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. 2003 Jul;36(7):464-71.
doi: 10.1046/j.1365-2591.2003.00627.x.

Inflammatory infiltrate of chronic periradicular lesions: an immunohistochemical study

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Inflammatory infiltrate of chronic periradicular lesions: an immunohistochemical study

S Liapatas et al. Int Endod J. 2003 Jul.

Abstract

Aim: To determine the cellular profile of human chronic periradicular lesions using immunohistochemical methods in order to study the differences in the cell infiltrate of periradicular granulomas and cysts.

Methodology: The study population consisted of 45 individuals without any systemic disease. Biopsies were obtained during periradicular surgery. Paraffin-embedded sections were stained by the avidin-biotin complex method (ABC), whilst cryostat tissue sections were stained using the alkaline phosphatase antialkaline phosphatase assay (APAAP). These methods are highly valid and sensitive using a panel of specific monoclonal antibodies: CD4, CD8, CD3, CD10, HLADR, CD20, CD45RO, CD68 and CD57. The 45 specimens were characterized by the use of both techniques.

Results: The 45 specimens were histologically diagnosed as: 25 periradicular granulomas, 17 periradicular cysts and 3 scar tissues. No statistically significant differences were detected in the inflammatory infiltrate between periradicular granulomas and cysts. Observation of the sections showed that the majority of inflammatory cells consisted of T and B lymphocytes and macrophages. T and B lymphocytes were equally distributed in 60% of the cases. The T4/T8 ratio ranged approximately from 1 to 3 and greater, being consistent with inflammation of periradicular tissues. The final differentiation of B lymphocytes to plasma cells was also detected, whilst natural killer (NK) cells were found in only 10 cases (22%). Moreover, antigen presenting cells and T suppressor/cytotoxic cells were found to be associated with both pre-existing and newly formed epithelium.

Conclusions: Periradicular granulomas and cysts represent two different stages in the development of chronic periradicular pathosis as a normal result of the process of immune reactions that cannot be inhibited.

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