The Nuts and Bolts of Root Resorption and How to Treat It

Today we'll be talking about root resorption. We've all seen it in our practice in one form or another, and it's something we need to understand in order to diagnose and treat it properly. So what's interesting about root resorption is that it utilizes our own soft tissue cells to work against us. It initiates its attack against the tooth from the inside out, as well as from the outside in. In this podcast, we'll learn about this insidious process and hopefully we'll get a better understanding of the fundamentals behind the different types of root resorption. And by doing so, we as clinicians can sharpen our diagnostic skills and optimally manage these conditions on a case-by-case basis. So several things have to happen in order to get tooth resorption. On the external surface of the tooth, there has to be some disruption or loss of pre-cementum. On the internal surface of the tooth, if the resorption is working inside out, and we're talking about within the pulp chamber in the root canal system, we need some disruption or loss of predentin. Okay, so outside we need something that disrupts the precementum, and on the inside we need something that disrupts the predentin. Now, related to both of these surfaces, we also need an inflammatory response. of the adjacent soft tissues. The reason for this is that the inflamed soft tissue allows for clastic cell invasion. So what are clastic cells? Clastic cells are responsible for mineralized tissue resorption. Bone resorbing cells, for instance, are called osteoclasts, as we learned in dental school. Cells that resorb mineralized dental tissues are called odontoclasts. Now, the location of this damage and the associated tissues determines the type of resorption that occurs. Internal root resorption is its own unique entity. Okay, so when you say internal root resorption, you're specifically talking about one kind of resorption. Now, on the other hand, external resorption can take on many forms. So, if you're talking about external resorption, it could be several different types. of resorptive processes that are going on. And we'll get into that shortly in this podcast. So let's begin with internal root resorption. But first, we all know that to achieve healthy, beautiful smiles, we sometimes need to align the teeth. And to do so, aligner therapy is a great option. So why not set your practice apart with 3M Clarity Aligners Flex from Solventum, formerly 3M Healthcare. Designed for comfort, Clarity Aligners Flex feature a thin, flexible design. yet they deliver excellent force persistence over a two-week period. Plus, they resist scratching and stains, and they're backed by a dedicated clinician team providing support every step of the way. With a variety of affordable case-type options, single or dual-arch, Clarity Aligners Flex offer a great value to your patients and practice. To learn more, visit 3M.com slash clarity dash aligners dash flex. So what kind of scenario do we need for internal root resorption to occur? Well, as we just mentioned, we need some degree of loss or damage to the pre-denton lining the pulp chamber or root canal spaces, depending on where it's happening. Combined with that, we need soft tissue inflammation. In this case, the soft tissue that's adjacent to the pre-denton is the pulp tissue. So the soft tissue that's going to be responsible for creating those clastic cells is the pulp tissue. in the case of internal root resorption. Pulpal inflammation is essentially responsible for activating odontoclasts. And that's according to Dr. Tronstad. And he did a lot of research on this. So keep in mind that we need some vital pulp tissue in order for this process to work. And that's really important to understand. Because without the vital pulp tissue, you will not have any clastic cell creation. There'll be no clastic cells that are generated. that will actually cause the dissolution of the predentin, all right? So you need vital pulp tissue. So if you have a completely necrotic pulp, then you might have problems with the tooth in other ways, but you're not going to have active internal root resorption, okay? You must have some vital pulp tissue present in order for this to happen. So now the question is, what causes the inflammatory response of the vital pulp, right? Remember, we need that combination. disruption of the predentin, and then we need that inflammatory response of the vital pulp. So what causes it? Well, typically we get pulpal inflammation following localized coronal pulp necrosis, which may occur secondary to trauma, coronal fractures, deep restorative dentistry without adequate cooling spray, placement of a pulp cap. So when one or more of these external factors leads to localized necrotic pulp tissue, This will inevitably incite an inflammatory reaction of the adjacent vital pulp tissue. So we now have all the ingredients for root resorption internally, which once it gets started will most likely progress continuously until complete pulp necrosis occurs. All right, so let me just reiterate that. We're