Gingival fibromatosis is an uncommon but benign oral disease which causes progressive and non-hemorrhagic enlargement of the gingiva. There are two types of
gingival fibromatosis: idiopathic
gingival fibromatosis (GF), which is of unknown cause and may be associated with hereditary factors, and
drug-induced
gingival fibromatosis which is caused primarily by
phenytoin intake. In cases of
gingival fibromatosis, either the teeth are delayed in emergence or most of the
crowns are embedded in the soft tissue even after full eruption. The objective of this study was to examine the basis of excess
collagen formation in the two types of
gingival fibromatosis in four patients admitted to the dental clinic at Kaohsiung Medical College Hospital, Kaohsiung, Taiwan. There were two male patients, aged ten (Case 1) and sixteen (Case 2), with idiopathic
gingival fibromatosis and
hypertrichosis, and two female patients, aged sixteen (Case 3) and eleven (Case 4), with
Dilantin-induced
gingival hyperplasia (DGH). Cultures of gingival fibroblast were established either from clinically excised hyperplastic tissues or from pre-orthodontic surgical normal gingiva. The synthesis of
collagen and levels of
prolyl hydroxylase, a key
enzyme in
collagen synthesis, were examined in the healthy and affected fibroblasts. Our studies showed that after two days in culture, fibroblasts from all four patients multiplied faster than healthy gingival fibroblasts, though the amount of
DNA and
protein per cell remained unchanged. In addition, all cultures (except Case 1) had a 2- to 3- fold increase of
prolyl hydroxylase activity over that of the controls. As in the cases of
prolyl hydroxylase activity, Case 1 did not show any change in
collagen synthesis when compared to the control. However, Cases 2, 3, and 4 showed appreciable
collagen increases in the cell and medium: 61% and 60% for Case 2; 16% and 36% for Case 3; and 21% and 80.7% for Case 4 respectively.