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Resorption of the root of the tooth, or root resorption, is the progressive loss of dentine and cementum by the action of . Root resorption is a normal physiological process that occurs in the exfoliation of the Deciduous teeth. However, pathological root resorption occurs in the permanent or Permanent teeth and sometimes in the primary dentition.
Root resorption most commonly occurs due to inflammation caused by pulp necrosis, trauma, periodontal treatment, Orthodontics tooth movement and tooth whitening. Less common causes include pressure from malpositioned ectopic teeth, , and .
Receptive activator of nuclear factor kappa-B ligand (RANKL), also called osteoclast differentiation factor (ODF) and osteoprotegerin ligand (OPGL), is a regulator of osteoclast function. (2025). 9780120884513, Elsevier. ISBN 9780120884513 In physiological bone turn over, and release RANKL, this acts on and which fuse and become osteoclasts. Osteoprotegerin (OPG) is also secreted by osteoclasts and stromal cells; this inhibits RANKL and therefore osteoclast activity.
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 between bone resorption and deposition. Damage to the periodontal ligament 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, are produced, the RANKL system is activated and osteoclasts are activated and 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.
It may also present as an incidental, radiographic finding. Radiographically, a radiolucent area of uniform density within the root canal may be visible with well-defined borders. Canal walls may appear sclerosed, thus the outline of pulp chambers or root canals may not be followed through the lesion. Lesions may also be oval radiolucencies that are continuous with the canal walls.
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 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.
Alternatively, pressure may also cause external inflammatory root resorption. Specifically, application of heavy, continuous, and intrusive (i.e. directed toward the bone) forces during orthodontic tooth movement are associated with external root resorption.
However, due to the lack of robust evidence in treatment of other forms of external root resorption, there is currently no single recommended best treatment for the management of external root resorption. Treatments are case-dependent and dependent on clinical judgment and experience. Therefore, more research is needed in this area.
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