M. Chandler1, DVM, MS, MANZCVSc, DACVN, DACVIM, DECVIM-CA, MRCVS; B. Niemiec2, DAVDC, DEVDC, FAVD
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 little to no outward clinical signs of the disease, and therefore, therapy typically comes very late. Consequently, periodontal disease may also be the most undertreated disease in our patients. Additionally, unchecked periodontal disease has numerous local as well as systemic consequences.
Periodontal disease is initiated by oral bacteria which adhere to the teeth in a substance called plaque. Plaque is a biofilm, made up almost entirely of oral bacteria and contained in a matrix composed of salivary glycoproteins and extracellular polysaccharides. Calculus (or tartar) is plaque which has secondarily become calcified by minerals in saliva. Plaque and calculus may contain up to 100,000,000,000 bacteria per gram. Bacteria within a biofilm do not act like free living or "planktonic" bacteria, and in fact are 1,000 to 1,500 times more resistant to antibiotics than planktonic bacteria. Plaque on the tooth surface is known as supragingival plaque. Once it extends under the free gingival margin and into 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 bacteria in the subgingival plaque secrete toxins as well as metabolic products. Also produced are cytotoxins and bacterial endotoxins which can invade tissues, and in turn cause inflammation to the gingival and periodontal tissues. This inflammation damages 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. 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.
The inflammation produced by the combination of the subgingival bacteria and 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 (towards the root tip). The end stage of periodontal disease is tooth loss; however, the disease has created significant problems prior to tooth exfoliation. 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. 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 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 it is possible to arrest its progression.
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. Normal sulcal depth in a dog is 0 to 3 mm and in a cat is 0 to 0.5 mm.
The first clinical sign of gingivitis is erythema of the gingiva. This is followed by edema, gingival bleeding during brushing or after chewing hard/rough toys, 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. As periodontitis progresses, alveolar bone is also lost. In some cases, the apical migration results in gingival recession. Consequently, tooth roots become exposed and the disease process is easily 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. 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 bone loss is permanent.
Severe Local Consequences
Oral-nasal fistula (ONF)
Class II perio-endo abscess
Severe Systemic Manifestations
Systemic ramifications of periodontal disease are 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. Recent animal studies suggest the possibility that these bacteria negatively affect the kidneys and liver, leading to decrease in function of these vital organs over time. Furthermore, it has been suggested that these bacteria can become attached to previously damaged heart valves (i.e., valvular dysplasias) and cause endocarditis. Other studies have linked oral bacteremias to cerebral and myocardial infarctions and other histological changes. Human studies have linked periodontal disease to an increased incidence of chronic respiratory disease (COPD) as well as pneumonia. There are many studies that strongly link periodontal disease to increased insulin resistance and poor control of diabetes mellitus as well as increased severity of diabetic complications (wound healing, microvascular disease). Additionally, diabetes is a risk factor for periodontal disease. Periodontal disease and diabetes have a bidirectional interrelationship where one worsens the other.
Nutritional Control of Periodontal Disease
Dry vs. Moist Pet Foods
A common perception in small animal practice is that feeding dry pet foods decreases plaque and calculus and canned foods promote plaque formation. It would seem that biting into a hard kibble should clean the teeth; actually moist foods may have a similar effect to a typical dry food on plaque and calculus accumulation. As the pet bites into a typical kibble, it shatters and crumbles, which provides no mechanical cleaning.
Dental Diets and Treats
Some foods and snacks for dental cleaning have a texture which maximizes the contact with the teeth. Foods with the right shape, size and physical structure can provide plaque, stain and calculus control. A 6-month study comparing feeding a dental diet to a typical maintenance diet showed about a third less plaque and gingival inflammation with the dental diet. A dental diet fed to Beagles significantly decreased pre-existing plaque, calculus and gingivitis, whereas these increased in Beagles eating a maintenance diet. The type of fibre in dental diets is thought to exercise gums, promote gingival keratinisation and clean teeth. Dental treats need to be very hard, and can sometimes fracture teeth.
Some diets and treats contain antibiotics or additives to retard or inhibit plaque or calculus; e.g., sodium hexametaphosphate (HMP) which forms soluble complexes with calcium and decreases the amount available for forming calculus. Adding HMP to a dry diet decreased calculus in dogs by nearly 80%, although another study showed no difference in plaque or calculus when HMP-coated biscuits were fed to dogs for 3 weeks.
Veterinary Oral Health Council (VOHC)
A way to check if a food or treat prevents or decreases plaque or calculus is its approval by the VOHC (vohc.org). The VOHC is a non-regulatory agency which includes representatives from professional dental associations, AVMA, AAHA, FDA, private practice and industry. The VOHC provides independent and objective reviews of tests of dental products submitted to it which are in accordance with their protocols, although they do not provide testing themselves. The VOHC awards a Seal of Acceptance for two categories: helps control plaque and helps control tartar.
Deficiencies in vitamin A, C, D and E and the B vitamins folic acid, niacin, pantothenic acid and riboflavin have been associated with gingival disease. These are adequate in diets which meet AAFCO or FEDIAF guidelines but can be deficient in other diets, such as many homemade diets.
Natural Diets and Feeding Raw Bones
Proponents of natural foods or feeding raw bones have claimed improvement in the cleanliness of pets' teeth; further claims are sometimes made that feeding commercial pet food contributes to the high prevalence of periodontal disease. However, a study in foxhounds fed raw carcasses, including raw bones, showed that they had varying degrees of periodontal disease as well as a high prevalence of tooth fractures. The skulls of 29 African wild dogs eating a "natural diet", mostly wild antelope, showed evidence of periodontal disease (41%), teeth wearing (83%) and fractured teeth (48%).
Small feral cats on Marion Island (South Africa) which had been eating a variety of natural foods (mostly birds) showed periodontal disease in 61%, although only 9% had evidence of calculus. Australian feral cats eating a mixed natural diet had less calculus compared to domestic cats fed dry or canned commercial food, although again there was no difference in the prevalence of periodontal disease. These studies show that a natural diet, or one containing raw bones, does appear to confer some protection against dental calculus, but not against the more destructive periodontal disease. There is also the risk of fractured teeth.
Nitric oxide (NO), an important inflammatory mediator, is increased in human periodontitis, and agents blocking the production of NO or its effects might be therapeutically valuable. Lactobacillus brevis (L. brevis) is a probiotic bacteria which contains high levels of arginine deiminase (AD). High levels of AD inhibit NO generation by competing with NO synthase for the arginine substrate. In humans, topical application of probiotics containing L. brevis decreased inflammatory mediators involved in periodontitis. Preliminary results of topical L. brevis CD2 in dogs showed reduced gingival inflammatory infiltrates.
While the common idea of dry food cleaning the teeth is appealing, many dry foods do not decrease the risk of periodontitis. Similarly, feeding natural foods or raw bones may decrease dental calculus but does not decrease the risk of periodontitis.
References are available upon request.