Fibromatosis

A Brazilian/American collaboration has found a gene mutation that is responsible for the rare disease, hereditary gingival fibromatosis, in which the gums grow over the teeth. The results, published in the April issue of American Journal of Human Genetics, may help researchers explain the mechanisms by which such gingival overgrowth occurs.

The research team, led by Thomas Hart, associate professor of oral pathology and medicine at the University of Pittsburgh School of Dental Medicine (Room 440, Salk Hall, 3501 Terrace St., Pittsburgh, PA 15261; Tel: 412/648-8880; Website: www.dental.pitt.edu), studied a large multigenerational Brazilian family with high incidence of HGF. They discovered that a mutation in the son of sevenless-1 (SOS1) gene causes HGF, type one. SOS1 codes for a protein that activates the ras pathway, which promotes cell growth and division.

"By understanding this gene and the mutation, we have the potential to understand what causes normal gingival growth and abnormal gingival overgrowth. We are now looking at the therapeutic potential of manipulating this pathway," says Hart. "Not only does this create the potential for new therapies to treat HGF, but also new avenues for investigation into common dental problems like periodontal disease and receding gums."

The only treatment for HGF currently available involves cutting away the gingival overgrowth and trying to regrow the tissue between the teeth through grafting, a process that is both difficult and painful.

This discovery may also have implications for the diagnosis and treatment of other related diseases, including drug-induced gingival fibromatosis. Researchers believe that by understanding what causes gingival overgrowth, they may ultimately be able to identify those predisposed to drug-induced gingival fibromatosis. This unwanted side effect occurs in approximately 15% of patients who take dilantin for seizures; 15% who take calcium-channel blockers; 30% who take cyclosporine for autoimmune disorders; and 40% of transplant patients who combine cyclosporine and nifedipine as anti-rejection medication.

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