Volume 4 Number 1 December 1999

Periodontic-Endodontic Lesions
Huan Xin Meng*
* Beijing Medical University, Beijing, China.

Lesions of the periodontal ligament and adjacent alveolar bone may originate from infections of the periodontium or tissues of the dental pulp. This review focuses on the relationship of lesions of endodontic origin with lesions of periodontal origin and their classication. Ann Periodontol 1999;4:84-89. KEY WORDS Dental pulp diseases/classication; dental pulp diseases/etiology; periodontal diseases/classication; periodontal diseases/etiology; lesions/endodontic; lesions/periodontic.

ulpal infection may cause a tissuedestructive process that proceeds from the apical region of a tooth toward the gingival margin. The term retrograde periodontitis was suggested in order to differentiate this from marginal periodontitis in which the infection spreads from the gingival margin toward the root apex.1,2 Another term, pulpodontic-periodontic syndrome, has been used to dene a syndrome involving inflammation or degeneration of the pulp with a periodontal pocket adjacent to the same tooth. This syndrome can be initiated by either pulpal or periodontal disease and may manifest pulpal and periodontal symptoms.3 In general, pulpal infection has the potential to initiate inammatory changes in the alveolus at both apical and non-apical locations of teeth.3 Combined lesions (previously referred to as true combined lesions) are those that occur where an endodontically induced periapical lesion exists on a tooth that is also periodontally involved.4 All of these conditions can be placed under the general term periodontitis associated with pulpal disease. This review focuses on the relation of lesions of endodontic origin with lesions of periodontal origin and their classication.

COMMUNICATION BETWEEN ENDODONTIC AND PERIODONTAL LESIONS The periodontium communicates with pulp tissues through many channels or pathways. These channels may be involved in extending pulpal infections to the periodontium, and vice versa.
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Lateral and Accessory Canals and Foramina Studies of human teeth have shown that lateral and accessory canals and foramina are present in great numbers, especially in the bifurcation and trifurcation regions of molars.3,5 Some investigators found accessory canals in molar furcations in 20% to 60% of permanent teeth,6 and in 23% of deciduous molars examined.7 In a study of 1,140 extracted adult human teeth, lateral canals were found in 27% of the teeth, and distributed at various levels of the root.8 The lateral canals were filled with capillaries, pulp cells, ground substance, and connective tissue bers that were continuous with the pulp tissue. In many cases the width of the accessory foramina or lateral canals was exceedingly small, permitting the presence of only small caliber vessels and their supporting stroma.3 In another report, 2% of the 100 teeth studied had accessory canals located within a periodontal pocket and 23% had 1 or 2 accessory canals.9 A fairly high prevalence of lateral canals in posterior teeth that communicate with the oor of the pulp chamber and the periodontal ligament has been reported in animals.10,11 Thus, there is ample evidence to indicate that infection of the pulp can potentially communicate with the periodontium at locations other than the apex of the tooth. Apical Foramen and Other Communications It has been shown that when apical granulomas from necrotic pulps are extensive, the granulomatous tissue can be present along the lateral aspects of roots, which may cause extensive resorption of the alveolar crest.3 Other communications between the periodontium and pulp may include dentinal tubules and common vasculolymphatic drainage.1,12 Although communication between pulp and periodontium can be focused on the vascular route, many other possible avenues exist. The following anatomical entities or pathways have also been mentioned in the literature as possible causes of periodontally derived endodontic lesions: lingual grooves, root/tooth fractures, cemental agenesis/hypoplasia, root anomalies, intermediate bifurcation ridges, brinous communications, and trauma-induced root resorption.13 Effect of Pulpal Diseases on the Periodontal Tissues Pulpal disease is known to cause periodontal changes in both animals3,10,11,14 and humans1,3,4,15,16 through lateral canals, accessory foramina, and crestal extension of granulomatous lesions. Several experimental animal studies have assessed the effect of pulpal injury on the periodontium.3,10,11 It has been noted that interradicular periodontal lesions can be initiated by inflamed or necrotic pulps after mechanical pulp exposures in posterior teeth of kittens, dogs, monkeys,3,10,11 and rats.14 In most instances, lateral canals were found to be associated