talking about the scenario where internal root resorption is active. We have all the ingredients for it. It's all happening. But it stops when the pulp is fully necrotic. That's it. Nothing else happens. Now, of course, that could progress into apical periodontitis through the apex of the tooth because the necrotic tissue will cause an apical rarefaction, which is typical for a necrotic tooth. But the internal part that we're talking about, which is destroying the tooth internally with that typical... circular or oval-looking destructive pattern radiographically, that will stop once the vital tissue dies. So knowing this, if we remove the necrotic pulp and the remaining vital pulp tissue that's still active, we can stop the process of internal resorption, stop it in its tracks. And that means doing non-surgical root canal therapy. Now, if the internal root resorption perforates the tooth, so now it's into the attachment apparatus. That's a different story. Now there's a whole different treatment plan for that, and of course the prognosis will come down. So we're talking about treating internal root resorption where there is no perforation present, and the treatment of choice would be non-surgical root canal therapy. And of course you'd have to use some sort of obturation technique where you can... warm the gutta percha and fill that big void that's sitting there from the resorption that occurred. And it's interesting to note that studies have been done using scanning electron microscopy that show that subclinical internal root resorption is found quite frequently in necrotic teeth. So what does this mean? It means that part of the normal pathophysiology of a pulp dying coronally down to the apex, there's a process of internal root resorption that's going on almost all the time, but it's subclinical. It's so small that you can only pick it up with an electron microscope in this study by Gabor and others. And what they found, as I mentioned, was that this is a typical process that goes on when it... tooth when a pulp dies. You get this internal resorption at the microscopic level. So it's relatively rare, internal root resorption. It's not something you find very often, but the scenario for it to actually progress where you see it radiographically means that it was a perfect storm. The necrotic pulp tissue causes the inflammation of the vital pulp tissue further down apically. and you have that disruption of the pre-denton, and then the odontoclasts take over and start dissolving the dentin around the pulp chamber and around the root, depending on where it is. It's usually the middle third of the root where this occurs. When visible clinically or radiographically, we'll see that the internal root resorption is continuous with the pulp chamber or root canal space. And as we know, in the absence of a perforation, internal root resorption is quite treatable with non-surgical root canal therapy. If internal root resorption is perforating, then the prognosis, of course, drops dramatically. And depending on the case, we need to decide whether we want to extract the tooth or possibly use some sort of bioceramic materials to seal it, as well as regenerative endodontic techniques to save that tooth. And that's a decision that has to be made by the general dentist and the specialist. So we covered internal root resorption to some extent. In a minute, we'll be back talking about external root resorption. But first, if you're on the lookout for a versatile material that serves as both a protective liner for composites and is ideal for direct and indirect pulp capping, let me introduce you to Theraquel LC from Bisco. Its unique hydrophilic resin-modified calcium silicate formulation provides a strong, stable liner that reduces post-op sensitivity. It's radiopaque and incredibly easy to apply. Once light-cured, Theracal-LC is ready for use with any bonding technique. What's even better, Theracal-LC is non-soluble, meaning it won't wash out over time. Plus, it promotes calcium release, which supports secondary dentin bridge formation. And that's perfect for those tricky pulp exposures. When you're working deep in a tooth prep, you want reliable protection for the dental pulpal complex. You want TheraCal LC, a top choice among independent evaluators and thousands of dental clinicians. For more information on Bisco's full line of pulp protection products, head on over to Bisco.com. Let's talk about external root resorption. Now, for the remainder of this podcast, I'll refer to this... as external inflammatory root resorption. And the reason that I use the word inflammatory in this case is because later in the podcast, I'll be discussing a form of external resorption that is non-inflammatory. So in general, external inflammatory root resorption takes on several forms depending on their etiology. So what do we need to happen for external inflammatory root resorption to occur? Well, we need the loss or damage to the precementum, lining of the root surface, as we discussed earlier, combined with the inflammation of the adjacent soft tissue, which is the periodontal