Management of tooth resorption
Dental resorption is a physiological or pathological process, which involves loss of dentine and/or cementum by hard tissue resorbing cells. As a physiological process on the root surface, it is dynamic and continual but is not clinically detectable. Occasionally, such resorption may be triggered to become transiently pathological but leaving no long-term consequences; it is usually detected only by chance. Progressive pathological resorption may also remain asymptomatic until it reaches an advanced stage. Early diagnosis and appropriate management is necessary if tooth loss is to be avoided or delayed. Depending on whether resorption is internal or external in nature, different treatment modalities are recommended. Understanding the aetiology and pathogenesis of the disease process is essential for appropriate management of teeth undergoing resorption.
Dentine and cementum are protected from resorption by their non-mineralized structural components (predentine and precementum) and cells (odontoblasts and cementoblasts). Secretion of an anti-invasion factor by predentine, precementum and intact periodontal ligament is thought to prevent attachment of multinucleated resorbing dentinoclasts to dental hard tissues. Anti-invasion factor has also been found in cartilage and blood vessel walls. It is believed that the highly mineralized intermediate cementum layer (hyaline layer of Hopewell-Smith) further prevents external root resorption by covering the dentinal tubules, acting as a protective barrier between root-canal irritants and the periodontal ligament.
The cells responsible for resorption of dental hard tissues are multinucleated giant cells classified as clasts (Fig. 11.1). These cells attach themselves to the mineralized tissues by the cell membrane adjacent to the part of the cytoplasm called the “clear zone”. Resorption takes place under the highly folded cell membrane, known as the ruffled border (Fig. 11.2) in this zone. The membrane releases a cocktail of enzymes capable of dissolving both organic and inorganic components of hard tissues. Osteoclasts are involved in resorption of bone and dentinoclasts resorb dentine and cementum. The latter are smaller, have fewer nuclei and their clear zone is minimal or non-existent.
Fig. 11.2 (a) Light micrograph of an osteoclast-like cell in close apposition to dentine, cementum and alveolar bone (×100); (b) electron micrograph of the osteooclast-like cell in (a) with its ruffled border along dentine, cementum, and alveolar bone (×5000); (c) electron micrograph showing the ruffled border of the osteoclast-like cell in (a) along dentine, cementum, and alveolar bone (×19 000). B = alveolar bone, C = cementum, D = dentine
For dental resorption to occur, there must be damage to the non-mineralized components (predentine and periodontal ligaments) and interference with the normal protection afforded by blast cells (odontoblasts, cementoblasts and fibroblasts), which allows colonization of the denuded surfaces by dentinoclasts. The causes of such damage are listed in Table 11.1. The concomitant acute inflammation during injury activates the dentinoclasts and initiates resorption. However, this process may be transient in the absence of a perpetuating or persistent stimulus for the dentinoclasts, allowing repair by hard tissue deposition to occur. Resorption becomes progressive if it is sustained by chronic inflammation, whether in the pulp or periodontium. The causes of persistent chronic inflammation are listed in Table 11.2.
Pathological resorption has been classified by site, aetiology and pathogenesis. The classification system presented below is based on all three aspects to facilitate diagnosis and treatment planning.
This type of resorption has a prevalence of 0.1–1.6% in permanent teeth. It is initiated by damage to or loss of the predentine and odontoblast layer (see Table 11.1) and sustained by pulpal inflammation (see Table 11.2). Dental trauma, overheating and dehydration during restorative procedures, use of cytotoxic restorative materials or dressing materials in pulpotomies, and orthodontic tooth movement are factors that may injure the protective predentine and odontoblast cells.
In the absence of persistent pulpal inflammation, initial resorption of dentine from the pulpal aspect is self-limiting with no clinical consequence (Fig. 11.3). It has been detected, for example, in boxers sustaining repetitive injury to anterior teeth.
In the early stages of internal resorption, microleakage of bacteria and their products via dentinal tubules and cracks sustain the inflammatory process. Eventually, the coronal pulp is invaded by bacteria and becomes necrotic. The former provides ongoing stimulus for resorption. The pulpal tissue in the resorptive defect and apical to it is vital and provides blood supply to the resorption area. The rate of progression of resorptive activity may be related to the strength of inflammatory stimulus. In the case of total pulp necrosis where the blood supply is cut off, the resorption ceases.
