Periodontitis is a lesser known but frequent complication of
diabetes mellitus and is the major cause of
tooth loss in patients with diabetes. Dental
therapy for this complication is primarily focused on the control of oral
infections. No current
therapy directly addresses the potential effects of diabetes itself on this complication. In studies conducted in young normal control and
streptozotocin diabetic rats (100 g) treated with and without the
aldose reductase inhibitor (ARI)
imirestat, experimental
periodontitis was induced in one side of the mouth by 3
injections of
lipopolysaccharide (LPS) from Escherichia coli 055:B5 9 into the palatal gingiva between the first and second maxillary molars at 48-hour intervals. The other control side was injected with
phosphate buffered saline (PBS). Fourteen days after the final injection, all rats were euthanized and the heads were defleshed. The maxillary area was separated from the remaining skull. The cleaned maxillary alveoli were stained in 5% aqueous
toluidine blue to identify the cemento-enamel junction (CEJ) on the molars.
Alveolar bone loss was measured according to standard methods by determining both the distance between the CEJ and the alveolar bone on the 2 molars between which the
injections were made, and by measuring the ratio of root area/enamel area in the same region. These measurements showed that LPS
injections resulted in significant bone loss compared with PBS
injections in both control and diabetic rats, and that this bone loss was not present in the ARI-treated diabetic rats (P < 0.05). These results suggest that the
sorbitol pathway plays a critical role in the pathophysiological mechanism(s) of diabetic
periodontitis and that AR may be a direct pharmacological target for the treatment for this disease.