Feline tooth resorption and caudal stomatitis (Proceedings)

Some of the known causes of external root resorption include inflammation related to infection (either marginal from periodontal disease or apical from endodontic disease), pressure secondary to expanding cysts, tumors, or impacted teeth, excessive orthodontic force, after any trauma to the periodontal ligament, and one component of the normal process of primary tooth exfoliation. One of the more common types of tooth resorption (TR) in dogs and cats is caused by local inflammation. These are seen at sites of inflammation such as severe gingivitis or in periodontal pockets. Another type, however, is an idiopathic resorption that often appears clinically at the cervical area of the tooth but frequently has already extensively involved the root by the time it is visible on the crown. This type of TR is very common in domestic cats, but also occurs in exotic felines, dogs, humans, rats, mice, marmosets, pigs, dolphins and others. TR in cats was first described and characterized in detail in the human dental literature in 1930. It was later described as "root caries" (a misnomer) in 1955 and then again recognized as non-caries-related odontoclastic resorption in the 70's. The syndrome was probably uncommon prior to the 20th century, but today has been reported to have a prevalence of between 30 to 60% (studies vary) in domestic cats. They are much less common in dogs and humans. Feline TR has been called many different things over the years, including resorptive lesions (RL), feline odontoclastic resorptive lesions (FORLS), neck lesions, root resorptions, cervical line lesions, cervical line erosions, buccal cervical root resorptions, external resorptions, cat caries, invasive resorptions, and initiocircocervical desmodentiopathy. Some of the terms used for them in humans include idiopathic root resorption, invasive resorption, abfraction, and non-carious cervical lesions. The term "tooth resorption" is currently considered to be the preferred term as determined by the Nomenclature Committee of the American Veterinary Dental College.

Etiology

Some TR lesions are clearly caused by inflammation as a result of marginal periodontitis. This is often seen in areas of periodontal pockets in cats, dogs and humans. These inflammatory resorptions affect the roots in the area of inflammation, usually close to the gingival margin or within a pocket. The remainder of the root and crown remote from the inflammation remains unaffected and appears normal on a radiograph. The more common type of TR in cats appears on radiographs as a more generalized decreased radiopacity affecting large areas of the root. The roots of these teeth often undergo a replacement resorption in which the osteoblastic reparative process occurs simultaneously with the odontoclastic tooth destruction, replacing the lost root with bone. Although these TRs have been well described in their clinical appearance, progression, and pathophysiology, their etiopathogenesis has not yet been proved. Some of the proposed theories for their etiology, such as the acidic pH of cat foods and their surface coatings, and acidity from regurgitation, have been disproved. One theory that is still being investigated is the possibility of abnormal forces generated when sectorial teeth, designed for slicing rather than masticating, bite down on hard cat foods. The resultant lateral forces on the crowns could cause abfraction as the stresses are transferred to the cervical area where the tooth is rigidly supported by bone. Repeated micro-flexure of the tooth at this location could cause crazing of the enamel or injury to the periodontal ligament (PDL) allowing odontoclasts access to the root dentin. Another theory under investigation is related to the high level of vitamin D in many cat foods.

Clinical findings

TR is diagnosed by direct visual observation combined with probing with a sharp dental explorer. Localized marginal gingivitis, often on the mid-buccal surface, should prompt further investigation. General anesthesia, removing calculus from the area, and examination with a dental explorer may be necessary to identify or rule out a lesion. TR that affects the crown commonly has a sharp ledge of undercut enamel around the margin. Lesions that appear clinically small may have extensive resorption apparent on a radiograph, and dental radiographs are often necessary to find extraoral (no clinically visible lesion in the mouth) lesions.

There are two radiographically distinct types of TR. Type 1 lesions are often associated with periodontitis and severe gingivitis, and many of them are likely to be inflammatory resorptions caused by adjacent inflammation and periodontal disease. Type 1 lesions are defined radiographically as lesions in which the roots maintain their normal general radiodensity and distinct periodontal ligament space except focally at the site of the lesion. Although the lesions may extend down onto the root, the remaining root does not seem to "disappear". Type 1 lesions also sometimes present with concurrent endodontic disease, unlike type 2 lesions. On the radiograph, the left mandibular molar (tooth on the right) has a large radiolucent area on the mesial (front) aspect of the mesial root at the marginal area of the root. This is a type 1 TR; the remainder of the tooth and root have normal radiopacity and the PDL is clearly visible.

