Perspectives On Medical Research
Volume 5, 1995
Aping Science
A Critical Analysis of Research at the Yerkes
Regional Primate Research Center
3. Dental Research
S. Offenbacher and colleagues have studied the association between experimental
periodontitis (inflammation of the gums adjacent to the teeth) in rhesus monkeys
and the concentration of certain mediators of inflammation in the saliva near
teeth.1,2 Their findings have accorded with previous human clinical
observations, including those by Offenbacher, that local increases in the concentrations
of certain prostaglandins known to incite inflammation elsewhere in the body
are strongly associated with periodontitis and tooth attachment loss.3-6 Similarly,
while Offenbacher et al. showed that a drug that blocks formation of these
prostaglandins reduces experimental periodontitis, again this merely accorded
with previous clinical studies of people with periodontitis who were taking
similar drugs for treatment of arthritis.7,8 These findings are
consistent with the Committee on Animal Models in Biomedical Research’s
general finding that human clinical investigation tends to inspire animal studies,
which then merely dramatize various observations but fail to provide novel
insights.
Because this animal model system differs considerably in pathogenesis
and natural history from human periodontitis, it is unlikely to provide
clinically useful hypotheses. The researchers induced periodontitis in
monkeys by placing suture material around the teeth to incite inflammation
and providing a soft diet to promote plaque formation. Their manipulations
did cause periodontitis, but its etiology was irritation rather
than infection. It is unlikely that this experimental disease
process models human periodontitis, which typically has a much slower
onset and is affected by factors such as dental care, sugared gum, and
diet, not implanted foreign materials. Therefore, the monkey studies,
at best, can only dramatize clinical findings. Should the clinical data
and the monkey data diverge, it would likely reflect differences between
normal human periodontitis and the experimental analogue. Ongoing clinical
research is the most efficient and reliable means of determining the
optimal treatment for human periodontal disease.9
1. Offenbacher S, Braswell LD, Loos AS, et al. Effects of flurbiprofen on the
progression of penodontitis in Macaca mulatta. Journal of Periodontal
Research 1987;22:473-481.
2. Offenbacher S, Odle BM, Braswell LD, et a!. Changes in cyclooxygenase metabolites in experimental periodontitis in Macaca Mulata. Journal of Periodontal Research 1989;24:63-74.
3. Offenbacher S, Farr DH, Goodson JM. Measurement of prostaglandin E in crevicular fluid. Journal of Clinical Periodontology 198 l;8:359-367.
4. Offenbacher S, Odle BM, Gray RC, Van Dyke TE. Crevicular fluid prostaglandin E levels as a measure of the periodontal disease status of adult and juvenile periodontitis patients. Journal of Periodontal Research 1984; 19: 1-13.
5. Offenbacher S, Odle BM, Van Dyke TE. The use of crevicular fluid prostaglandin E2 levels as a predictor of periodontal attachment loss. Journal of Periodontal Research 1986;21: 101-112.
6. Goodson JM, Dewhirst FE, Brunetti A. Prostaglandins levels and human periodontal disease. Prostaglandins 1974;6:81-85.
7. Waite IM, Saxton CA, Young A, Wagg BJ, Corbett M. The periodontal status of subjects receiving non-steroidal anti-inflammatory drugs. Journal of Periodontal Research 1981; 16:100-108.
8. Feldman RS, Szeto B, Chauncey HH, Goldhaber P. Non-steroidal anti-inflammatory drugs in the reduction of human alveolar bone loss. Journal of Clinical Periodontology 1983;10:131-136.
9. Offenbacher S, Odle BM, Green MD, et al. Inhibition of human periodontal prostaglandin E2 synthesis with selected agents. Agents and Actions 1990;29:232-238.