Burkitts lymphoma), causing rapid deterioration and death. However, most of the aggressive lymphomas respond well to treatment and are curable. The prognosis, therefore, depends on the correct diagnosis and classification of the disease, which is established after examination of a biopsy by a pathologist (usually a hematopathologist). Previous classifications
Several previous classifications have been used, including Rappaport 1956, Lennert/Kiel 1974, BNLI, Working formulation (1982), and REAL (1994). The Working Formulation of 1982 was a classification of non-Hodgkin lymphoma. It excluded the Hodgkin lymphomas and divided the remaining lymphomas into four grades (low, intermediate, high, and miscellaneous) related to prognosis, with some further subdivisions based on the size and shape of affected cells. This purely histological classification included no information about cell surface markers, or genetics, and it made no distinction between T-cell lymphomas and B-cell lymphomas. It was widely accepted at the time of its publication but is now obsolete.In 1994, the Revised European-American Lymphoma (REAL) classification applied immunophenotypic and genetic features in identifying distinct clinicopathologic entities among all the lymphomas except Hodgkin lymphoma. For coding purposes, the ICD-O (codes 9590–9999) and ICD-10 (codes C81-C96) are available. Staging
After a diagnosis and before treatment, cancer is staged. This refers to determining if the cancer has spread, and if so, whether locally or to distant sites. Staging is reported as a grade between I (confined) and IV (spread).
Complementary response to inflammation
Chemical reaction with Interleukin and Prostaglandin

Mechanisms
Periapical cysts develop due to an inflammatory stimulus in 3 stages:
Initial stage: Epithelial cells from the rests of Malassez at the apex of the roots of a non-vital tooth (one where the nerve and blood supply in the tooth have degenerated and no longer exist) become stimulated due to the bodys inflammatory response to bacterial endotoxins infecting the pulp or as a direct response to necrotic pulp tissue, therefore re-entering the growth phase. Bacterial byproducts then are able to seep into the periapical region through the infected pulp. Cyst development stage:  Epithelial cells form strands and are attracted to the area which contains exposed connective tissue and foreign substances. Several strands from each rest converge and surround the abscess or foreign body. Cyst growth stage: Fluid flows into the cavity where the forming cyst is growing due to the increased osmolality of the cavity in relation to surrounding serum in capillaries. Pressure and size increase.The definitive mechanism by which cysts grow is under debate; several theories exist. Biomechanical theory
Pressure and concentration differences between the cystic cavity and the growth surroundings influence fluid movement into the cyst, causing size increase. Biochemical theories
a. Collagenase (breakdown of collagen) in the jaw bone leads to bone degeneration, providing room for cysts to develop. Substances released by the bodys immune system as a result of the connective tissue breakdown, such as cytokines and growth factors, contribute to the mobilization and proliferation of epithelial cells in the area. b.