Tooth resorptions in cats (TR) were first called caries (because of the human lesions), then cavities (because there is a hole), cervical line lesions (because they occur near the cervix of the tooth), feline neck lesions (because they occur at the neck of the tooth in cats), and more recently, feline odontoclastic resorptive lesions (FORL). More recently, they were called resorptive lesion (RL). The feline term was dropped as the same lesions were found in human, dog, chinchilla, Guinea pig and marmoset. It describes the lesion in some detail but still does not tell us what starts this destructive process. The latest term better represents the actual pathology.
The cellular process at work is now quite well understood. It starts when plaque bacteria cause an inflammatory reaction in the gingival tissues. Chemotactic compounds attract stem cells that transform into odontoclasts. This is the active phase of the disease, where numerous odontoclasts resorb enamel or cementum and create a lacuna in the dentin. Odontoblast numbers do not increase proportionally with the odontoclasts. Instead, inflammatory cells and granulation tissue migrate to the defect. Granulation tissue matures; the blood vessels enlarge and ensure a good blood supply. This is a prerequisite for the reparative phase, where odontoblasts produce new bone/cementum to replace the lost dentin. In areas where blood supply is marginal, the lesion continues to erode dentin and penetrate the pulp canal. A recent study has shown that teeth normal grossly and radiographically, in cats with other teeth affected, have resorptive lesions starting on the root surfaces. These lesions, at first, are not inflammatory. The PDL degenerates and loses the horizontal alignment of Sharpey's fibers. The PDL space narrows, resulting in dentoalveolar ankylosis.
Incidence of the disease remained low until the 1960s. Since, multiple causes have been proposed, such as canned diet, pH in the diet, texture of the diet, neutering, vaccination programs, etc. None have proven true. Eight years ago, Dr. A. Reiter started a research looking at the level of calciotropic hormones in affected cats as opposed to normal cats. Serum levels of parathyroid hormone (PTH), parathyroid hormone related peptide (PTHrP), calcitonin (CT), 25-hydroxyvitamin D (25OHD), and tetraiodothyronine (T4) were assessed.
TR-affected cats showed increased BUN, increased phosphorus, decreased urine specific gravity, but still within normal ranges. The only statistically significant difference was that affected cats had a higher concentration of 25O HD. 25O HD increased the risk of TR by 2% per nmol/l.
Odontoclasts may attach to or may be attracted only to mineralized tissue. Normally PDL, cementoblasts, cementoid, odontoblasts and predentin are uncalcified and protect the root surface from resorption. In affected cats, one sees hypercementosis, osteoid formation along the alveolar socket wall, and gradual calcification of PDL. These factors result in narrowing of the PDL space. Once dentoalveolar ankylosis is established, the root becomes incorporated in the bone remodeling process common in the rest of the body.
Dogs and cats do not synthesize vitamin D3, they depend on dietary intake. Research showed that 250 to 500 IU/kg of ingested dry matter was ample to supply their needs. Twenty out of 49 canned diets evaluated were found to contain in excess of 30 times the vitamin D3 requirements of 250 IU/kg of dry matter. Fifteen of those contained over 10,000 IU/kg dry matter. Hypervitaminosis D studied in lab species discovered that is caused: unusual structures in dentin, edematous degeneration of PDL, hypercementosis, increased osteoid formation, calcification of the PDL, dentoalveolar ankylosis, granulation tissue formation, root resorption, and a mixed pattern of alveolar bone resorption and osteosclerosis.
Now the principle has not been proven yet, but one can conclude from these facts that excess vitamin D3 in cats could play an important part in the development of TR. Now a few years later, a French study did not find any relationship between serum levels of vitamin D and occurrence of tooth resorption.
A PhD study just completed this year shows that vitamin D seems to be involved in the formation of tooth resorption but at the cellular level rather than the serum level. The final word is that we still do not know exactly why some cats get TR and some don't.
