Feline Tooth Resorption (TR)
TRs are a very common malady. Reports vary as to their incidence, but approximately 60% of cats over 6 years of age have at least one, and those that have one typically have more. These lesions are caused by odontoclasts which are cells that are responsible for the normal remodelling of tooth structure. These cells are activated and do not down regulate, resulting in tooth destruction.
There are currently two recognized forms of resorptive lesions, type 1 and type 2. Clinically, they appear very similar, as dental defects that are first noted at the gingival margin. However, advanced cases will show significant tooth destruction and may appear to be a fractured tooth. The best diagnostic tool for differentiating between types is dental radiology. With type 1 lesions, there is no replacement of the lost root structure by bone, whereas with type 2 there is generally marked replacement of the lost tooth structure.
Type 1 TRs are typically associated with inflammation such as caudal stomatitis or periodontal disease. In these cases, it is thought that the soft tissue inflammation has activated the odontoclasts. The inciting cause of class lesions is a cemental defect. Odontoclasts move in and destroy the dentin, leading to secondary enamel loss and a resorption lacuna. The weakened crown will eventually fracture, and in these cases the root canal system stays intact resulting in continued pain and infection for the patient.
Type 2 lesions are generally seen in otherwise healthy mouths; however, the lesions will create local gingivitis. The etiology of type 2 TRs remains unproven. The two major current theories are abfraction injuries from eating hard food and excess vitamin D in the diet. Type 2 TRs show histological evidence of simultaneous repair of the defect by osteoblasts at the same time that tooth is being resorbed by odontoclasts.
Historically, restoration was a recommended therapy, however, due to the progressive nature of the disease; extraction is now the treatment of choice. Extractions can be very difficult in these cases due to tooth weakening and ankylosis. Additionally, in some cases, there is little to no tooth structure remaining. In cases with significant weakening and or ankylosis, performing the extractions via a surgical approach is recommended to speed the procedure and decrease the incidence of fractured and retained roots.
Recently, crown amputation has been suggested as an acceptable treatment option for advanced type 2 lesions as it results in significantly less trauma and faster healing than complete extraction. This procedure, although widely accepted, is still controversial. Most veterinary dentists employ this technique, however, in widely varying frequency. Veterinary dentists typically employ this treatment option only when there is significant or complete root replacement by bone. Unfortunately, the majority of general practitioners use this technique far too often. Crown amputation should only be performed on teeth with radiographically confirmed advanced type 2 TRs which show no peri-apical or periodontal bone loss. Crown amputation should not be performed on teeth with: type 1 TRs, radiographic or clinical evidence of endodontic or periodontal pathology, inflammation, or infection; or in patients with L/P stomatitis. Those practitioners without dental radiology capability should not perform crown amputation. In these cases, the teeth should either be fully extracted or the patient referred to a facility with dental radiology.
This is very similar to canine endodontics. However, true fractures are rare in any teeth except the canines. Teeth with direct pulp exposure are painful and/or infected and require root canal therapy or extraction. Root canal therapy is always recommended if possible as extraction of the maxillary canines is challenging and maxillary canine extraction carries a high risk of lip catching (see below).
There are two main differences between dogs and cats with regard to endodontic disease. First, the pulp chamber of the canine teeth extends very close to the cusp tip. This means that any fracture (no matter how small) is suspect for endodontic disease. Anesthesia for careful probing and dental radiographs should be performed for any fracture. Secondly, cats will tend to resorb the root apex when a tooth has a chronic infection.
Lip Trauma Following Maxillary Canine Extraction
In my experience, approximately 1/3 of cats that have maxillary cuspids extracted surgically will develop lip trauma from the mandibular canine. For this reason, we try to avoid extracting maxillary canines when possible preferring to perform root canal therapy or periodontal surgery if indicated.
Many of these cats will show no clinical signs, however, if the lip is examined, ulcers will be present. These cats are painful and are in need of therapy. Other patients may show mild to severe evidence of discomfort.
The options for therapy include coronal amputation and vital pulp therapy or extraction of the offending mandibular canine.
Case report: “Sid” had both maxillary canines extracted elsewhere due to periodontal disease. He presented with a complaint of having difficulty eating and the owner was concerned about a TMJ problem because of the way he moved his jaw after eating. Oral exam revealed significant trauma to the lips secondary to the mandibular canines.
