FORLs

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Stage 1 - FORL lesion affecting only the root cementum
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Stage 1 - FORL lesion affecting only the root cementum
Stage 2 - FORL lesion progressing into the dentin
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Stage 2 - FORL lesion progressing into the dentin
Stage 3 - FORL lesion entering the pulp cavity
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Stage 3 - FORL lesion entering the pulp cavity
Stage 4 - FORL lesion with extensive structural damage and dento-alveolar ankylosis
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Stage 4 - FORL lesion with extensive structural damage and dento-alveolar ankylosis
Stage 5a - FORL lesion with an absent crown and retained root structure
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Stage 5a - FORL lesion with an absent crown and retained root structure
Stage 5b - FORL lesion with extensive root replacement resorption and a nearly intact crown
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Stage 5b - FORL lesion with extensive root replacement resorption and a nearly intact crown

Feline odontoclastic resorptive lesions (FORLs) occur in 39-67% of domestic cats and are a leading cause of gingivitis, chronic faucitis and tooth loss[1]. They have been reported in captive felids and domestic dogs. FORLs are considered to be progressive defects of the calcified tooth substance of permanent teeth, which results from the destructive activity of odontoclasts on the root cementum. This often is called external resorption because the destruction is occurring on the external tooth surface. Internal resorption refers to the odontoclastic activity that occurs in detin adjacent to the pulp canal[2]. The roots of permanent teeth do not normally undergo resorption. The cementum and periodontal ligaments are organic, uncalcified components, Two conditions must be present for local tooth resorption:

  • the protective covering of the root must be missing or altered
  • a stimulus for the resorbing cells must be present.

Periodontal disease (plaque bacteria and their toxins) and other possible causes of local inflammatory activity then may provide the inflammatory stimulus (cytokines) for resorption of alveolar bone and teeth[3][4][5].

Contents

Causes

The underlying cause of this dental lesion in cats is not well understood. DeLaurier et al (2009)[6] recently investigated the origin and progression of early tooth resorption lesions in teeth with no clinical signs of disease. The surfaces of 138 teeth from 13 adult cats were analyzed using electron microscopy. At least one resorptive lesion was found in 53% of the teeth. Most cats (85%) had tooth lesions, and there was a significant association between increasing age and incidence of lesions. The most commonly affected teeth were the mandibular molars. Resorptive lesions were found at the cemento-enamel junction in 38% of teeth. Evidence of repair limited to the root surface was found in 23% of teeth. When lesions occurred at the cemento-enamel junction, there was no evidence of repair. The researchers conclude that resorptive lesions are common in feline teeth, even when no signs of disease are obvious. Lesions can be found anywhere on the tooth surface, but there seems to be absent or compromised repair mechanisms at the cemento-enamel junction.

The introduction of commercial diets paralleling the rising incidence of FORLs, and the relative absence of FORLs in wild felidae suggests domestication factors (e.g. diet, increased frequency for feeding, etc) have played a significant role in the rising incidence of this disease.

Dietary factors

Cats with FORLs have significantly higher serum 25-hydroxyvitamin D concentrations than cats without FORLs[7]. Cats with FORLs are significantly more likely to have detectable calcitonin in their serum. Cats are not able to synthesize vitamin D3 in the skin sufficiently, and a direct linear relationship exists between serum concentration of 25-hydroxyvitamin D and dietary intake of vitamin D. In the results of one study, concentrations of 25-hydroxyvitamin D indicated that cats with resorptive lesions had ingested higher amounts of vitamin D or vitamin D metabolites, compared with cats without resorptive lesions[8]. Many commercial cat foods contain excess concentrations of vitamin D.

Periodontal disease

Plaque bacteria are the cause of chronic periodontal disease[9]. The focus in understanding recurrent oral disease is on determination of the impact of these bacteria on the immune response and the interaction of the host's defense mechanisms. Periodontal disease results from an imbalance between the host and the local microflora. A good immune response results in no evidence of progressive disease despite the presence of calculus and plaque. A patient with an impaired immune system (e.g. FIV or FeLV infection) may have generalised or localised evidence of disease.

Inflammation of the periodontium leads to the release of bacterial byproducts such as lipopolysaccharides and inflammatory mediators, especially cytokines [10]. Epithelial, endothelial and inflammatory cells secrete cytokines. Inflammatory cells often are found associated with resorptive lesions in cats., although no significant correlation exists between resorptive lesions and periodontitis. The inflammation associated with resorptive lesions more likely is a secondary reaction related to the plaque accumulation that occurs at the site of the resorptive lesion.

