Chew on This - Nutrition for Dental Disease
World Small Animal Veterinary Association Congress Proceedings, 2018
1Vets Now Referrals, Clinical Nutrition, Glasgow, UK; 2Veterinary Dental Specialists, Veterinary Dentistry, San Diego, CA, USA

Implications Of Nutrition And Dental Health


Periodontal disease is the number one health problem in small animals. By two years of age, 70% of cats and 80% of dogs have periodontal disease. There are generally little to no outward signs of early disease process, so therapy typically comes late. Consequently, periodontal disease may be the most undertreated disease in our patients. Unchecked periodontal disease has numerous local and systemic consequences.


Periodontal disease is initiated by oral bacteria which adhere to teeth in a substance called plaque. Plaque is a biofilm, made up almost entirely of oral bacteria, contained in a matrix of salivary glycoproteins and extracellular polysaccharides. Calculus (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. Bacteria within a biofilm do not act like free living or “planktonic” bacteria; they are 1,000 to 1,500 times more resistant to antibiotics than planktonic bacteria. Plaque on the tooth surface is 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 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 supragingival plaque and calculus is minimal. Therefore, control of supragingival plaque alone is ineffective in controlling the progression of periodontal disease.

Bacteria in the subgingival plaque secrete toxins as well as metabolic products. Cytotoxins and bacterial endotoxins can invade tissues causing inflammation of 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, bacterial metabolites elicit a host inflammatory response. 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 periodontal tissues.

The inflammation produced by the combination of the subgingival bacteria and host response damages the tooth’s soft tissue attachment and decreases bony support via osteoclastic activity. This causes the tooth’s periodontal attachment to move apically (towards the root tip). The end stage of periodontal disease is tooth loss; however, the disease creates significant prior problems.

Periodontal disease is generally in two stages, gingivitis and periodontitis. Gingivitis is the initial, reversible stage in which 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 process 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.

Clinical Features

Normal gingival tissues are coral pink in color (allowing for normal pigmentation), have a thin, knife-like edge, and a smooth and regular texture. There should be no demonstrable plaque or calculus on the dentition. Normal sulcal depth in a dog is 0–3 mm and in a cat is 0–0.5 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 dental calculus but is primarily elicited by plaque and can be seen in the absence of calculus. Alternatively, widespread supragingival calculus may be present with little to no gingivitis. 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 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, resulting in tooth exfoliation. After this occurs, the area generally returns to an uninfected state, but the bone loss is permanent.

Severe Local Consequences

  • Oral-nasal fistula (ONF)
  • Class II perio-endo abscess
  • Pathologic fracture
  • Blindness
  • Oral cancer
  • Osteomyelitis

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. Studies suggest these bacteria negatively affect the kidneys and liver leading to decreased function. Furthermore, it has been suggested that these bacteria can become attached to previously damaged heart valves (i.e., valvular dysplasias) and cause endocarditis. Oral bacteremias have also been linked to cerebral and myocardial infarctions. Human studies have linked periodontal disease to an increased incidence of chronic obstructive respiratory disease, pneumonia and increased insulin resistance, resulting in poor diabetic control and increased severity of diabetic complications (wound healing, microvascular disease). Diabetes is also a risk factor for periodontal disease. Periodontal disease and diabetes appear to have a bidirectional interrelationship where one worsens the other.

Diet and Periodontal Disease

Dry vs. Moist Pet Foods

A common perception is that feeding dry pet foods decrease plaque and calculus and canned foods promote them. It would seem that the crunching action of biting into a hard kibble should clean the teeth. 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.

In a study of 10 cats, those consuming a dry cereal-based kibble compared to a higher protein/lower carbohydrate wet diet had a more diverse oral microbiome, but with an enrichment of bacteria associated with both gingival health and periodontal disease.

Dental Diets and Treats

Some dental foods and snacks 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 a dental diet to a typical maintenance diet showed about a third less plaque and gingival inflammation with the dental diet. When a dental diet was fed to Beagles with preexisting plaque, calculus and gingivitis, there was a significant decrease in these, whereas they increased in the Beagles eating a maintenance diet. The type of fibre in the dental diets exercises the gums, promotes gingival keratinisation and cleans the 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) 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.

Vitamin Deficiencies

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 diets which don’t meet those guidelines, such as many homemade diets.

Natural Diets and Feeding Raw Bones

Proponents of natural foods or of feeding raw bones have claimed that this will improve the cleanliness of pet’s teeth; further claims are sometimes made that feeding commercial pet food contributes to the high prevalence of periodontal disease in cats and dogs. However, a study in foxhounds fed raw carcasses, including raw bones, showed that they had varying degrees of periodontal disease and 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% cats, although only 9% had calculus. In Australia feral cats eating a mixed natural 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 of 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, has been shown to be increased in human periodontitis and agents blocking the production of NO or its effects might be valuable. Lactobacillus brevis (L. brevis), is a probiotic bacteria containing high levels of arginine deiminase (AD). High levels of AD inhibit NO generation by competing with NO synthase for the same arginine substrate. In people, topical application of probiotics containing L. brevis decreased inflammatory mediators involved in periodontitis. Topical L. brevis CD2 in dogs showed reduction of 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.


Speaker Information
(click the speaker's name to view other papers and abstracts submitted by this speaker)

Marge Chandler
Vets Now Referrals
Clinical Nutrition
Glasgow, UK

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