Familial gingival fibromatosis; no correlation with HLA-antigen A family study J. Katz', A. Ben-Yehuda^ E. MachteiS J. Goultschin' and Y. L. Danon^ ^IDF Dental and Oral Medicine Center; ^Department of Periodontology, Hadassah School of Dental Medicine; ^Beiiinson Medical Center, Department of Pediatrics, Isr&et Kalz J, Ben-Yehuda A. Machtei E, GouUschin J and Danon YL: Familial gingival fibromaiosis; no correlation with HLA-antigen. A family study. J Clin Periodontol 1989: 16: 660^61. Abstract. Familial gingival fibromatosis is generally reported to be inherited as an autosomal dominant trait. We investigated 2 families with few siblings affected with gingival fibromatosis. No linkage between HLA antigen and the phenomenon was found. These results support the idea of the autosomal dominant nature of familial gingival fibromatosis. Key words: familial gingival fibromatosis; HLA-antigens. Accepted for publication 27 December 1998 Gingival fibromatosis is an uncotnmon benign oral disease which has been re- ported in the literature under at least 25 different names (Jorgenson & Cocker 1974). It is characterized by a slowly progressive, non-hemorrhagic enlarge- ment of the maxillary and mandibular gingivae (Fig. 1). The familial nature of gingival fibromatosis has been sug- gested as being of an autosomal domi- nant mode (Rushton 1957. Hartsfield et al. 1985). In a few cases, autosomal recessive itiheritance has been reported (McKusick et al. 1968). We investigated 2 families with familial fibromatosis; a study of class I (HLA-A. B. C) determi- nants and CI-TI antigens (HLA-DR, DQ) was conducted in order to deter- mine the role of HLA in predisposing the disease. Material and Methods 2 families with a diagnosis of familial fibromatosis, one originating from Morroceo and the other from Yemen. were investigated in the department of Periodontology, Hadassah School of Dental Medicine. 10 ml of venous blood was collected in heparinized test tubes from each subject of the 2 families. Tis- sue typing for HLA-A. B, C antigens was performed using the standard two- Fig. 2. Pedigree of family no. i. Fig. 1. Fig. 3. Pedigree of family no. 2. Stage microcytotoxicity assay. HLA- ODR typing was performed on T cell depleted B cell enriched lymphocytes by extended incubation microtoxicity test- ing (Terasaki 1978). The HLA sera used were the alloantisera utilized for disease and genetic studies in the 8th Histocom- patibility Workshop (1980), and sera of local origin. HLA D typing was per- formed using the standard MLC tech- nique {Amar 1982). A selected panel of 80 European. American and local HTCs was employed to determine DW, to Results The pedigrees of Family 1, of Mor- roccan origin, are shown in Fig. 2. 3 affected siblings {1 female and 2 male) of this family do not share both HLA haplotypes (2 of the 3 affected siblings share haplotype A). The pedigree of family no. 2, of Ye- menite origin, are shown in Fig. 3, 4 siblings (3 male and 1 female) are affected. In this case too, the affected siblings do not share both HLA haplo- types (3 of 4 share haplotype A). Discussion and Summary In order to ascertain whether familial fibromatosis is inherited in linkage with HLA antigens, 2 families with few af- fected siblings were examined for HLA haplotypes. The results do not support the hypothesis that the disease suscepti- bility gene is in close linkage to the ma- jor histocompatibiiity antigen. In none