In contrast, the Type 2 lesions are often not associated with endodontic disease or periodontitis other than mild localized gingivitis or a local gingival granuloma filling the resorption lacuna. They commonly show generalized root resorption on radiographs, as indicated by loss of radiopacity of the roots of the involved tooth. This replacement resorption is most easily appreciated by comparing the radiopacity of affected roots with those of adjacent unaffected teeth. On the radiograph the right mandibular third premolar (tooth on the right) is undergoing type 2 resorption. The radiopacity of the roots is approximating that of the supportive bone and is much less than that of the unaffected teeth. The PDL is difficult to identify as the roots are replaced by bone.

When a tooth has characteristics of both type 1 and type 2 resorption in the same tooth (and sometimes in the same root) it is categorized as a type 3 lesion. On this radiograph, the left mandibular third premolar (tooth on the left) has generalized loss of radiopacity and lack of a discernable PDL on the distal (back) root while the mesial root maintains a normal radiopacity and PDL space.

TR has been reported to cause anorexia, ptyalism, lethargy, depression, dysphagia, halitosis, and discomfort. However humans with type 2 resorption that is completely extraoral usually report no discomfort. It is likely that we can use humans as a model for this syndrome in cats, at least regarding symptoms, since they appear radiographically and clinically identical. However, once a lesion is exposed to the oral cavity then tooth sensitivity and discomfort are likely.

TR is staged by severity, with stage 1 being a very early resorption involving only the cementum. Stage 1 lesions are rarely clinically recognized. Stage 2 lesions extend visibly into the dentin but do not involve the pulp. Stage 3 lesions involve the pulp. Stage 4 resorption has destroyed enough crown to significantly weaken the tooth. Stage 5 lesions have no remaining supragingival crown with normal gingiva completely covering the site.

Treatment

Due to the progressive nature of the lesions even after restoration, affected teeth should be removed. All teeth with type 1 lesions should be completely extracted with no root remnants left behind. A gingival or mucogingival flap is elevated bucally and lingually, reflected with a Pritchard PR3, marginal buccal bone is removed, multiroot teeth are sectioned, and the periodontal ligaments are fatigued using dental elevators and patience. Only very gentle pressure is used to avoid fracturing roots. Mandibular canines require an extra measure of patience to avoid fracturing the mandible. After the tooth is delivered from the alveolus, the alveolar bone is smoothed with a #2 round bur, the alveoli flushed, and the gingiva sutured primarily with absorbable suture. The author's preference remains 4-0 chromic gut (with a 3/8 reverse cutting ophthalmic needle) due to its quick absorption, knot security, and soft texture for patient comfort.

An alternative treatment to complete tooth extraction for type 2 lesions that are stages 2 through 4 involves amputating the remaining crown and leaving the roots to continue their replacement resorption. This can only be performed on type 2 lesions. This procedure is less traumatic for the cat, allows for quicker healing and less loss of alveolar bone, and is much easier for the operator since type 2 lesions have ankylosis that complicates extraction and increases the chances of fracturing a root.

The procedure of crown amputation with intentional root retention is quick and simple; a very limited gingival envelope flap is developed, consisting only of minimal elevation of the gingiva from the tooth and marginal alveolar bone. The gingiva is reflected and protected with the flat end of the Pritchard PR3 elevator while a #2 round bur in a high-speed handpiece is used to remove the crown of the tooth to a level slightly below the level of the marginal bone. Any sharp bony projections are smoothed, and the gingiva is closed with a single 4-0 suture. Gentle digital pressure is placed on the gingiva for 30 seconds to stabilize the clot and to adapt the gingiva to the underlying structures. The entire procedure takes only a few minutes.

When deciding to amputate a tooth crown rather than completely extract the tooth, it is very important that selected cases have no buried pathology. Pre-procedural radiographs must be made. There should be no periodontitis, no clinical deep periodontal probing defects, no abnormal tooth mobility, and no radiographic evidence of endodontic disease or apical pathology. The roots should be exhibiting generalized loss of radiopacity on a radiograph. The roots that can be retained are those that are already turning into normal healthy bone. Another very important selection criterion is that there must be no clinical evidence of feline caudal stomatitis. For these patients, it is critical that all fragments of all roots are completely removed, and ideally also the associated periodontal ligaments. A final selection criterion is that roots should not be left behind on a patient that is known to be positive for FIV or FeLV.

Canine teeth with resorption are sometimes treated with a restorative to keep them functional and comfortable a little longer while the resorption process continues. This allows time for the process to progress more obviously to a type 1 requiring full extraction, or a type 2 allowing crown resection. The restoration is considered a temporary treatment. The material of choice for restoring TR is a glass ionomer. Glass ionomers release fluoride to the surrounding tooth structure, self bond to dentin minimizing the amount of tooth that must be removed in preparation, and have a modulus of elasticity similar to the tooth to allow the restoration to flex along with the tooth. The lesion is first debrided of granulation tissue using a bur. No tooth structure is removed except what is necessary to remove the soft tissue from the resorption lacuna and to remove any unsupported enamel along the defect margin. The lesion is etched, rinsed, slightly dried, the material mixed and placed, and immediately covered with a barrier to dessication and moisture.

