Current Concepts in Periodontal Disease and Therapy
World Small Animal Veterinary Association Congress Proceedings, 2018
B. Niemiec, DVM, DAVDC, DEVDC, Fellow AVD
Veterinary Dental Specialties and Oral Surgery, Dentistry, San Diego, CA, USA

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 outward clinical signs, and therefore therapy typically comes very late in the disease. Consequently, periodontal disease may also be the most undertreated disease in our patients.


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.

It is important to note that rough tooth surfaces will greatly increase the speed of plaque and calculus formation. Therefore any condition which detracts from the smooth tooth surface should be addressed. This can be as simple as a bonded sealant or in some cases can be better treated by a composite restoration. Another condition which commonly hastens the onset of periodontal disease is crowding. This will impair not only the homecare efforts, but also the natural cleaning ability of the patient.

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.

Initial plaque bacteria consist of predominately non-motile, gram-positive, aerobic facultative rods and cocci. Gingivitis is initiated by an increase in the overall number of bacteria, which are primarily motile gram-negative rods and anaerobes. The specific plaque hypothesis is based on the fact that these few species are seen in virtually all cases of chronic periodontal disease.

The bacteria in the subgingival plaque secrete toxins as well as metabolic products. Also produced are cytotoxins and bacterial endotoxins which can invade tissues on their own, and in turn cause inflammation to the gingival and periodontal tissues. This inflammation causes damage to the gingival tissues and initially results in gingivitis. Eventually, the inflammation can lead to periodontitis (i.e., the destruction of the attachment between the periodontal tissues and the teeth).

In addition to directly stimulating inflammation, the bacterial metabolic byproducts also elicit an inflammatory response from the animal. White blood cells and other inflammatory mediators migrate out of the periodontal soft tissues and into the periodontal space due to increased vascular permeability and increased space between the crevicular epithelial cells. White blood cells fight the infection by phagocytizing bacteria, but may also release enzymes to destroy the bacterial invaders either by design or after their death. When released into the sulcus, these enzymes will cause further inflammation of the delicate gingival and periodontal tissues. In fact, the progression of periodontal disease is determined by the virulence of the bacteria combined with the host response. It is the host response that often damages the periodontal tissues. However, patients with deficient immune systems typically have more severe periodontal disease than those individuals in good health.

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. In addition, 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.

The development of halitosis in pets is almost always due to periodontal disease. As previously stated, periodontal disease is caused by an increase in anaerobic bacteria. Certain strains of these bacteria will digest protein as their energy source (generally provided by the host). Some amino acids contain sulfur and this digestion creates products called volatile sulfur compounds (VSCs). One of these is hydrogen sulfide, which creates the “rotten egg smell.” VSCs are proinflammatory and actually contribute to periodontal inflammation and attachment loss. Therefore, not only are the VSCs produced by periodontal disease, they also directly increase the level of periodontal disease. Consequently, control of halitosis should be part of the treatment for periodontal disease.

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

The most common severe local consequence of periodontal disease is an oral-nasal fistula (ONF). ONFs are typically seen in older, small-breed dogs; however, they can occur in any breed as well as felines. ONFs are created by the progression of periodontal disease up the palatal surface of the maxillary canines however; any maxillary tooth is a candidate. This results in a communication between the oral and nasal cavities, creating an infection (sinusitis). Clinical signs include chronic nasal discharge, sneezing, and occasionally anorexia and halitosis. Definitive diagnosis of an oronasal fistula often requires general anesthesia. The diagnosis is made by introducing a periodontal probe into the periodontal space on the palatal surface of the tooth. Interestingly, this condition can occur even when the remainder of the patient’s periodontal tissues are relatively healthy (including other surfaces of the affected tooth). Appropriate treatment of an ONF requires extraction of the tooth and closure of the defect with a mucogingival flap. However, if a deep periodontal pocket is discovered prior to development of a fistula, periodontal surgery with guided tissue regeneration can be performed to save the tooth.

Another potential severe consequence of periodontal disease can be seen in multirooted teeth, and is called a class II perio-endo abscess. This occurs when the periodontal loss progresses apically and gains access to the endodontic system through the apical blood supply, thereby causing endodontic disease via bacterial contamination. The endodontic infection subsequently spreads through the tooth via the common pulp chamber and causes periapical infection on the other roots.

This condition is also most common in older small- and toy-breed dogs; however, this author has personally treated a case in a Labrador retriever. The most common site for a class II perio-endo lesion to occur in small animal patients is the distal root of the mandibular first molars.

