Summary

The term ‘endodontic-periodontal’ (endo-perio) lesions has been used to describe lesions that involve the pulp and periodontal tissues either in a separate or a combined pattern. The diagnosis, management, and prognosis of teeth with endo-perio lesions are challenging for the clinician. The complexity of endo-perio lesions reflects the close developmental relation between the pulp and periodontal tissues. The last decade has witnessed a change in the perspective of endo-perio lesions and our understanding of the condition. This chapter addresses the complex and dynamic nature of normal anatomical and pathological pulp and periodontal inter-communication pathways. In addition, it presents new classification systems for endo-perio lesions together with methods for diagnosis, management, and assessing the prognosis following treatment.

22.1 Communication Pathways Between the Pulp and Periodontal Tissues

The inter-relationship between the dental pulp and periodontium has been investigated widely [1–4]. The complexity of normal anatomical variations and pathological conditions, together with the ability of these tissues to provide a well-protected environment to deter/repel invading microorganisms and their toxins, requires dentists to have a thorough knowledge and understanding of pulp and periodontal relationships for proper treatment planning and management of lesions involving these two tissues.

The apical foramen and accessory canals (lateral canals, chamber canals, and apical deltas) are the most common anatomical pathways of communication between the pulp and periodontal tissues that provide the necessary vascular, lymphatic, neural, and connective tissue communications [4–6] (Figure 22.1). Exposed cervical dentine, where the cementum and enamel do not meet at the normal cemento-enamel junction (CEJ), can also provide tubular communications through patent dentinal tubules [7, 8]. Dentinal tubule exposure because of physiological root resorption in the external furcation areas of primary molar teeth might also play a role in facilitating toxin diffusion [9]. In addition, the permeability of cementum together with cytoplasmic processes of cementocytes may provide another avenue for communication between the pulp and periodontal tissues [10–12]. Sharpey’s fibres may provide another communication since they are surrounded by an uncalcified central core in the cellular cementum; the breakdown of these fibres would leave a sieve-like surface full of micro-channels that has the potential to facilitate the invasion of microorganisms and/or their toxins to the underlying dentine [8, 13–15].

Root dentine has good thermal insulating properties [16]; however, considerable thermal conductivity from the radicular dentine/cementum complex to the periodontium during root canal treatment procedures has been reported [17–21]. Interestingly, it seems that there is no correlation between the tubular anatomy of dentine and its thermal transmission property because enamel, which has less water content and contains no tubular morphology, has greater thermal conductivity and diffusivity than dentine [22, 23].

Notably, such anatomical communications are subject to dynamic changes by age:

• Apical foramina decrease in diameter, and their deviation from the long axis of the root increases because of cementum apposition [24, 25];
• Accessory canals gradually decrease in diameter because of continuous deposition of secondary dentine and cementum [26];
• Radicular dentine becomes less permeable because of the formation of sclerotic dentine [27–29]; and
• Cementum becomes less permeable [30].

Besides these normal anatomical and physiological avenues, the pulp and periodontal tissues may communicate through pathways created by a variety of pathological conditions. Developmental anomalies such as palato-gingival grooves [31], facial radicular grooves [32], cemental hypoplasia and/or resorption due to developmental diseases [12, 33], radicular dens invaginatus [34, 35], dentine dysplasia type I [36], and extended radicular grooves due to teeth gemination or fusion [37–39] are examples of developmental pathological communication pathways. Nondevelopmental factors are related to either disease, trauma, or an iatrogenic procedure such as furcation perforations because of caries [40] (Figure 22.2a), vertical and horizontal root fractures [41, 42] (Figure 22.2b), perforating internal/external root resorption defects [2, 43] (Figure 22.2c–f) and accidental root perforations during treatment [44].

22.1.1 Endo-perio Lesions: A Terminological Controversy

There is confusion and controversy associated with the terminology of ‘periodontal-endodontic (endodontic-periodontal) lesions’ often refered to as ‘endo-perio (perio-endo) lesions.’ Many authors have defined those lesions as primary endodontic or primary periodontal lesions causing secondary periodontal or secondary endodontic involvement, respectively, that can also be presented independently and may coalesce [2, 15, 45–47]. These lesions may require endodontic or periodontal treatment or a combined interdisciplinary treatment approach. Abbott and Salgado [4] highlighted that endo-perio lesions should be limited to those teeth that have both independent endodontic and periodontal diseases occurring at the same time, which can be with or without communication. Ahmed [48] defined endo-perio lesions as the dependent and/or independent involvement of the pulp (or the pulp space in case of endodontically treated teeth) and periodontal tissues of an individual tooth.

Classification of a disease (as presented by its clinical profile) is fundamental; the identification of its causes allows appropriate treatment. A typical endo-perio lesion presents with apico-coronal involvement of the periodontium as observed both through clinical and radiologic examinations. Periodontal lesions are always present but must be distinguished separately [49, 50]; namely, periodontal lesions of endodontic origin and plaque-induced periodontal lesions must be categorised accurately. Due to their different aetiology and pathogenesis [49, 50], periodontal lesions occur at different locations. Those deriving from pulp infection are found at or near the root apex although they may also originate laterally where infection drains via lateral canal foramina [51, 52]. Conversely, periodontitis caused by bacterial plaque (biofilm) at the periodontal margin is usually identified at a more coronal level of the root (Figure 22.3).

