Gingivitis, as opposed to normal dental decay associated with age, is an inflammatory disease of the gums leading to premature tooth loss and gum disease that is both painful and detrimental to cat health. A significant number of cats with gingivitis are prone to chronic renal disease because of the constant insult by bacterial antigens which are absorbed into the blood and their byproducts deposited in the renal glomerulus[1][2][3].

Gingivitis can also lead to faucitis, which involves inflammation and infection to the entire rear region of the mouth involving the palatine tonsils, pharynx and sometimes larynx, leading to pain, inappetance and considerable weight loss[4][5].

This disease appears to have a genetic predisposition as it commonly ocurs in certain purebred cats including British, Siamese, Burmese, Bengal and Abyssinian cats. Gingivitis occurs from 12-18 months of age and normally progresses in spite of treatment. Dental extractions are common by 2 years of age. There are two types of results from gingivitis in cats; resorptive lesions (shrinking tooth roots) and stomatitis (inflammation of the mouth) and these are discussed below[6][7].


Gingivitis may begin with or without tartar (calculus) present on the teeth. Dental calculus is composed by diverse bacteria and organic substances attached to an inorganic matrix composed by hydroxyapatite, calcium and phosphorus (from the saliva), forming a mineralized plaque[8][9]. Some bacteria located within the gingival sulcus produce toxins (hyaluronidase and lysosomal enzymes) which, combined to the great influx of inflammatory cells, irritate the gingiva and unchain an inflammatory reaction which yields swelling and reddening of the gingiva as well as development of friable tissue[10][11]. Plasmocytes and linfocytes are the more common cells present in this type of gingival inflammation. Plasmocytes produce antibodies against the bacterial endotoxins, and this antigen/antibody complex activates the complement system. These substances attract a great number of inflammatory cells via chemotactic factors and increase local vascular permeability, causing smooth muscle contraction and intense gingival retraction[12][13][14][15].

  • Diet – resulting in formation of FORLs – often attributed to commercial food (high starch and Vit D content)
  • Oral conformation – common in Persian cats with Brachycephalic syndrome
  • Poor oral hygiene – daily brushing reduces calculus formation and bacterial adherence to tooth cementum
  • Genetic – juvenile gingivitis of Abyssinian, Persian and Maine coon breeds)
  • Bacteria – gingivitis starts by deposition of microorganisms in the dental-gingival interface, predisposing the formation of dental calculi which is characteristic of this disease. Common bacteria include Bacteroides sppActinobacillus sppStaphylococcus spp., Streptococcus sppPseudomonas spp. It appears evident that Bartonella spp does not appear to be associated with this disease[16].
  • Viruses – of all infectious agents, feline calicivirus (FCV) is the most commonly associated with gingivitis and lymphocytic plasmacytic stomatitis[17]. More rare causes include FHV, FIV and FeLV[18][19]
  • Anodontia/Oligodontia – reduced or complete absence of teeth (no inflammatory process, present since juvenile)
  • Eosinophilic granuloma complex – usually perioral lesions (e.g. rodent ulcer) and other skin lesions.
  • Mandibular osteosarcoma
  • Oral carcinoma
  • Oral melanoma

Clinical signs

Gingivitis appears clinically as reddened, inflammed gums that are tender to touch and cause pain during eating in cats. Often, the cat with claw at its face while attempting to eat, and there may be shuddering of the jaw, and occasionally, screaming in pain. Anorexia is seen when gingivitis is severe.

Severe gingivitis is a common cause of euthanasia due to the intractable, often unresponsive nature of the disease.


First line therapy involves teeth cleaning above and below the gingiva as well as strict home care and treatment (extraction) for those teeth affected with grades 3 and 4 periodontal disease and/or feline odontoclastic resorptive lesions.

  • Surgery
Currently, the only treatment that will deliver consistent results of 70% cure without the use of follow up medications, are extractions of all the teeth distal to the canines. In addition to extraction, all quadrants are flapped and a bur is used to remove a trough of bone where the roots were, thus removing most of the keratinised gingiva, periodontal ligament and periradicular alveolar bone. In those non-responding, all teeth are removed. When extracting the teeth meticulous attention must be paid that, all tooth substance is removed. Intraoral radiographs should be taken before and after surgery. Additionally, the alveolar socket should be “smoothed down” with a high-speed drill bur before resuturing the gingiva. Postoperative application of flucinonide 0.05% (Lidex Gel) to the gingival margin helps in the healing process.
  • Drugs
Antibiotics – most antibiotics have been trialled in chronic gingivitis in cats. Good responses are usually seen with broad-spectrum classes of drugs, including clindamycin, Metronidazole, amoxicillin, ampicillin, enrofloxacin and tetracycline
Steroidal anti-inflammatories – corticosteroids such as Prednisolone, Methylprednisolone acetate have been shown to be beneficial in the short term (6-12 months).
Non-steroidal anti-inflammatory drugs – daily doses of Metacam and its generic offspring have been trialled with good results in long-term pain and disease management in chronic gingivitis.
Immunomodulatory drugs – Gold Salts (Solganol: Shering 1mg/kg im every week until improvement (up to four months) then every 14-35 days), Megestrol acetate 1mg/kg, levamisole, cyclophosphamide, Cyclosporin-A, chlorambucil, Bovine Lactoferrin, and CO2 laser therapy have been used with inconsistent long term results.