ligament. This scenario facilitates the activation of odontoclasts. Now, keep in mind, external inflammatory root resorption relates to endodontic pathosis. So there's an endodontic pathology related to external inflammatory root resorption. That means it involves, or should I say requires, necrotic pulp tissue to exist. So we must have necrotic pulp tissue for external inflammatory root resorption to occur. Now, for instance, apical external inflammatory root resorption is often present subclinically in cases of apical periodontitis, secondary to pulp necrosis. In other words, when we see the typical area of rarefaction around the root apex, we can be sure there is some level of external inflammatory root resorption on the root of the infected tooth. So we just covered a form of external inflammatory root resorption known as apical external inflammatory root resorption. And that's very common. When you see a rarefaction on the x-ray, which is an indication of bone loss around the apex of the tooth, you will... certainly have some level of resorption of the root itself. So that can be referred to as apical external inflammatory root resorption. Now, when we talk about lateral external inflammatory root resorption, this is usually a condition that is more extensive than apical and occurs following severe luxation type injuries. Okay, the tooth is luxated or even an avulsion. Okay, the tooth's knocked out of the mouth. and replaced. These injuries are associated with both pulp necrosis and direct damage to the root surface, including the precementum and adjacent PDL. So there are transient forms of lateral external inflammatory root resorption, and they're called surface resorption, and they could occur in early stages of healing post-trauma, but typically resolve as long as the pulp tissue remains vital. So if the pulp tissue remains vital after an avulsion and the tooth is replaced, or a luxation where the tooth is traumatized and it's luxated, we could get transient surface resorption, but that resolves, assuming that the pulp stays vital, okay? Now, when we're talking about apical external inflammatory root resorption, which we talked about earlier about the necrotic pulp, and lateral external inflammatory root resorption, they resolve typically after non-surgical root canal therapy, all right? So other than the transient forms, which resolve on their own because the pulp remains vital, when we start to see necrotic tissue in the pulp, we need to do root canal therapy, and that usually stops the apical and lateral external inflammatory root resorption process, all right? If lateral external inflammatory resorption becomes progressive where it continues, it has the potential to progress to what we call replacement resorption or ankylosis. We've all heard about ankylosis. That's where bone actually replaces the PDL and just starts dissolving the tooth. Now, replacement resorption occurs due to bony remodeling, and this occurs directly following the resorptive process. So what we'll see clinically are teeth that lack physiologic mobility. So when you tap on them, they have somewhat of a metallic tone. Now radiographically, the periodontal ligament and laminadora defining the root are replaced by osseous ingrowth. So your typical PDL space with the laminadora, which is the more cortical bone, tends to be replaced by just osseous ingrowth. So when you take an x-ray, you won't see that typical PDL space on the x-ray. That will all be filled in with bone. Now, currently, there's no treatment for replacement resorption, as we know. Once that process starts eating the tooth away and replacing it with bone, the prognosis is not good. If enough root surface is replaced that the tooth reaches one millimeter of infra-occlusion, typically a decoronation protocol is advised to preempt coronal fracture. And then we'll be looking towards implant replacement. So once the tooth becomes weakened to that level, you just cut the crown off so that you prevent it from fracturing. and then you plan for an implant. So now let's talk about a non-inflammatory type of external resorption. Now this is commonly referred to as pressure resorption. Every other resorptive process we've just discussed has to do with inflammation of the soft tissue adjacent to it. This is non-inflammatory. Now pressure resorption is associated with the same originating tissues as external inflammatory resorption, but the etiology is different. And as the name states, and I'm sure everyone who's listening figured it out, the main causes are orthodontic movement, right? Orthodontic movement is the main cause for pressure resorption. Also, misaligned tooth eruption is another cause or pressure from slow-growing tumors or cysts of the jaw. But those are less common, obviously. Now, again, to reiterate, for pressure resorption to occur, we need to have direct damage to the pre-cementum, right, on the outside of the root, and periodontal ligament. Removing the causative agent by stopping orthodontic movement or removing the misaligned tooth or jaw lesion will halt pressure resorption. However, resorbed