Calcified substance (osteo-dentine) similar to bone may be present within the inflammatory tissue in the resorptive defect and this type of presentation has been classified separately as “internal replacement resorption”, “root-canal replacement resorption”, or “metaplastic resorption”.
Clinically, the early stages of internal resorption are usually asymptomatic. A pink spot may be present on the crown if resorption takes place in the pulp chamber (Fig. 11.4). The pink discoloration associated with internal resorption is caused by the highly vascularized inflammatory tissue undermining the coronal enamel. Vital pulp tissue is required for internal resorption to progress, therefore, such teeth will give positive responses to pulp tests. However, a negative response could not rule out the progression of resorption because only the pulp tissue coronal to the lesion may be necrotic. Progression of inflammation fuelling the resorption may result in total necrosis of the pulp and, therefore, cessation of internal resorption. The necrotic pulp may then become infected and symptomatic, discoloured and give negative responses to pulp tests (Fig. 11.5).
Radiographically, the appearance of internal resorption has been classically described as a well-circumscribed, symmetrical, oval or circular shaped radiolucency continuous with the root canal (Fig. 11.6). The radiolucency has a uniform density and the pulp chamber or canal cannot be followed through the lesion. The position of the radiolucency remains the same in mesial or distal angled radiographic views. However, a radiopaque mass resembling calcification may be present within the lesion or in the canal space apical to the internal resorption. A periradicular radiolucency may be associated with perforation of the root or total necrosis of the pulp in advanced cases (Fig. 11.7). This may pose difficulty in differentiation from external inflammatory resorption associated with root-canal infection (Fig. 11.8). Occasionally, internal resorptive lesions remain undetected and may only appear incidentally on a post-obturation radiograph (Fig. 11.9).
Management of progressive internal resorption varies according to the extent of the lesion, presence of calcification and perforation. Root-canal treatment should be carried out immediately after detection in order to prevent further disease progression leading to root perforation.
It may be difficult to control haemorrhage and to remove completely the severely inflamed tissue from the resorptive defect. Therefore, debridement should be carried out using copious amounts of sodium hypochlorite irrigant. In addition to its antibacterial properties, sodium hypochlorite also possesses tissue-dissolving ability. Use of higher concentration (5%) of sodium hypochlorite in combination with ultrasonic agitation has been recommended and may enhance debridement. The canal should be checked for perforation by exploring with a curved file attached to an apex locator. Care should be taken to prevent extrusion of sodium hypochlorite irrigant through any perforation. An extensive lesion with calcification may render canal location and complete debridement of the resorptive defect impossible (Figs 11.4, 11.10). Calcium hydroxide dressing should be used between appointments to prevent recolonization by bacteria and to facilitate removal of any residual inflamed tissue within the irregular resorptive defect. Long-term dressing with calcium hydroxide is indicated to induce hard tissue repair if a perforation is present (see Figs 11.7, 11.11). It may be prudent to delay root-canal obturation until complete bone healing has occurred to ensure minimum extrusion of filling material.
Fig. 11.10 (a,b) Extensive internal resorption defect with calcification of the tooth in Figure 11.4 rendered complete debridement impossible
Fig. 11.11 (a) Internal resorption in a maxillary central incisor; (b) calcium hydroxide dressing filling the defect incompletely and inadequately; (c) apical part of the root canal obturated with laterally compacted gutta-percha and sealer; (d) the resorption cavity and coronal part of the canal obturated with warm gutta-percha and sealer
Complete obturation of the defect may be achieved by using a thermoplasticized root-filling technique, such as injection of molten gutta-percha using an Obtura II system (see Chapter 8) after filling the canal apical to the defect using lateral or vertical compaction technique (Fig. 11.11).
A surgical approach is indicated when a large perforation is present and or excess root-filling material has been extruded into the periodontal tissue. However, these cases have compromised prognosis and are prone to root fracture.
Resorption of the root surface is commonly seen in association with severe dental trauma, apical periodontitis or orthodontic treatment. The apical region is generally affected but lateral and cervical aspects of the root may also be involved.