Hard tissues are protected from resorption by their surface layers of blast cells. It appears that as long as these layers are intact, resorption cannot occur. Although bone, dentine and cementum are mesenchymal mineralised tissues composed mainly of collagen and hydroxyapatite, they differ markedly in their susceptibility to resorption.
Two mechanisms are involved in resorption of hard tissue:
2. Reason for the resorption to continue
The trigger mechanism in root resorption is a root surface detached from its protective blast cell layer. Detachment may follow any damage to the protective blast layer. For the resorption to continue, a stimulus is required, e.g., infection or a continuous mechanical force.
Root resorption always starts at a surface and is termed internal if emanating from the root canal wall and as external if emanating from the root surface.
INTERNAL ROOT RESORPTION
Internal resorption is rare in permanent teeth. Radiographically, it is characterised by an oval shaped enlargement of the root canal space. Histological examination reveals resorption of the internal aspect of the root by multinucleated giant cells adjacent to granulation tissue in the pulp. There are different theories regarding the origin of the pulpal granulation tissue involved in internal resorption. The most logical explanation is that it is pulp tissue that is inflamed because of an infected coronal pulp space. In addition to the requirement of the presence of granulation tissue root resorption takes place only if the odontoblast layer and predentine are lost or altered. Trauma has been suggested as a cause for loss of predentine adjacent to the granulation tissue1.
Traditionally, a pink tooth has been thought pathognomonic of internal root resorption; the pink colour is caused by granulation tissue in the coronal dentine undermining the crown enamel. However, a pink tooth can also be a feature of a specific type of external root resorption, namely peripheral inflammatory external root resorption (detailed later in this manuscript), which must be ruled out before a diagnosis of internal root resorption is made. Also, a pink tooth can also be due to pulpal haemorrhage.
EXTERNAL ROOT RESORPTION
There are different forms of external root resorption described in man. The underlying mechanism is understood for some of these, whereas other forms are still unexplained and, therefore, termed idiopathic. A classification system for external root resorptions that have a known mechanism has been proposed in man2 and is as follows:
Replacement resorption associated with ankylosis
A surface resorption is initiated subsequent to injury of the cementoblast layer. The denuded root surface attracts clast cells, which will resorb the cementum for as long as osteoclast-activating factors are released at the site of injury, usually a few days. When the resorption stops, cells from the periodontal ligament will proliferate and populate the resorbed area resulting in deposition of reparative dental tissue2-4.
It is thought that minor traumata caused by unintentional biting on hard objects, bruxism etc. can cause localized damage to the periodontal ligament and trigger this type of resorption. The process is self-limiting and reversible.
This type of resorption results in replacement of the dental hard tissue by bone. When a surface resorption stops, cells from the periodontal ligament will proliferate and populate the resorbed area. If the resorption is large it will take some time for these cells to cover the entire surface. Cells from the nearby bone may then arrive first and establish themselves on the resorbed surface5. Bone will thus be formed directly upon the dental hard tissue. This results in fusion between bone and tooth, i.e., ankylosis. This can be seen as a form of healing, the bone has accepted the dental hard tissue as part of itself and the tooth becomes involved in the normal skeletal turnover6. So during consequent remodeling of bone, both dental hard tissue and bone will be resorbed. When the resorptive process is over, the osteoblasts will form bone in the resorbed area. In this way the dental tissues will gradually be replaced by bone. In short, ankylosis is a form of healing of root surface resorption, which from a clinical standpoint may be undesirable.
In addition to apical root resorption caused by apical periodontitis as a consequence of pulpal necrosis, there are two main forms of external resorption associated with inflammation in the periodontal tissues, namely:
Peripheral inflammatory root resorption (PIRR)
External inflammatory root resorption (EIRR)
Both forms are triggered by destruction of the cementoblasts. In PIRR, the osteoclast activating factors, which perpetuate the resorptive process, are provided by an inflammatory lesion in the adjacent periodontal tissues7,8. EIRR, on the other hand, receives its stimulus for continued resorption from an infected necrotic pulp7. In other words, the common factor for these two types of resorption is inflammation in the adjacent tissues. As far as PIRR is concerned the periradicular inflammation per se keeps the resorptive process going, while the stimulus for EIRR is periradicular inflammation caused by products released from the necrotic pulp by way of the dentinal tubules exposed by the resorption.
Peripheral Inflammatory Root Resorption (PIRR)
A damaged cervical root surface (e.g., due to excessive scaling or other trauma) is usually covered by junctional epithelium. Sometimes this does not occur, instead the damaged area will be repopulated by connective tissue. In the presence of a periodontal lesion the onset of a resorptive process is triggered8. It is conceivable that the inflammatory cells in the lesion recognize the osteoclast activating factors of the denuded root surface and, thus, initiate and maintain clastic activity. This type of resorption is found immediately apical to the marginal tissues and is thus is often situated cervically and has therefore been termed cervical root resorption. However, the location is related to the level of the marginal tissues and the pocket depth and may thus not always be cervical in position.
External Inflammatory Root Resorption (EIRR)
This type of root resorption is a complication that can follow dental trauma. It begins as a surface resorption due to damage to the periodontal ligament in conjunction with the traumatic injury. The pulp is also damaged and becomes necrotic. As the surface resorption approaches the dentine, the osteoclasts will carry on their resorptive activity, as necrotic and possible infected pulp matter is released from the thus exposed dentine tubules7. The pulp products will then maintain an inflammatory process in the adjacent periodontal tissues that in turn will trigger the continuance of the resorption.
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2. Andreasen, JO. (1981). Relationship between surface and inflammatory resorption and changes in the pulp after replantation of permanent incisors in monkeys. Journal of Endodontics 7, 294.
3. Lindskog S, Blomlof L, Hammarstrom L. (1983b). Repair of periodontal tissues in vivo and in vitro. Journal of Periodontology 10, 188.
4. Lindskog S, Blomlof L, Hammarstrom L. (1987). Comparative effects of parathyroid hormone on osteoblasts and cementoblasts. Journal of clinical periodontology 14, 386-389.
5. Andreasen JO, Kristersson L. (1981). The effect of limited drying or removal of the periodontal ligament: periodontal healing after replantation of mature permanent incisors in monkeys. Acta Odontol Scand 39, 1.
6. Hammarstrom L, et al. (1986). Tooth avulsion and replantation: a review. Endodont Dent Traumatol 2, 1.
7. Andreasen JO. (1985). External root resorptions: its implication in dental traumatology, paedodontics periodontics, orthodontics and endodontics. International Journal of Endodontics 8, 109.
8. Gold S, Hasselgren G. (1992). Peripheral inflammatory root resorption; a review of the literature with some case reports. Journal of Clinical Periodontology 19, 523.