Huang J S, Ho K Y, Chen C C, Wu Y M, Wang C C, Ho Y P, Liu C S
Department of Periodontology, School of Dentistry, Kaohsiung Medical College, Taiwan, Republic of China.
Kaohsiung J Med Sci. 1997 Mar;13(3):141-8.
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.
牙龈纤维瘤病是一种罕见的良性口腔疾病，可导致牙龈进行性、非出血性肿大。牙龈纤维瘤病有两种类型：特发性牙龈纤维瘤病（GF），病因不明，可能与遗传因素有关；药物性牙龈纤维瘤病，主要由服用苯妥英引起。在牙龈纤维瘤病病例中，牙齿萌出延迟，或者即使在完全萌出后，大部分牙冠仍埋于软组织中。本研究的目的是，对台湾高雄医学院附设医院牙科门诊收治的4例患者的两种牙龈纤维瘤病中胶原蛋白过度形成的基础进行研究。有2例男性患者，分别为10岁（病例1）和16岁（病例2），患有特发性牙龈纤维瘤病并伴有多毛症；2例女性患者，分别为16岁（病例3）和11岁（病例4），患有苯妥英钠引起的牙龈增生（DGH）。牙龈成纤维细胞培养物，取自临床切除的增生组织或正畸手术前的正常牙龈。对健康和患病成纤维细胞中的胶原蛋白合成及胶原蛋白合成关键酶脯氨酰羟化酶的水平进行了检测。我们的研究表明，培养两天后，4例患者的成纤维细胞比健康牙龈成纤维细胞增殖更快，尽管每个细胞的DNA和蛋白质含量保持不变。此外，所有培养物（病例1除外）的脯氨酰羟化酶活性比对照组增加了2至3倍。与脯氨酰羟化酶活性情况一样，病例1与对照组相比，胶原蛋白合成未显示任何变化。然而，病例2、3和4的细胞及培养基中的胶原蛋白有明显增加：病例2分别增加61%和60%；病例3分别增加16%和36%；病例4分别增加21%和80.7%。
