This presentation provides an in-depth review of current knowledge on tooth resorption, with a particular focus on feline tooth resorption. It offers a comprehensive overview of the pathomechanisms involved, questions the existing classification of TR in cats, and suggests an adaptation to align with the classification used in human dentistry. A decision-making strategy based on the inflammatory component present at the time of investigation is proposed. Treatment methods are not covered in this presentation.

Feline Tooth Resorption: actual knowledge and new classification

 1. Introduction
Tooth resorption refers to the loss of dental hard tissue due to the activity of odontoclasts. It is a common condition in cats, affecting between 29% and 72% of the feline population. Despite progress in understanding the pathomechanism of tooth resorption, identifying the causative factors remains challenging. Currently, the official nomenclature distinguishes three types of tooth resorption in cats based on the radiographic appearance of the lesion. In humans, tooth resorption is rare and there is no universally accepted classification. However, a recent publication by Abbott (2022) proposed eleven different types based on causative factors, pathomechanisms, and location. One type is physiological resorption, which occurs during the shedding of deciduous teeth. Resorption is due to the action of immune cells; the distinction between physiological and pathological resorption lies in the inducing factor. Physiological resorption is induced by the growth of permanent teeth, whereas pathological resorption is triggered by predisposing, inflammatory and non-inflammatory factors. Bone resorption, similar to tooth resorption, can be physiological or pathological. Physiological bone resorption is part of the continuous turnover of bone, while pathological bone resorption is associated with bone infection or necrosis, like in periodontal disease. Tooth resorption is an immune-mediated process that can be activated by various stimulating factors. It serves to eliminate modified, infected, or necrotic hard tissue, but under certain conditions, it can become destructive. To better understand tooth resorption, it is essential to focus on its pathomechanism and compare the different types observed in humans and cats.

2. Pathomechanism of Tooth Resorption
Tooth resorption is an immune-mediated mechanism driven by odontoclastic activity. Odontoclasts are large, multinucleated cells that originate from blood-borne leukocytes derived from the bone marrow. They are similar to osteoclasts but have fewer nuclei and are smaller in size. Odontoclasts come from hematopoietic stem cells in the bone marrow and are part of the monocyte/macrophage lineage. Precursor cells migrate to the site of action and fuse to form multinucleated odontoclasts under the influence of signaling molecules like RANKL, M-CSF, and other inflammatory cytokines. Odontoclasts adhere to the dental hard tissue via integrin receptors, forming a sealed zone. This attachment creates a microenvironment between the odontoclast membrane and the dental hard tissue. Odontoclasts secrete hydrogen ions (H+) through proton pumps (H+-ATPase) into the resorption lacuna, acidifying the microenvironment to dissolve the inorganic components (hydroxyapatite) of dentin and cementum. They also release lysosomal enzymes, such as cathepsins and matrix metalloproteinases (MMPs), to degrade the organic matrix, which is primarily collagen. The odontoclasts then digest the resorbed material. Their activity is regulated by the RANK/RANKL/OPG signaling pathway, where RANKL promotes differentiation and activation, while OPG inhibits the process.

Dental hard tissues are inherently resistant to resorption. The first barrier is the periodontal ligament (PDL), which separates the alveolar bone from the root surface. The second barrier is the root surface, protected by a layer of cementum, which is covered by cementoblasts and a non-mineralized cementoid layer. Internally, dentin is protected by a predentin matrix and odontoblasts. Clastic cells do not adhere to or resorb unmineralized matrix. Three general requirements, referred to as the “Resorption Triad,” must be met for resorption to occur: (a) Breakdown of natural barriers (b) Continuous presence of a stimulating factor (c) Viable blood supply for clastic cells. In external resorption, the cementoid layer can be damaged by factors such as curettage, surgical or restorative procedures, or congenital defects. Sometimes dentine is congenitaly exposed due to some defect at the cemento- enamel junction where the two tissues do not meet or do not overlap. Little is known about the causes of internal resorption. In most cases, the pulp will necrose very quickly, which removes the blood supply to the resorbing cells and, this, in turn, protects the root against extensive resorption. This probably explain why internal resorption are rare in dogs and cats.

The resorption process can be broken down into several phases: a. Alteration of the protective layer b. Resorption as long as stimuli are present c. Reparation by cementoblast or bone remodeling activity. In human, various factors can initiate tooth resorption, including pulpal necrosis, trauma, periodontal treatment, orthodontic treatment, the use of tooth whitening agents, necrosis of the PDL, developmental defects, impacted teeth, or the presence of cysts or tumors. Regardless of the initial cause, the process is predominantly inflammatory. Resorption is a dynamic process, starting microscopically, evolving slowly and potentially leading to the loss of the crown and replacement of the root by bone. Active resorption requires constant stimuli, and upon cessation of the stimulus, a reparative phase begins. It is crucial to consider the disease stage when evaluating a lesion.

