Influence of diet consistency on periodontal disease
in captive carnivores

David A. Fagan, D.D.S., Dental Consultant, and
Mark S. Edwards, Ph.D., Nutritionist

Zoological Society of San Diego, Department of Veterinary Services
P.O. Box 120551, San Diego, CA 92112-0551 USA

Over one hundred years ago, British scientist Sir Frank Colyer began research resulting in an exhaustive text concerning dental disease in animals. In that document, Colyer addresses the topic of the progressive periodontal destruction of the animal’s masticatory apparatus, where he says:

“In my opinion there is abundant evidence to show that, in animals, parodontal (sic) disease is attributable to injury of the gums caused by food.”.

Colyer analyzed the problem at length in domestic animals, in wild animals in captivity, and in wild animals in their natural habitat. He observed that the relocation of the wild animal from its natural habitat into a captive environment brought about a radical change in the environment of its oral cavity, and this change resulted in the development of a wide variety of oral diseases.

Following many years of very thorough examination of individual exotic animals in museums worldwide, he concluded:

1. “The disease starts as an injury to the gum margins caused by food. This injury may be of a traumatic or of a chemical nature; when traumatic, the food in the process of mastication penerates the soft tissues; when chemical, the products of stagnant food injure the epithelial surface and thus expose the deeper tissues to infection.”
2. “The bone lesion is a progressive, rarefying osteitis commencing at the margin of the bone.”
3. “The disease is caused by an alteration in the character of the diet of the animal of either a physical or of a chemical nature–in other words, by a departure from natural diet and conditions.”

During the past 100 years since Colyer’s exhaustive study, there have been untold millions of dollars and man-hours spent investigating the etiology, pathogenesis, treatment, and prevention of oral disease in mammals. The American Dental Association tells us that oral and dental disease of humans is the single most common pathology. They estimate that 99% of the population have oral disease in one form or another. Extensive analysis of the mechanisms of periodontal disease, one of the most common and destructive manifestations of all oral disorders, suggests and now confirms that it is predominantly a bacterial problem, and that the bacteria in the oral cavity affect mammalian periodontium in four ways:

1. direct invasion of the oral tissues
2. release of harmful toxins into these tissues
3. production of destructive enzymes
4. initiation of antigen/antibody reactions within the local soft tissues.

The bacteria accomplish all of this by forming an amorphous colonial microbial mass, which is commonly refer to as dental plaque. The pathogenesis of oral disease has been extensively described in detail elsewhere. Much is known and has been published about the relationships between dental plaque, diet, nutrition, and oral disease. A wealth of useful information is readily available to all via the Internet.

What is also very well known but not widely accepted is that:

1. The consistency and / or texture of food has a direct affect upon the composition of, and the rate of formation of dental plaque.
2. Soft diets tend to produce more bacterial plaque than do firm diets.
3. Excessively course, granular diets can produce periodontal disease through the action of abrasive overuse of, and by direct traumatic injury to the supporting tissues of the oral cavity.
4. Foods of firm consistency will increase the number, distribution, and tone of the capillaries in the gingival tissue; which improves the metabolism and vitality of all of the supporting and surrounding structures of the oral cavity.
5. The degree of keratinization of the stratified squamous epithelium in the mouth, which affords protection against trauma and other injurious agents, is affected by the frictional qualities of the diet.
6. Chewing, by its mechanical action produces a compression and expansion of the periodontal ligament space around the teeth which, in turn, promotes formation of a dense fibrous suspensory structure by increasing both circulation and fibroblastic activity.
7. The width of the periodontal ligament, a measure of its health, is directly related to the intensity of the mastication function.
8. Regarding the maintenance of the alveolar bone itself, the proper balance between bone resorption and new bone formation is materially aided by hard foods, and that inadequate masticatory function induced by soft foods will produce atropic changes in the surrounding tissues, and lower the threshold of bone activity.
9. And, finally, although there is not an abundance of good evidence that oral disease can be initiated by diet consistency and/or texture alone, texture is generally accepted to be a major secondary contributor or modifier of the oral disease process. In short, diet consistency and texture more than likely play a regulatory role in the etiology of oral disease.

It is clearly difficult, and often misleading, to extrapolate data developed in human medicine directly to a similar problem in animals. This is particularly true with exotic animals. But, it is also equally true that significant results found in one species, cannot be completely ignored when considering other similar species. Actual clinical trials are required to completely document the interactive relationships between diet, texture and oral disease as it relates to a specific species. However, the clinical test that will meet with universal approval has not yet been devised. Problems faced at the present time by those individuals involved the task of maintaining reproduction in endangered species are urgent, and solutions are needed now.