Viral infections

Systemic immunosuppressive diseases stimulated by viral infections may aggravate resorption processes, but their ability to initiate resorptive lesions is unlikely. Few cats with resorptive lesions are infected with FIV or FeLV (August, 2006). No evidence exists that these viruses contribute to the development of FORLs. Because viral infections can stimulate oral disease and lead to chronicity, immunosuppression has been mentioned as a possible cause of resorptive lesions[11].

Calicivirus has been mentioned as a factor in the development of FORLs related to the oral manifestation of calicivirus infection such as gingivostomatitis, however studies have shown that only a small number of cats with resorptive lesions have chronic gingivostomatitis[12].

Endocrine factors

Root resorption has not been seen with primary hyperparathyroidism or renal secondary hyperparathyroidism[13]. Tooth roots appear to be resistant to resorption even when significant bone resorption occurs elsewhere in the body as a result of systemic disease.

The effect of hormone changes associated with neutering has also be investigated as a possible cause of FORLs,. Estrogens are produced primarily in the ovaries and in small amounts in the testicles and adrenal cortex. Routine neutering of domestic animals has not been associated with the development of resorptive lesions[14].

Diagnosis

Diagnosis is usually made by visualisation of the teeth, often under general anaesthesia, in order to allow full examination. Radiographs may help assess the health of the tooth root.

Treatment

Treatment of FORLs is usually simplistic due to financial constraints of many cat care-givers. Therapies in most cases is aimed at alleviating pain associated with dental root-canal disease through use of daily NSAIDs and broad-spectrum antibiotics, to limit further FORL development. In advanced cases, dental extractions are the norm.

Rarely are cosmetic changes, such as tooth root canals and fillings, made to the tooth. That cats can eat equally well without teeth underlies the importance of palliative care and long-term renal protection by avoiding chronic gingivostomatitis.

The implication of commercial diets as a likely contributor to FORLs necessitates a drastic rethink of feline diets in cases of FORL or chronic gingivitis.

References

  1. August, JR (2006) Consultations in feline internal medicine. Vol 5. Elsevier Saunders, USA
  2. Ne, RF, Witherspoon, DE & Gutman, JL (1999) Tooth resorption. Quintessence Int 30:9-25
  3. Johnston, N (2000) Acquired feline oral cavity disease. Part 2: feline odontoclastic resorptive lesions. In Practice 22:188-197
  4. Deihl K, Rosychuk RAW (1993). Feline gingivitis-stomatitis-pharyngitis. Veterinary Clinics of North America :Small Animal Practice 23:139-153M
  5. Frost P, Willians CA (1986). Feline Dental Disease. Veterinary Clinics of North America Small Animal Practice 16:851-873
  6. DeLaurier A, Boyde A, Jackson B et al: Identifying early osteoclastic resorptive lesions in feline teeth: a model for understanding the origin of multiple idiopathic root resorption, J Periodontal Res 44:248, 2009
  7. Reiter, AM (2004) The role of calciotropic factors in the etiology of feline odontoclastic resorptive lesions (FORL). Thesis, University of Veterinary Medicine, Vienna, Austria
  8. How, KL, Hazewinkel, AW & Mol, JA (1994) Dietary vitamin D dependence of cat and dog due to inadequate cutaneous synthesis of vitamin D. Gen Comp Endocrinol 96:12-18
  9. Frost, P & Williams, CAA (1986) Feline dental disease. Vet Clin North Amer Small Anim Hosp 16:851-873
  10. Harley, R et al (1999) Cytokine mRNA expression in lesions in cats with chronic gingivostomatitis. Clin Diagn Lab Immunol 6(4):471-478
  11. Williams, CA & Aller, MS (1992) Gingivitis/Stomatitis in cats. Vet Clin North Am Small Anim Pract 22:1361-1383
  12. Crossley, DA (1991) Survey of feline dental problems encountered in a small animal practice in NW England. Br Vet Dent Assoc J 2:3-6
  13. Tomsa, K et al (1999) Nutritional secondary hyperparathyroidism in six cats. J Small Anim Pract 40:533-539
  14. Reiter, AM & Mendoza, K (2002) Feline odontoclastic resorptive lesions. An unsolved enigma in veterinary dentistry. Vet Clin North Amer Small Anim Pract 32:791-837
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