[2] This type of odontogenic neoplasm was designated as an adamantinoma in 1885 by the French physician Louis-Charles Malassez.

Additionally, as abnormal cell growth easily infiltrates and destroys surrounding bony tissues, wide surgical excision is required to treat this disorder.

If an aggressive tumor is left untreated, it can obstruct the nasal and oral airways making it impossible to breathe without oropharyngeal intervention.

As the swelling gets progressively larger it can impinge on other structures resulting in loose teeth and malocclusion.

Due to thin bone and weak barriers, the neoplasm can extend into the sinonasal passages, pterygomaxillary fossa and eventually into the cranium and brain.

Resemble a fibro-osseous lesion with no obvious ameloblasts whilst dominated by dense collagenous tissue (desmoplastic).

[8] Radiographically, the tumour area appears as a rounded and well-defined lucency in the bone with varying size and features.

Numerous cyst-like radiolucent areas can be seen in larger tumours (multi-locular) giving a characteristic "soap bubble" appearance.

[10] While chemotherapy, radiation therapy, curettage and liquid nitrogen have been rarely effective in cases of ameloblastoma, surgical resection or enucleation remains the most definitive treatment for this condition.

However, in a detailed study of 345 patients, chemotherapy and radiation therapy was contraindicated for the treatment of ameloblastomas.

A case of giant ameloblastoma was recently reported and managed with total mandibulectomy and pectoralis major myocutaneous flap reconstruction.

[8] The aim of treatment and surgery is to remove the entire tumour with a margin of surrounding tissue (block resection) for a good prognosis.

[13] Smaller mandibular neoplasms have been enucleated where the cavity of the tumour is curetted, allowing preservation of the bone cortex and the lower border of the mandible.

[25] To reduce the likelihood of recurrence within grafted bone, meticulous surgery[23] with attention to the adjacent soft tissues is required.

[7] A recent study discovered a high frequency of BRAF V600E mutations (15 of 24 samples, 63%) in conventional ameloblastoma.

These data suggests drugs targeting mutant BRAF as potential novel therapies for ameloblastoma.

[26] SMO mutations lead to the activation of the hedgehog pathway giving similar results as V600E but is less frequently seen.

[7] Evidence shows that suppression of matrix metalloproteinase-2 may inhibit the local invasiveness of ameloblastoma, however, this was only demonstrated in vitro.

[28] People with African heritage have been shown to have a higher incidence compared to Caucasians, with the site often being in the midline of the mandible.