Summary

Root resorption is the loss of the dental hard tissues (cementum, dentine and/or enamel). Whilst this is a necessary process for the exfoliation of primary teeth, odontoclastic resorption is an undesirable event in permanent teeth, resulting in irreversible tooth structure loss which usually requires orthograde and/or surgical management. This chapter provides an overview of the different types of resorption that affect the dental hard tissues. The aetiology, pathogenesises, diagnosis and management of internal (inflammatory, replacement) and external (inflammatory, replacement, surface, cervical) resorption will be discussed.

5.1 Introduction

Dental resorption is defined as the loss of dental hard tissues as a result of clastic activities [1]. Root resorption in the primary dentition is a physiological process unless it occurs prematurely. It is not yet completely understood how this process occurs, although it is believed that it is regulated by cytokines and transcription factors which are also involved in bone remodelling [2, 3]. Root resorption of permanent teeth is a pathological process, which if left untreated, may result in premature loss of the affected teeth.

Depending on its location in relation to the root (or canal) surface, root resorption may be classified as internal or external [4, 5]. Internal root resorption (IRR) was reported as early as 1830 [6]. The aetiology and pathogenesis of IRR is not completely understood [7]. The diagnosis of IRR may be challenging and is often confused with external cervical resorption (ECR). An incorrect diagnosis may result in inappropriate treatment [7].

There are three phases to root resorption; initiation, resorption and repair [8]. Root resorption may be detected during routine clinical examination, or as an incidental radiographic finding, as the process may be self-limiting and the patient may be asymptomatic. If the initial surface resorptive process is sustained, for example, by infection and/or pressure, then dental hard tissue destruction will continue and substantial tooth tissue loss may occur. This may result in the tooth becoming untreatable.

The aim of this chapter is to provide a practical guide to the diagnosis of root resorption lesions using a simple classification (Figure 5.1), and aid the management of these defects in everyday practice (Table 5.1).

5.2 Histopathology of Root Resorption

The dentine is protected from internal and external root resorption by the non-collagenous organic outer surface of the root canal wall consisting of the odontoblast layer and predentine, and the root surface (precementum and periodontal ligament). Once the non-collagenous layer is damaged or irritated, odontoclasts are recruited to the site of injury by the release of several inflammatory cytokines. The recruited odontoclasts then bind to the extracellular protein containing arginine-glycine-aspartic acid (RGD) sequence of amino acids present on the surface of mineralized tissues by means of integrins [10]. Root resorption involves the activation of the Osteoprotegerin (OPG)/Receptor activator of factor kappa B (RANK)/RANK Ligand (RANKL) transcription factor system which is responsible for bone remodelling [11]. Several studies have identified the ability of periodontal ligament, cementum, and dental pulp to express RANKL which are paramount in the differentiation of odontoclasts during root resorption [12–14].

5.3 Internal Root Resorption

This form of resorption affects the root canal wall [7]. It is further classified as either inflammatory or replacement. The replacement type is associated with the deposition of mineralised tissue in the root canal space after the initial loss of dentine (initial dentine loss is a feature of both types) [7]. However, the inflammatory type is associated with the loss of predentine. Histologically, internal root resorption occurs due to the activation of odontoclasts which are responsible for resorbing dental hard tissue. The odontoclasts are small in size and also have small nuclei and sealing zones. These cells have enzymatic properties and cytologic features. Furthermore, odontoclasts create resorption depressions on the surface of the mineralized tissue, known as Howship lacunae. Odontoclasts are polarized in relation to the dental tissues and have a ruffled border, located inside a clear zone, that is in intimate contact with their dental substratum [15, 16]. When observing odontoclasts using an electron microscope, a large number of mitochondria and vacuoles are evident in the cytoplasm, whilst there is scarcity of endoplasmic reticulum. In a study assessing the histological appearance of internal root resorption, Wedenberg and Zetterqvist [17] reported that the pulpal tissue was predominantly composed of lymphocytes and macrophages, with some neutrophils. The connective tissue within the pulp spaces was less vascular than healthy pulpal tissue and resembled periodontal membrane connective tissue with relatively more cells and fibres. The odontoblast layer and predentine were absent from the affected dentinal walls, which were populated by large, multinucleated odontoclasts occupying resorption lacunae. The odontoclasts showed evidence of active resorption. They were accompanied by mononuclear cells, believed to be odontoclast precursors, which populated the connective tissue adjacent to the site of resorption. Both types of cells displayed tartarate-resistant acid phosphatase (TRAP) activity.