Lack of permanent response to conventional oral hygiene, antibiotics, anti-inflammatory drugs, and immunosupressives is typical[20][21].

In mild cases of gingivitis that respond to corrective dental hygiene (descaling, antibiotics, etc), prognosis is good. In chronic gingivitis and lymphocytic-plasmacytic stomatitis, full dental extractions are required, and in many cases, euthanasia is necessary despite aggressive therapy.


  1. ↑ Gaskell RM, Gruffydd-Jones TJ (1977) Intractable feline stomatits. Veterinary Annual 17:195-199
  2. ↑ Gaskell RM, Bennet M (2001). Doenças Infecciosas Felinas In Dunn JK. Tratado de Medicina de Pequenos Animais pp:953-978
  3. ↑ Gruffyd-Jones TJ (1991). Gingivitis and Stomatitis. In August JR. Consultations in Feline Internal Medicine Vol 3 pp:397-402
  4. ↑ Andrade, M (2002) Antiinflamatórios esteroidais. In Spinosa HS, Górniak SL, Bernardi MM: Farmacologia aplicada à medicina veterinária. Rio de Janeiro, Guanabara Koogan, pp:240-252
  5. ↑ August JR (1992), Moléstias virais felinas. In: Ettinger SJ: Tratado de Medicina Interna Veterinária. 3 ed. São Paulo p 340-6.
  6. ↑ Barlough JE, et al (1991). Acquired immune dysfunction in cats with experimentally induced feline immunodeficiency virus infection: comparison of short-term and long-term infections. Journal of Acquired Immune Deficiency Syndrome 4(3):219-27
  7. ↑ Barr MC, et al (2000). Exogenous glucocorticoids alter parameters of early feline immunodeficiency virus infection. Journal of Infectious Diseases 181(2):576-586
  8. ↑ Holzangel E, et al (1998) The role of in vitro-induced lymphocyte apoptosis in feline immunodeficiency virus infection: correlation with different markers of disease progression. Journal of Virology 72:9025-33
  9. ↑ Knowles JO, Gaskell RM, Gaskell CJ, Harvey CE, Lutz H (1989). Prevalence of feline calicivirus, feline leukemia virus and antibodies to FIV in cats with chronic stomatits. The Veterinary Record 1:336-338
  10. ↑ Harvey CE (1991) Oral inflammatory diseases in cats. Journal of American Animal Hospital Association 27:585-591
  11. ↑ Harvey CE (1994) Oral and dental diseases. In Sherding RG. The Cat: Diseases and Clinical Management 2nd Ed: pp:1117-1151
  12. ↑ Beebe AM, Dua N, Faith TG, Moore PF, Pedersen NC, Dandekar S (1994). Primary stage of feline immunodeficiency virus infection: viral dissemination and cellular targets. Journal of Virology 68:3080-91
  13. ↑ Bendinelli M, et al (1995) Feline immunodeficiency virus: an interesting model for AIDS studies and an important cat pathogen. Clinical Microbiology Review 8:87-112
  14. ↑ Ceballos-Salobrena A, et al (2000). Oral lesions in HIV/AIDS patients undergoing highly active antiretroviral treatment including protease inhibitors: a new face of oral AIDS? AIDS Patient Care 14:627-635
  15. ↑
  16. ↑ Dowers, KL et al (2010) Association of Bartonella species, feline calicivirus, and feline herpesvirus 1 infection with gingivostomatitis in cats. JFMS 12:314-321
  17. ↑ Belgard S et al (2010) Relevance of feline calicivirus, feline immunodeficiency virus, feline leukemia virus, feline herpesvirus and Bartonella henselae in cats with chronic gingivostomatitis. Berl Munch Tierarztl Wochenschr 123(9-10):369-376
  18. ↑ Hartmann K (2005). Feline immunodeficiency virus and related diseases. In Ettinger SJ & Feldman EC. Textbook of Veterinary Internal Medicine 6th Edn: pp:659-662
  19. ↑ Hartmann K (1998) Feline immunodeficiency virus infection: an Overview. The Veterinary Journal 155:123 – 137
  20. ↑ Cohn LA (1997). Glucocorticosteroids as immunosuppressive agents. Seminars in Veterinary Medicine and Surgery (Small Animal) 12:150-156
  21. ↑ Daniel AGT, Reche Jr A (2005). Oral bacteria from cats with gingivitis and feline immunodeficiency virus. Online Journal of Veterinary Research 9:74-78

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