Feline chronic gingivostomatitis (FCGS)
Diane D. Addie
This lecture has 4 sections with 4 key messages:
1. Feline chronic gingivostomatitis (FCGS) is NOT the gingivitis associated with ordinary tooth decay and is NOT juvenile periodontitis. It IS a refractory immune-mediated inflammatory condition involving the gingivae and the palatoglossal folds.
2. The aetiology is complex, the role of feline calicivirus(FCV) uncertain, and, in my view, the role of nutrition is underestimated and all cats with gingivitis should be taken off from cereal-based cat foods, at least until they are healed
3. Many treatments may need to be attempted, but CORTICOSTEROIDS SHOULD BE AVOIDED.
4. Avoid vaccinating cats with FCGS with live FCV vaccines
Oral disease is one of the commonest reasons cats are presented to veterinarians
Periodontal disease is a common oral disease in cats. In the United States, the two most common disorders reportedfor cats examined at private veterinary practices weredental calculus (24.2% of cats) and gingivitis (13% of cats).Also, it has been reported that 70% of cats in the age range of20 –27 mo have signs of periodontal disease. (Ingham et al, 2002)
Periodontaldisease is a plaque-induced inflammatory disease of the sup-
porting tissue of the tooth and includes both gingivitis andperiodontitis. If plaque is left undisturbed, gingivitis developsrapidly. Gingivitis is reversible if plaque is removed from thetooth surface. If gingivitis is left untreated, the cat may develop periodontitis. Periodontitis is irreversible and involvesthe destruction of the periodontal ligament and the alveolarbone. This leads eventually to tooth loss. Periodontal diseasein the cat is a debilitating condition and severely affected catsare reluctant to eat or drink. (Ingham et al, 2002)
What feline chronic gingivostomatitis IS NOT
FCGS is NOT ordinary dental disease with tartar and calculus
Ordinary dental disease – i.e. calculus - isrelatively easily cured by doing a dental: removing decayed and loose teeth, scaling the tartar off the others and giving broad spectrum antibiotics pre and post-operatively to prevent bacteraemia and bacterial endocarditis.[1]
Mild or moderate concurrent dental disease was found in 71% of FCGS cases (Healey et al, 2007) so how does one differentiate ordinary dental disease from FCGS? In the latter, the extent of gingivitis is exaggerated relative to the amount of tartar present, and the palatoglossal folds may be involved. In addition, FCGS cases continue to suffer from inflamed gingivae after the routine dental procedure.
FCGS is NOT juvenile periodontitis
Juvenile onset gingivitis-periodontitis appears in cats less than 9 months of age. Initial signs occur just before or at the time of eruption of the adult teeth (Williams and Aller, 1992) and may be noted at time of presentation for vaccination or neutering, as a thin red line along the margin of the gums or as a more severe gingivitis.
Williams and Aller (1992) noticed a breed predilection in Siamese, Maine Coon and domestic shorthair cats.
Less severe cases may spontaneously regress. Addie documented recovery of one Somali kitten on changing the food from cereal-based dry foods to a mixed wet and meat-based dry food (Applaws, MPM products, Cheshire, UK) in a YouTube video ( Some cases respond favourably after removal of any retained deciduous teeth and plaque. However, these cases can progress to FCGS.
FCGS is NOT feline juvenile hyperplastic gingivitis
Juvenile hyperplasticgingivitis appears in cats less than 9 months of age, often first appearing at the time of eruption of the adult teeth (Williams and Aller, 1992). Williams and Aller (1992) noticed a breed predilection in Abbysinnians and Persians. These cases require gingivectomy to eliminate the pseudopockets formed by the gingical hyperplasia (Williams and Aller, 1992). Teeth with resorptive lesions will require removal.
What feline chronic gingivostomatitisIS
Feline chronic gingivostomatitis (FCGS or FCGS), also sometimes referred to as lymphocytic plasmacytic gingivitis and/or stomatitis, faucitis or pharyngitis is a painful inflammatory condition of the palatoglossal folds (fauces) with or without involvement of the gingivae.