The treatment was to perform coronal amputation and vital pulp therapy on the mandibular canines. This is much less painful for the patient and will maintain the strength in the rostral mandible.
Eosinophilic Granuloma Complex
The true etiology of these conditions is unknown; however, a local accumulation of eosinophils is thought to initiate the inflammation and necrosis. The accumulation may result from a local (food) or systemic allergies; although these lesions have been seen in cases where allergic disease has been ruled out. Additional causes include a response to irritation, such as chronic grooming or traumatic malocclusion. There may also be a genetic predisposition.
Indolent ulcers are the most common oral manifestation, and they will present as brownish-red lesions on the upper lip or around the maxillary canine teeth.
Linear granulomas can be single or multiple; the most common sites are the lips, gingiva, palate and tongue. They are generally non-painful, but can become secondarily infected. The typical presentation is a raised, lobulated yellow-pink mass; however, they can also appear ulcerative causing severe damage to the oral mucosa and underlying bone. This may lead to severe periodontal loss, pathologic fractures, or oronasal fistulas.
Histopathology should be performed to confirm the diagnosis. Following confirmation of the diagnosis, a thorough allergy evaluation should be conducted including food trial, flea treatment, +/- allergy testing.
The acute disease process is best treated with systemic corticosteroids; however, corticosteroids should not be used for long-term disease control due to the significant systemic side effects. The typical initial protocol is prednisone 2 mg/kg q 12 hours for 3–4 weeks. Additional options include intralesional triamcinolone (3 mg weekly) or methyl prednisone injections. Antibiotic therapy is required occasionally to induce remission and/or treat secondary infection. There are also cases that appear to respond to antibiotic therapy alone. Therefore, we initially treat mild cases with antibiotics alone and more severe cases with a combination of antibiotics and corticosteroids.
Many cases remain idiopathic, requiring lifelong therapy; options for this include antibiotics and cyclosporine. Fewer side effects may be expected with cyclosporine in comparison to steroids, but there are reports of opportunistic fungal and fatal protozoal infections associated with its chronic use. Use the lowest effective dose, and perform regular therapeutic levels and routine blood testing.
This is another frustrating oral inflammatory disease. The best description is a severe immune mediated reaction to dental tissues. Some feel that this may actually be a group of disease processes that look the same clinically which is why they can be very frustrating to treat.
The history will generally include anorexia, drooling, gagging, and pain during mastication. Physical exam will typically include a thin pet with unkempt fur. The oral exam will reveal severe stomatitis usually over all teeth. The inflammation will most commonly be worse on cheek teeth than canines and incisors. However, faucitis is the key clinical finding. Severe hyperplastic inflammation to the gingiva can result from periodontal disease, however faucitis will not be present.
A pre-operative blood panel will generally show a marked elevation in globulins (polyclonal gammopathy) and total protein.
Most medical therapies will work for a while, however, in general resistance will start within a year or less. In addition, most therapies have side effects worse than the disease process in and of itself. In general, medical therapy is very frustrating to the practitioner and client.
Corticosteroids are the mainstay of most medical therapy today. It is generally very effective at first and is relatively inexpensive for the client. In my experience, injectable (Depo-Medrol 10 mg IM) is much more effective than oral preparations in my experience. However, they will typically loose effectiveness after a year or so requiring higher and higher doses at shorter increments. This generally results in significant deleterious effects. About 10% of stomatitis cases we treat are already diabetic!
Antibiotics are safer than steroids but much less effective, especially in long-term therapy. They are generally disappointing in their success. Metronidazole and clindamycin are the mainstays of therapy; however Clavamox and amoxicillin can be used as well. Metronidazole may be the antibiotic of choice due to its anti-inflammatory effect.
Other immune suppressive such as Imuran, Cytoxan, Gold Salts, Cyclosporine have been used. However, they are all very expensive with numerous adverse side effects (myelosuppression). Cyclosporine is currently the most commonly prescribed immune modulatory drug (other than steroids) for this disease process. However, its chronic use is somewhat expensive and has been implicated in severe fungal and protozoal infections. Starting dose is 5–10 mg/kg. Look for a trough level of about 500 ng/ml on regular basis. In most dentists opinion it is only really effective after teeth are removed. However, it has shown promise in resistant cases.
