Male patient, black, 21 years of age, who consulted the Maxillofacial Surgery Department of the Hospital Universitario San Vicente Fundación de Medellín attached to the Universidad de Antioquia, referred by a dentist from a public health institution for presenting an asymptomatic increase in the volume of the mandible, with unknown evolution.
Intraorally, excellent dental integrity and good dental occlusion were observed, but there was an increase in volume in the vestibular region involving the body and the symphysis, while lingually, the expansion of the table was only in the area of the lower right canine and bicuspids.
The initial panoramic X-ray showed a radiolucent image 10 cm long, multiloculated, located from distal tooth 46 to mesial tooth 33. The mesial root of tooth 46 and the root of tooth 45 showed rhizolysis, with possible pulp necrosis. Teeth 46, 45 and 44 had minimal mobility; the other teeth had normal vitality and the lower dental canal was rejected. There is no alteration in the sensitivity of the mentonian nerve.

The patient consented to the entire treatment by signing the informed consent form. Prior to the initial biopsy an aspirate was taken producing a citrine fluid and the first histopathological study found a lax connective tissue, some multinucleated giant cells with few nuclei and a thin band of keratin; there was no evidence of epithelial tissue but it was considered as insufficient sample. Nevertheless, a diagnosis of keratocystic odontogenic tumour was made, due to the presence of a keratin band. After this procedure, the lesion became superinfected and the patient had to be hospitalised due to the severity of the clinical picture; this condition was used to perform a second biopsy under general anaesthesia 8 days later, in which a capsule made up of connective tissue with an intense inflammatory infiltrate and epithelial tissue with several layers of cells was found, which gave the diagnosis: inflammatory root cyst. Given the ambiguity of the diagnosis and the aggressiveness of the lesion, it was decided to perform the intervention with the first diagnosis (keratocystic odontogenic tumour -exkeratocyst-). With this diagnosis it was decided to plan an aggressive surgical treatment and it was decided to order endodontic treatment from 46 to 33 (9 teeth) prior to the surgical procedure, as the dental apices were immersed in the cavity and the curettage itself would cause amputation of the pulp vascular bundles, in addition, according to the diagnosis, it is a very recurrent lesion. This endodontic treatment lasted 3 months due to the difficulty of sealing the canals due to the presence of an amber-coloured liquid draining through the pulp chambers. After this time, the production of liquid content ceased and the endodontic treatment was completed.

The surgical phase was performed under general anaesthesia. A trapezoidal flap was raised from distal 46 to distal 33. When the flap was reflected, it was found to be expanded in its entire length and perforated in the bicuspid area (teeth 44 and 45), where the biopsies had previously been taken. We proceeded to remove all the expanded vestibular cortex until we had complete access to the cystic cavity. The thick fibrous capsule covering the osseous defect was found and removed. The bone cavity is reamed with rotary cutting instruments and the entire bone defect is brushed with Carnoy's solution. Some perforations of the lingual cortex are visible, which are cauterised with an electroscalpel due to the risk of invasion of the tumour lesion into the lingual soft tissues. Due to the weakening of the mandibular basilar border, a reconstruction plate is placed to avoid intra- or postoperative fracture. Before suturing the flap, the bone defect is filled with fibrillar collagen and medicated with analgesics and antibiotics. The tissue obtained is sent to pathology. The histopathological report of the surgical specimen shows fibroconnective tissue devoid of epithelium and a post-surgical diagnosis of an aneurysmal bone cyst was obtained.
Because the second biopsy showed an epithelium, the diagnosis was misleading but, evaluating the three histopathological samples, it was considered that the epithelial tissue of the second biopsy was the product of the inflammatory reaction, while the initial biopsy and the surgical specimen showed no epithelial component; it was decided to consider it an aneurysmal bone cyst.
The patient was evaluated at 8 and 15 days and then at 2 months, 10 months and 2 years. At the follow-up appointment at 2 months pulp necrosis and fistula were found at the level of 47, which was adjacent to the lesion and the mesial root apex had been amputated during the surgical procedure. Endodontics was performed and the infection resolved. He also presented with right mentonian nerve paraesthesia and was prescribed B-complex tablets for one month. A new post-surgical assessment was carried out 10 months later and adequate bone healing was found, but there was an occlusal sequela, as the teeth that were left without bone support due to being immersed in the bone defect (teeth 44 to 33) were intruded and produced an open bite. Two years later a new clinical and radiographic check-up was carried out where it was found that: teeth 44 to 33 remained in open bite, tooth 44 was also slightly vestibularised. The panoramic radiograph shows good bone filling, but the three-dimensional tomography shows that there is a defect of about 6 mm in diameter that compromises the apex of 44 and 43, and that the bone has yet to regenerate, and the paraesthesia still persists two years later. The intraoral image shows that the enlargement produced by the expansion of the lesion of the lingual plate at the level of teeth 43, 44 and 45 still persists.