Periodontal disease is the most common infectious disease in both humans and pets. It is by far the most commonly seen oral problem, suggesting that our current preventive measures are either not widely practiced, or are not widely successful. Periodontal disease can be briefly described as inflammation leading to recession of the periodontium (tissues surrounding the teeth). However, the process that causes this disease is complex.

The Pathology of Periodontal Disease

After a meal, naturally-occurring microorganisms in the mouth mix with salivary glycoproteins (the pellicle), polysaccharides from ingested food, and other oral contents such as sloughed epithelial cells and white blood cells. This mixture forms plaque, a soft, sticky substance (or biofilm) that adheres to the tooth’s surface. This soft plaque is initially confined to the tooth’s crown, and contains predominantly gram-positive, non-motile, aerobic cocci. When these gram-positive, non-motile, aerobic cocci contact the gingiva, they stimulate an inflammatory response. Neutrophils engulf the bacteria, and when they become full, they burst, releasing toxins and enzymes that begin irritating the patient’s periodontal tissues, causing inflammation of the gingival margin. This inflammation causes the attached gingiva to loosen from the tooth, creating a space between the tooth and the gingiva known as a periodontal pocket. The bacteria also secrete substances that improve the biofilm’s adhesion to the tooth and protect the bacteria from antimicrobial agents—making the bacteria within this biofilm up to 1500 times more resistant to antiseptics and antibiotics than the same bacteria would be by itself. Oxygen is no longer able to reach the deepest layers of this thick matrix, so now the bacterial population begins to shift, with gram-negative, anaerobic, mobile rods and filamentous organisms taking over. These anaerobes are more virulent than the surface-dwelling aerobes, producing endotoxins, which, along with the patient’s own defense mechanisms, lead initially to soft tissue loss (or sometimes, gingival hyperplasia), progressing to bone loss, and eventually, tooth loss. This is known as attachment loss.

If plaque is not brushed off, within as little as 2–3 days calcium from food and saliva begin to mineralize it into a hard substance called calculusor tartar. Calculus itself doesn’t cause periodontal disease, but it does have a very rough, porous surface that makes a great home for disease-causing bacteria.

Stages of Periodontal Disease

Periodontal disease index is scored by the amount of attachment loss. It is primarily determined by periodontal pocket depths and radiographic assessment of bone loss. There may be (and usually are) teeth with different periodontal indices within the same mouth.

PD0: Normal

• Attachment loss is 0%.
• No inflammation of the gingiva, it is pink, smooth, and lies flat against the teeth.
• No treatment is required, but homecare should be initiated to maintain oral health.

PD1: Gingivitis

• Attachment loss is 0%.
• Gingivitis only.
• There may be a slight increase in sulcus depth because of gingival swelling (pseudopocket) though no actual attachment loss has yet occurred.
• Bacteria at this stage are gram-positive, aerobic, non-motile cocci.
• This is the only stage of periodontal disease that is reversible!
• Treatment: dental prophylaxis to remove all biofilm and reverse inflammation, homecare.

PD2: Early Periodontitis

• Attachment loss is <25%.
• Bacteria in subgingival regions are gram-negative, anaerobic, motile rods.
• Pocket depth increases due to attachment loss.
• Crestal bone starts to deteriorate.
• Treatment: dental prophylaxis and closed root planing. Periceutical scan be placed within the periodontal pockets to kill bacteria and help relieve inflammation.
• Homecare.

PD3: Moderate Periodontitis

• Attachment loss is 25–50%.
• Bacterial population is almost entirely anaerobic.
• Alveolar bone starts to deteriorate, leading to vertical bone loss and horizontal bone loss.
• Tooth roots may be exposed, and furcation exposure may be evident.
• Alveolitis or osteomyelitis may be present.
• Treatment: frequent dental prophylaxis and periodontal therapy including open root planing.
• Homecare.

PD4: Severe Periodontitis

• Attachment loss is >50%.
• Bacterial population is similar to PD3.
• Tooth roots and root furcations are exposed.
• Teeth may be mobile, some only held in position by calculus or granulation tissue.
• Teeth with more than 50% attachment loss may not be able to be salvaged.
• Treatment: assess whether each tooth can or should be saved.

