Disease Info Card

Gingival Hyperplasia

Information about Gingival Hyperplasia: characteristics, related genes and pathways, plus antibodies you can use for research. This page is being enriched constantly, if you see some information you would like this page to include please send your suggestions to us.

Overview of Gingival Hyperplasia

Most recent studies have shown that Gingival Hyperplasia shares some biological mechanisms with decreased-immunologic-activity-[pe], dental-plaque, epilepsy, fibromatosis, fibromatosis-gingival, gingival-diseases, gingival-neoplasms, gingivitis, hemorrhage, hyperplasia, hypertensive-disease, hypertrichosis, hypertrophy, inflammation, mouth-diseases, neoplasms, oral-manifestations, periodontal-diseases, periodontitis, ulcer.

Among the many pathways, these few ones have gauged particular interests from scientists studying Gingival Hyperplasia, and have been seen in publications frequently: Amelogenesis, Bone Resorption, Cell Proliferation, Coagulation, Excretion, Fibroblast Proliferation, Glomerular Filtration, Hypersensitivity, Immune Response, Inflammatory Response, Localization, Mastication, Ossification, Pathogenesis, Phagocytosis, Pigmentation, Reverse Transcription, Secretion, Tooth Eruption, Wound Healing

Quite a number of genes have been found to play important roles in Gingival Hyperplasia, such as ALB, ANTXR2, CRP, CSH1, EGF, ERCC8, FGF2, FGF7, FN1, GCFC2, GGH, GH1, GNAI1, GORAB, HSPA9, IL1B, IL2, IL6, SOS1, TNF. See what Boster has to offer for the research of these genes by clicking the gene name links below and view a more detailed info card/product listing for that gene.

In a later update, we will include information such as current drugs and therapy solutions as well as on-going and past clinical trials for this disease. Plesae stay updated.