Odontogenesis happens by means of a complex interaction between oral epithelium and surrounding mesenchymal tissue. Abnormal tissue interaction during this process can result in ectopic tooth development. Ectopic tooth eruption may result due to pathological process, such as a tumor or cyst or developmental disturbance. The pathogenesis of<unk>  is still controversial. The accumulation of fluid either between the reduced enamel epithelium and enamel or in between the layers of enamel organ seems to be the key to the formation of<unk> s. A potentially erupting tooth on an impacted follicle can obstruct the venous outflow, inducing rapid transudation of serum across the capillary walls. Main suggested that this may exert pressure, causing the accumulation of fluid. On the contrary, Toiler suggested that the breakdown of proliferating cells of the follicle after impeded eruption is likely to be the origin of the<unk> . The breakdown products may result in increased osmotic tension, resulting in cyst formation. The exact histogenesis of<unk> s remains unknown, but most authors favor a developmental origin from the tooth follicle. In 1928, Bloch-Jorgensen suggested that the overlying necrotic deciduous tooth is the origin of all<unk> s. The resultant periapical inflammation might spread to involve the follicle of the unerupted permanent successor, an inflammatory exudate ensued with resultant<unk>  formation. He reported 22 cases of follicular cysts and stated that in each case a deciduous tooth or the remnants thereof was found in direct contact with the cyst cavity and that the related deciduous tooth always was diseased. Azaz and Shteyer similarly suggested that the persistent and prolonged periapical inflammation caused chronic irritation to the follicle of the successors. This may trigger and hasten the formation of a<unk>  developing around the permanent teeth. They reported five cases of<unk> s which involved the second mandibular premolar in four children aged 8 to 11 years old. These children were referred for extraction of carious, nonvital primary molars with swelling of the surrounding soft tissue. Occlusal radiographs showed buccal expansion of bone at the affected site. The primary teeth were not in direct contact with the underlying<unk> . It has been suggested that<unk> s may be either extrafollicular or intrafollicular in origin. There were three possible mechanisms exist. Firstly, surrounding the crowns of affected teeth, the intrafollicular developmental<unk> s may be formed. These cysts may be secondarily inflamed and infected as a result of periapical inflammation spreading from non vital deciduous predecessors. Benn and Altini (1996) claimed that this possibility was unlikely as all the cases reported were not associated with tooth impaction. Secondly, radicular cysts developed at the apices of non vital primary teeth. These radicular cysts may fuse with the follicles of the unerupted successors, causing the eruption of the successors into the cyst cavity. This may result in the formation of extrafollicular<unk> . Shear regarded this to be exceptionally rare because radicular cyst is uncommon in the primary dentition. The third possibility is that periapical inflammation could be of any source but usually from a non vital deciduous tooth spreading to involve the follicles of unerupted permanent successors. The inflammatory exudate causes separation of reduced enamel epithelium from the enamel with resultant cyst formation.
Dentigerous cyst
Tornwaldt cyst
Paradental cyst
Tarlov cyst
Nuchal fibroma
Odontogenic cyst
Ganglion cyst
Acrospiroma