Early Detection of Dietary-Induced Periodontal Bone Loss and the Effect of Flurbiprofen Administration in the Syrian Hamster

Abstract

Root surface caries is an increasing problem in the United States as more of the population are retaining their teeth to an older age. The disease requires the recession of gingival tissue and resorption of alveolar bone prior to exposure of the root surface. Animal models for root surface caries provide a means to investigate the etiology and treatment of the disease. The Golden Syrian hamster has been used as a model, and alveolar bone loss and root exposure are induced by feeding the animals a high glucose diet. Significant bone loss, when compared to control groups, is usually detected within five weeks. At present, the use of non-steroidal anti-inflammatory drugs in the treatment of periodontal disease is an area of great interest. As there is a role of host response in the alveolar bone destruction seen in periodontitis, inhibition of this prostaglandin-mediated process may provide a means of treatment. Flurbiprofen (Ansaid™, Upjohn Co., Kalamazoo, Ml) has been widely studied and appears to inhibit this bone loss in a variety of animals, including man. The purposes of the study were to determine if the early alveolar bone loss occurring after three, four and five weeks' exposure to the high carbohydrate diet could be quantitated with fluorescent bone labels, and if this bone loss could be inhibited by daily administration of flurbiprofen. The animals received a series of four intraperitoneally-injected fluorochrome labels over a one-month period, then were fed ground lab chow, the high carbohydrate MIT-200GI diet or the MIT-200GI diet plus flurbiprofen. At the end of three, four and five weeks, animals were euthanized, and the mandibles were prepared for analysis. Statistical analysis of gross and histomorphometric measurements detected no significant differences between the experimental groups. It is suspected that the diets failed to produce periodontal disease in this experiment, possibly due to changes in the oral microflora caused by administration of tetracycline as the final bone label. There was much variation in the presence of bone labels, but they were able to provide the growth velocity of the alveolar complex. Flurbiprofen administration produced no measurable effects, but the animals did tolerate the dosage given. Future studies should consider variation of the labels and a different route of administration.