Plaque-induced periodontal lesions are of bacterial aetiology and inflammatory pathogenesis. In general, the clinical examination and radiographic findings reveal tissue alterations at locations and with characteristics that are easily recognised and make diagnosis straightforward. In other cases where the tooth is affected both apically and coronally, the clinical and radiologic examinations may indicate a dual nature of the lesions, which requires a differential diagnosis that allows their aetiology to be defined accurately. Not only do they present different signs and symptoms but these are frequently hidden and/or misleading (Figure 22.4).

It is obvious that endo-perio lesions require a more intensive analysis to distinguish their origin and progress. Do symptoms involving the periodontium originate from the pulp, affecting the periodontal margin, and draining via a sinus tract? Or are they indicative of a plaque-related marginal lesion that has progressed more deeply into the apical periodontium and affected the pulp? In both cases, there is a primary cause involving one tissue leading to secondary involvement of another tissue. A third alternative may be encountered in which both primary conditions originate independently and subsequently merge as they evolve. The latter represents a combined endo-periodontal lesion also known as a true endo-periodontal lesion. All diagnostic steps must seek to clarify whether the lesion originates from a single cause, and the nature of this cause, or to what extent different causes have contributed to the overall pathosis.

22.1.2 Classifications of Endo-perio Lesions

As mentioned above, endo-perio lesions can present with many clinical and radiological patterns. This diversity in presentation is always accompanied with challenging diagnostic landmarks that require thorough knowledge and special attention from dental practitioners to provide the best treatment outcomes for the patient. Table 22.1 describes classifications for endo-perio lesions [2, 4, 15, 47–49, 53–57], which is based on either the aetiological factors and pathological patterns [2, 4, 48, 49, 53] or the treatment strategies and prognosis [47, 54]. As an attempt to introduce a more generalised classification, some authors tended not to follow a single criterion and classified endo-perio lesions on the basis of aetiological factors, pathological patterns, and treatment strategies. For instance, Hiatt [15] introduced endo-perio lesions of short and long duration, and added other classes for periodontal diseases that are treated by either hemisection or root amputation, and included endodontic and periodontic iatrogenic factors causing periodontal and pulpal diseases, respectively. Similarly, Weine [55] followed this approach by adding class III (Table 22.1) that refers to teeth having no pulpal problems but require endodontic therapy plus root amputation to gain periodontal healing. However, in classes I and IV (Table 22.1), he described the simulating clinical and radiographic landmarks of pulpal and periodontal lesions originated from periodontal and pulpal tissues, respectively.

Despite these efforts, the considerable variability of the aetiological factors and patterns of presentation of endo-perio lesions do not correspond with a satisfactory, evidence-based classification that can place endo-perio lesions precisely into clear and accurate categories. This arises from the incomplete identification of all aetiological factors and patterns of presentation related to endo-perio lesions. In addition, the relevance of considering the treatment strategy and prognosis in some classifications [47, 54] is debatable as all endo-perio lesions should be diagnosed first before considering the treatment plan that usually varies according to each case [4]. It would also be more confusing when the treatment strategies include teeth having only periodontal diseases with no pulpal involvement that require either hemisection or root amputation [15, 55]. Although intentional root canal treatment may be required, the pathological pattern is not related to endo-perio lesions. Foce [49, 50] and Ahmed [48] introduced classification systems for endo-perio lesions, which will be discussed in detail in the following sections.

22.1.3 Foce Classification System for Endo-perio Lesions

22.1.3.1 Class 1 – Crown-down Plaque-induced Periodontal Lesions

Crown-down plaque-induced periodontal lesions start from the crown and propagate along the root apically and may extend to deep periradicular areas (Figure 22.5). This extension may lead to signs and symptoms mimicking pulp disease, but in fact there is no pulp involvement and it requires only periodontal treatment or at a later stage it may involve the pulp tissues via lateral canals or the apical foramen that requires root canal treatment followed by periodontal treatment.

22.1.3.2 Class 2 – Down-crown Periodontal Lesions of Endodontic Origin

These lesions start from the apical foramen and/or patent accessory canals of the root and progress in an apico-coronal direction. They spread within the limited space of the periodontal ligament before progressing to the surrounding alveolar bone. Down-crown lesions are capable of causing periodontal tissue inflammation but will not lead to irreversible loss of the periodontal ligament attachment unless left untreated, which will allow plaque and calculus to form subsequently to initiate disease independently (Figure 22.6).

22.1.3.3 Class 3 – Combined Endo-perio Lesions

What appears clinically and radiographically as a single lesion extending apico-coronally may in fact be a combination of two separate lesions that have developed independently (Figure 22.7). Their distinct aetiologies and pathogeneses have created conditions that encroach on one another from opposite directions: a plaque-generated pocket that extends apically to merge with a periodontal lesion of endodontic origin that developed at the root end before progressing coronally toward the pocket. From a clinical standpoint, however, it makes no difference to the diagnosis and subsequent treatment plan how the true combined lesion developed.