The critical factor in determining the outcome is the type of cells that repopulate the root surface during the healing phase. If cementoblasts cover the damaged root surface, a type of healing called cemental healing, resulting in a favorable outcome. Conversely, if bone-producing cells cover the root surface, the healing conditions will be unfavorable. This leads to direct contact between bone and root over some areas of the root surface, a phenomenon known as ankylosis. Bone is resorbed and formed physiologically throughout life. As a result, the root is resorbed by osteoclasts, but during the reforming stage, bone is laid down instead of dentin, slowly replacing the root with bone. This process is termed replacement resorption or osseous replacement. It has been reported that destruction of more than 20% of the root surface is required for osseous replacement to occur.

Cervical resorption: Because the source of stimulation (infection) is not the pulp, it is postulated that bacteria in the sulcus of the tooth stimulate and sustain an inflammatory response in the periodontium at the attachment level of the root.

When evaluating radiographs of feline tooth resorption, it is essential to determine if the lesion is in the active resorptive phase or the reparative phase. Sometimes, it can even be a mixture of both. In the active resorptive phase, the radiograph shows a radiolucent, well-circumscribed area in the dental hard tissue. The size, form, extent, and location of the lesion do not play a role, as the lesion can be at the very beginning or at an advanced stage of resorptive activity. The active resorptive phase will not stop as long as the stimulating factors of resorption are present. Inflammatory cytokines contribute to the destruction of dental hard tissue by promoting osteoclast activity and inhibiting osteoblast function. The reparative phase cannot start as long as inflammation is present.

If the lesion is small (surface resorption), the reparative tissue can be cementoid (external surface resorption) or odontoblast (internal surface resorption). If the lesion is large or if the alveolar bone is in contact with the cement/dentine (ankylosis), the reparative mechanism will result in bone replacement, progressively replacing dental hard tissue with bone. This bone replacement mechanism is only possible in a non-inflammatory environment. When bone replacement of the tooth root progresses coronally, it will eventually get close enough to the oral cavity for bacteria to colonize the newly formed bone, reactivating the resorption process and halting the reparative phase.

The starting point of the lesion is extremely important. If the lesion starts coronally, close to the gingival sulcus, secondary inflammation will start very early in the process, possibly before the reparative phase begins. If, on the other hand, the lesion starts apically in a non-inflammatory environment, the reparative phase and bone replacement can progress along most of the root length before becoming secondarily inflamed. A study on the location of the central point (speculated starting point of a resorptive lesion) on the root surface related to tooth type revealed that resorption has a higher tendency to start apically on canine teeth, while it tends to start more coronally on premolars and molars (Harvey 2004). Interestingly, canines often show more advanced root replacement along the entire root compared to premolars and molars, which have a greater tendency for cervical resorption

3. Classification
Human dental resorption is classified into several types, as outlined by Abbott (2022): • External surface resorption: localized injury-induced and self-limiting.
• External inflammatory resorption: associated with necrotic pulp and traumatic injury.
• External replacement resorption: bone replaces resorbed cementum and dentin following severe injuries.
• External invasive resorption: commonly called “cervical resorption”. Caused by defects or trauma at the cemento-enamel junction.
• External pressure resorption: due to pressure from impacted teeth, tumors, or cysts. • Orthodontic resorption: apical root resorption resulting from orthodontic treatment.
• Physiological resorption: natural shedding of deciduous teeth.
• Idiopathic resorption: no apparent cause. Internal resorption includes:
• Internal surface resorption: minor and self-limiting.
• Internal inflammatory resorption: inflammatory process within the pulp leading to dentin loss.
• Replacement internal resorption: rare, typically trauma-induced without bacterial infection. Surface resorption, whether external or internal, often presents as very shallow lesions that are frequently overlooked in routine X-rays. These lesions are typically discovered accidentally during histological studies. They can be self-limiting when the underlying stimuli cease, leading to the lesion being covered by cementoblasts, with the periodontal ligament healing completely. However, these lesions can also serve as the initial stage for deeper resorption over time, potentially evolving into invasive or replacement resorption In cats, three types of tooth resorption are recognized (Dupont 2002, AVDC Nomenclature):
1. Type I: Focal or multifocal radiolucency with normal radiopacity and periodontal ligament space. 72% of type I lesion are associated with periodontitis.
2. Type II: Narrowing or disappearance of the periodontal ligament space and decreased tooth radiopacity. 15% of type II lesion are associated with periodontitis.
3. Type III: Combination of Type I and II in the same tooth. The severity of resorption is classified into five stages:
• Stage 1: Mild dental hard tissue loss(cementum or cementum and enamel).
• Stage 2: Moderate loss of dentin without involvement of the pulp cavity.
• Stage 3: Deep loss extending into the pulp cavity.
• Stage 4: Extensive loss compromising the integrity of the tooth.
• Stage 5: Irregular radiopacities with complete gingival covering.

