Quality Resource Guide l Tooth Root Resorption 4th Edition 4 www.metdental.com External Resorption Etiology and Clinical and Conventional Radiographic Presentation External resorption is a much more difficult condition to diagnose and manage. It has been described by a variety of names, which may describe the location, etiology, or pathogenesis of the lesion. External resorption may be caused by physical damage to the external protective layer of precementum; by trauma, infection, or both. In certain cases, the etiology is of unknown origin. Mild physical damage due to trauma ( i.e., concussion or subluxation), may result in recruitment of clastic cells to the area with resultant isolated foci of resorption. However, without persistent irritation, these resorptive lacunae may be repaired with new cementum as healing takes place. This condition is termed surface resorption, and requires no treatment. In fact, it is only discovered on histologic examination of teeth extracted for other reasons. Pressure from ectopically erupting teeth or excessive orthodontic forces may also cause external resorption that is self-limiting; once the pressure stimulus is removed (the ectopically erupting tooth is extracted, or orthodontic forces are discontinued), the resorptive process halts. Infection alone may damage the external root surface and allow initiation of the resorptive process. This is commonly seen in teeth with necrotic, infected pulps with resultant apical periodontitis. Not only have clastic cells resorbed bone to the point where radiolucency can be seen apically, but the root surface can be resorbed in the area as well. This is usually seen as a shortened root adjacent to a periapical bony lesion (Figure 4A). While the root length cannot be regained, nonsurgical root canal therapy with adequate debridement and disinfection will allow healing of the bone, and halt the root resorptive process. A normal periodontal ligament space will be reestablished ( Figure 4B). Because resorption of the root apex often results in the loss of the natural apical constriction, the clinician must take care not to over-extend the obturation material. Interim radiographs can help with length control. When damage occurs to the cementum layer and bacterial infection is present, the external resorption that ensues is called inflammatory root resorption, and often has devastating effects. A typical case scenario involving inflammatory resorption would be a mature avulsed tooth that is replanted, but does not receive root canal therapy within 7-10 days. The clastic cells that inhabit the root surface as part of the normal wound healing process are stimulated by bacteria and their by products that arrive on the scene by way of dentinal tubules extending from the necrotic pulp (Figure 5). If an avulsed tooth is not replanted within minutes, and is transported in a manner that does not allow survival of periodontal ligament cells on the root surface, the entire root surface becomes devoid of vital cementum. When dentin is in apposition to alveolar bone without a protective layer of cementum (ankylosis), a different type of resorption takes place. In effect, the root dentin is resorbed by alveolar osteoclasts, and is replaced by bone produced by resident osteoblasts. Accordingly, this type of external root resorption is called replacement resorption (Figure 6). A final category of external root resorption originates beneath the junctional epithelium of the periodontium, and has been called invasive cervical resorption, or extra canal invasive resorption. This condition is particularly confusing, as it often extends in a coronal direction, undermining enamel, and results in what is commonly called the ‘pink tooth’ (Figure 7). The cause of the damage to the precementum layer is often obscure; the patient may not recall an episode of trauma, and there may be no other obvious predisposing factors, such as excessive orthodontic forces, periodontal therapy or tooth bleaching. Extra canal invasive resorption is often asymptomatic, and typically discovered only during routine radiographic examinations. The lesion is usually seen as a diffuse radiolucency with ill-defined borders, and because the defect is external to the pulp canal space, it is seen to be superimposed on normal root canal anatomy. That is, the pulp canal space can be seen through Figure 4 Root-end resorption caused by chronic inflammation in the periapical tissues resulting from a necrotic, infected dental pulp (panel A). Following adequate root canal therapy, the resorptive process is halted, and the bony lesion has healed (panel B) (17 month recall). Figure 5 Inflammatory root resorption. The root dentin is very quickly consumed by clastic cells that are stimulated by bacteria and their by- products. This tooth was avulsed and quickly replanted, however, endodontic therapy was delayed for 4 weeks following the injury. Figure 6 Replacement resorption. Note the replace- ment of the root structure by trabecular bone.