Laser therapy is not proven at all, most clients and RDVMs are very unhappy with the long term results. It is very expensive and short-term relief only.
Extraction is currently the only effective long-term treatment for this disease process in cats. In our experience, the sooner this is done, the better that cats do both post-operatively as well as long term.
For extractions to be successful, the teeth must be completely removed. Therefore post-operative radiographic confirmation of complete extraction of the tooth roots is recommended. Following the insurance of complete removal of the teeth, perform alveoplasty to remove the periodontal ligament and smooth rough bony edges. This is typically performed do this with a rough diamond bur. Studies report a 60% success rate when all teeth caudal to the canines are extracted, however, our experience has not been as good. Whole mouth extractions have a success rate of approximately 90–95% for clinical remission. Slight faucitis may remain, but pets are comfortable. In addition, the rare cases that don’t completely respond are generally much more responsive to medical therapy. If there is no inflammation to the canines or incisors (which is rare), then the owner is given the option of leaving the canines. However, if these are inflamed, all teeth should be extracted.
In the rare cases where the teeth have been fully extracted but inflammation and pain continues, other therapies are needed. The current treatment of choice in the USA is cyclosporine. Another option, which appears to work better in Europe is feline interferon. Finally, UC Davis has had some success with stem cell therapy.
Feline Juvenile (Puberty) Gingivitis/Periodontitis
Juvenile periodontal disease is inflammation which occurs soon after permanent tooth eruption. This syndrome can be described in two categories, feline hyperplastic gingivitis and juvenile onset periodontitis.
The etiology of this condition is unknown. However, in humans there is a period of increased susceptibility to gingivitis during the pubertal period. A genetic predisposition towards feline juvenile onset periodontitis has been reported in Siamese, Somali, and Maine Coon cats.
Hyperplastic gingivitis appears as gingival enlargement and significant inflammation which is confined to the gingiva and begins during the eruptive period of the permanent dentition. Bleeding during mastication and on oral exam are common findings. While occasionally seen in dogs, this condition has a much higher incidence in cats. It is generally a non-painful condition for the patient, and halitosis is a common complaint. If left untreated, it typically proceeds quickly to periodontal disease, which may result in early exfoliation of the teeth. This disease is commonly mistaken for caudal stomatitis. The distinguishing clinical sign is the lack of caudal inflammation in this disease process. As the patient matures, susceptibility appears to subside at approximately two years of age.
In contrast, juvenile periodontitis does not involve enlargement of the gingiva and usually leads to the rapid proliferation of plaque and calculus and subsequent inflammation. This in turn results in significant early bone loss, periodontal pocket formation, and furcation exposure. This is generally the worst around the mandibular first molars. Treatment and effective management of these cases is often exceedingly difficult.
Histopathology (via incisional biopsy) should be considered to rule out other causes of gingival inflammation. Culture and sensitivity testing is generally unrewarding, but may be of value in non-responsive cases. Dental radiographs should be performed to evaluate the quality of the alveolar bone and also for early tooth resorption. Finally, Bartonella testing may be beneficial in some cases, especially in patients who do not respond to traditional management practices.
In the management of both of these conditions, early (9 months of age) and frequent (q 6–9 months) dental prophylaxis (even if only minimal plaque is present) along with strict homecare is critical to decrease inflammation. Ideally, homecare consists of daily brushing, as it is the gold standard of plaque control. Other homecare alternatives include chlorhexidine rinses as well as plaque control diets and treats. In cases where gingival hyperplasia is present, early gingivectomy is recommended to remove pseudopockets, decrease inflammation, and facilitate plaque control (both professional and homecare). Finally, extraction of any significantly diseased teeth is warranted to decrease the degree of inflammation.
- The diagnostic key between caudal stomatitis and periodontal disease is the presence of inflammation in the caudal area.
- All fractured teeth in cats are suspect for endodontic disease.
- Extraction is the treatment of choice for caudal stomatitis and tooth resorption.
- Dental extractions are critical for proper therapy.
1. Niemiec BA: Dental, Oral, and Maxillofacial Pathology, a Color Handbook. (Manson).
2. Niemiec BA: Dental Applications in Emergency Medicine (Practical Veterinary Publishing) www.practicalvetpublishing.com.
3. Bellows, J: Feline Dentistry (Wiley Blackwell).