The feline classification, which is based primarily on radiographic modifications, is limited and does not adequately represent the diversity of resorption types. To adopt a classification system for cats similar to that used in humans, we propose modifying and adapting the Abbott classification as follows:
1. Internal Inflammatory Resorption
2. External Inflammatory Resorption
3. External Replacement Resorption
4. External Invasive Resorption
5. External Pressure Resorption
6. Physiological Resorption Additionally, we simplify the staging system:
• Stage 1: Resorption without clinical or radiographic signs of inflammation
• Stage 2: Resorption with clinical or radiographic signs of inflammation
This proposed system, based on human classifications, offers improved differentiation of resorption types by considering pathomechanisms and causative factors, and it simplifies the staging process.

However, even if other resorptive type may be encountered in the cat, we must admit that two types dominate: external replacement resorption (former Type II) and external invasive resorption (cervical resorption)( former Type I). External replacement resorption in cats appears to be associated with modern life. A study of 256 cats from Switzerland that died between 1973 and 1974 revealed the presence of type I resorption but found no cases of type II external replacement resorption (Cao 2010). Conversely, research from the early 2000s indicated that type II resorption was diagnosed almost as frequently as type I (Girard 2008; Dupont 2002). Thus, between 1970 and 2000, type II resorption has increased dramatically, coinciding with significant changes in cats’ lifestyles due to modern conditions. These studies suggest that type I and II resorptions have different origins in cats. Another underappreciated aspect of feline external replacement resorption was published by two different authors in the early 2000s. They described a degeneration of the periodontal ligament (PDL) associated with early resorptive lesions, showing that this degeneration was present in some teeth before the resorption process began (Gorrel 2002; Roux 2005).

In humans, the etiology of replacement resorption is related to the absence of a vital periodontal ligament covering the root surface (Andreasen 1985). While the role of PDL degeneration in cats is acknowledged, its etiology remains unknown. Type I resorption in cats is strongly associated with inflammation. Two aetiologies are considered. The first hypothesis suggests primary inflammation, where gingivitis and early periodontitis stimulate odontoclasts at the most coronal aspect of the PDL near the cervix. Inflammatory by-products continuously stimulate the resorptive process, leading to typical radiolucent cavities at the cervix. The second hypothesis suggests secondary inflammation, where non-inflammatory resorption starts near the cervix. Once the lesion extends into the oral cavity, a secondary infection from dental plaque occurs, and inflammatory factors maintain the resorptive process.
A prospective study on teeth with no clinical or radiographic signs of resorption demonstrated that the lesions varied in their location along the root but were always below the level of the alveolar crest and not associated with inflammation in the adjacent PDL (Gorrel 2002).

 Complicating the issue further, similar etiologies may evolve differently, and similar radiographic appearances may have different etiologies.

4. Decision-making Strategy
Resorptive lesions are progressive and rarely reversible. Key considerations include prevention, determining the appropriate timing for intervention, and assessing pain. Physiological resorption is not painful. Non-inflammatory resorption is painless until secondary inflammation occurs. A retrospective study in humans found that replanted teeth with necrotic periodontal ligaments survived for 3 to 7 years in younger patients (ages 8-16), while ankylosed teeth in older patients (ages 17-39) could function for decades or even for life (Gunnraj 1999). This suggests that older cats might tolerate replacement resorption without experiencing pain over the long term. The etiology or type of resorptive lesion does not significantly impact the treatment approach. However, even if resorption begins without inflammation, it can develop into secondary inflammation over time. This distinction is crucial for treatment strategies, as inflammatory resorption is painful and requires immediate attention, whereas non-inflammatory resorption remains pain-free until secondary inflammation occurs. Teeth with non-inflammatory resorption may be maintained as long as they are not painful. In conclusion, a thorough understanding of the pathomechanisms and classifications of tooth resorption in both humans and cats can aid in better diagnosis and management of this condition. By adapting the human classification system to feline cases and focusing on the inflammatory component, more effective strategies for decision-making and treatment can be developed.

References available upon request.