[9] It includes: A thin, uniform lining of stratified squamous epithelium with tendency to detach from the underlying connective tissue capsule; a thin corrugated surface http://www.selleckchem.com/products/INCB18424.html layer of parakeratin; a spinous cell layer 8 to 4 cells in thickness, often showing intracellular oedema; a flat epithelial-fibrous tissue junction, usually devoid of epithelial rete ridges; and a relatively thin fibrous capsule that lacks inflammatory cell infiltrate. Benign neoplasm? Pindborg and Hansen[10] were the first to point out the aggressive behavior of OKC. Toller[4] as early as 1967 suggested that OKC should be considered as a benign neoplasm rather than a conventional cyst mainly because of their clinical behavior. Ahlfors and others[11] in 1984 suggested OKC to be classified as a true benign cystic epithelial neoplasm and suggested modified treatment schedules.
Shear[12] published his extensive work on the aggressive nature of the odontogenic keratocyst and finally labeled it as a benign cystic neoplasm. Shear aggressively used the term ��keratocystoma�� in naming this cyst. Regezi and others[13] have attempted to explain the pathogenetic mechanisms of OKC. They mention the mechanisms that favor growth and expansion of OKCs are high proliferation rate, over expression of antiapoptotic proteins (bcl-2) and expression of matrix metalloproteinase (MMPs 2 and 9). Mutation in PTCH 1 (��patched��) gene has also been considered as responsible for the pathogenesis of this cyst.[12,13,14] Recurrences The incidence of recurrence of OKC has varied from 2.5% to 62%.
[14] The great degree of variation in these reports are mainly because some series included cysts from patients with Nevoid Basal cell carcinoma syndrome (NBCCS), while other reasons for this variation can be due to duration of the follow-up period and method of treatment used.[14] In 1976, Brannon[15] proposed three mechanisms for OKC recurrence: Incomplete removal of the cyst lining, growth of a new OKC from satellite cysts (or odontogenic rests left behind after surgery), and development of a new OKC in an adjacent area. Histopathological features that predict recurrences. The major features that can be considered to predict recurrences in OKC are Higher level of cell proliferative activity in the epithelium Budding in the basal layer of the epithelium Parakeratinization of the surface layer Supraepithelial split of the epithelial lining Subepithelial split of the epithelial lining Presence of remnants/cell rests as well as daughter cysts.
Rechristened Meanwhile, Reichart and Philipsen[16] reclassified the odontogenic tumors in 2002 and renamed OKC as keratinizing cystic odontogenic tumor (KCOT) and placed it under the subheading of ��benign neoplasm of odontogenic epithelium with mature, fibrous AV-951 stroma; odontogenic ectomesenchyme not present.