Tooth resorption

Resorption of the root of the tooth, or root resorption, is the progressive loss of dentin and cementum by the action of odontoclasts. Root resorption is a normal physiological process that occurs in the exfoliation of the primary dentition. However, pathological root resorption occurs in the permanent or secondary dentition and sometimes in the primary dentition. While resorption of bone is a normal physiological response to stimuli throughout the body, root resorption in permanent dentition and sometimes in the primary dentition is pathological. The root is protected internally (endodontium) by pre-dentin and externally on the root surface by cementum and the periodontal ligament. Chronic stimuli that damage these protective layers expose underlying dentin to the action of osteoclasts. Root resorption most commonly occurs due to inflammation caused by pulp necrosis, trauma, periodontal treatment, orthodontic tooth movement and tooth whitening. Less common causes include pressure from malpositioned ectopic teeth, cysts, and tumors. Calcium metabolism The pathophysiology of root resorption is not completely understood. It is postulated that osteoclasts are the cells responsible for the resorption of the root surface. Osteoclasts can break down bone, cartilage and dentin. 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. In physiological bone turn over, osteoblasts and stromal cells release RANKL, this acts on macrophages and monocytes 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.