Stomatitis is where the inflammation extends beyond the mucogingival junction into the oral mucosa and in which, as well as hyperemia, oedema and bleeding, there may also be proliferation of granulation tissue. (Williams & Aller, 1992) Most authors agree that a diagnosis of FCGS usually requires involvement of the palatoglossal folds (sometimes referred to as the fauces). Other areas that can be affected are the palate, pharynx, tongue and lips (Healey et al, 2007). Dental disease is completely absent in 29% of FCGS cases, and only mild to moderate where present. (Healey et al, 2007). The immune response of a cat with FCGS is abnormal, with an imbalance in the inflamed gingivae and palatoglossal folds towards a mixed Th1 and Th2 instead of a predominantly Th1 response (Harley et al,1999)
Clinical signs, generally caused by the inflammation which induces pain when opening the mouth, are dysphagia, weight loss, loss of grooming behaviour, ptyalism (excessive salivation), pawing at the mouth and halitosis (Dolieslageret al, 2011). In one study some cats suffering from FCGS were extremely fractious, likely due to the pain from which they were suffering: they returned to their “normal” personalities as their lesions healed(Addie, unpublished observation). Thus such cats may first be presented as behaviour problem cases rather than as dental cases.
The prevalence of FCGS in the UK is 0.7% (Healey et al, 2007). Although any age of cat can be affected, Healey et al(2007) noticed two age peaks: between 1 and 4 years of age, and between 10 and 13 years of age. Male and female cats were equally likely to be affected.Although Healey et al (2007) noticed no breed predisposition, Maine Coon cats seem to be predisposed to FCGS (Addie unpublished observation).
Many cats suffering from FCGS are euthanased due to refractoriness to treatment and possibly because of aggressive behaviour due to the extreme pain of their mouths.
The aetiology of FCGS is complex and multifactorial: a brief summary is presented in table 1.
Does feline calicivirushave to be present to diagnosefeline chronic gingivostomatitis?
The short answer to this question is no – FCV does not have to be present to make a diagnosis of FCGS. FCV was present in a great many cats without FCGS (10 – 25% in cats visiting veterinary surgeries and at cat shows (Coutts et al 1994; Porter et al, 2008) and absent in 46% (Belgard et al) and 30% (Harbour 1991) of cats with FCGS.
The question of the role of FCV in the aetiology of FCGS remains: is FCV a causal organism or merely an opportunistic pathogen? Recovery from clinical signs coincided with cessation of FCV excretion (Addie et al, 2003). However, strains of FCV taken from FCGS cases were unable to reproduce the disease in specific pathogen free cats (Knowles et al 1991) thus FCV fails to fulfil Koch’s postulates.
The question remains – is FCV a causal organism or merely an opportunistic pathogen? What is clear is that the presence of FCV in FCGS cases is not to their benefit: Dolieslageret al (2013) stated: “A positive correlation was observed between clinical disease severity and the presence of FCV (p=0.001).” In addition, there are growing numbers of reports of clinical response to recombinant interferon omega therapy (Leal et al, 2013; Mihaljevic 2003; Mihaljevic 2004; Southerdenet al, 2007) though it is not clear whether this is due to its anti-viral or anti-inflammatory activity, likely both.
The role of food in the aetiology of FCGS is underestimated
Food is a very important feature in this condition: prior to the recovery of one case, the cat had been changed to Classic Cat Food (Addie et al, 2003). In addition, after dentistry, cats fed on Hills a/d diet gained more weight and had smaller lesions than those fed on a control diet (Theyseet al, 2003). A FCGS-recovered cat can be made to relapse by feeding him on some dry food such as Friskies or Royal Canin, and to recover again when those foods are withheld (Addie, unpublished observation). The possible explanations are:
1. Allergy / intolerance to some component
2. Micronutrient deficiency
3. Omega 6:3 ratio
4. Exposure to toxins
Many of the larger cat food companies uses poor quality, cereal based, protein in their foods (Hodgkins 2007). Most pet food is made by a process called extrusion, which was developed decades ago to make puffed breakfast cereals. ( When I visited a pet food manufacturer in England, I was shocked to learn that almost all pet foods were the same, basic, kibble. I was told that individual brands differed only in a mix that is sprayed onto the kibble at the penultimate stage of manufacture: just before packaging. Thus high end, expensive veterinary brands sat side by side with the cheapest supermarket own brands, a huge difference in price, a small difference in whatever was sprayed on to the same basic, carbohydrate kibble. The plant had to shut down, clean out the machines and put in a completely different set of contents for just two brands: Applaws and Almo Nature.
1. Allergy / intolerance to some food component
Contact allergy is recognised as a cause of human gingivostomatitis, (Endo & Rees, 2006). Ironically,the culprit isoften cinnamon in toothpaste or chewing gum. Most modern cat food is completely unnatural and completely processed: is it not possible that some component is triggering allergic responses in cats?
