By John R. Lewis, VMD, DAVDC, Founding Fellow, AVDC OMFS

In last month's column, I discussed the epidemic of tooth resorption (TR) and how to diagnose it. Multiple etiologies have been proposed to explain tooth resorption, including extension of periodontal disease, genetic or anatomic anomalies, mechanical trauma due to forces placed on the teeth, endocrine abnormalities, infectious disease,¹ age-related changes, and dietary aspects.

TR is seen with advanced age. In one study, cats in the age group of 10 to 15 years had a 6.6 times higher occurrence of TR compared to the 0 to 4 years age group.² A histological study of clinically and radiographically normal teeth of cats showed histological signs of periodontal ligament degeneration, hypercementosis, dentoalveolar ankyloses, and resorption, suggesting TR is a generalized disorder of all teeth rather than a focal disease of isolated teeth.³

An archival study of feline skulls suggests the prevalence of TR has increased over the past five decades at a rate that cannot be entirely explained by increased awareness and improved diagnostics.⁴ Also, feral cats exhibited a much lower prevalence rate compared to domestic cats.⁵ It is difficult to explain the increased prevalence of TR by physiological degradation associated with aging.

The cause of tooth resorption likely resides in an environmental change or aspect of domestication that 1) has increased in popularity since the 1960s, and 2) is capable of causing changes to the entire periodontium of multiple, if not all, permanent teeth.

Studies from the University of Pennsylvania suggest an aspect of domestication related to diet might possibly be associated with the development of TR. A statistically significant increase in serum 25-hydroxyvitamin D concentrations has been found to be present in cats with TR compared to cats with no clinical or radiographic evidence of TR. Experimental oversupplementation of vitamin D and its metabolites in dogs and rats has revealed marked periodontal ligament degeneration, hypercementosis, hyperosteoidosis, and alveolar bone expansion, and several other histological changes that parallel those seen in cats with TR.⁶

Cats are unable to produce vitamin D in their skin. Nutritional research has shown plasma concentrations of 25-hydroxyvitamin D in kittens is directly related to the dietary intake of vitamin D.

Vitamin D is obtained from food, although the requirement for cats appears to be low. Based upon mean plasma concentrations obtained after feeding a diet of known vitamin D level, a minimum vitamin D concentration of 250 IU/kg dry matter has been recommended for commercial diets.⁷

Fish is common source of protein in dry and canned cat food, and contains substantial levels of vitamin D. Mackerel flesh contains a mean of 9,500 IU/kg dry matter, whereas mackerel viscera contains a mean of 144,000 IU/kg dry matter. Therefore, whole minced fish often contains 25,000 IU/kg dry matter. It has previously been determined 36 of 49 (73 percent) of canned cat foods tested had vitamin D concentrations greater than 1,500 IU/kg dry matter, and 15 of 49 (31 percent) foods tested were in excess of the Association of American Feed Control Officials' (AAFCO) recommended maximum level of 10,000 IU/kg dry matter.⁸

Though this evidence supports a role of vitamin D causing changes to the periodontium, a cause-and-effect relationship between chronic increased dietary intake of vitamin D and development of tooth resorption has not yet been proven. Indeed, experimental long-term feeding studies would be necessary.

There may be a connection between TR and other common feline oral pathologies, including alveolar (buccal) bone expansion and tooth extrusion (supereruption), as cats with TR are significantly more likely to exhibit extrusion of their maxillary canine teeth.⁹

Treatment of tooth resorption

In the past, these lesions have been treated by restoration with glass ionomer cements, but follow-up studies have shown poor long-term results with restoration due to progression of the lesions. Therefore, extraction has been the treatment of choice.

Sometimes it is not possible to perform a complete tooth extraction due to severe root resorption where a portion of the root has been replaced by a reparative bone-cementum material. When this occurs, the tooth root becomes incorporated into the adjacent alveolar bone.

Radiographs in this case suggest a non-inflammatory evidence of resorption, referred to as root replacement. Radiographic signs include loss of periodontal ligament space and decreased root density, approximating the surrounding bone density. When this radiographic appearance is seen, in the absence of: 1) significant periodontal pockets of the affected tooth, 2) endodontic disease, 3) stomatitis, or 4) immunosuppressive disease, it is possible to perform a crown amputation (also known as coronectomy).

Hard tissue with clinical and radiographic characteristics of tooth root is removed, while resorbed root, which has been replaced by bone, is left in place. The tooth crown and coronal root segment are removed with a dental bur in a high-speed hand-piece. The crestal alveolar bone is smoothed with a dental bur, and the gingiva is closed with absorbable suture over the site.

Without dental radiographs, a determination cannot be made as to whether crown amputation is an acceptable technique. Recall from last month's column the radiographic types of tooth resorption referred to as Type 1 and Type 2. Roots affected by Type 1 tooth resorption are treated via full extraction, whereas roots affected by Type 2 tooth resorption may be treated by coronectomy.

What about dogs?

Some feel the prevalence of tooth resorption in dogs is also on the rise. Middle-aged and older dogs that are heavy chewers often have widespread tooth resorption of multiple premolar teeth.

One study looked at 224 dogs via full-mouth radiography and found 53.6 percent had some form of tooth resorption. This study found older large-breed dogs to be most frequently affected.¹⁰  

John Lewis, VMD, DAVDC, FF-OMFS practices and teaches at Veterinary Dentistry Specialists and Silo Academy Education Center, both located in Chadds Ford, Pa.

References

1. Thomas S, Lappin DF, Nile CJ, et al. Microbiome analysis of feline odontoclastic resorptive lesion (FORL) and feline oral health. J Med Microbiol. 2021;70(4):001353.
2. Mestrinho LA, Runhau J, Bragança M, Niza MM. Risk assessment of feline tooth resorption: a Portuguese clinical case control study. J Vet Dent. 2013;30(2):78-83. 
3. Gorrel C, Larsson A. Feline odontoclastic resorptive lesions: unveiling the early lesion. J Small Anim Pract. 2002;43(11):482-8. 
4. Harvey CE. Dental disease in cat skulls acquired before 1960. Proc 4th Annual Vet Dent Forum. 1990: 41.
5. Verstraete FJ, van Aarde RJ, et al. The dental pathology of feral cats on Marion Island, part II: Periodontitis, external odontoclastic resorption lesions and mandibular thickening. J Comp Pathol 1996; 115: 283-297.
6. Reiter AM, Lewis JR, Okuda A. Update on the etiology of tooth resorption in domestic cats. Vet Clin North Am Small Anim Pract. 2005;35(4):913-42.
7. Morris JG, Earle KE. Vitamin D and calcium requirements of kittens. J Clin Nutrition 1996;3:93-96.
8. Morris JG. Vitamin D synthesis by kittens. Vet Clin Nutrition 1996;3:88-92.
9. Lewis JR, Okuda A, Shofer FS, Pachtinger G, Harvey CE, Reiter AM. Significant association between tooth extrusion and tooth resorption in domestic cats. J Vet Dent. 2008;25(2):86-95.
10. Peralta S, Verstraete FJ, Kass PH. Radiographic evaluation of the types of tooth resorption in dogs. Am J Vet Res. 2010;71(7):784-93