Introduction

Pathological tooth resorption occurs in many species, and is common in domestic cats. Lesions were described on cat teeth in 1930 but the aetiology remains unproven. As a result it has many names including resorptive lesions, feline odontoclastic resorptive lesions (FORLs), neck or cervical lesions and others. A similar type of non-carious cervical lesion (NCCL) in humans has also had many terms including idiopathic resorption, invasive resorption and abfraction. In veterinary dentistry the currently recommended term is 'tooth resorption' (TR).

TR is characterised histologically by odontoclasts in resorption lacunae. Many defects are filled with granulation tissue. Inflammation is usually absent or mild in many lesions that have extensive and generalised involvement. Osteoblastic bone repair occurs simultaneously with resorption in these lesions.

A very different picture is seen on some lesions in which inflammation is prominent. There is no repair occurring, and the roots do not show the same generalised involvement.

Clinical Findings

TR has been reported to cause discomfort. Humans who have TR affecting the root but not the crown ('extraoral lesion') found as incidental findings on radiographs do not report discomfort. When TR is exposed to the oral cavity ('intraoral lesion') people describe tooth sensitivity. It seems likely to be similar in our patients. Clinically, an early lesion often appears as a loss of tooth substance close to the gingival margin. They can also begin in the alveolus. When the resorption lacuna is filled with granulation tissue the gingiva appears to extend on to the crown. The vestibular surfaces of the lower third premolar teeth are often the first affected. Lesions that begin under the gingival margin in the furcation area can mimic periodontal involvement. A lesion can progress through dentine to affect the enamel. In end stages the crown is absent and it may appear as an area of raised gingiva.

Aetiology

There are many well known types of external root resorption. It is a component of deciduous tooth exfoliation. It can also occur after damage to the periodontal ligament, such as after traumatic tooth luxation, from infection (periodontal or endodontic disease), from pressure secondary to expansile lesions (cysts, slowly growing tumours) or impacted teeth tipped towards an adjacent root and from excessive orthodontic force. It has been shown that the periodontal ligaments of cat roots may spontaneously develop microscopic defects that are generally repaired uneventfully and do not progress to overt TR.

Some questions we need to answer include:

 Is there something that causes some of these normally formed defects to progress into large lesions?

 Is TR caused by some force or factor that is new or unnatural to cats, or is it caused by a change in the cat's ability to respond to normal forces or factors?

 Is there a different aetiology for each of the two very different types seen on histopathology evaluation, or do they reflect two different responses to a single initial cause?

 Is TR in cats a valid model for that subgroup of NCCLs seen in humans?

Some of the proposed theories for the aetiology of TR include:

 The abnormal force applied to teeth when cats bite on hard food. The resultant horizontal force may cause abfraction when stresses that are transferred to the cervical area damage the periodontal ligament.

 Inflammation from poor dental hygiene can damage the cementum and periodontal ligament, exposing the dentine to odontoclastic activity.

 The vitamin or mineral content or balance of cats' diets, i.e., excessive vitamin D.

 The acid pH of cat foods.

Types

There are two radiographically distinct types of TR. Roots of type 1 lesions maintain normal general radio-opacity and a distinct periodontal ligament space. Type 1 lesions are more commonly associated with periodontitis and endodontic disease than type 2 lesions. They may be similar to inflammation-induced root resorption in dogs and humans caused by periodontitis. Alternatively, concurrent inflammation might interfere with repair, preventing a type 1 lesion from progressing to a type 2.

The roots of teeth with type 2 lesions have generalised loss of radio-opacity compared to the roots of adjacent teeth. Affected roots appear to 'disappear'. Type 2 lesions are not generally associated with endodontic disease or periodontitis. They frequently have only a mild localised gingivitis.

We believe (this is opinion and has not been shown) that there are at least two causes. The less common form of TR is likely to be caused by periodontal inflammation (most type 1 lesions). The more common form of TR may be caused by abnormal mechanical stresses on the teeth (abfraction) with or without a metabolic facilitator (type 2 lesions).

