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Association of Periodontal Disease and Histologic Lesions in

Multiple Organs from 45 Dogs
Linda J. DeBowes, DVM, MS, Department of Clinical Sciences, Kansas State University
Derek Mosier, DVM, PhD, Diagnostic Medicine/Pathobiology, Kansas State University
Ellen Logan, DVM, PhD, Science and Technology Center, Hill’s Pet Nutrition, Inc.*
Colin E. Harvey, BVSc, FRCVS, Department of Clinical Studies, School of Veterinary Medicine, University
of Pennsylvania
Stephen Lowry, PhD, Science and Technology Center, Hill’s Pet Nutrition, Inc.
Daniel C. Richardson, DVM, Science and Technology Center, Hill’s Pet Nutrition, Inc.
*(Dr. Logan was at Kansas State University Animal Resource Facility at the time this study was
conducted.)
Introduction
Periodontal disease is a common problem in dogs that may affect their health and
quality of life. A greater than 75% incidence of periodontal disease has been reported
in dogs 1. The presence of systemic disease in dogs with chronic periodontal disease
has been attributed to bacteremia and absorption of bacterial toxins from the oral cavity
1-9. Problems suggested to be associated with chronic periodontal disease in dogs
include chronic bronchitis, pulmonary fibrosis, endocardiosis, endocarditis, interstitial
nephritis, glomerulonephritis, and hepatitis1-9.
Periodontal disease in human beings may affect their general health and lead to
systemic disease 10. A significant relationship in human beings between dental disease,
cardiovascular disease, and total mortality has been reported 11. Bacteremia is
sometimes attributed to poor dental hygiene, periodontal infections, and periapical
infections in human beings 12. Additionally, infective endocarditis can be associated
with tooth brushing and mastication, as well as dental procedures 13, 14. During
mastication, bacteria enter the blood stream via the lymphatics at a predicted
cumulative rate about 1,000 times greater than that which occurs from a single tooth
extraction 15. Additional concerns for human beings with oral infection are the
potential for development of acute bacterial myocarditis, brain abscesses, uveitis,
“fever of unknown origin”, and other problems 16. The purpose of the present study
was to evaluate the relationship between periodontal disease and pathologic changes in
various tissues in dogs.
Materials and methods
Forty-five dogs were obtained from the Animal Resource Facility at Kansas State
University, College of Veterinary Medicine. Dogs ranged in age from 5 months to 14
years (mean = 2 years, median = 3.9 years) and weighed between 3.2 and 27.3 kg
(mean = 12.5 kg, median = 13.6 kg). All dogs were presented to the Animal Resource
Facility for euthanasia. All components of the study were conducted following humane
euthanasia with a lethal injection of Beuthanasia-D (Schering-Plough Animal Health).
Following euthanasia, a periodontal disease score (PDS) was determined for each dog.
The individual tooth PDS was the sum of the scores for the following criteria for each
tooth: plaque index, calculus index, mobility, furcation exposure, true pocket depth,
pseudopocket depth, and gingival recession. The animal PDS was the sum of the tooth
periodontal disease scores. Criteria used to determine the plaque index, calculus index,
mobility, and furcation exposure scores are listed in Table 1 17. True pocket depth was
measured (millimeters) from the cementum-enamel junction (CEJ) to the bottom of the
pocket. Gingival recession was measured (millimeters) from the CEJ to the gingival
margin. Pseudopockets were measured (millimeters) from the CEJ to the free gingival
margin. Teeth that were missing and concluded to be missing due to periodontal
disease, were assigned a tooth PDS based on an estimated score compatible with
severe periodontal disease. Assigned PDSs for individual teeth presumed lost
secondary to periodontal disease were: incisor, first premolars, mandibular third molar
teeth - 15; second, third, fourth premolar and first, second molar teeth - 18; canines -
20.
All collected tissues were observed for evidence of gross pathologic change. The
mitral valves were specifically evaluated for gross evidence of endocardiosis.
Organs evaluated microscopically were lungs, heart, kidneys, liver, spleen,
tracheobronchial lymph node, submandibular lymph node, and tonsil. Lung specimens
were obtained from the apical, middle, and diaphragmatic lobes of both lungs and the
accessory lung lobe. Papillary muscle from the left ventricle was obtained from the
heart. Histopathology scores were determined for each tissue based on the criteria
listed in Table 2. Scores from zero to five were assigned for each criterion, with zero
equaling normal and five being the most severely affected. Kidney scores were based
on the sum of the score for both kidneys from each dog. Organ specimens were
collected by a single person (EL) and histopathology was performed by a single
pathologist (DM) who was unaware of the PDS.
Multiple regression analysis was performed to determine if PDS was a predictor of
histopathologic changes (organ histopathology score) or mitral valve endocardiosis
while accounting for changes due to age. Statistical significance was set at p < 0.05.
Results
Eleven of the 45 dogs studied had gross changes on their mitral valve leaflets consistent
with endocardiosis. However, there was no significant relationship between PDS and
mitral valve endocardiosis in the 45 dogs studied.
A statistically significant relationship (p = 0.027) was present between PDS and the
histopathology score for criteria included under the category “myocardial
degeneration” (Tables 2, 3). Statistically significant relationships were also present
between PDS and histopathology scores for the criteria included under the categories
“kidney -glomerulus” (P = 0.0001), “kidney - interstitium” (P = 0.042) (Tables 2, 4),
and “liver parenchyma” (P = 0.035) (Tables 2, 5). The PDS was not a significant
predictor of organ histopathologic score in lungs (Table 6), spleen, tonsil,
tracheobronchial or submandibular lymph nodes (Table 7). All results were adjusted
for differences in age of the dogs.
Discussion
In dogs, kidney disease, particularly glomerulonephritis, is considered a potential
consequence of chronic low-grade bacteremia associated with periodontal disease
1,4,6,8,18,19. Pyelonephritis and interstitial nephritis may also result from bacteremia
or sepsis related to oral infection 5,9. The results of this study demonstrate an
association between periodontal disease and morphologic changes in renal glomeruli
and interstitium. Glomerular changes were mild, variable thickening of the mesangia
and were interpreted as being non-specific alterations suggestive of immune complex-
mediated damage. The interstitial change was an increase in lymphocytes and plasma
cells in the interstitium of the cortex, medulla, and pelvis. Collectively, these findings
suggest that periodontal disease may contribute to the development of chronic lesions
compatible with low-grade but persistent insult to the kidney. In extreme cases, where a
disease process sufficiently injures the glomeruli and/or interstitium, chronic renal
failure may result 20.

