Root resorption following traumatic dental injuries.

Abstract

Permanent teeth are usually not attacked by osteoclasts despite their situation in a site where active bone resorption constantly takes place as a result of local and systemic osteoclast activating factors. This fact points to antiresorption factors residing in both the periodontal ligament (PDL) and the pulp. Concerning the PDL homeostasis factor (i.e. permanency of a separation between the alveolar socket and the root surface and protection of the root surface against osteoclastic activity), recent studies have shown that this factor, at least with respect to trauma and wound healing, is linked to, and probably resides in, the cementoblast layer and/or the cells next to this layer. If there is loss of this tissue integrity, root resorption may occur; especially if non-PDL derived cells gain access to the site. With respect to the pulp, no systematic research has been performed regarding the homeostasis of this structure (i.e. permanency of the pulpal organ with its specific anatomy and functional stability). In evaluating the events where resorption does occur, it appears that the loss of tissue components within the pulp (including odontoblasts) implies a risk of root canal resorption if nonpulpally derived cells gain access to the site. Root resorption following traumatic dental injuries, whether located along the root surface or within the root canal appears to be a sequel to wound healing events, where a significant amount of the PDL or pulp has been lost due to the effect of acute trauma. The goal of these processes is removal of injured tissue from zones of trauma, space creation for neovascularization or control of infection. Irrespective of the goal, these processes have a potential for root resorption. The type of tissue repair, i.e. repair originating from the dental pulp, the PDL or bone or a combination, seems to be of importance in determining the risk of root resorption during the healing process.