Stages

This seems to be the most logical and functional grading system:

 Stage 1: very early resorption involving only the cementum but not extending into the dentine

 Stage 2: the resorption extends into the dentine but not to the pulp

 Stage 3: the resorption involves the pulp

 Stage 4: crown destruction has significantly weakened the tooth

 Stage 5: there is no remaining supragingival crown; the gingiva completely covers the site

Stage 4 lesions can be subcategorised depending on whether the crown or root is more affected but this is unimportant information once the type and stage are noted.

Diagnosis

Most TR can be diagnosed by direct visual observation or by probing with a sharp dental explorer. Localised marginal gingivitis suggests there may be an underling TR. If an affected area is probed with a fingernail or dental explorer, cats may react with an immediate jaw chatter movement, but this also occurs in the absence of TR and is not a reliable test. In humans there is considerable interest in cervical dental hypersensitivity since it may be an early indicator of a lesion. In cats this sensitivity can occur whenever dentine is exposed and does not distinguish between TR and exposed root from periodontitis. Many lesions are hidden from view under accumulated calculus. Lesions that are completely subgingival require deep subgingival probing or radiographs to detect them. Lesions that appear small clinically may have extensive resorption on a radiograph. It is easy to over-diagnose TR in furcation areas where an inflamed furcation can mimic a lesion.

Treatment

Extraoral TR found as an incidental finding on a radiograph does not require immediate treatment unless there is evidence of associated pathology. However, TR that is visible on the crowns of teeth should be treated since it may cause discomfort. Extraction is the current most common recommendation for treatment. An alternate treatment for type 2 lesions that are stages 2-4 is crown amputation with root retention. The roots of these teeth already show radiographic evidence of replacement. Their weakened root structure and alveolar ankylosis make them difficult to extract without fracturing the roots.

The procedure of crown amputation is quick and simple. The gingiva is slightly elevated using a small periosteal elevator. The gingiva is reflected with the flat end of a Pritchard PR4 while the crown is removed to, or just below, the alveolar marginal bone using a number 2 round burr in a high-speed hand piece. The bone is smoothed, and the gingiva is closed with 1.5 metric (4-0 USP) suture. Gentle digital pressure on the gingiva for 30 seconds stabilises the clot and adapts the gingiva to the bone. The procedure is more comfortable for the cat than extraction. It is also faster for the operator, less damaging to alveolar bone and surrounding tissues, and facilitates the conversion of the root to normal bone instead of delaying it. When it is performed, the client should be informed of the procedure and the rationale behind it.

Important caveats must be followed when crown amputation is performed rather than extraction. There must be no buried pathology. Preprocedural radiographs must be made. There should be no periodontitis, no clinical deep periodontal probing defects, no tooth mobility and no radiographic evidence of endodontic disease or periapical lucency. On a radiograph the roots should have generalised loss of radio-opacity; the roots that can be retained are those that are already turning into bone. Another very important selection criterion is that there must be no inflammation in the region of the pterygomandibular raphe (evidence of ulceroproliferative caudal stomatitis). Currently, patients affected with this syndrome require full extraction of all the premolars and molars to cure or improve their inflammation. For these patients all fragments of all roots must be completely removed, ideally with alveolar curettage to remove the periodontal ligament. Additionally, roots should not be left behind if a patient is known to be positive for feline immunodeficiency virus (FIV) or feline leukaemia virus (FeLV).

Restorations are rarely placed; most clients do not choose them given the 2-year success rate of 60% or less. Restoratives are sometimes placed in canine teeth to retain them while the lesion becomes more clearly a type 1 or type 2. When a restoration is placed, the clients are advised that it is temporary. Granulation tissue is removed with a burr. Our choice for restorative material is glass ionomer because it requires little-to-no tooth removal, self-bonds to dentine and has a modulus of elasticity similar to the tooth.

Prevention

Prevention will be difficult until we know the cause(s) of TR. Oral hygiene will minimise periodontitis and may prevent inflammatory-type TR. We recommend dental diets for cats, formulated to help tooth self-cleaning during mastication. Plaque control by this method could decrease inflammation that may predispose to some TR. Some of the dental diets allow more tooth penetration than many of the dry diets, possibly decreasing abfractive forces on the teeth.