Diseases of the feline oral cavity (Proceedings)

This lecture will be focusing on inflammatory diseases of the feline oral cavity. For the most part, these diseases can be diagnosed and treated in the general practice. The diseases we will discuss are periodontal disease, odontoclastic resorptive lesions, and gingivostomatitis.

When working up inflammatory diseases in the cat, it is important to know that at various stages of the disease process, they can display pathogenic behavior that is similar when compared to one another. Hence, diagnosing these diseases requires a wide variety of diagnostic tests and a thorough patient history. Finally, with all of these diseases, submitting tissue samples for histopathological analysis is a vital tool towards piecing together the diagnostic puzzle.

Treatment of these diseases requires a multimodal approach. This approach involves home care, medical therapy and surgical intervention. Oral hygiene provided by a good home care regimen can prevent or slow the progression of the inflammation. Medical therapy uses antibiotics, antimicrobials, antiseptics, antiinflammatories and antivirals. Surgical intervention usually means extraction in these cases.

Periodontal Disease

The first disease we will explore is periodontal disease. The pathogenesis of periodontal disease is pretty much the same when compared with the dog. In the cat, there are a couple of interesting manifestations of this disease.

Periodontal disease affects 85-95% of cats over 2 years of age Persians, Maine Coons, Burmese and Siamese tend to be more prone to early onset or severe periodontal disease. Geriatric, immunocompromised, or patients suffering from chronic systemic disease have a more difficult time fighting the disease.

Pathogenesis of Periodontal Disease

Pellicle - the oral cavity is a constantly moist environment. The pellicle is a thin film consisting of salivary proteins and glycoproteins. The pellicle protects and lubricates. Pellicle deposition occurs immediately after a dental cleaning. As the pellicle ages, it gives the oral bacteria a surface to adhere.

Dental Plaque - as bacteria colonize on the pellicle, it forms a biofilm on the inert surfaces of the tooth, namely the crown and becomes mature plaque. It forms within 24 hours of a dental cleaning. It is difficult to see but can be visualized using a plaque disclosing solution. The biofilm thickens as the aerobic bacteria consume oxygen and multiply, making the environment more suitable for anaerobic bacteria. An important thing to remember here is that dental plaque is not a disease, but is the cause of periodontal disease. Plaque that is allowed to accumulate will result in gingivitis.

Dental calculus - dog and cat mouths, unlike humans are slightly alkaline, an environment in which calcium salts are more likely to be deposited. Calcium carbonate and calcium phosphate salts are found in the salivary fluid. These calcium products crystallize on the surface of the teeth and mineralize the soft plaque. Calculus contributes to periodontal disease by keeping the plaque in close contact with periodontal tissues. The formation of dental calculus takes 2-14 days. The deep crevices along the surface of the calculus promote further growth of anaerobic bacteria because oxygen is low to unavailable. Calculus cannot be removed except by mechanical action (hand or power scaling).

Gingivitis - plaque extends subgingivally and the mixture of bacteria and cell degradation products become destructive on the periodontal soft tissues and inflammation occurs and gingivitis develops. Sulcus depths are usually normal. There are two forms of gingivitis - acute gingivitis and chronicgingivitis. Acute gingivitis is presents with red, swollen gums that easily bleed. Chronic gingivitis has calculus and plaque present with halitosis being the main complaint. Gingivitis is considered reversible, meaning that once the bacterial laden dental plaque is removed, the inflammation disappears. Not all sites with gingivitis proceed to periodontitis. Gingivitis can become more severe in patients with local or systemic conditions.

Periodontitis - inflammatory destruction of the coronal part of the periodontal ligament allows the apical migration of the bacteria. This causes the destruction of the periodontal attachment tissue (periodontal ligament, alveolar bone). In order to make a diagnosis of periodontitis, bone loss must be present. Periodontitis can have active and quiescent periods, which explains why you could see some teeth with root exposure or increased periodontal pocket depth, but no inflammation

Pathogenic bacteria cause the body to activate immune and non-immune reactions that are responsible for the tissue damage. It is the host response to plaque bacteria and not the virulence of the bacteria that causes the tissue damage. So, all cats will develop plaque, but not all will that plaque develop into periodontitis.

Purebred Cats and Periodontal Disease

In certain purebred cats there are unique forms of periodontal diseases.

Juvenile hyperplastic gingivitis - this commonly affects Abyssinian and Persian kittens. The patient will present with proliferative tissue that covers the teeth. This condition appears at 6-8 months of age. The lesions cause the patient to have difficulty chewing and brushing the teeth is hindered. The treatment is to perform a gingivectomy on the proliferative tissue with submission of a tissue sample for histopath.

