The disease process known as Invasive Cervical Resorption (ICR) can be quite devastating for a tooth. The big problem for us as practitioners is that it’s difficult to identify ICR early. By far the most comprehensive article on ICR is by Geoff Hiethersay, (an Australian Endodontic legend) and this is the one article you need to read if you want more information than is contained in this post (Hiethersay 2004).
For dental resorption to occur, we need three things: 1. blood supply; 2. a stimulus; 3. breakdown or loss of the protective layer. When I refer to the protective layer, what I’m referring to is the pre-cementum externally, and the pre-dentine internally. It might seem odd that these seemingly frail tissues are able to protect tooth structure. The reason this protection occurs is that specific peptides named RGD peptides provide binding sites for the resorptive cells. These RGD peptides are bound to calcium salt crystals on mineralised surfaces. So when the resorbing cells reach the unmineralised pre-dentine or pre-cementum, they are unable to bind as no RGD peptides are present and thus, no resorption occurs.
So, it would seem that a lack of pre-cementum on the surface of a root may predispose to the development of ICR. This could happen due to trauma via a number of mechanisms such as scaling/root planing, internal bleaching, physical trauma or perhaps orthodontic movement of teeth. Dental trauma, internal bleaching and orthodontics have been associated with the development of ICR (Heithersay 1990). The condition also occurs without any pre-disposing factors, and it is suggested that a genetic lack of cementum (and therefore pre-cementum) may be present in those cases.
ICR is known by a number of other names and one of these is External Invasive Cervical Resorption. The “External” label is a reasonable addition as ICR is always external in nature. The resorption develops from cells in the periodontal ligament in the cervical region. This is the area that is most likely to have an absence of cementum from a developmental point of view at least. I mentioned that pre-dentine is also protective against ICR. The reason we know this is that in extensive cases the external resorption reaches the pulp, but the pulp is spared, protected by the pre-dentine. For this reason, even in extensive cases of ICR, the pulp usually remains vital. The resorptive tissue which invades the tooth seems to resist bacterial invasion. Certainly, you will not usually find a traditional periodontal pocket adjacent to the resorption.
I mentioned the three things that are required for resorption to occur. It’s obvious we have a blood supply and lack of protection, but where does the stimulus come from? The answer is that we don’t know. It has been hypothesised to be either inflammatory due to sulcular infection or a benign proliferative fibrovascular or fibro-ossesous disorder. That’s quite a mouth-full and I’ll leave it up to somebody much smarter than me to work out which one is correct. The cell that does the resorbing is similar in morphology to the osteoclast and may represent a functional variant of the same lineage.
Clincially, the tooth is usually completely asymptomatic. There may be a pink (or sometimes grey) discolouration of the crown but often the radiograph is the only indication that resorption is occuring. Radiographically, a mottled lucency is present and in advanced cases, there is a radiopaque line bordering the pulp chamber. Taking mesial and distal angled images will see the lesion move in relation to the pulp and this will differentiate the resorption from an internal resorption, as well as tell you if it’s positioned buccaly or lingually. Of course cone beam CT will also provide useful information.
Heithersay’s clinical classification is as follows:
Class 1 – small lesion with shallow penetration
Class 2 – well defined lesion close to coronal pulp
Class 3 – Deeper invasion to include the coronal third of radicular dentine
Class 4 – Large invasive lesion extending beyond the coronal third of the root
Class 1 and 2 lesions can be treated predictably, but the success rate in treating class 3 and 4 lesions drops dramatically. Treatment usually consist of using trichloracetic acid (TCA) to attempt to destroy the resorptive tissue via coagulation necrosis. The difficulty comes from the fact that the resorption is not usually confined to a discrete area and can have multiple feeding channels from well below the gingival margin. The lesion can also be treated surgically, but in practice it can be difficult to access and may even require bone removal to gain direct vision of the lesion. This rapidly gets destructive of both tooth structure and periodontal tissues which is why it is important to identify and treat (if indicated) the disease as early as possible. See Heithersay’s article for a description of the use of TCA and also other treatment options.
Hiethersay G. Invasive Cervical Resorption. Endodontic Topics 2004, 7, 73–92