with the production of the periodontal lesions and led to destruction of much of the interradicular bone and bone in bifurcations.3,10 Periodontal lesions induced by pulp diseases have also been noted in humans.1,3-5,15-17 In a case series of 109 teeth considered to have a hopeless periodontal prognosis, 89% of the teeth were successfully retained after endodontic therapy.1 These results suggest that the cases were affected by a retrograde periodontitis. In another study, 80% of the teeth (42/53) subjected to pulpal and periodontal irritants had a greater incidence of inammatory reactions than those teeth with periodontal disease alone.3 Several recent retrospective clinical studies have shown a correlation between degree of marginal periodontal breakdown and presence of periapical pathology in periodontitisprone patients.18-20 In an experimental study in monkeys, an intra-canal infection with endodontic pathogens stimulated epithelial downgrowth along denuded dentin surfaces.21 Based on this nding it has been suggested that endodontic infections in periodontitis-prone patients may contribute to the progression of periodontitis.21 Periodontal damage of pulpal origin has the potential to occur in the early stages of pulpal disease. Furthermore, an apical endodontic lesion may also extend and drain along the periodontium (previously referred to as retrograde periodontitis). In molar teeth this pathway usually follows a track to the furcation, but may reach the crevice on any aspect of the tooth.22 The inflammation from inflamed and necrotic pulps can readily spread through lateral canals and accessory foramina into the periodontal ligament. EFFECT OF PERIODONTAL INFLAMMATION ON THE PULP Although dental plaque bacteria have the potential to induce pathologic changes in the pulp along the same pathways as an endodontic infection can affect the periodontium in the opposite direction, the effect of periodontal disease on the pulp is not as clear-cut as the effect of pulpal disease on the periodontium. It has been found that inammatory alterations or localized necrosis of pulp tissue were adjacent to lateral canals in roots exposed by periodontal disease.5 The direct inflammatory extension of periodontal inflammation through the apical foramen or lateral canals to the pulp, including subsequent pulpal necrosis, has been demonstrated.23,24 However, normal pulps have also been observed in teeth with advanced periodontal disease.25,26 The initial effect of periodontal inammation on the pulp may be degenerative. Fibrosis, calcications, and collagen resorption have been reported in pulps of teeth with long-standing periodontal disease.24,27 Irregular or reparative dentin formation has also been found
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with some resorption of dentin in periodontally diseased teeth.23 During scaling and root planing, cementum and supercial dentin are removed from the root surface by instrumentation. In one study, chronic pulpitis with bacterial penetration of dentinal tubules was found adjacent to roots of teeth that had been scaled and root planed.28 MICROBIOLOGY Early microbiological studies29 that assessed the microflora associated with acute suppurative dental infections implicated streptococci or staphylococci as the causative microorganisms, but more recent studies suggest that the microbiota of an acute dentoalveolar abscess is usually polymicrobial,6,29,30 similar to periodontal disease. Fusobacterium, Prevotella, Porphyromonas, Peptostreptococcus, and Streptococcus are the predominant genera that have been isolated.30-34 Spirochetes also reside in infected root canals.35,36 Acute exacerbations of chronic perapical infections are frequently associated with specic anaerobes, particularly Porphyromonas gingivalis and Porphyromonas endodontalis.30 The microbiota in necrotic pulps are not as complex as those in deep periodontal pockets. The former is usually comprised of a limited number of bacterial species of which one or two may predominate,6 such as blackpigmented Bacteroides.37,38 Depending on the microbiota and capacity of the host to resist the infection, an acute abscess or a chronic inammatory reaction may develop at any site along the periodontium, where there are direct communications with the pulpal chamber.6 CLINICAL FEATURES In contrast to supercial periodontal lesions extending from gingivitis, pulpal diseases have the potential to initiate inammatory changes deep in the alveolus at both apical and non-apical locations of involved teeth. Effect of Acute Endodontic Lesions on the Marginal Periodontium Acute manifestations of root canal infections can result in rapid and extensive destruction of the attachment apparatus.6 Dental abscesses can form at any level of the periodontium, from the tooth neck to the apex and may drain anywhere along this path; i.e., a sinus tract along the periodontal ligament space or an extraosseous stula into the gingival sulcus/pocket. Transalveolar abscesses may be caused by seeping of purulent exudate from an adjacent periapical abscess into the empty tooth socket39 and in deciduous molars, dental abscesses frequently develop at bifurcation areas.17 The periodontium can be extensively damaged at sites of periapical infection. Following proper endodontic therapy, such lesions frequently heal without a persistent periodontal defect.6
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Endodontic and periodontal abscesses may resemble each other clinically, differing only in the point of origin and specic path of infection. In most instances, periapical abscesses occur singly, the involved teeth may be extruded and exhibit tenderness to percussion and hypermobility. Marked lymphadenopathy is common, as is facial swelling and extension of the infection along tissue planes to points of drainage (either intraoral or extraoral). Fever and malaise commonly occur, which may be due to the action of the endogenous pyrogen interleukin-1, which is found in high levels in exudates from periapical abscesses. A range of significant complications may arise from untreated endodontic abscesses.40 Persistent fever has been reported due to an occult dental abscess.41 Root Perforations Inammatory lesions in the marginal periodontium as manifested by increased probing depth, suppuration, increased tooth mobility, and loss of brous attachment may result from an undetected or unsuccessfully treated root perforation.6,42 A periodontal abscess may also occur in the absence of any previous periodontal disease, following perforation of the lateral wall of the root during endodontic therapy.1,33 Vertical Root Fracture In general, vertical root fractures occur most often on endodontically treated teeth. However, spontaneous vertical root fractures of non-endodontically treated teeth can also occur and more than 500 cases have been reported in the Chinese population.43-52 The clinical features of vertical root fractures in non-endodontically treated teeth can sometimes appear as combined endodontic and periodontal lesions.45,46,52-54 Pain during occlusion or mastication is the principal symptom. Thermal sensitivity, gingival swelling, and periodontal abscess or sinus tracts are also common. Upon clinical examination pulps of fractured teeth may or may not be responsive to electric pulp testing.50,52-54 Narrow or localized deep pockets are usually detected by periodontal probing. Widening of the root canal space and periapical and/or periodontal radiolucencies are radiographic characteristics which may aid in diagnosis.46,50,54 One study indicated that vertical root fractures are often associated with traumatic occlusal contacts or severe abrasion which increased the occlusal load during chewing.50 Another study found that most of the fractures passed along incremental lines in dentine, and fractures frequently occurred on at roots with 2 canals,51 suggesting that they may be related to developmental or anatomic defects. Root fractures frequently occur on endodontically treated teeth and are associated with a deep pocket on a surface of the tooth which may or may not be abscessed.6 Symptoms and signs associated with vertical root fractures show a variety of characteristics and