2. Micronutrient deficiency
The most famous micronutrient deficiency resulting in gingivitis is surely scurvy of the human, resulting from vitamin C deficiency? However cats, unlike humans and guinea pigs, can make their own vitamin C. They do require a nutritional source of arginine though and arginine is essential for the healthy function of the immune system: cats evolved as obligate carnivores and I believe that although many of the nutritional needs of cats have been discovered, we do not yet know them all sufficiently to be able to fabricate a diet, based on cereals, which meets all of their nutritional needs. In addition, combinations of components can have unforeseen consequences, for example rice is often used in hyposensitive diets, but rice bran decreases taurine, (Stratton-Phelps et al, 2002) another essential amino acid for the cat (and dog), deficiency of which leads to dilated cardiomyopathy, blindness and infertility.
3. Omega 6:3 ratio
The imbalance of omega-6 to omega-2 polyunsaturated fatty acids in the modern human diet are widely accepted as a cause of the increase in chronic inflammatory diseases such as arthritis, asthma, and inflammatory bowel disease (Simopolous, 2008). Corbeeet al (2012) hypothesized that a catfoodwith an omega-6 polyunsaturated fatty acid (ω6 PUFA) to ω3 PUFA ratio of 10:1 would reduce inflammation of the FCGS and accelerate soft tissue wound healing of the gingiva after dental extractions, compared to a catfood with a ω6:ω3 PUFA ratio of 40:1. The cats were fed diets with chicken fat and fish oil as sources of fatty acids. In one diet, part of the fish oil was replaced by safflower oil, resulting in two diets with ω6:ω3 PUFA ratios of 10:1 and 40:1. This double-blinded study in two groups of seven cats revealed that dietary fatty acids influence the composition of plasma cholesteryl esters and plasma levels of inflammatory cytokines. The diet with the 10:1 ratio lowered some pro-inflammatory cytokine plasma levels significantly, compared to the diet with the 40:1 ratio. However, feeding diets with dietary ω6:ω3 PUFA ratios of 10:1 and 40:1, given to cats with FCGS for 4 weeks after extraction of all premolars and molars, did not alter the degree of inflammation or wound healing.The reasons for the lack of clinical response, in my view, are that 4 weeks isn’t long enough, and that the ratio wasn’t low enough: for example a ratio of 2.5:1 reduced rectal cell proliferation in patients with colorectal cancer, whereas a ratio of 4:1 with the same amount of omega-3 PUFA had no effect (Simopolous, 2008). Really the ideal is to get to about 1:1.
4. Exposure to toxins
Cats are uniquely sensitive to certain plant based toxins, notably phenols. Cats evolved with a uniquely carnivorous diet and, as a result of lack of exposure to plant-based toxins (phytoalexins), have presumably lost the need to metabolise these toxins via glucuronidation, which is common in most herbivores and omnivores (Shrestha et al, 2011). It is possible that a plant based (or other) toxin irritates the feline oral mucosa.Grains and cereals can be contaminated with mycotoxins. Most mycotoxins are stable under normal food processing conditions, including sterilization temperatures (120°C). Therefore, if the toxins are present in the raw material used for manufacture they will still be present in the kibble. (Hughes et al, 1999) Some manufacturers do screen deliveries of wheat and other grains for mycotoxinsprior to using it (Hughes et al, 1999) though it is possible that there exists some unrecognised toxin irritant to oral mucosa.
Table 1. The multifactorial aetiology of FCGS has not been clearly elucidated and the following have been implicated:
Possible instigator of FCGS / CommentsFeline calicivirus / Instigator or passenger? Present in up to 76% of cases.
Cat’s immune response / Shift from predominantly Th1 to mixed Th1 and Th2 in lesions
Food / Allergic or intolerant response to a food component: this is a recognised cause of human stomatitis
Micronutrient deficiency?
Omega 3:6 ratio – too much omega 6 in cereal based diets leads to a chronic pro-inflammatory state
Feline leukaemia virus (FeLV) / Belgard et al (2010) found no association. FeLV is immunosuppressive though, so while you need not test a FCGS cat for FeLV, it is wise to check the mouth of a FeLV positive cat for FCGS.
Feline immunodeficiency virus (FIV) / Present in ~5% of the general cat population and the FCGS population too. Belgard et al (2010) found no association. So you need not test a FCGS cat for FIV, but it is wise to check the mouth of a FIV positive cat for FCGS.At least 4 studies in FIV positive cats have shown a life span equal to uninfected cats.
Bartonellahenselae / The causative organism of cat scratch disease in humans: there are conflicting reports regarding its relevance in FCGS: e.g. Sykes et al (2010) found an association but Belgard et al (2010) found no association.
