However, treatment is necessary to maintain a healthy lifestyle. If left untreated
The following can occur if left untreated:

Too much gingiva exposure

Oral morbidity

Chronic infection of areas between the gums and teeth, or at the gum line

various degrees of Periodontitis - most likely due to the inability and difficulty of keeping the gingival margin and surrounding tissue clean due to the overgrowth

Improper tooth eruption and/or complete prevention of tooth eruption as a result of too much gingiva exposure

Systemic every-day troubles including functional and aesthetic problems of the mouth

Malocclusion

Treatment
Most recent methods of treatment take the form of surgeries such as oral prophylaxis, followed by post-surgical therapies to monitor, provide proper oral hygiene, and correct the deformity. Although, the nature of recurrence post-treatment is virtually unknown, let alone what type of treatment is most effective for HGF. (SOURCE 2) In some cases, there is re-growth after surgical removal of the excess gingival tissues, in others there is minimal. No cases yet have shown any particular treatment or form of medicine to permanently remove HGF.One type of procedure that can be executed is as follows: Removal of excess tissue under anesthesia through an internal bevel gingivectomy or undisplaced flap followed by gingivoplasty and continuous sling suture placements and periodontal dressing; after about a week of recovery after the surgery, remove sutures and periodically do observational evaluations to look for any signs of re-occurrence. Recent research
Some researchers suggest that HGF is transmitted as a Mendelian trait since both autosomal dominant and autosomal recessive transmission has been reported since the early 1970s.
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.