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are difcult to distinguish from those associated with periodontal and endodontic lesions. Pain on selective loading of cusps may be an indication of a root fracture. Combined Lesions This lesion occurs as the result of the interaction between diseases of endodontic and periodontal origin, on the same tooth, irrespective of the sequence in which they occur. The clinical and radiographic examinations do not permit identification of the primary cause of the lesion. DIAGNOSIS The diagnosis of periodontal lesions associated with pulpal diseases may be relatively simple if a patient has been monitored over a period of time and records (e.g., radiographs) are available. The diagnosis becomes more difficult when a complete history is unavailable. A growing periapical area with secondary formation of a deep periodontal pocket may be similar in clinical and radiographic appearance to a longstanding periodontal lesion that has progressed to the root apex.2 The radiographic image of bone resorption, including the apical and furcal or marginal regions, may confuse rather than aid in making a diagnosis. However, if radiographs taken during the progression of bone resorption reveal it to be extending from the apex to the crest, the apical region can be positively identied as the origin of the infection.55 In general, it is easier to determine the origin of the lesion when a vital pulp test is obtained, because the test results usually will rule out an endodontic etiology. However, pulp tests may not always be reliable.56 This consideration is particularly relevant when challenges to pulpal status arise from periodontal diseases.57 Partial necrosis of a pulp, especially in a multirooted tooth, may be a result.5,23,58 This may allow for positive responses to pulp testing suggesting vitality, despite the existence of a combined lesion.59 It has been suggested that when doubt exists about a pulps status, a test cavity can be made.2 However, this may not always provide a more exact determination of pulpal status once partial pulpal necrosis has occurred. A non-vital or endodontically-treated tooth associated with a combined lesion presents a greater diagnostic problem.2,4 In this situation, pulpal necrosis is frequently associated with inammatory involvement of the periodontal tissue. The location of these pulpal lesions is most often at the apex of the tooth, but they may also occur at any site where lateral and furcal canals exit into the periodontium. Differential Diagnosis Determination of pulp vitality is essential for a differential diagnosis and for selection of primary measures for treatment of inammatory lesions in the marginal