Tannerella forsythia(and other bacteria) / “Although the number of cats harbouring T. forsythia was low, 80% of samples in which it was present were from cases with the highest clinical disease severity” (Dolieslager et al, 2013).
Feline herpesvirus / Ruled out as a cause of FCGS, but steroid treatment or the chronic pain of the mouth in FCGS cats can cause recrudescence of latent FHV in FCGS cases, causing secondary ocular signs, such as serous discharge, conjunctivitis.In all refractory conjunctivitis and nasal discharge cases, I recommend checking the mouth as a source of underlying chronic stress.
Leishmaniainfantum / “Clinical manifestations compatible withfelineleishmaniosis include lymph node enlargement, skin and mucocutaneous lesions, ocular lesions,chronicgingivostomatitis, hypergammaglobulinemia, and normocyticnormochromic anaemia.” (Pennisi 2015)
Diagnosis
Biopsy is the definitive diagnostic technique and helps differentiate FCGS from possibly similar appearing lesions such as squamous cell carcinoma or eosinophilicgranuloma. Virus isolation is the method of choice to detect FCV (PCR is less reliable because FCV is an RNA virus, so it is more difficult to design primers and probes which will detect all isolates.) Obtain three negative tests a month apart before declaring the cat FCV free. Cats with FCGS can be unusually fractious (Addie, manuscript in preparation) and clipnosis can help you obtain a sample without recourse to using a sedative (Pozzaet al, 2008).
Treating FCGS
See table 2. At the outset of treating FCGS, it is vital to give the client realistic expectations – to explain that there currently is no single cure for this condition and that you may have to attempt many different strategies before a successful outcome is established. Owners are more likely to elect for euthanasia if they perceive the problem to be intractable or to change veterinary surgeons if they have not been warned in advance that you will likely have to try more than one treatment. It is often a good idea to prepare a practice leaflet explaining the procedure.
Full dental extraction, antibiotics and non-steroidal anti-inflammatory drugs
The only treatment to claim a high cure rate (about 80%) remains full dental extraction by a specialised veterinary dentist. However, the risk of iatrogenic damage to the eyes has to be considered (Smithet al, 2003). Non-surgical treatment is aimed at trying to eliminate FCV, if present; shifting the immune response back to type 1 and restoring normal mouth flora (healthy cat’s mouths have predominantly Pasteurellamultocida, cats with stomatitis have abnormal flora, including, in cats most severely affected,Tannerella forsythia (Dolieslager et al, 2013), which, along withTreponema. denticola and Porphyromonasgingivalis, form a bacterial consortium, often referred to as the ‘Red Complex’, that is strongly associated with the clinical progression of chronic periodontitis (Dashperet al, 2011)). Rather creepily, identical strains of T. forsythia were isolated from a human and their cat, (Booij-Vrieling et al, 2010) so don’t kiss your cats unless your oral hygiene habits are excellent – we don’t want you infecting the little furries. Antibiotics of choice include cefavexin (Convenia, Pfizer) and clindamycin hydrochloride (Antirobe, Pfizer) although the latter must be used with caution as oesophagitis has been suspected after its use (as with many tablets in the cat) (Beatty et al, 2006).
Key message: DO NOT USE corticosteroids
Corticosteroids give a misleading initial response due to their ability to diminish pain and inflammation and increase appetite. However, the benefits are short-lived and adverse effects are far more serious and may disable the cat from ever being able to recover from FCGS. In his PhD study, Ross Harley found a “bounce back” effect of corticosteroid use: that not only did FCGS return but itcame back worse and more intractable following corticosteroids. These are some of the problems associated with corticosteroid use:
- corticosteroids thin the mucosal epithelium of the mouth, causing gums to be more friable and less able to withstand bacterial onslaught
- they decrease both Th1 and Th2 immune response, stopping the cat from ever clearing the FCV infection
- corticosteroids have been documented to induce feline infectious peritonitis in cats who were otherwise asymptomatically infected with feline coronavirus
- corticosteroid treatment of a dental case led to fatal leishmaniosis (Leivaet al, 2005)
- corticosteroids can re-activate dormant toxoplasma infection with fatal consequences
- corticosteroid treatment may lead to recrudescence of latent herpesvirus infection, causing conjunctivitis and upper respiratory tract signs
- long term use of corticosteroids predisposes to obesity
- long term use of corticosteroids predisposes to diabetes mellitus
Pain relief is essential