Introduction

Periodontal disease is the number one medical condition in small animal veterinary medicine. We will begin this presentation with an overview of the current knowledge as to the pathogenesis of periodontal disease. This will allow us to properly treat the condition. Following this is a discussion of the local and systemic effects of periodontal disease. This will give attendees the ability to improve client compliance with dental recommendations. In addition, a firm grasp of the disease process will improve practitioner understanding of proper treatment modalities.

Due to the plethora of new and concerning information about this condition, treatment and prevention is the subject of significant research. This focus has resulted in numerous new products and procedures to prevent and treat periodontal disease and this presentation is designed as an introduction to these new and future therapies.

Periodontal Disease Overview

Periodontal disease is the number one health problem in small animal patients. By two years of age, 70% of cats and 80% of dogs have some form of periodontal disease. However, there are generally few to no visible clinical signs, and, therefore, therapy typically comes very late in the disease. Consequently, periodontal disease may also the most undertreated disease in our patients.

Pathogenesis

Periodontal disease is generally described in two stages, gingivitis and periodontitis. Gingivitis is the initial, reversible stage in which the inflammation is confined to the gingiva. The gingival inflammation is created by plaque bacteria and may be reversed with a thorough dental prophylaxis and consistent homecare. Periodontitis is the later stage of the disease process and is defined as an inflammatory disease of the deeper supporting structures of the tooth (periodontal ligament and alveolar bone) caused by microorganisms. The inflammation results in the progressive destruction of the periodontal tissues, leading to attachment loss.

This can be seen as gingival recession, periodontal pocket formation, or both. Mild to moderate periodontal pockets may be reduced or eliminated by proper plaque and calculus removal, however, periodontal bone loss is irreversible (without regenerative surgery). Although bone loss is irreversible, it is possible to arrest its progression.

However, it is more difficult to maintain periodontally diseased teeth in comparison to healthy teeth. Additionally, periodontal attachment loss may be present with or without active inflammation.

Periodontal disease is initiated by oral bacteria which adhere to the teeth in a substance called plaque. Plaque is a biofilm, which is made up almost entirely of oral bacteria, contained in a matrix composed of salivary glycoproteins and extracellular polysaccharides. Calculus (or tartar) is basically plaque which has secondarily become calcified by the minerals in saliva.

Plaque and calculus may contain up to 100,000,000,000 bacteria per gram. More importantly, bacteria become much more resistant to antiseptics and antibiotics than their free living or “planktonic” counterparts. In fact, they are 1,000 to 1,500 times more resistant to antibiotics and antiseptic concentrations need to be up to 500,000 times that which would kill singular bacteria.

Plaque on the tooth surface is known as supragingival plaque. Once it extends under the free gingival margin and into the area known as the gingival sulcus (between the gingiva and the teeth or alveolar bone), it is called subgingival plaque. Supragingival plaque likely affects the pathogenicity of the subgingival plaque in the early stages of periodontal disease. However, once the periodontal pocket forms, the effect of the supragingival plaque and calculus is minimal. Therefore, control of supragingival plaque alone is ineffective in controlling the progression of periodontal disease.

The inflammation produced by the combination of the subgingival bacteria and the host response damages the soft tissue attachment of the tooth, and decreases the bony support via osteoclastic activity. This causes the periodontal attachment of the tooth to move apically. The end stage of periodontal disease is tooth loss; however, the disease has created significant problems prior to tooth exfoliation.

Clinical Features

It is important to be familiar with normal features in order to identify abnormal findings. Normal gingival tissues are coral pink in color (allowing for normal pigmentation), and have a thin, knife-like edge, with a smooth and regular texture. There should be no demonstrable plaque or calculus on the dentition.

The first obvious clinical sign of gingivitis is erythema followed by edema of the gingiva. However, it is now known that the first evidence of gingivitis is bleeding during brushing, probing, or after chewing hard/rough toys. Therefore, it is important to realize that normal appearing teeth/gums can actually be infected. If the first stages of gingivitis are not treated, it will progress into edema, spontaneous bleeding, and halitosis.

