Hereditary gingival fibromatosis (HGF), also known as idiopathic gingival hyperplasia, is a rare condition of gingival overgrowth. HGF is characterized as a benign, slowly progressive, nonhemorrhagic, fibrous enlargement of keratinized gingiva. It can cover teeth in various degrees, and can lead to aesthetic disfigurement. Fibrous enlargement is most common in areas of maxillary and mandibular tissues of both arches in the mouth. Phenotype and genotype frequency of HGF is 1:175,000 where males and females are equally affected but the cause is not entirely known. It mainly exists as an isolated abnormality but can also be associated with a multi-system syndrome. Signs and symptoms
There may or may not be any evidence of history of HGF in the family nor any usage of taking long-term medicines for any particular disease when it comes to diagnosing HGF. There also may or may not be any signs of medical and/or family history of mental retardation, hypertrichosis, nor clinical symptoms that can be associated with gingival enlargement. Although, enlargement of gingiva, interdental papilla, hindered speech, and secondary inflammatory changes taking place in the mouth commonly at the marginal gingiva are all very indicative of this condition. Commonly the patient will have mandibular and maxilliary inflammation and overgrowth as opposed to the traditional pink, firm, and fleshy consistency of healthy gingiva. The patients jaw may also appear distorted because of the gingiva enlargements. Overgrowth of the gingiva can range from slightly covering the surface of teeth or it can even completely cover the surrounding teeth.
Inflammation
Hormonal Imbalance
Neoplasia
More commonly associated with an autosomal dominant gene inheritance
Multi-system syndromes: Zimmerman-Laband syndrome, Jones syndrome, Ramon syndrome, Rutherford syndrome, juvenile hyaline fibromatosis, systemic infantile hyalinosis, and mannosidosis
Some unknown causes

Mechanism
Genetic linkage studies are among the most popular methods of study to look at the mechanism of this HGF. Genetic linkage studies have found to localize genetic loci for autosomal dominant forms of HGF to chromosome 2p21-p22 (indicative of HGF1) and chromosome 5q13-q22 (indicative of HGF2). Chromosome 2p21-p22 has been refined to an interval of ~2.3 Mb to construct an integrated physical and genetic map of the 16 genes interval. Here, a mutation is found in sequencing these 16 genes.There is an insertion of a cytosine between nucleotides 126,142 and 126,143 in codon 1083 of the SOS1 gene, meaning there is a mutation in SOS1. This causes a problem because SOS1 introduces a frameshift mutation and creates a premature stop codon. Also, it can segregate over generations, most commonly four. Once it causes a premature stop codon, the chromosome loses four important proline-rich SH-3 binding domains in the carboxyl-terminal region of the SOS1 protein. As a result, the N-terminal amino acids for SOS1 is fused into a 22–amino acid carboxyl terminus. Researchers claim that this mutation in the SOS1 gene is a probable primary cause of this disease but limited information supports the mechanism of this claim. Diagnosis
There are very few ways to test a patient for HGF. Currently, the most common way to diagnose a patient is by means of a physical evaluation.