The role of inflammation in the pathogenesis of gingival enlargement during the administration of diphenylhydantoin sodium in cats

Abstract

In order to determine the role of gingival inflammation in the pathogenesis of the gingival enlargment seen in individuals taking diphenylhydantoin sodium (DPH), thirteen female and ten male adult mongrel cats were subjected to a coarse diet, irritating plastic bands around selected teeth, and a daily tooth brushing routine. Fourteen days after initiating the diet, bands, and brushing, 12 of the cats were randomly selected to receive a daily intramuscular injection, 10 mg/kg body weight, of DPH. The remaining cats received the equivalent amount of inert solvent. The maxillary quadrants containing banded teeth were not brushed whilst the maxillary quadrants containing no banded teeth were brushed daily. This combination produced grossly inflamed (banded) and non‐inflamed (non‐banded) maxillary quadrants in two groups of animals; one group receiving DPH, the other receiving vehicle only. The mandibular gingiva were not used in this study. It was possible to reproduce the clinical and histological appearance of DPH gingival enlargement in 11 of the 12 cats receiving DPH and whose gingiva were subjected to local irritation and no oral hygiene. Animals receiving DPH and oral hygiene care, but with no bands on adjacent teeth and thus no local irritation, showed no overt gingival enlargement. Analysis of the results reveals that in the presence of local irritants, producing inflammation, gingival enlargement develops after DPH administration. In the absence of irritants no enlargement occurs.

Factors influencing phenytoin‐induced gingival enlargement

“…Firm evidence of the involvement of phenytoin as the principal iatrogenic factor in the development of gingival enlargement has been presented in the literature (Hassell et al 1976, Nuki & Cooper 1972, Seymour et al 1985, Dahllof et al 1993. Duration of treatment and phenytoin plasma levels have also shown a significant correlation to gingival enlargement in some studies (Panuska et al 1961, Little et al 1975.…”

Phenytoin induced gingival overgrowth in institutionalized epileptics

“…However, Aas (1963) found no statistically significant relationship between IQ and level of oral hygiene, but reported a statistically significant correlation between severity of inflammation and severity of gum overgrowth, a finding corroborated by the present investigation. Glickman & Lewitus stated in 1941 that focal irritation is a secondary phenomenon; in the interim, well controlled experiments in tnan, in monkeys and in cats have demonstrated that in the absence of the frank irritation and ensuing inflammation caused by plaque, PHT induced gingival overgrowth can be minimized (Hall 1969, Nuki & Cooper 1972, King et al 1976, Staple & Reed 1976, Pihistrom et al 1980, Steinberg & Steinberg 1982. Furthermore, patients without teeth, and thus without gingival sulci which harbor plaque, almost never develop the lesions (Glickman & Lewitus 1941, Ziskin et al 1941, Aas 1963).…”

The effect of a plaque control program on the development of phenytoin‐induced gingival overgrowth

“…Several itivesligators have suggested that gingival overgrowth can be prevented or minimized with good oral hygiene, but there is little information concerning the effectiveness of specific preventive programs on the development of gingival overgrowth. Nuki & Cooper (1972) studied the role of inflammation on the development of the PHT-lesion in an animal model and concluded that gingival inflammation associated with dental plaque is a prerequisite for the development of the lesion. Accorditig to Pihlstrom et al (1980).…”