of Endodontic-Periodontic Lesions

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© Springer Nature Switzerland AG 2020

S. Nares (ed.)Advances in Periodontal Surgerydoi.org/10.1007/978-3-030-12310-9_15

15. Management of Endodontic-Periodontic Lesions

Bradford R. Johnson1  
(1)

Department of Endodontics (MC 642), University of Illinois at Chicago, Chicago, IL, USA
 
 
Bradford R. Johnson
Keywords

Endodontic-periodontic lesionsTreatment planningEndo-perioOutcomes of endo-perio lesions

15.1 Introduction

Although endodontology and periodontology are often viewed as two separate areas of oral science and clinical practice, the intimate association between diseases of the pulp and diseases of the periodontium creates areas of significant overlap. The relationship between the pulp and periodontium has embryologic origins and continues as a functional relationship in the mature dentition [1]. Oxygen saturation was found to be lower in pulps of teeth with periodontal attachment loss and recession, and there is a negative correlation between markers of periodontal disease and pulp oxygen saturation [2]. Diagnosis and management of endodontic-periodontic (endo-perio) lesions often involves interdisciplinary consultation and shared treatment planning. The purpose of this chapter is to provide a brief overview of endodontic-periodontic lesions, with a primary focus on endodontic considerations in diagnosis and treatment planning.

15.2 Pathways Connecting the Pulp and Periodontium

There are three primary paths of communication between the pulp and periodontium. First, the largest opening in an intact permanent tooth is the apical foramen, typically measuring between 0.2 and 0.4 mm [3]. The spread of inflammatory by-products and microorganisms from the pulp to the periodontium via the apical foramen is a well-documented sequelae of infection of the root canal space. The resulting apical periodontitis may range in degree from completely asymptomatic to acute pain and swelling. Nonsurgical root canal therapy is usually the treatment of first choice for apical periodontitis in a restorable tooth with adequate periodontal support. Alternatives include no treatment and extraction, and, for teeth that have already received initial root canal therapy, revision of initial therapy and/or endodontic microsurgery should be considered. Spread of infection from the periodontium to the pulp via the apical foramen is believed to occur only when attachment loss reaches the foramen. The second pathway of potential communication between the pulp and periodontium is lateral or accessory canals (Fig. 15.1a), which are most common in the apical third of the root but can also be found in the middle and cervical third, as well as the furcation of molars (Fig. 15.1b) [4]. Finally, exposed dentinal tubules in an area of the root with no cementum layer can also allow for communication between the pulp and periodontium. Dentinal tubules extend from the pulp to the external root surface, with a mean diameter of approximately 2.5 μ at the pulp-dentin interface and narrowing to a mean diameter of 0.9 μ at the root surface [5]. Since most oral bacteria are smaller in diameter than 0.9 μ, penetration into the tubules and eventually the pulp is possible if the protective cementum layer on the root surface is absent. The predominant microorganisms found in infected root canals, Porphyromonas sp. (13.9%), Filifactor sp. (12.5%), and Parvimonas sp. (11.1%), are similar to those identified in periodontal pockets, suggesting the periodontal pocket could be a source of infection in the root canal space, and vice versa [6].

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Fig. 15.1

Accessory canals and periodontal defects. (a) The blue arrow demonstrates sealer in an accessory canal. This accessory canal, a fairly common finding in the apical third of many roots, is large enough to allow spread of bacteria and bacterial by-products from the pulp to periodontium and vice versa. (b) A buccal sinus tract was present and traced with gutta-percha (orange arrow) to the furcation of #30. The location of the lesion is suggestive of a primary perio lesion, but this is actually a primary endo lesion (previously treated with chronic periradicular abscess) due to coronal microleakage secondary to recurrent caries at the distal crown margin (red arrow). Since accessory canals are not uncommon in the furcation area of molars, bone destruction can occasionally appear first in the furcation area rather than the more common presentation at the root apices

15.3 Classification and Diagnosis

A practical way to classify endo-perio lesions for treatment planning purposes is to separate into three broad categories: (1) primary endodontic, (2) primary periodontal, and (3) combined endo-perio lesion [7]. The combined endo-perio lesion category can be further subdivided into primary endodontic with secondary periodontal disease, primary periodontal with secondary endodontic disease, and true combined endo-perio lesions. Proper classification will help guide treatment sequence and determine prognosis.

15.4 Primary Endodontic Lesion (Fig. 15.2)

  • Pain is often absent (drainage may occur through the sulcus and/or sinus tract; sinus tracts should be traced with gutta-percha although this is not always a reliable test [Fig. 15.3a]).

  • No response to pulp sensibility testing (thermal and electric pulp test).

  • Periodontal probings within normal limits (WNL) except one isolated defect that may probe to the apex.

  • Response to percussion and palpation is variable.

  • Treatment: prognosis is favorable with RCT (root canal therapy) only (nonsurgical or surgical).

