Bacterial plaque associated periodontal disease is the most common chronic infection in man and dogs. In man, there is an association between periodontal disease and myocardial infarction and stroke, while in dogs it has also been associated with changes in internal organs. Inflamed periodontal tissues present a 'periodontal disease burden' to the host and the extent of this inflammatory disease burden is likely to affect the degree of associated pathological change in distant organs. This hypothesis was investigated in dogs with naturally occurring periodontal disease. Post-mortem investigations including periodontal assessment, standard necropsy, and organ histology were performed on 44 mature toy and miniature Poodles (related, periodontitis predisposed breeds) that died naturally or were euthanized based on clinical disease. Animals with gross primary organ pathology were excluded. The periodontal disease burden was estimated from the total surface area of periodontal pocket epithelium using six measurements of probing depth for each tooth and the tooth circumferences. Ordinal logistic regression (OR) analysis established that for each square centimeter of periodontal disease burden there was a 1.4-times higher likelihood of greater changes being present in the left atrio-ventricular valves (OR = 1.43), plus 1.2 and 1.4 times higher likelihoodfor greater liver and kidney pathology (OR = 1.21; OR = 1.42), respectively The results show that there is a link between the estimated 'periodontal disease burden' resulting from plaque-bacteria associated periodontal disease and the level of internal pathology in this population, implying that periodontitis might contribute to the development of systemic pathology in dogs.

Transforming growth factor-beta (TGF-beta) represents a family of polypeptide growth factors, involved in embryogenesis, inflammation, regulation of immune responses and wound healing. To determine whether TGF-beta contributes to the evolution of periodontal disease, we assayed TGF-beta levels in gingiva and crevicular fluid of patients with gingivitis and periodontitis. In parallel, TGF-beta was quantified in gingival fluid and serum of beagles with experimentally-induced periodontitis. Disease was monitored by several clinical parameters including Plaque Index, Gingival Index, probing depth, and epithelial attachment loss. Gingival tissues were obtained from 9 patients at the time of periodontal surgery, and gingival fluid samples were collected from an additional population of 10 periodontal patients. In 14 beagles, experimental periodontitis was induced and gingival fluids collected 6 months later. Fluid was collected by paper strips and volume measured by Periotron. Additionally, sera was collected before and 9 months after the ligature-induced periodontitis in 7 beagles. The levels of TGF-beta 1 were measured by ELISA. In the patients, a significantly higher concentration of TGF-beta 1 was observed both in the gingival tissues and fluid samples obtained from the sites with deeper periodontal pockets than in the less involved sites. In beagles, TGF-beta 1 levels measured in gingival fluid were elevated in moderate disease, declining in fluid samples obtained from the pockets during more advanced experimental periodontitis. Furthermore, with the progression of experimental periodontitis, a decrease in TGF-beta 1 occurred in the sera of the beagle dogs. These data suggest that TGF-beta 1 may play a rôle in the pathogenesis and diagnosis of periodontal disease, and that its actions can be further explored in an animal model.

TAC in GCF is related to the degree of severity of periodontal disease in dogs. This is likely the result of release of reactive oxygen species by activated phagocytes and fibroblasts in the inflamed periodontal tissues. The results of our study suggest that the local delivery of antioxidants may be a useful adjunctive treatment for periodontitis in dogs.