Juvenile early onset gingivitis - this condition is seen in the deciduous and permanent dentition of young Persians. The sign is an erythematous line along the gingival margin that extends from the incisors to the molars. The treatment for this condition is regular professional cleanings and rigorous home care

Juvenile early onset gingivitis-periodontitis - this is commonly seen in Maine Coons, Siamese, and DSH kittens. The teeth will have heavy deposits of plaque and calculus with red and swollen gingiva. You will see on oral examination attachment loss, periodontal pockets, gingival recession and bone loss. The gum tissue bleeds so difficulty chewing will be expected. As in the previous disease professional cleanings and rigorous home care are advised in order to slow the progression of this disease. Some cases will not respond to treatment and extractions with oral biopsies will need to be performed.

Odontoclastic Resorptive Lesions (ORL)

Introduction

Since most of the current research focuses on cats, this discussion will also focus on cats. Feline odontoclastic resorptive lesions or FORLS are one of the most common oral lesions seen in the cat mouth. During the oral exam these lesions are usually seen on the buccal and labial tooth surfaces at the cementoenamel junction with granulation tissue filling the affected area. The maxillary and mandibular third premolars, the maxillary fourth premolar and the mandibular first molar are the most commonly affected teeth with the canines and incisors being less commonly affected.

Etiology, Predisposition

While there are countless volumes of research on this topic, the etiology of this disease is unknown. The research thus far has shown that FORLs are seen in cats starting at 2 years of age. It affects 25-75% of cats.1 The number of lesions increases with age. There is also no clear breed disposition, except that there may be a higher occurrence in purebred cats with longhaired Persians and Siamese being at the forefront. Neutering is also not found to be a factor. There has been an increase in the prevalence of FORLs since the 1970s. It is thought that with the domestication of the cat, which has brought changes in diet, neutering and vaccinations that this has had an influence on feline tooth development, causing the tooth surface to be less resistant to resorption.6 There is also some new research that is looking into the role of hypervitaminosis D causing root surface, and periodontal changes which could alter the resorption inhibiting capabilities of the root surface.

Progression

Normal odontoclastic activity is seen with the resorption of deciduous tooth roots preceding exfoliation. Odontoclastic resorptive lesions are a form of external and internal root resorption. Odontoclastic activity occurs on the surface of the cementum and in the dentinal layer which is adjacent to the pulp chamber.

The disease starts in the hard tissues of the root surface or cementum. Normally, the external covering of the root has a resorption inhibiting characteristic. It can be said that some form of trauma might be causing damage to the periodontal ligament and the cementoblast layer and trigger resorption at the site of injury.6 Hence, in order for odontoclastic activity to occur, a part of the protective covering must be missing and, secondly something must provide a stimulus. These defective areas on the surface become mineralized which can attract odontoclasts.

Resorption in the cementum progresses to the dentin and spreads via the dentinal tubules and thus eventually involves the pulp, the dentin of the crown and then the crown. The enamel of the crown either resorbs or loses its attachment to the previously intact dentin and fractures off. Hence, when one sees the lesions in the mouth on oral exam, we are in the late stages of the disease.

The resorption phase is self limiting. When the resorption stops, the cells from the periodontal ligament deposit bony reparative dental tissue to replace the lost dentin. This causes a fusion between root and bone called ankylosis. As this reparative phase progresses, the contour of the root becomes more and more irregular or disappears leaving "ghost roots."

Classification

Lesions are graded by severity in 5 levels. The grading system is useful for developing a treatment plan. An accurate classification of a resorptive lesion is attained through a combination of a thorough oral exam and dental radiographs.

Class 1 - cementum only

Class 2 - cementum and dentin

Class 3 - cementum, dentin and pulp chamber, crown intact, bleed when probed, painful.

Class 4 - extensive tooth damage, ankylosis of roots

Class 5a- no crown remaining, gingiva is in various stages of repair over the former tooth site.

Class 5b- crown may be present with extensive root replacement resorption

Recently there has been a further diagnostic typing of ORLs in order to help match the correct treatment option with the lesion.

Type 1 - seem to have infection or inflammation associated with them. The roots are not resorbed and show normal root radiodensity.

Type 2 - inflammation is minimal with occasional hyperplastic gingiva or granuloma. On radiographs, these lesions show generalized root resorption by increased radiopacity of the roots. When this is evident, the root is being replaced by cementum like tissue which eventually converts to bone.

Diagnosis

An accurate diagnosis and classification is achieved through a combination of a good history, visual inspection, examination using a dental explorer and radiographs.

Patients will present with multiple clinical symptoms or no symptoms. Symptoms can include dysphagia, ptyalism, anorexia, dehydration. The owner may see symptoms such as head shaking, sneezing, dropping food or outright refusal to eat or hissing and/or running from the food bowl when attempting to eat. The pain associated comes from the exposed dentinal tubules and pulpal irritation.