The weight of observational evidence from the authors clinical practice with exotic animals is overwhelming. There is more than sufficient evidence at this point in time to declare that oral disease has been, and in many cases still is, a major problem and serious medical concern associated with maintenance of exotic species in captive environments – particularly among carnivores. The authors have personally treated numerous cases from the Order Carnivora – including: dingo, dhole, cape hunting dog, maned wolf, hyenas, wolverine, binturong, most all of the bears – polar, black, Kodiak, sun, specticled; many felids such as sand cat, fishing cat, serval, caracal, leopard, jaguar, cheetah, leopard, lion, tiger; otters, both the red and giant panda, and on and on.

The etiology of much of their oral disease is related to the physical characteristics of their diet and the chemical changes those diets induce, as described above. There are sufficient data and clinical examples – now published in the literature – to cause concern among clinicians.

In humans, the incidence of spontaneous infectious agents appearing in the individual’s blood stream, or bacteremia, appears to be directly related to the severity of existing oral disease, as well as to the amount of tissue trauma which normally occurs during eating, chewing or mastication. It is well known that transient bacteremias occur spontaneously in normal, healthy persons in day-to-day living. For example, 24% of 305 persons while brushing their teeth and 17% of 225 persons chewing hard candy produced bacteremia.

Procedures such as gastrointestinal tract endoscopy, percutaneous liver biopsy, and urethral catheterization also cause significant transient bacteremias in humans. Numerous studies have shown that almost all dental procedures produce intermittant bacteremia, and that the very common oral Streptococcus viridans group of organisms are responsible for over 50% of the infective endocarditis reported in the literature. Of the two factors responsible, trauma and infection, one study described infection as the more important, and noted that bacteremia occurred in 86% of the patients with marked gingivitis with such slight trauma as biting on a tooth. Therefore, it is possible that exotic animals with oral disease, particularly periodontal disease, experience transient bacteremias during their daily routine. Although there is not adequate evidence in free ranging animals, there is sufficient data from analysis of a variety of zoo maintained mammalian species, to show that periodontal disease is plaque-related, and from the bacterial analysis of the plaque of zoo animals, it has been shown that diet does influence-the diversity of the bacterial content and the composition of the plaque.

We would like to make it clear that we are not suggesting that diet or dietary husbandry is the sole cause of periodontal disease or oral disease in captive exotic species. However, what we are proposing, is that from the perspective of 30 years of investigative analysis and treatment of a great deal of oral disease in a wide variety of exotic animals, one of the authors has seen a direct relationship between the texture of the diet, oral problems, and systemic health. We also see a direct cause and effect relationship, which is a relatively easily controllable factor in the maintenance of animals in captivity.

Diet related oral disease affects the body of an animal in one of three ways:

1. Through immediate contact from adjacent tissues, the infection spreads from one local area to another, i.e. cellulitis to local osteomyelitis.
2. Via natural pathways, it spreads through the trachea, into the lungs; through the esophagus into the stomach; through the eustachian tubes to the inner ear; etc., and
3. Through the lymphatic and circulatory system the infection spreads to the entire body by continuous passage of bacteria, toxins, and harmful and metabolic byproducts.

Following repeated treatment of severe oral disease in association with arthritic problems, acute renal failure, pancreatic, and hepatic infections, it appears that our task as medical personnel caring for exotic animals can be defined as maintaining a healthy, active, and reproducing group of animals. That is no small task, and there are still enormous voids in our knowledge. It is important to minimize variables that have been more clearly characterized. The etiology between diet, oral disease and systemic health is fairly well known and understood. The veterinary medical staff caring for any group of captive exotic animals must of necessity examine diet from a variety of viewpoints, including:

1. the reported food preferences in the wild,
2. known nutritional requirements of related domestic species,
3. occupational therapy value of food items not necessarily related to nutritional value,
4. practical considerations relating to the foodstuff’s availability, perishability, and/or economy.

In reality, zoo diets tend to remain rather variable to accommodate changes in foodstuff availability, additions or deletions to the collection, and newly available nutritional information. Of course, the diet must provide suitable nutrients for growth, maintenance, reproduction, lactation, and the changing needs of the individual animal or group. From a purely administrative perspective, the major emphasis appears to be on the nutritional composition of the diet, and the economy of acquisition, storage, and transport. But captive animals need wear and tear on the dentition. The masticatory apparatus of carnivores was designed to be used, and used aggressively and ferociously. If the animals don’t use their dentition and mastictory apparatus, they will in time lose it. The systemic health of any individual animal will not be adequately maintained with the loss of the primary entry mechanism to the digestive system. Moreover, as the average age of captive breeding groups increases, which it certainly should as our reproductive research program prove successful – we will be faced with the oral disease problems of the geriatric individual, which can be considerably more complex.