tooth structures will not regrow, obviously. Whatever is lost is lost. We all know that. It is important to understand all this because as pulpal disease does not cause pressure resorption, endodontic therapy is not indicated in its management, right? So if the pulp has nothing to do with this type of a resorption, so we do not want to do a root canal on a tooth that looks like it has resorption going on on the side of it, but it has nothing to do with the pulp. And obviously you'll do a pulp vitality test and realize whether the tooth is undergoing any kind of orthodontic movement, et cetera. The final resorptive category that I will talk about today is external cervical resorption. This is another type of external resorption. This type of resorption occurs at the cemento-enamel junction, the CEJ, and it is believed that external cervical resorption is the most often seen form of resorption in clinical dentistry. So this is the most common one. So what do we need for external cervical resorption to happen? We've all probably seen it on an x-ray. At the CEJ, we need developmentally missing, lost, or damaged precementum combined with inflammatory tissues. But the inflammatory tissue is not the pulp as it is in internal resorption, and it's not the PDL as it is in inflammatory external resorption. But the soft tissue that we're talking about now that needs to be inflamed in order for external cervical resorption to occur is the junctional epithelium. of the periodontal attachment apparatus, the junctional epithelium. And we remember that from dental school when we learned about the periodontal attachment apparatus. It's the tissue at the base of the gingival sulcus. So again, we need damaged precementum at the CEJ along with inflamed junctional epithelium, which is the tissue at the base of the sulcus. So what are the possible etiologies for this? Well, they include a history. of orthodontics, trauma, periodontal therapy, or even in some cases, research has shown that internal bleaching with caustic agents leaking down into the sulcus could cause this. So bleaching with caustic agents that get down into the sulcus could cause inflammation to the junctional epithelium, and that combined with some lost or damaged precementum. will activate clastic cells that will start resorbing the neck of the tooth, the cervix of the tooth. And having said that, keep in mind, this type of resorption often presents idiopathically and has been associated with a wide variety of other conditions, including viruses, for instance. So even though they never had bleaching, maybe they never had orthodontic treatment, no history of trauma, no periodontal therapy whatsoever, Sure enough, we take an x-ray and there's an obvious cervical resorption occurring. The tooth is vital. You know, we don't know why it started. So as dentists, what should we be aware of clinically when it comes to external cervical resorption? You may see significant soft tissue ingrowth in the area of the CEJ. This can be seen clinically as vascular tissue that is growing in the cervical concavity of the tooth or... can be picked up as a pink discoloration seen within the crown. In other cases, osseous ingrowth can occur, and in those cases, the lesions will be clinically undetectable. Radiographically, lesions present as mixed radiolucencies with a kind of like a ground glass appearance as the lesions extend inward. And as we know, the dental pulp has its own protective predentin, so pulpal involvement is rare in cases of cervical resorption. Okay, so I'll repeat that. Pulpal involvement is rare, so we should detect a vital pulp when we do pulp testing on that tooth. And that's a great way to rule out other forms of resorption because if that tooth is completely vital and no pain and responds normally to pulp testing, then it's highly likely that we're looking at external cervical resorption. There are cases where pulpal involvement does exist with external cervical resorption, and that's usually related to secondary caries or infection that develops within the resorptive cavity and the pulp becomes necrotic, but that's not that common. Now, assuming the tooth is restorable, lesions are generally managed surgically with application of some form of debridement medicament like trichloroacidic acid that can be used to debride the area. followed by the restoration of the defect. In the cases of secondary pulp involvement, of course, root canal therapy is necessary. So in the cases of asymptomatic osseous ingrowth, if the tooth is still structurally sound, there is no rush to extract the tooth, but the patient should be told that the prognosis is guarded and the tooth should be actively monitored. So as I mentioned in the beginning of this podcast, it's important for dentists to understand the fundamentals behind the different types of root resorption and be able to differentiate their clinical signs, radiographic appearances, and etiologic factors so they can properly diagnose and manage these conditions appropriately. Thanks for listening to the Vivo Podcast Show. I'm Dr. Phil Klein.