The third potential local consequence of severe periodontal disease is a pathologic fracture. These fractures typically occur in the mandible (especially the area of the canines and first molars), due to chronic periodontal loss, which weakens the bone in affected areas. This condition is again, most commonly seen in small-breed dogs, mostly because their teeth (especially the mandibular first molar) are larger in proportion to their jaws as in comparison to large-breed dogs. Pathologic fractures occur most commonly as a result of mild trauma, or during dental extraction procedures. Although this is typically considered a disease of older patients, this author has personally treated three cases in dogs less than three years of age.

Pathologic fractures carry a guarded prognosis for several reasons including lack of remaining bone, low oxygen tension in the area, and difficulty in rigidly fixating the caudal mandible. There are numerous options for fixation, but the use of wires, pins or plates is generally required. Regardless of the method of fixation, the periodontally diseased root (s) must be extracted.

Awareness of the risk of pathologic fractures can help the practitioner avoid problems in at-risk patients during dental procedures. If one root of an affected multirooted tooth is periodontally healthy, there is an even greater chance of mandibular fracture due to the increased force needed to extract the healthy root. An alternate form of treatment for these cases is to section the tooth, extract the periodontally diseased root, and perform root canal therapy on the periodontally healthy root. In cases where periodontitis involving a mandibular canine or first molar is identified during a routine prophy, it is best to inform the owners of the possibility of a jaw fracture prior to attempting extraction of the offending tooth.

The fourth local consequence of severe periodontal disease results from inflammation close to the orbit, which could potentially lead to blindness. The proximity of the tooth root apices of the maxillary molars and fourth premolars, places the delicate optic tissues in jeopardy.

The fifth local consequence is described in recent studies which have linked chronic periodontal disease to oral cancer. The association in this case is likely due to the chronic inflammatory state that exists with periodontitis. In this way, periodontal inflammation acts as a ‘promoter’ of cancer, similar to the chronic inflammation from smoking increases the incidence of lung cancer.

The final significant local consequence of periodontal disease is chronic osteomyelitis, which is an area of dead, infected bone. Dental disease is the number one cause of oral osteomyelitis. Furthermore, once an area of bone is necrotic, it does not respond effectively to antibiotic therapy. Therefore, definitive therapy generally requires aggressive surgical debridement.

In some cases, the bacterial infection may also result in a septicemia. In one case treated by this author, the patient presented with an entire hemi-mandible which was necrotic secondary to osteomyelitis. In this case, the patient required a complete hemi-mandibulectomy.

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 is 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 (IE valvular dysplasias) 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 effects.

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:

1.  Control the infection (pathogen control)

2.  Decrease the amount of inflammation and/or bone destruction by the host (host modulation)

3.  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:

  • Dental prophylaxis
  • Home care
  • Periodontal surgery
  • Extraction

A. Complete dental prophylaxis should include the following steps:

1.  Presurgical exam

a.  Decreases “surprises” under anesthesia

2.  Proper and balanced anesthesia

3.  Supragingival scaling

a.  Mostly with a ultrasonic scaler

b.  Hand scaling ideally follows the ultrasonic step

4.  Subgingival scaling

a.  Generally with a curette or subgingival tip

b.  Hand instruments must be sharp

5.  Polishing

6.  Sulcal lavage

7.  Oral exam and charting

8.  Dental radiology

B. Homecare

Homecare is an absolutely critical part of periodontal therapy. This is because plaque forms in 24 hours, tartar in 3 days and gingivitis in 2 weeks. This means that even with annual cleaning, patients are infected 50 weeks a year. In fact, human studies show that professional cleanings without homecare are essentially worthless.

There are 2 major divisions of homecare, active and passive. Active homecare is defined that the client actually needs to perform work as opposed to feeding a diet or treat, the latter is considered passive.

Active homecare

As far as homecare is concerned, tooth brushing is still the gold standard. Educate your clients early about the benefits and compliance will increase. Brushing is performed with a toothbrush and veterinary toothpaste. However, mechanical removal of plaque by the brush is the most important part of periodontal care. The toothpastes typically only provide flavorings and antitartar agents, neither of which is actually helpful for control of periodontal disease.

Antiseptics such as chlorhexidine and zinc ascorbate can be good adjunct therapy for periodontal disease. However, as above, plaque bacteria are very resistant to antiseptics and therefore mechanical removal of plaque is the most important part of periodontal care.

