2020 Volume 41 Issue 4 Pages 340-346
It is well known that gingival hyperplasia is caused by hereditary gingival fibromatosis and drugs such as phenytoin, calcium antagonists of nifedipine and amlodipine, and cyclosporine. We report a case of a severely mentally and physically disordered child who was found to have gingival hyperplasia with no drugs and who had no genetic factor.
A 7-year 8-month-old girl had cerebral palsy (spastic type), intellectual disability, epilepsy, and vascular Ehlers-Danlos syndrome. She was not taking any drug that could cause gingival hyperplasia and she also did not have any genetic predisposition to hereditary gingival fibromatosis. Horizontal ridge-like gingival hyperplasia was prominent inside the molars on both the upper and lower jaws. No findings of inflammation were observed in the hyperplasia gingiva. There were no bones inside the gingival hyperplasia. Impacted milk teeth and permanent teeth inside her gingival hyperplasia were observed. Narrowing of the tongue space and vertical positioning of the tongue were also observed. Due to the vertical gingiva expansion, the gingiva at the posterior part of the upper and lower molars came into contact, resulting in open bite with three-finger breadth. After gingival resection, eruption of permanent teeth and reduction of open bite width were observed. However, over time, gingival hyperplasia grew large again. Five years later, gingival hyperplasia was observed to the extent that the gingiva of the left and right lower molars contacted each other. Due to the difficulty of establishing an airway and hemorrhagic diathesis with vascular Ehlers-Danlos syndrome, we could not perform gingival resection. We referred her to another hospital where advanced medical management was possible.