With the patient under anesthesia, the teeth can be thoroughly inspected. Plaque and dental calculus need to be removed, because lesions can be hidden underneath. The lesions will most likely be found at the cementoenamel junction. Defects in the enamel, dentin and cementum are found using the dental explorer. The explorer will make a "pinging" sound as it catches on the edge of the lesion. Granulation tissue can also be found filling the lesion. It is important to remember that lesions that are found clinically usually mean that the tooth is in the late stages of the disease process. Radiographs must be taken in order to evaluate the extent of the disease.

Radiographic evaluation includes the assessment of the lamina dura which surrounds the root of the tooth. The lamina dura of ORL affected teeth seems to disappear, and in advanced cases the root will also be involved.10 On the radiographs, FORLs are visible as notched radiolucencies with sharp or scalloped margins at the cementoenamel junction and/or in the furcation. During the reparative phase you might see dentoalveolar ankylosis between the root and the alveolar bone which would indicate that the root dentin is being replaced by bone. Very late stage FORLs cause the tooth to appear moth-eaten or striated.

Treatment

Odontoclastic resorption is a progressive disease. At this time there is no known treatment that stops the progression. The current treatment options are conservative management, tooth extraction or coronal amputation.

Conservative management is done on those lesions that are not able to be found on examination, but are rather seen on radiograph on a patient that is not exhibiting any pain. This treatment involves regularly monitoring the lesions clinically and radiographically.

Extraction is the treatment of choice with resorptive lesions. You must take radiographs before attempting the extraction. A full tooth extraction can only be done easily if there is an intact root and periodontal ligament. Extraction gets more and more difficult as the dentin and periodontal ligament are destroyed. The tooth becomes fragile and hence you are usually dealing with extracting the tooth in fragments. An option for extraction was to pulverize the root tips using a high speed handpiece. This technique has been found to not completely remove root tips, damage the alveolar bone, injure the neurovascular bundles, possibly cause sublingual emphysema, air emboli, and salivary extravasation syndrome and may transport root remnants into the mandibular canal or nasal cavity.6

In the case of a Class 5 FORL where the gingiva has healed over the root remnants, if there is no periapical pathology and the gingiva is not inflamed, the roots can be left where they are.

Coronal amputation with intentional root retention is used when the tooth roots become incorporated into the alveolus or are being incorporated into bone. This can only be seen on radiographs. This procedure involves raising a mucogingival flap, amputating the crown to just below the level of the alveolus and replacing and suturing the flap. This procedure needs regular radiographic monitoring to ensure the roots are resorbing and the amputation site is healing. Contraindications for this procedure are the presence of periodontal disease, presence of endodontic disease, and no evidence of stomatitis. If these conditions are present, a full extraction must be performed.

In conclusion, statistically one-third of all domestic cats may develop FORLs during their lifetime. As the cat ages, their chance of developing the disease increases. We can assume that this disease may cause discomfort. The aim of treatment is to stop the progression before suffering can occur. The veterinary technician should be able to recognize the symptoms and signs perform the testing needed to classify these lesions, and assist in the carrying out of the treatment plan and follow up contacts.

Gingivostomatitis

Gingivostomatitis is the chronic active inflammation of the mucosa and submucosa. The disease presents with erythematous, ulcerative and/or proliferative lesions. Lesions are commonly found on the gingiva, buccal mucosa, lips, palatal glossal folds, lateral pharyngeal walls, and the lateral aspects of the tongue.

Etiology and Predisposition

The etiology of this disease is currently unknown. Bacterial, viral, and immunological causes are being investigated, namely plaque bacteria, calicivirus, herpes, coronavirus, Hemobartonella henseale, FeLV, FIV, and immune reaction.

There is no sex, age, or breed predilectation, but purebred cats such as Persians, Abyssinians, Siamese, Burmese and Himalayans develop a more severe form of the disease. The median age is 7 years.

Clinical Presentation

The most common symptoms of patients that suffer from this are: halitosis, blood-tinged saliva, ptyalism, and dysphagia, difficulty opening the mouth and weight loss. These cats also become less active, are reluctant to groom themselves and can show signs of aggression.1 It is important to remember that these patients are painful and caution must be taken when performing the oral exam.

There are two types of this disease. Type 1 is almost congenital and signs begin to appear as soon as the deciduous teeth erupt. This form continues through life. It is believed that the condition is passed transplacentally or is a hereditary immune condition. Type 2 presents at around 7 years of age and continues through life.

Diagnostics

Prior to treatment, it is important to get a thorough history from the owner to establish a timeline and assess any previous treatments. Bloodwork should consist of CBC and serum chemistry. This will establish a baseline, as some of the drugs that will be given will need to be monitored to assess their effects on the body and their levels in the bloodstream. Testing for the presence of FeLV, FIV, Calicivirus, and Hemobartonella henselae can rule out other causes which may hinder control.