Feline stomatitis and caudal stomatitis

Stomatitis is a general term for oral inflammation. The term generally refers to an overall inflammation of the oral cavity, including gingivitis caused by plaque (a normal response to bacterial biofilm on the tooth surface), or any of the various mucosal inflammations that can occur. Each individual inflammatory syndrome is treated or prevented by addressing its identifiable etiological agent. However, cats sometimes suffer from a specific idiopathic syndrome that affects the tissues in the region of the pterygomandibular raphe, and is unrelated to gingivitis or inflammation in other areas. This is the tissue in the back of the mouth that extends between the upper and the lower retromolar areas in the region of the palatoglossal folds that is stretched when a cat opens its mouth. The etiology is not known, but is suspected to be related to an immunopathy that causes the patient's immune system to over respond to one or more antigens. Many patients are positive for calici virus infection. Many other associations have been sporadically reported (herpes virus, food or other allergy, Bartonella infection) but studies have not definitively shown an association with any of them.

Clinical signs

Affected cats suffer extreme pain when they open their mouth. The pain worsens over time. The first sign noticed by an owner might be exaggerated jaw motions during or after eating, or hesitance to eat in spite of an apparent hunger and interest in food. However, many owners will not notice a problem until later in the course when the cat might exhibit increased salivation or saliva staining on the fur, vocalization during eating or yawning, or animated avoidance of food with complete lack of grooming or yawning. Cats will sometimes develop approach-avoidance behavior with food, as hunger drives them to eat while the anticipation of pain-on-eating drives them away. Clinical observation of bilateral ulcero-proliferative changes affecting the caudal tissues along with severe pain on opening the mouth is pathognomonic.

Treatment

The only treatment that can potentially provide ongoing relief is extraction of all the premolar and molar teeth. For emergency use, immune suppressants provide immediate relief from pain. An injection of cortisone can bring a cat suffering from severe pain back to near-normal behavior. However, steroids tend to be less effective over time and should not be used to manage a patient except for emergency relief. Many treatments for caudal stomatitis have been recommended, including cyclosporine, laser or radiosurgical ablation of affected tissue, long term antibiotic therapy, bovine lactoferrin, azathioprine, staph phage lysate, and cortisone. Oral lactoferrin, bovine colostrum and Transfer Factor have been used with anecdotal reports of temporary improvement, possibly related to local activity in the oral cavity. Some of the other listed treatments also help while the patient is receiving them, but none provide a permanent solution.

Extraction of the premolars and molars must be done early and meticulously, removing all parts of every root. Ideally, the periodontal ligament should also be removed from each socket, the alveolar bone carefully smoothed, and the gingiva should always be completely sutured for primary healing. Extremely meticulous technique is important.

Patients should be tested for potential concomitant problems (feline leukemia, feline immunodeficiency virus, oral calici virus) to rule out complicating or contributing factors. It is important that patients with caudal involvement be treated immediately, and not maintained on medical treatment for any length of time. Anecdotally, it seems that those patients that have had the inflammation present for longer periods and that have received multiple steroid treatments have a significantly poorer prognosis for resolution once the surgical extractions have been done.

Surgical removal of the premolars and molars, done early and correctly, has a success rate of over 90% for comfort without the need for further mediations, and around 70% for complete resolution of symptoms including inflammation. The prognosis drops with chronicity and with previous incomplete extractions. Patients that suffer pain even after extraction surgery have a guarded prognosis at best. Radiographs should be made to identify any possible persistent root remnants or areas of abnormal bone. Adjunctive treatments with 30mg CoQ placed on the food daily, alternating therapy with 0.12% chlorhexidine solution and vitamin C and zinc products, topical medications, and water additives may provide some help. The current best hope for these patients is treatment with feline omega interferon. Unfortunately this is not currently available in the United States. It has been imported from the U.K. or Europe through use of appropriate paperwork for import into the U.S. but this compassionate exemption may have been discontinued. Anecdotal reports from the U.K. are encouraging. While treatment does not completely resolve the inflammation, the patients have been reported to improve clinically in regards to their discomfort. It is used by first giving an intralesional injection of half the contents of a 10MU vial diluted to 2 mls with sterile saline. The other half is diluted in 100 ml sterile saline and frozen in 10 ml aliquots in syringes. Each syringe is thawed as needed, with the client administering 1 ml po daily alternating sides of the mouth. There are no data on this, and there have been reports of failures of this as well.