serum levels following treatment of adult periodontitis (AP n ј 40; control group n ј 35).
Crucial data have been collected in the field of periodontology, where chronic periodontitis is considered a risk factor for cardiovascular disease, atherosclerosis, bacterial pneumonia, and premature births (Debelian et al. 1994, DeBowes 1998, Murray & Saunders 2000, Garcia et al. 2001). The Gram-negative bacteria seem to be particular important in this context in that they cause secondary systemic effects – formation of endotoxins, cytokines, and inflammation mediators.
To what extent latent endodontic processes - along with haematogenic infection (e.g. risk of endocarditis) - have a systemic impact needs to be elucidated by further studies. For example, an influence on rheumatoid arthritis is under consideration. Infected endodontic tissue has been shown to contain a high percentage of the Gram-negative bacteria (Debelian et al. 1994, Murray & Saunders 2000, Garcia et al. 2001), so that secondary effects via endotoxins and inflammation mediators appear possible.
To summarize, it would certainly be useful to collect case reports and clinical studies and to conduct endodontological intervention studies to improve our current understanding of how oral microorganisms are linked to systemic health.


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