and apical periodontium. Deep restorations, dental trauma, endodontic treatment, previous pulp capping, and pulp vitality testing are factors to be considered when assessing the need for endodontic treatment as a part of overall periodontal therapy.6 Location and extent of pockets, probing depth, and furcation invasions are also essential for the differential diagnosis.60 If the pulp reacts clinically normal, but a periodontal pocket can be located, then periodontal tissues should be suspected as the origin of either the acute or chronic inammatory process. On the other hand, when the pulp is found to test nonvital, the inammatory process which passes through a lateral canal or the apical foramen will cause a lesion of endodontic origin. When pulpitis is clinically recognized in a tooth with pre-existing periodontal disease, the pulpitis may be secondary to the periodontal disease, particularly in the absence of any other obvious cause of pulpitis. The presence of subgingival calculus deposits and the degree and location of inflammation are important to note in determining the primary source of the disease. When severe or angular localized lesions of the periodontium are detected, the differential diagnosis between pulpal and periodontal origins should be made. Severe localized periodontal lesions are well documented periodontal consequences of pulpal pathoses.22 However, destruction of the periodontium near or about the apical area of a tooth does not necessarily indicate that the lesion is of pulpal origin. Large and diffuse areas of radiographically evident periapical destruction can occur without compromising the health of the pulpal tissues.61 Such lesions can occur in the following circumstances: 1) direct extension of an active periodontal lesion; 2) interproximal channel lesion, generally seen in the mandibular cuspid area; 3) cystic lesions derived from epithelial remnants of tooth-forming tissues; 4) localized sites of rapidly advancing periodontitis; or 5) localized lesions of osteomyelitis involving the periodontium.61 It has been suggested that the percentage of spirochetes as seen by darkeld microscopy might be of value in the differential diagnosis of periodontal and endodontic abscesses.62 In this study it was reported that, in periodontal abscesses, spirochetes were the predominant cell (mean, 40.6 10.9%) with coccoid cells present in significantly lower numbers (mean, 19.7 10.9%). In endodontic abscesses the reverse was true, where coccoid cells dominated (mean, 44.3 19.7%) and only few spirochetes were present (mean, 5.6 4.7 %).62 The clinical value of this observation has not yet been determined. CONCLUSION Pulpal disease may cause periodontal changes in both animals and humans through lateral canals, accessory
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canals, accessory and apical foramina, and gingival extension of endodontic lesions. Periodontal diseases may cause pulpal changes through communications between the pulp and the root surface. These pathologies (i.e., endodontic or periodontal) may exist independently of each other on the same tooth. It is proposed that the combined lesion is where there is an interaction between diseases of endodontic origin and periodontal diseases on a tooth. Thus the combined lesion is the lesion to be classied. ACKNOWLEDGMENT The author expresses her appreciation to Dr. Esmonde Corbet for his generous assistance in the preparation of this paper. REFERENCES
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55. Christie WH, Holthius AF. The endo-perio problem in dental practice: Diagnosis and prognosis. J Can Dent Assoc 1990;56:1005-1011. 56. Belk CE, Gutmann JL. Perspectives, controversies and directives on pulpal-periodontal relationships. J Can Dent Assoc 1990;56:1013-1017. 57. Petersson K, Soderstrom C, Kiani AM, Levy G. Evaluation of the ability of thermal and electrical tests to register pulp vitality. Endod Dent Traumatol 1999;15:127131. 58. Hirsch RS, Clarke NG, Srikandi W. Pulpal pathosis and severe alveolar lesions: a clinical study. Endod Dent Traumatol 1989;5:48-54. 59. Kipioti A, Nakou M, Legakis N, Mitsis F. Microbiological ndings of infected root canals and adjacent periodontal pockets in teeth with advanced periodontitis. Oral Surg Oral Med Oral Pathol 1984;58:213-220. 60. Peters DD, Baumgartner JC, Lorton L. Adult pulpal diagnosis. I. Evaluation of the positive and negative responses to cold and electrical pulp tests. J Endod 1994;20:506511. 61. Gold SI, Moskow BS. Periodontal repair of periapical lesions: the borderland between pulpal and periodontal disease. J Clin Periodontol 1987;14:251-256. 62. Trope M, Tronstad L, Rosenberg ES, Listgarten M. Darkfield microscopy as a diagnostic aid in differentiating exudates from endodontic and periodontal abscesses. J Endod 1988;14:35-38. Send reprint requests to: Dr. Huan Xin Meng, Beijing Medical University, School of Stomatology, Weigongcun, Haidian District, Beijing 100081 China. Fax: 86-10-6217-3402; email: hxmeng@public.east.cn.net

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