Gingivitis is typically associated with calculus on the involved dentition, but is primarily elicited by plaque and thus can be seen in the absence of calculus. Alternatively, widespread supragingival calculus may be present with little to no gingivitis. It is critical to remember that calculus itself is essentially non-pathogenic. Therefore, the degree of gingival inflammation should be used to judge the need for professional therapy.

As gingivitis progresses to periodontitis, the oral inflammatory changes intensify. The hallmark clinical feature of established periodontitis is attachment loss. In other words, the periodontal attachment to the tooth migrates apically. As periodontitis progresses, alveolar bone is also lost. On oral exam, there are two different presentations of attachment loss. In some cases, the apical migration results in gingival recession while the sulcal depth remains the same. Consequently, tooth roots become exposed and the disease process may be identified on conscious exam. In other cases, the gingiva remains at the same height while the area of attachment moves apically, thus creating a periodontal pocket. This form is typically diagnosed only under general anesthesia with a periodontal probe. It is important to note that both presentations of attachment loss can occur in the same patient, as well as the same tooth. As attachment loss progresses, alveolar bone loss continues, until tooth exfoliation in most cases. After tooth exfoliation occurs, the area generally returns to an uninfected state, but the bone loss is permanent.

Severe Local Consequences

There are numerous recognized potential local effects of periodontal disease including:

• Oral-nasal fistulas (ONFs)
• Class II perio-endo abscesses
• Pathologic fractures
• Ocular disease and blindness
• Oral cancer
• Osteomyelitis

Severe Systemic Manifestations

Systemic ramifications of periodontal disease are also well documented. The inflammation of the gingiva and periodontal tissues that allows the body’s defenses to attack the invaders also allows these bacteria to gain access to the body. It is important to note that just established gingivitis (i.e., no attachment loss) is enough to create these systemic effects. In humans, the periodontal surface area comprises a surface area the size of the palm of your hand. This is a large area of infection for the body to deal with. However, if you consider the size of the mouth and teeth of a small breed dog in relation to their body, there is actually a far greater level of infection affecting these patients.

There are a plethora of studies both in the human and veterinary literature which document a link between periodontal inflammation and organ dysfunction. Affected organs include the kidneys and liver, leading to decrease in function of these vital organs over time. Furthermore, it has also been suggested that these bacteria can become attached to previously damaged heart valves (i.e., valvular dysplasia) and cause endocarditis, which in turn can result in intermittent infections, and potentially thromboembolic disease. Other studies have linked oral bacteremias to cerebral and myocardial infarctions and other histological changes. Additional human studies have linked periodontal disease to an increased incidence of chronic respiratory disease (COPD) as well as pneumonia. Oral bacteremias have also been linked to arthritis and adverse pregnancy affects.

There are many studies that strongly link periodontal disease to an increase in insulin resistance, resulting in poor control of diabetes mellitus as well as increased severity of diabetic complications (wound healing, microvascular disease). Additionally, it has been shown that diabetes is also a risk factor for periodontal disease. Periodontal disease and diabetes are currently viewed as having a bidirectional interrelationship where one worsens the other.

Most critically, periodontal disease is now associated with early mortality. In other words, humans with bad periodontal disease die earlier than those in good periodontal health. In fact, periodontal disease is now viewed as a higher risk factor for early death than smoking!

Conversely, proper therapy of periodontal disease has been shown to have beneficial effects on systemic maladies. The kidney, liver, and heart function have all been shown to improve when periodontal disease is properly treated. Further, glycemic control is increased in patients with good periodontal health.

Periodontal Therapy

Methods and products for periodontal disease treatment and prevention can be grouped into three distinct treatment areas: control infection (pathogen control), decrease the amount of inflammation and/or bone destruction by the host (host modulation), and re-grow lost bone (guided tissue regeneration).

Pathogen Control

It is well known that periodontal disease is initiated by plaque bacteria. Therefore, the basis for periodontal therapy is, and likely always will, be plaque control.

Proper plaque control is a four-pronged attack based on the level of disease:

1.  Dental prophylaxis

2.  Home care

3.  Periodontal surgery

4.  Extraction