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failure may result 20.

Bacterial endocarditis in dogs may result from bacteremia associated with dental
manipulations or severe periodontal disease 19,21. A cause and effect relationship is
supported by the isolation of the same bacteria from the gingival sulcus and from
infected, fibrosed mitral valves 9,22. Endocardiosis and myocardial fibrosis occur
with increased frequency in aged dogs and it has been suggested that geriatric dogs with
periodontal disease have a higher incidence and greater severity of cardiac disease
compared to those with healthy teeth 22. In the current study, the focal fibrosis and mild
degenerative changes found in myocytes are compatible with past episodes of mild
ischemic or inflammatory insult. The significance of the thickening of myocardial
vessels is unknown.
Chronic bronchitis, chronic obstructive pulmonary disease, fibrosis, and emphysema
are often present in dogs with periodontal disease 7, 22-24. Periodontal disease may be
an initiating, contributing, or exacerbating factor for these conditions. It has been
postulated that chronic periodontal disease exposes the lower respiratory tract to large
numbers of bacteria which may cause chronic, recurrent, low-grade infections and
subsequent pulmonary damage 7,22. The same bacteria have been cultured from the
gingival sulcus and the small airways of the lungs, suggesting a cause and effect
relationship 22. In geriatric patients with periodontal disease, an increase in the
incidence and severity of pulmonary diseases compared to geriatric patients with
healthy teeth has been suggested 22. However, in the current study there was no
significant association between the PDS and the lung histopathology scores.
Bacteremia associated with periodontal disease is a suspected cause of some hepatic
disorders, including hepatitis in dogs 1,3,4,6,8. There was a significant relationship
between PDS and hepatic parenchymal inflammation score in this study. This
inflammation was generally mild, multifocal, and of minimal clinical significance.
The results of this study indicate a significant relationship between periodontal disease
and morphologic alterations in the kidney (glomerulus, interstitium), myocardium, and
hepatic parenchyma. These results support the hypothesis that periodontal disease can
have systemic effects on other organs.

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