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Endodontic Treatment In The Management Of Endodontic-Periodontic Lesions - A Case Report
K. Balakoti Reddy a*, Nagesh. Bollaa, Indira Priyadarshinia
Department of Conservative Dentistry & Endodontics, SIBAR Institute of Dental Sciences, Guntur, India.
Article History : Received : 8 July 2009 Received in revised form : 7 August 2009 Accepted : 28 August 2009 Key Words : Endo-Perio Lesion Differential Diagnosis Periodontal Disease
Occasionally periradicular lesions of endodontic origin may be radiographically indistinguishable from periodontal disease. Infected pulpal tissue and microbial by-products may move through accessory and furcal canals and cause loss of attachment in those areas. Accurate diagnosis may be particularly difficult when a sinus tract originating from the endodontic lesion drains along the periodontal ligament space, giving the appearance of periodontal disease. Thorough diagnostic testing to confirm pulp necrosis or periodontal disease becomes critical when attempting to diagnose the specific disease entity accurately and then deliver suitable treatment. This article describes the management of a patient presenting with a combined endo-perio problem that was apparently treated adequately. However, successful healing was obtained after thorough disinfection and sealing of the root canal system.
©2009 SIDS.All Rights Reserved
INTRODUCTION : Endodontic periodontic relationship was first described by Simring and Goldberg in 1964.Its the spread of inflammation and infection from one component to the other. 1 Pulpal and Periodontal problems are responsible for more than 50% of tooth mortality.2,3 The relationship between the pulp tooth and the attachment apparatus of a tooth has been widely documented (Simon et al, 1972; Paul B, Hutter JW, 1997; American Association of Endodontists newsletter, 2001). Most of the time periodontal inflammation due to pulp space toxins occur in the apical region and thus can readily be distinguished from a periodontal pocket. However, occasionally necrotic infected tissue byproducts move through accessory or furcal canals, * Corresponding author : Dr. K. Balakoti Reddy Professor,
Department Of Conservative Dentistry & Endodontics, SIBAR Institute of Dental Sciences, Takkellapadu, Guntur - 522 509.
producing inflammation that is indistinguishable from periodontal disease9. The amount of tissue destruction is directly correlated with the total microbial content in the root canal system (Bystrom et al, 1987) and to the length of time these tissues are exposed to the infecting organism (Korzen et al, 1974). Differential diagnosis is particularly difficult when a sinus tract originating from the endodontic lesion may drain along the periodontal ligament, giving the appearance of periodontal breakdown (Simring M, Goldberg M, 1964; Seltzer et al, 1967). Yamasaki et al (1994) have reported that periradicular lesions may initially expand horizontally through cancellous bone and then proceed vertically.Analyzing a series of retrospective studies, Blomlof et al (1993) concluded that endodontic infection promotes periodontal pocket formation and should be regarded as a risk factor in periodontitis progression.4 Therefore, a primary endodontic lesion draining through the attachment apparatus should be treated initially by endodontic therapy (Zehnder M, Hasselgren G, 2002)5. This must be confirmed by
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accurate diagnostic tests to confirm pulp necrosis and diagnostic probing (usually a precipitous drop in probe depth is detected around a tooth) (Harrington, 1979). CASE REPORT : A 45 year old male patient was referred to the Department of Conservative Dentistry & Endodontics with a chief complaint of discomfort in mandibular right first molar. He was known diabetic and was under medication. On intra oral examination the tooth was heavily restored and the tooth was tender on vertical percussion with no mobility and there was a sudden drop of periodontal probe indicating a deep periodontal pocket of 10mm. The tooth was found to be not responding to pulp testing. On radiographic examination the tooth was heavily restored involving enamel, dentine & pulp with periapical radiolucency. There was evidence of bone loss on the distal root and the furcation area (Fig 1). Thus a diagnosis of primary endodontic lesion was established. Local anesthesia was given by inferior alveolar nerve block of lidocaine 2% with epinephrine 1:100 000 (Lidocadren; Teva Ltd, Jerusalem, Israel) and medium thickness rubber dam of 6x6 inches (Hygienic; Coltene Whaledent) was placed. Access was achieved using a round diamond bur (ISO 801001016, Komet, and Lemgo, Switzerland). The pulp chamber was opened & the canal was located. Working length determined electronically using Dentaport ZX Apex locator (J. Morita Mfg. Corp.japan) & confirmed radiographically (Fig.2) as 21mm (Fig 2). Cleaning and shaping was initiated using the crown-down technique with GatesGlidden drills (Dentsply-Maillefer, Ballaigues, Switzerland) numbers 2-5 at the cervical and middlethirds of the root canals. The manual instrument size 15 was used to apical patency. The canal was negotiated to the working length, as indicated by an apex locator (Root ZX, J.Morita MFG Corp, Kyoto, Japan), with a stainless steel size 15 hand file. Apical preparation was performed by using ProFile (Tulsa Dental Products, Tulsa, USA). The master apical file was size #30 for all the root canals. Interappointment dressing of calcium hydroxide was given. In the second appointment, as the subjective symptoms were relived all canals were filled with gutta-percha and AH26 sealer (Fig. 3) and the opening cavity was sealed with Fuji IX (GC Corp., Tokyo, Japan). The post operative follow up after 6 months revealed no signs of pathosis with a pocket depth of 3-4mm & radiographic evaluation showed radiopacity
at the distal root & furcation area that indicated favourable healing and bone formation. (Fig:4).