Treatment11

The goal of therapy is to control the disease. The response to the disease is temporary and relapses are normal.

Dental therapy - since the presence of plaque bacteria may stimulate the inflammation, providing regular dental cleanings to regularly remove the plaque bacteria with home care can provide temporary comfort.

Treatment of teeth with ORL - since these lesions can also be caused by inflammation, treatment of these teeth by extraction is indicated.

Gingivoplasty - if the proliferative form of this disease is present, removal of the excess tissue is beneficial.

Antibiotics - effective antibiotics are azithromycin, amoxiciilin, amoxicillin/clavulanic acid, metronidazole and doxycycline. The choice of the antibiotic should be based on the results of your diagnostic testing. Treatment will last several weeks.

Corticosteroids - these are beneficial about 70-80% of the time. They should be given over a 4-6 month period gradually decreasing the amount until the lowest effective dose is reached.

Pain management - analgesics such as buprenorphine, butorphanol, and fentanyl patches will bring some comfort.

Secondary therapies - the use of gold salts, immunostimulants like alpha interferon, bovine lactoferrin, shark cartilage, laser surgery to remove inflamed tissue, and immunosuppressant drugs such as azathioprine and cyclophosphamide.

Tooth extraction - this should be considered when medical treatment is no longer bringing any improvement to the patient. The aim of surgical treatment is to remove plaque bacteria and to treat any diseased teeth in order to decrease inflammation. It is important to note that it is impossible to remove all plaque bacteria from the mouth permanently. The bacteria along the base of the tongue are enough to cause an inflammatory response. In general, 60% of these cases will have complete resolution, 20% will have minimal inflammation, 13% will have partial improvement but will require continued medical therapy, and 7% will show no improvement.

Tooth Extraction Procedure

The majority of the inflammation occurs along the premolar and molar teeth. The procedure can be staged extracting only the teeth that have inflammation.

Pre and post-operative radiographs must be taken to plan the extraction procedure for each tooth. All roots must be removed. Provide multimodal pain management using nerve blocks and injectable medications. Remove any proliferative tissue. Any teeth that will be left behind must be cleaned, polished and flushed with an oral antiseptic.

All extraction sites must be closed with an absorbable monofilament suture material.

If the patient is having any difficulty eating, place an esophagostomy feeding tube. This will allow food and medications to be given during the healing process. Pain management and antibiotic therapy should be provided at home. Once the patient is eating comfortably and taking in the daily required amount of food, the tube can be removed.

A recheck appointment should be planned at 1 month and at 3 months. At the 3 month recheck, one should have a good idea about how the patient will react to the treatment. If teeth are left behind, 6 month recheck exams +/- dental cleanings should be done. Rigorous home care must be practiced between visits once the mouth has healed. It can take up to 2 years to know what the full response will be.

Conclusion

While inflammatory diseases of the feline oral cavity are difficult and sometimes frustrating to treat, research has brought some promising new treatment protocols. These new protocols have given our feline patients a more pain free life.

References

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2. Roudebush, P., Logan, E., & Hale, F. (2005). Evidence based veterinary dentistry: a systemic review of homecare for the prevention of periodontal disease in dogs and cats. J Vet Dent, 22 (1), 6-15.

3. Gorrel, C., & Derbyshire, S. (2005). Periodontal disease. In Veterinary Dentistry for the Nurse and Technician (pp. 69-85). Edinburgh: Elsevier Butterworth Heinemann.

4. Harvey, C. (2005). Management of periodontal disease: understanding the options. Vet Clin North Anim Small Anim Pract, 35 (4), 819-836.

5. DuPont, G. (1995). Crown amputation with intentional root retention for advanced feline resorptive lesions - a clinical study. J Vet Dent, 12 (1), 9-13.

6. Reiter, A., & Mendoza, K. (2002). Feline odontoclastic resorptive lesions: an unusual enigma in veterinary dentistry. Vet Clin Small Anim, 32, 791-837.

7. Okuda, A., & Harvey, C. (1992). Etiopathogenesis of feline dental resorptive lesions. Feline Dentistry: Vet Clin Small Anim, 1385-1404.

8. Gorrel, C. (2004). Odontoclastic resorptive lesions. In Veterinary Dentistry for the General Practitioner (pp. 119-128). Edinburgh: Saunders.

9. DuPont, G. (2005). Radiographic evaluation and treatment of feline dental resorptive lesions. Vet Clin Small Anim, 35 (4), 943-962.

10. Lyon, K. (2006). Odontoclastic resorptive lesions. In e. August JR, Consultations In Feline Internal Medicine, volume 5 (pp. 67-80). St Louis: Elsevier Saunders.

11. Wiggs, R. (2006). Lymphocytic plasmacytic stomatitis. In e. Noseworthy GD, The Feline Patient, 3rd edition (pp. 631-633). Ames: Blackwell.