As great as effective toothbrushing is, this is rarely the case. Toothbrushing needs to be performed correctly on a very regular basis. If a client stops brushing even for a short time, gingivitis will return. Since it has been shown that less than 1% of clients brush their pets daily, this is rarely a great choice. Further, it is very difficult to access the distal teeth as well as the linguopalatal surfaces. It has been shown that brushing is effective on rostral teeth (canines and incisors) but less so on premolar and molar teeth. Chew-based “passive” homecare is more effective on the chewing teeth. Therefore, a combination of the two is likely best.

Passive homecare

Passive homecare is mostly chew-based removal of plaque. As far as “passive” methods of homecare are concerned, many available products have no scientific evidence behind them. Essentially, all pet store products have no studies.

Further, most studies just look at overall plaque and calculus reduction, not where the reduction occurs. This may or may not indicate true effectiveness against periodontal disease. This is because the decrease is generally at only the incisal edge to middle of the tooth and does not reach to the gingival margin where the disease actually occurs. This may or may not indicate true effectiveness against periodontal disease Therefore, when you are determining what products to recommend to your clients, ideally look beyond just plaque and calculus control and determine where that control occurs.

Softer and more pliable products are not only safer in general, they should clean all the way to the gumline.

C. Periodontal Surgery

The other “new” form of pathogen control should be periodontal surgery. As discussed in the last article, pockets greater than 3 mm are pathologic and in need of therapy. All pockets between 3 and 6 mm should be treated with closed root planing and ideally the administration of a sustained-release local antimicrobial. Pockets greater than 6 mm or furcation level II and III require periodontal flap surgery to effectively clean the root surface and allow for reattachment and infection control. These procedures can be learned by a general practitioner and require minimal investment in equipment. If this is not an option, these teeth should be extracted.

D. Extraction

While extreme, the ultimate in plaque control is extraction. This will completely remove the plaque retentive surface of the tooth. It is the actual cure for gum disease. Dental radiographs will greatly facilitate the procedure.

This author is a big believer in minimally invasive surgery. Use small, sharp luxating elevators, minimal bone removal, and envelope flaps for extractions.

Bone Regeneration

Regenerating bone lost via periodontal disease is another weapon in the fight against periodontal disease. This is combined with periodontal flap surgery to clean and regenerate the lost bone. The technique of guided tissue regeneration (GTR) has been around for decades, but recent advances in barriers and bone grafting have markedly improved the success rates. Regardless, there is only a handful of conditions which carry a good prognosis for bone regeneration. The best prognosis is seen with 3-walled periodontal pockets (typically seen on the palatal aspect of the maxillary canine and distal aspect of the distal root of the mandibular first molar) and class II furcation lesions. Since these are quite common in small-breed dogs, there is a large number of patients who would benefit from these procedures.

The theory of GTR is that the down growth of faster healing soft tissue must be prevented to allow the slower growing bone and periodontal ligament to repopulate the periodontally induced bony defect. GTR involves creating a periodontal flap and performing open root planning to create a clean root surface for healing. After this is accomplished, the defect is filled with bone augmentation and a barrier membrane placed. There are numerous products currently utilized on the human side; however, currently the products of choice for most veterinary dentists are cancellous freeze-dried demineralized bone for the graft and demineralized laminar bone sheets as the membrane.

Host Modulation

This is an exciting new area of periodontal therapy. It is the use of products to decrease the inflammatory response to bacterial plaque. In this way it can lessen gingivitis and in some cases decrease the amount of alveolar bone loss. Some products are drugs, but there is an increasing number of nutraceuticals in this segment.

Probiotics have been shown to be very effective at improving oral health. They can be administered orally, but are more effective when rubbed on the gums. Additionally, they have been shown to decrease pocket depths when injected into a periodontal pocket.

Fatty acids are well known for their anti-inflammatory effect on skin and joints. They have also been shown to be effective against periodontal disease. In particular, a veterinary-labelled product can be topically applied for maximum local effect, but, when swallowed, also provides joint support.

Other agents in this category are CoQ10, antioxidants, and proper overall nutrition.


Periodontal disease is by far the most common disease process in small animal veterinary patients. It is particularly common in small- and toy-breed dogs. Not only does it create local infection and can lead to tooth loss, but there are numerous negative local and systemic effects of untreated periodontal disease. In fact, on the human side periodontal disease is known as the “silent killer.” Proper care of periodontal disease is critical for the overall health of the patient.

The basis for therapy of periodontal disease is plaque control. This is achieved by a combination of professional cleanings, periodontal surgery, extractions, and most critically homecare. It is critical to select therapies (particularly homecare) which are effective at and below the gumline. Recently, guided tissue regeneration and host modulation have emerged as additional options for combatting periodontal disease.


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Veterinary Dental Specialties and Oral Surgery, Dentistry
San Diego, CA, USA

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