Grossly, the lesions start as a small dot of inflamed tissue at the gingival margin. The resorption starts near the cementoenamel junction. The erosion progresses through the enamel or through the cementum to reach the dentin. Once there, it can spread in any direction. If left untreated, it will reach the endodontic system, at which point the tooth is lost. Grossly, as the lesion enlarges, the granulation tissue follows to try to fill the defect.
Stages of their progression are classified as follows:
Stage 1 (TR1). The lesions appear as shallow depressions in the enamel or the cementum near the CEJ; mild dental hard tissue loss (cementum or cementum and enamel)
Stage 2 (TR2). Moderate dental hard tissue loss (cementum or cementum and enamel with loss of dentin that does not extend to the pulp cavity); the lesion is very sensitive. Granulation tissue often grows over the lesion in an attempt to protect the area.
Stage 3 (TR3). Deep dental hard tissue loss (cementum or cementum and enamel with loss of dentin that extends to the pulp cavity); most of the tooth retains its integrity. Bleeding is obvious if the lesion is probed. This stage is very painful.
Stage 4 (TR4). Extensive dental hard tissue loss (cementum or cementum and enamel with loss of dentin that extends to the pulp cavity); most of the tooth has lost its integrity.
(TR4a) Crown and root are equally affected
(TR4b) Crown is more severely affected than the root
(TR4c) Root is more severely affected than the crown
There is also extensive inflammation of the surrounding gingival tissue.
Stage 5 (TR5). Remnants of dental hard tissue are visible only as irregular radiopacities, and gingival covering is complete.
It has changed in the last few years. At first, affected teeth were ignored or extracted because we did not know what to do with them. Then we started to fill them, using glass ionomers. We filled them all, as long as the endodontic system was intact. Next, we realized that a large proportion of them had signs of root resorption accompanying the odontoclastic resorptive lesions. The recommendations became to radiograph all affected teeth first, and to fill only the ones where the endodontic system and the root system were intact. Even with these restrictions, reports came back that only 60% of these teeth remained asymptomatic 12 months post restoration; quite disappointing. So, we are back to extracting them.
In early cases, there is no problem, but in advanced cases, the teeth and their roots may be very difficult to elevate intact. With type II or replacement resorption, it is even more difficult to remove the retained fragments. The reason for this is that the affected dentin is replaced by new bone/cementum/dentin, which grossly is identical to alveolar bone. The operator is thus unable to distinguish the margins of the roots and, as a result, ends up damaging the supporting bone during the extraction procedure. Today, another choice may be possible. Radiographs are essential for this technique. They often show the roots to be disappearing into the bony background without any sign of inflammation. In these cases, the granulation tissue is cut away and the crown is ablated using a high-speed handpiece with a cutting bur. Make sure no spurs are left. The gingiva is elevated gently and sutured closed on top of the retained root fragments (elevation of the gingival envelope flap can be done before sectioning the crown off). It is very important to tell the owner that root fragments have been left in, and to recheck these fragments, six months later, by taking a follow up radiograph.
Why leave the roots in? By doing so you minimize the amount of trauma associated with extraction. Moreover, there is less recession of the crestal bone because the alveolus remains filled with tissue. If your original diagnosis was correct and the dentin in the roots is being replaced by new bone/cementum/dentin, your follow up radiograph will show only bone, no shadows of roots left. If you were wrong, and there was some inflammation, the radiograph will now show periapical pathosis. You now must go back and remove the remnants of roots. The good news is that the infection has loosened the roots, making them easier to extract. With type I or inflammatory resorption, the only choice is to extract, as the periodontal ligament is still present and there is a periapical infection.
Working with feline tooth resorption has been and remains a dynamic process. We have a better understanding of the pathological processes at work, but we are still not certain of what initiates the disease. Consequently, we can control the damage and the pain caused by the lesions, but we are still powerless to prevent their occurrence. This new technique, reserved for advanced cases of root resorption, is a prime example; it shows that our ongoing research helps us deal with the defects and the associated inflammation, but does nothing to prevent their occurrence. Nevertheless, it has the advantages of being quicker, easier on both patient and operator, and better in the long run for preservation of alveolar bone.