Interestingly, the root canal wall was incompletely lined with a mineralized tissue resembling bone or cementum in all of the examined teeth [17]. Furthermore, islands of calcified tissue of a similar nature occupied the pulpal space in three of the cases. Islands of mineralized tissue occupying the root canal space are the defining feature of internal replacement resorption [18]. The authors suggested that deposition of this mineralized tissue is likely to be part of a coupling process, at the end of a period of resorption, in which osteoblasts are attracted to the affected site and participate in bone formation [17].

5.3.1 Internal Inflammatory Root Resorption

The exact cause of such damage is not clearly understood. Several aetiological factors are thought to cause the loss of predentine (Table 5.2). In an advancing lesion, the pulp coronal to the resorptive lesion will be necrotic, whilst apically the pulp is vital, thus providing nutrients to the progressing lesion [5].

Clinically, teeth with internal inflammatory root resorption are asymptomatic and lesions are usually detected during a routine clinical examination. However, these teeth may exhibit signs of reversible or irreversible pulpitis. Furthermore, in infected root canal systems with necrotic pulps, symptoms and/or signs of apical periodontitis may arise (Table 5.2).

The radiographic presentation of internal inflammatory resorption lesions has been classically described as symmetrical radiolucent round or oval “ballooning” of the canal wall, typically in the middle third of the root. However, in reality, the radiographic appearance of these lesions may vary, both in location and nature [7].

The use of cone beam computed tomography (CBCT) as a diagnostic and treatment planning tool in the diagnosis and management of internal root resorption has been well documented [19]. It allows the clinician to appreciate the exact location and nature of the lesion, as well as the presence of a perforation, particularly in the bucco-lingual plane, which is not possible with conventional radiographic views. These considerations will have a significant impact on management and prognosis [19–21].

Root canal treatment of teeth diagnosed with internal inflammatory resorption is usually complicated by profuse bleeding from the granulomatous tissue within the root canal system. This will cease once the pulp and granulation tissue are removed. As a result of the irregular anatomy of internal root resorption lesions, techniques such as passive ultrasonic irrigation [19] or the use of a three-dimensionally adaptive file system such as the XP-endo Finisher (FKG, La Chaux-de-Fonds, Switzerland) [22] have been advocated to facilitate cleaning of the inaccessible regions of the resorptive defect. For the same reason, the use of an inter-appointment dressing such as calcium hydroxide may be of benefit although it may be challenging to completely remove the medication at the follow-up appointment.

In cases where the internal root resorption lesion has not perforated the root, it is desirable to fill the canal with a thermoplasticised technique to ensure optimum adaptation and compaction. However, in cases where a perforation is present, root canal filling is best performed with a bioceramic material such as mineral trioxide aggregate (MTA) or Biodentine [19]. Furthermore, the challenges of cleaning and sealing perforating defects may require additional surgical management.

5.3.2 Internal Replacement Resorption

Internal replacement resorption is uncommon with an unknown aetiology. However, it could be associated with the factors listed in (Table 5.2).

Clinical signs and symptoms are similar to internal inflammatory root resorption. Radiographically, these resorptive defects and the adjacent root canal wall usually have a mottled appearance due to the inclusion of hard tissue. The exact nature of the defect, as well as its location and extent, can only be accurately determined using CBCT (Figure 5.2 ).

Management of teeth with internal replacement resorption is similar to the management of teeth with internal inflammatory root resorption. However, the management of such cases may require the use of endodontic ultrasonic files and/or tips to navigate through the osteoid-like hard tissue.

5.4 External Root Resorption

5.4.1 External Inflammatory Resorption

External inflammatory root resorption is a common finding in almost all teeth diagnosed with apical periodontitis [7]. These lesions are also observed following severe traumatic injuries such as luxation injuries and avulsion. The progression of these lesions is related to the presence of root canal infection [5, 23, 24