Internal resorption is a relatively rare dental condition where the inner structure of a tooth is progressively dissolved and broken down by cells that originate from the tooth’s internal soft tissue, known as the pulp. This process begins within the pulp chamber or root canal system, slowly consuming the internal dentin. Because the condition develops from the inside out, it is often asymptomatic, meaning it causes no pain or noticeable symptoms for long periods. The gradual destruction of the tooth structure frequently leads to its incidental discovery during routine dental X-ray examinations.
What Internal Resorption Is
Internal resorption involves a pathological process where the hard tissue of the tooth is destroyed by specialized cells called odontoclasts or dentinoclasts. These cells are biologically similar to osteoclasts, which are responsible for bone resorption throughout the body. For internal resorption to occur, the protective layer lining the pulp chamber, composed of predentin and odontoblasts, must first be damaged. This damage allows the underlying connective tissue of the pulp to become inflamed and activate the clastic cells.
Once activated, the odontoclasts dissolve the dentin concentrically by releasing acidic enzymes, causing tissue loss to expand outward from the pulp space. The process is sustained by the presence of vital, inflamed pulp tissue that provides the necessary blood supply and cells to continue the destructive activity. The location of this process is confined to the inner walls of the root canal or pulp chamber. Radiographically, this destruction appears as a uniform, symmetrical widening or “ballooning” of the root canal space, which weakens the tooth structure and increases the risk of fracture.
Primary Causes and Risk Factors
The initiation of internal resorption requires two distinct factors: an injury that breaches the protective predentin layer, followed by persistent low-grade inflammation within the pulp tissue. Dental trauma is one of the most common precursors, particularly injuries that cause displacement or luxation of the tooth, as physical impact can damage the delicate tissue barrier and activate clastic cells.
Chronic inflammation stemming from deep decay or long-standing bacterial infection can also stimulate the resorptive process, as bacteria and their byproducts provide sustained irritation. Additionally, certain dental procedures, such as extensive restorative work or prior attempts at pulp capping, may cause localized heat or chemical irritation. If this irritation is not fully resolved, it can trigger the destructive cellular mechanism.
Identification and Diagnostic Features
The vast majority of internal resorption cases are discovered incidentally during routine dental examinations that include radiographs. The condition is often non-symptomatic, only causing discomfort if the lesion approaches the outer surface of the tooth. A classic, though infrequent, clinical sign is the appearance of a reddish or pink spot on the crown, often called the “Pink Tooth of Mummery.” This coloration occurs because the hyperplastic, vascular tissue filling the resorptive defect expands and becomes visible through the thinned enamel.
The definitive diagnosis relies on specific radiographic features seen on X-rays. Internal resorption presents as a distinct, well-defined radiolucency—an area that appears darker because the dense tooth structure has been lost—that is continuous with the pulp chamber or root canal. The borders of this lesion are typically smooth and symmetrical, differentiating it from the irregular borders of external resorption.
To confirm the internal origin and distinguish it from an overlapping external defect, dentists often take a second X-ray at a different angle. If the radiolucent area remains centered over the root canal space when the angle of the X-ray tube is shifted, it confirms the lesion is internal. For a more precise three-dimensional understanding of the defect’s size and location, Cone-Beam Computed Tomography (CBCT) imaging is often used, providing cross-sectional views invaluable for treatment planning.
Treatment Pathways
The primary goal of treating internal resorption is to immediately stop the destructive activity by eliminating the inflamed, vital pulp tissue that sustains the odontoclasts. Non-surgical root canal therapy (endodontic treatment) is the standard approach. This procedure involves accessing the pulp chamber, removing all the tissue, and thoroughly disinfecting the entire root canal system, including the resorptive defect.
Specialized chemical irrigants, such as sodium hypochlorite, are used to dissolve the remaining pulp and granulation tissue from the complex contours of the defect. An intracanal medication, such as calcium hydroxide, is often placed within the tooth for several weeks to further disinfect the area and deactivate any remaining clastic cells. Once the resorptive activity has ceased and the tooth is clean, the defect and the root canal are filled and sealed.
For smaller lesions, the canal space is usually filled with gutta-percha. If the resorptive defect is very large or has caused a perforation through the side of the root, specialized biocompatible materials like Mineral Trioxide Aggregate (MTA) may be used to repair and seal the defect. In cases where the internal destruction has significantly compromised the structural integrity of the tooth, surgical intervention or even tooth extraction may become necessary.