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Fig. 15.2

Lesions of primary endodontic origin periodontal status. (a) Preoperative radiograph of tooth #31. The tooth was nonresponsive to pulp sensibility testing and exhibited grade 2 mobility. Although probing depths ranged from 3.0 to 5.0 mm, the cervical periodontal attachment appeared to be intact circumferentially. A draining buccal sinus tract was present. The diagnosis was primary endo lesion (pulp necrosis with chronic apical abscess) with an unfavorable prognosis. The patient was highly motivated to try to save the tooth, and initial response to pulp debridement and placement of interim calcium hydroxide paste was favorable. RCT was completed in two appointments. (b) Good healing and bone regeneration are apparent at the 18-month posttreatment evaluation (Case courtesy of Dr. Cristina Olarov). (c) Heavily restored tooth #30 was nonresponsive to pulp sensibility testing. The tooth was slightly sensitive to percussion, palpation, and biting. Mobility was WNL. A periodontal probe could be inserted to full length of probe in a single, isolated mid-buccal defect. The diagnosis was primary endo lesion (pulp necrosis and chronic apical abscess). (d) Favorable initial healing was observed at the 1-year posttreatment evaluation and all probing depths are now WNL

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Fig. 15.3

Palatal sinus tract. A palatal sinus tract adjacent to tooth #15 was traced with gutta-percha (arrow) and suggested a primary endo lesion associated with recently erupted #15 (a). Teeth #13, 14, and 15 all responded positively to cold testing. A limited field of view CBCT of the area (without gutta-percha in the sinus tract) demonstrated a distinct periapical lesion associated with the P root of #14 (b and c; arrows pointing to the P root apex, in coronal and axial views, respectively). On endodontic access of #14, some vital tissue was found in the MB and DB roots (explaining the positive response to cold), and the P root was completely necrotic. The sinus tract resolved after initial canal space debridement and placement of calcium hydroxide paste as an interim intra-appointment medication in tooth #14

15.5 Primary Periodontal Lesion (Fig. 15.4)

  • Usually evidence of advanced periodontal disease.

  • May observe widened PDL secondary to occlusal trauma (can be confused with lesion of primary endo origin).

  • Normal response to pulp sensibility testing (thermal and electric pulp test).

  • Plaque and calculus present on root surfaces.

  • Treatment: prognosis depends completely on ability to manage periodontal disease; RCT may be indicated if periodontal therapy could lead to devitalization of the pulp or pulp status is uncertain.

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Fig. 15.4

Primary periodontal lesions. Two periapical images from an 18-year-old female referred to an endodontist for evaluation. All teeth responded WNL to pulp sensibility testing. The diagnosis was localized aggressive periodontitis, and prognosis depends entirely on ability to manage periodontal disease

15.6 Combined Endodontic-Periodontal Lesion

  • In early stages, endo and perio lesions are separate and may later connect.

  • Non-vital pulp and periapical lesion of endodontic origin.

  • Crestal bone and attachment loss; deep periodontal probings; plaque and calculus.

  • Need to rule out vertical root fracture (hopeless prognosis) (Fig. 15.5).

  • Treatment: Periodontal consult, if periodontal condition is manageable, then RCT, followed by periodontal therapy; prognosis is typically questionable.

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Fig. 15.5

Vertical root fracture. (a) Tooth #31 was nonresponsive to pulp sensibility tests and sensitive to percussion and biting. A 10+ mm periodontal probing depth was noted on the distal aspect (red arrow). Transillumination with a light source and visual examination revealed an incomplete vertical root fracture. This is an example of a true combined endo-perio lesion, and the tooth was extracted due to unfavorable prognosis (b)

Radiographic imaging is an essential first step although, as can be seen by numerous examples presented in this chapter, radiographs alone do not provide a defintive diagnosis. The recent introduction of cone beam computed tomography (CBCT) has greatly enhanced diagnosis and treatment planning in all areas of dentistry and gained rapid acceptance in endodontics [810]. Of the commonly used pulp sensibility tests for establishing pulp vitality, cold is generally the most useful and accurate [11, 12]. Electric pulp testing (EPT) may be useful for teeth with calcified and/or receded canals since these teeth often do not respond to cold but will respond to EPT. Heat testing is not as commonly used but can be very helpful when the chief complaint is sensitivity to hot foods or liquids. Laser Doppler flowmetry (LDF) and pulse oximetry (PO) have been proposed as alternative pulp sensibility tests and have the advantage of being able to measure pulp blood flow [1315]. However, even though these tests perform very well in limited benchtop and clinical experimental models, currently there are no commercially available and practical devices for this type of pulp testing. A small test cavity is considered to be highly accurate for determining pulp vitality but is invasive (albeit, minimally) and not routinely used.

Percussion is useful for generic identification of a tooth with inflammation in the periodontal ligament and especially apical tissues, but is not specific to endodontic vs. periodontic pathosis. Likewise, palpation sensitivity may help localize a problem but is not particularly useful for differential diagnosis of endo-perio lesions. Complete periodontal pocket depth probings are an essential part of any endo-perio diagnostic process and can help distinguish generalized periodontal attachment loss (suggestive of a primary perio lesion) from a single isolated deep probing pocket, which is more suggestive of a primary endo lesion.

15.7 Root Resorption

Pathologic root resorption can be broadly classified into two categories—internal and external. Internal resorption is primarily an endodontic only problem with unknown etiology and, in the early stages, requires the presence of active clastic cells in a vital pulp. The presence of an incomplete vertical root fracture or herpesvirus outbreak along a branch of the trigeminal nerve serving the affected tooth or teeth have both been suggested as possible causes of internal resorption [16, 17]. A possible genetic component has also been proposed and requires further investigation [18]. Regardless of etiology, root canal therapy is usually recommended when internal resorption is first diagnosed since progression of the disease process is unpredictable and the condition may remain inactive for years before a sudden increase in resorptive activity, leading to extensive loss of root dentin and often tooth loss. An example of internal resorption and management with nonsurgical root canal treatment is shown in Fig. 15.6. In this more advanced case, the pulp became necrotic and an endo-perio lesion developed.

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