Oral disease should be recognized as a serious problem in the care and maintenance of exotic animals. Today the clinical practice of veterinary medical and dental care has sufficient solutions to manage the problem. But, the application of those solutions to captive exotic animals represents a time consuming, and expensive effort. The authors propose that a great deal can be accomplished to eliminate and / or reduce the incidence of oral disease as a clinical consideration in exotic animal medicine by the means of prevention. It is possible to do something immediately and significantly to minimize oral problems of captive exotic carnivores. That “something” is to reevaluate the diet and dietary husbandry of the specimens. Animals need more “hassle factor” per mouthful of nutrients. The literature contains hundreds of references to the food habits of feral carnivores and, therefore, the appropriate menu is readily available. Convenient prepared diets, those without sufficient “hassle factor,” are ruining the mouths and compromising the health of our animals. Carnivores, in their natural habitat, eat rabbits, mice, rodents, birds, etc., in toto (i.e., connective tissues, viscera, organs).

We have attempted, with this presentation to outline a long-standing oral health problem from a clinical perspective. Our primary purpose has been to stimulate more discussion to better define the problem, and then to encourage group effort to resolve the matter by establishing norms for more appropriate diets.

References

Auskaps, A. M., Gupta, O.P. and Shaw, J.H.T. Peridontal disease in the rice rat. Ill. Survey of dietary influences. J. Nutr. 63:325, 1957.

Black, A. P., Crichlow, A. M., et al: Bacteremia during ultrasonic teeth cleaning and extraction in the dog. J. Dent. Res. 16:4, p.611-616, 1980.

Brekhus, P. J., Armstrong, W. D., and Simon, W. J.: Stimulation of muscles of mastication. J. Dent. Res. 20:87, 1941.

Burwasser, P., and Hill, T. J.: The effect of hard and soft diets on the gingival tissues of dogs. J. Dent. Res. 18:398, 1939.

Cobe, H. M., Transitory bacteremia. Oral Surg. 7:609, 1954.

Cohen,, B.: Comparative studies in peridontal disease. Proc. Roy. Soc. Med. 5:275, 1960.

Colyer, F.: Dental disease in its relation to general medicine, p.130. Longmans, Green & Co., London, 1911.

Colyer, F.: Variations and diseases of the teeth of animals, p.677. John Bale, London, 1936.

Coolidge, E. D.: The thickness of the human peridontal membrane. J. Amer. Dent. Ass. 24:1260, 1937.

Dent, V. E.: The bacteriology of dental plaque from a variety of zoo-maintained matmualian species, Archs. Oral Biol., Vol.24. 1979. p.277-282.

Engelberg, J.: Local effect of diet on plaque formation and development of gingivitis in dogs. 1. Effect of hard and soft diets. Odont. Rev. 16:31, 1965.

Hall, R. K.: Dental management of the chronically ill child, Aust. Dent J.; Vol.24, No.5, Oct. 1979.

Landry, S. M., Van Kruiningen, H. J.: Food habits of feral carnivores: A review of stomach content analysis. Jol. Ani. Hosp. Assoc. 15:6, 1979. p.775-782.

LeFrock, J. L., Ellis, C. A., et al: Transient bacteremia associated with percutaneous liver biopsy. Clin. Res. 21:8433, 1973.

Nizel, A.: Nutrition in preventive dentistry: Science and Practice, p.387. W. B. Saunders Co. Philadelphia.

O’Rourke, J. T.: The relation of the physical character of the diet to the health of the periodontal tissues. Amer. J. Orth. Oral Surg. 33:687, 1947.

Pelzer, R.: A study of the local oral effects of diet on the periodontal tissues and the gingival capillary structure. J. Amer. Dent. Assoc. 27:13, 1940.

Person, P.: Diet-consistency and periodontal disease in old albino rats. J. Periodont. 32:308, 1961.

Quie, P. G.: Streptococcus viridans and Streptococcus faecalis endocarditia. Zbl. Bakt., I. Abt. Orig., 214:298.

Shull, H. J., Green, B. M., et al: Bacteremia with upper gastrointestinal tract. Endoscopy, Ann Intern Med. 83:212, 1975.

Stahl, S. S., Miller, C. S. and Goldsmith, E. D.: Effect of various diets on the periodontal structure of hamsters. J. Periodont. 29:7, 1958.

Sullivan, N. M., Sutter, V. L., et al: Bacteremla following genito-urinary tract manipulation. Bacteriol Proe. M. 210:98 (Abstract), 1971.

Weinmann, J.: Keratinization of the human oral mucosa. J. Dent. Res. 19:57, 1940.