Fig 1: Pre operative radiograph
Fig 2: Working length radiograph
Fig 3: Post obturation radiograph
Fig 4: Post operative radiograph after six months
DISCUSSION : The periodontium and the pulpal have embryonic, anatomic and functional interrelationship. They are ectomesenchymal in origin, from which the cells proliferate to form the dental papilla and follicle, which are the precursors of the periodontium and the pulp respectively. The embryonic development gives rise to anatomical connections which remain throughout the life of the tooth.6 As the tooth matures and the root is formed, three main avenues for exchange of infectious elements and other irritants between the two compartments are created by (1) dentinal tubules, (2) lateral and accessory canals, and (3) the apical foramen.7 Classification of perio-endo lesions6 There are four types of perio-endo lesions and they are classified due to their pathogenesis. 1. Endodontic lesions -an inflammatory process in the periodontal tissues resulting from noxious agents present in the root canal system of the tooth. 2. Periodontal lesions - an inflammatory process in the pulpal tissues resulting from accumulation of dental plaque on the external root surfaces. 3. True-combined lesions -both an endodontic and periodontal lesion developing independently and progressing concurrently which meet and merge at a point along the root surface. 4. Iatrogenic lesions - Usually endodontic lesions produced as a result of treatment modalities.6
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Differentiating between periodontal and endodontic problems can be difficult. A symptomatic tooth may have pain of periodontal and/or pulpal origin. The nature of that pain often is the first clue in determining the etiology of such a problem. Radiographic and clinical evaluation can further clarify the nature of the problem. In the preponderance of endodontic lesions, microflora is the etiologic vector that dictates the clinical course of the disease and therefore the treatment plan (Zehnder M, Hasselgren G, 2002). On occasion, a sinus tract originating from diseased apical tissues may drain alongside the periodontal ligament, giving the appearance of a periodontal pocket. After ruling out fracture as the etiology, careful examination with a periodontal probe should be done, not only at the site of the lesion but also in the rest of the mouth. In addition, a negative response to thermal challenge and lack of mobility of the tooth may indicate that the lesion is purely of endodontic origin. Thus root canal therapy should be performed and periodontal therapy avoided, or at least delayed, until one or two months after the root canal has been performed (Blomlof et al, 1993), and then only if the attachment apparatus does not seem to be improving. Follow-up examination is crucial when attempting to evaluate the prognosis of the treated tooth. For primary endodontic lesions conventional endodontic therapy alone will resolve the lesion. A review 4-6 months post-operatively should show healing of the periodontal pocket and bony repair. Surgical endodontic therapy has been shown to be unnecessary even in the presence of large periradicular radiolucencies and periodontal abscesses. Invasive periodontal procedures should be avoided as this may cause further injury to the attachment - possibly delaying healing. If primary endodontic lesions persist despite extensive endodontic treatment it should arouse suspicions of an incorrect diagnosis. The lesion may have secondary periodontal involvement or be a true-combined lesion, the treatment for which is outlined later. Primary endodontic lesions with secondary periodontal involvement will not completely resolve with endodontic treatment alone. Root/re-root canal treatment is instituted immediately and the cleaned and shaped root canal filled with calcium hydroxide paste. As it is bactericidal, anti-inflammatory and proteolytic it inhibits resorption and favours repair. It also inhibits periodontal contamination of instrumented canals via patent channels connecting the pulp and periodontium before periodontal treatment
removes the contaminants. The canals are eventually filled with a conventional obturation when there is clinical evidence of improvement. Conclusion: In combined endodontic-periodontic lesions, it is generally wise to treat the Endodontic component first, because in many cases this will lead to complete resolution of the problem. We can conclude that endodontic lesions with involvement of the attachment apparatus can be successfully healed by performing adequate root canal treatment with great emphasis on disinfection of the root canal system. Understanding the mechanisms of bone destruction in these types of lesions is of great importance when trying to achieve successful healing.
1) Simring M, Goldberg M. The pulp pocket approach: retrograde periodontitis. J periodontal 1964:35:22-48. 2) Bender IB. Factors influencing radiographic appearance of bony lesions. J Endod 8; 161-170,1982. 3) Chen SY,Wang HI,Clickman GN. The influence of endodontic treatment upon periodontal wound healing. J Clin periodontal24; 449-456,1997. 4) Blomlof L (1993) Relationship between periapical and periodontal status. J Clin Periodontol 20: 117-23. 5) Jorge Vera, Martin Trope, Frederic Barnett and Kenneth S Serota Endodontic Practice May 2006. 6) Mhairi R. Walker. The pathogenesis and treatment of endoperio lesions. CPD dentistry 2001: 2 (3): 9-95. 7) Ilan Roststein & James H. Simon .The endo-perio lesion: a critical appraisal of the disease condition. Endodontic Topics 2006, 13, 34–56. 8) P. Carrotte F. Endodontics: Part 9 Calcium hydroxide, root resorption, endo-perio lesions. British Dental Journal Volume 197 no. 12 December 25, 2004. 9) Gunnar Bernholtz. Interactions between pulpal and Periodontal disease conditions: introduction. Endodontic Topics 2006, 13, 1–2. 10)Pradeep S. Anand,Nandakumar. Management of Periodontitis Associated with Endodontically Involved Teeth: A Case Series. The Journal of Contemporary Dental Practice, Volume 6, No. 2, May 15, 2005.
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