|Classification and external resources|
Root resorption is the progressive loss of dentine and cementum by the action of osteoclasts. This is a physiological process in the exfoliation of the primary dentition, caused by osteoclast differentiation due to pressure exerted by the erupting permanent tooth. However, in the secondary dentition the process is pathological.
Pulp necrosis, trauma, periodontal treatment, orthodontics and tooth whitening are the most common stimulants of inflammatory resorption. Some other less common causes include pressure from ectopic teeth, cysts, and tumours.
Osteoclasts are the cells responsible for the resorption of the root surface. Osteoclasts can break down bone, cartilage and dentine.
Osteoclast differentiation factor, osteoprotegerin ligand, receptive activator of nuclear factor kappa-B ligand (ODF, OPGL, RANKL), are all regulators of osteoclast function. In physiological bone turn over osteoblasts and stromal cells release RANK-L, this acts on macrophages and monocytes which fuse and become osteoclasts. OPG is also secreted by osteoclasts and stromal cells this inhibits RANK-L and therefore osteoclast activity.
The pathophysiology of stimulation of osteoclasts in the process of inflammatory resorption is unknown.
One thought is that the presence of bacteria plays a role. Bacterial presence leads to pulpal or peri-periapical inflammation. These bacteria are not mediators of osteoclast activity but do cause leukocyte chemotaxis. Leukocytes differentiate into osteoclasts in the presence of lipopolysaccharide antigens found in Porphyromonas, Prevotella and Treponema species (these are all bacterial species associated with pulpal or periapical inflammation).
Osteoclasts are active during bone regulation, there is constant equilibrium of bone resorption and deposition. Damage to the PDL can lead to RANKL release activating osteoclasts. Osteoclasts in close proximity to the root surface will resorb the root surface cementum and underlying root dentin. This can vary in severity from evidence of microscopic pits in the root surface to complete devastation of the root surface.
When there is insult leading to inflammation (trauma, bacteria, tooth whitening, orthodontic movement, periodontal treatment) in the root canal/s or beside the external surface of the root, cytokines are produced, the RANKL system is activated and osteoclasts are activated resorb the root surface.
If the insult is transient, resorption will stop and healing will occur, this is known as transient inflammatory resorption. If the insult is persistent, then resorption continues, and if the tooth tissue is irretrievably damaged, complete resorption may occur.
Internal resorption defines the loss of tooth structure from within the root canal/s of a tooth.
It may present initially as a pink-hued area on the crown of the tooth; the hyperplastic, vascular pulp tissue filling in the resorbed areas. This condition is referred to as a pink tooth of Mummery, after the 19th century anatomist James Howard Mummery. It may also present as an incidental, radiographic finding. Radiographically a radiolucent area within the root canal may be visible and/or the canal may appear sclerosed.
Chronic pulpal inflammation is thought to be a cause of internal resorption. The pulp must be vital below the area of resorption to provide osteoclasts with nutrients. If the pulp becomes totally necrosed the resorption will cease unless lateral canals are present to supply osteoclasts with nutrients.
If the condition is discovered before perforation of the crown or root has occurred, endodontic therapy (root canal therapy) may be carried out with the expectation of a fairly high success rate. Removing the stimulus (inflamed pulp) results in cessation of the resorptive process.
External resorption is the loss of tooth structure from the external surface of the tooth. It can be further divided it the following classifications:
External inflammatory resorption
Occurs following prolonged insult leading to continuing pathological resorption.
Commonly caused by damage to the PDL, drying of root surface (following avulsion), exposure of dentine tubules, and pressure.
This process can occur rapidly.
External cervical resorption
A localised resorptive lesion in the cervical area of the tooth, below the epithelial attachment. This rarely involves the pulp.
Prolonged insult leads to vertical and horizontal growth of the lesion.
Commonly caused by trauma, periodontal treatment, tooth whitening.
Multiple idiopathic cervical resorption is when a minimum of 3 teeth are affected by cervical resorption for no evident cause.
External replacement resorption
Occurs following ankylosis of the root of the alveolar bone. The tooth tissue is resorbed and replaced with bone. This process is poorly understood.
It is thought that following the union of bone and tooth and the obliteration of the PDL, the protective regulators released by the PDL to protect the root from resorption are no longer present. This results in the tooth tissue being resorbed by osteoclasts and replaced with bone like it was part of the continuous homeostatic process of bone turnover.
Transient inflammatory resorption
Also known as external surface resorption. It is a self-limiting process and is often and incidental radiographic finding. Transient inflammatory resorption undergoes healing and should be monitored only.
It is caused by localised and limited injury to root surface or surrounding tissues. There is 2–3 weeks of osteoclast activity before healing then occurs. If cementum alone is involved in the resorptive process then complete healing will occur, but if dentine is involved there will be re-contouring in the area of lost dentine.
- Kahn, Michael A. Basic Oral and Maxillofacial Pathology. Volume 1. 2001.
- Internal Resorption Research Project website http://internalresorption.com accessed February 17, 2014.
- Patel, Shanon; Ford, Thomas Pitt (2007). "Is the resorption internal or external?". Dental Update. 34: 218–229.
- Fuss, Z; Tsesis, I; Lin, S (2003). "Root resorption - diagnosis, classification and treatment choices based on stimulation factors". Dental Traumatology. 19: 175–182.
- Andreasen, J, O (1985). "External root resorption: its implication in dental traumatology, pedodontics, periodontics, orthodontics and endodontics". International Endodontic Journal. 18: 109–118.
- Darcey, J; Qualtrough, A (2013). "Resorption: part 1. Pathology, classification and aetiology". British dental journal. 214: 439–451.
- Boyle, W, J; Simonet, W, S; Lacey, D, L (2003). "Osteoclast differentiation and activation". Nature. 423: 337–342.
- Yasuda, H; Shima, N; Nakagawa, N (1998). "Osteoclast differentiation factor is a ligand for osteoprotegrin/ osteoclastogenisis-inhibitory factor and is identical to TRANCE/RANKL". Proceedings of the National Academy of Sciences USA. 95: 3597–3602.
- Nakamura, I; Takahashi, N; Jimi, E; Udagawa, N; Suda, T (2012). "Regulation of osteoclast function". Rheumatology. 22: 167–177.
- Choi, B, K; Moon, S, Y; Cha, J, H; Kim, K, W; Yoo, Y, J (2005). "Prostaglandin E(2) is a main mediator in receptor activator of nuclear factor kappaB ligand-dependent osteoclastogenesis induced by Porphyromonas gingivalis, Treponema denticola and Treponema sockranskii". Journal of Periodontology. 76: 813–820.
- Trope, M (2002). "Root resorption due to dental trauma". Endodontic Topics. 1: 79–100.
- Andreasen, J, O (1981). "Relationship between cell damage in the periodontal ligament after replantation and subsequent development of root resorption". Acta Odontologic Scandinavic. 39: 15–25.
- Lossdorfer, S (2002). "Immunohistological localization of receptor activator of nuclear factor kappaB (RANK) and its ligand (RANKL) in human deciduous teeth". Calcified tissue International. 71: 45–52.
- Majorana, A; Bardellini, E; Conti, G; Keller, E; Passini, S (2003). "Root resorption in dental trauma: 45 cases followed for 5 years". Dental Traumatology. 19: 262–265.