Without intervention, periodontal disease will progress until the teeth exfoliate. At this point, since there is no longer any tooth surface for bacteria to cling to, the periodontal tissues can heal. Until such time, however, the patient suffers with chronic infection and oral pain. Bacterial infection in the mouth has also been shown to cause disease elsewhere in the body, such as endocarditis. Every time an animal with periodontal disease chews, tiny abrasions occur in the fragile, infected periodontal tissues. Capillaries in these abrasions rupture, allowing bacteria to enter the bloodstream and settle in the valves of the heart, the kidneys, or the liver. This is especially dangerous in patients whose health is already comprised, such as diabetics, the immunosuppressed, or those in poor body condition.

Contributors to Periodontal Disease

There are several factors which can predispose a pet to periodontal disease or worsen existing disease.

1.  Crowded teeth: Most often seen in small or short-faced breeds such as Yorkshire terriers, pugs, shih tzu’s, Chihuahua’s, and cats such as Persians and Himalayans. These pets have been selectively bred by humans for their small size or flat faces, but unfortunately the size of their teeth has not decreased sufficiently to fit well within these smaller mouths. Because the jaws are too short to contain all of their teeth, the teeth are often rotated and crowded together. Crowded teeth tend to develop more tartar, and severely crowded teeth often do not have enough room between them for gingival tissue, allowing food particles and bacteria a path straight to the bone.

2.  Retained (persistent) deciduous teeth: Most often seen in canine teeth. This is a variation of crowded teeth, since the adult canine tooth and its deciduous counterpart erupt extremely close together. We have all seen the tartar (and often hair or other debris) that gathers between a permanent canine tooth and its retained deciduous. As in the case of severely crowded teeth, no protective gingiva exists between these teeth, and infection can quickly spread to the bone around the root of the adult tooth.

3.  Malocclusions: Teeth that are not in their proper position in the mouth can develop more tartar, as the forces of chewing and saliva flow help keep the teeth cleaner in a mouth which has a normal “pinking shears” occlusion.

4.  Supernumerary teeth: Extra teeth in the mouth, which is a common genetic abnormality in some dogs such as boxers, can cause crowding and all of the problems that go along with it.

5.  Enamel hypocalcification (also referred to as enamel hypoplasia): A condition of poorly mineralized tooth enamel, usually due to the young animal developing a high fever or illness during enamel formation. This hypocalcified enamel is often soft, discolored yellow or brown, and prone to flaking or pitting. Teeth with enamel hypocalcification tend to accumulate plaque and tartar faster than teeth with normal enamel because of their rough surfaces. Note: animals with enamel hypocalcification may also have highly sensitive teeth because of exposed dentin, and often do not tolerate tooth brushing.

6.  Diet: Animals fed soft food only may have a higher incidence of periodontal disease than animals fed a dry or mixed diet (in the absence of dental home care).

7.  Malnutrition, physical or psychological stress: these factors have been implicated in impairing the body’s ability to mount an immune response.

8.  Genetics: some pets appear to have a natural resistance to periodontal disease, while others have extreme susceptibility. This may be due to the immune system’s ability to cope with oral bacteria.

9.  Other factors: include chewing habits, architecture of the mouth, saliva flow, and general health status.

Clinical Signs of Periodontal Disease

• Halitosis (this is by far the most common reason pet owners present their animals for oral examination).
• Red, inflamed gingiva (common, less often noted by owners).
• Increased drooling, or blood in the saliva (not common).
• Pawing at mouth (rare).
• Difficulty eating (very rare, though many animals will prefer soft food if available).

Most pets hide their pain (a survival trait that pet owners often mistake for a lack of pain—don’t make this assumption!) and will continue to eat even while their teeth are rotting out of their mouths. Their drive to eat will only lessen when they are in unbearable pain or are becoming acutely ill. Many owners believe that halitosis and tartar accumulation are natural for their pets and have no idea that this indicates a disease process is occurring. It’s our job to educate them.