Abstract

To investigate the causes of hypertrophy in recurrent tonsillitis with hypertrophy (RTTH). An immunohistochemical study of recurrent tonsillitis with or without hypertrophy and adenoid tissue. Academic medical center. The study population comprised 15 patients with RTTH, 15 patients with recurrent tonsillitis (RT), 9 patients with adenoid vegetation, and 6 controls. The following outcome measures were investigated: follicle number and follicular area and circumference; degree of papillary arrangement and keratin cyst in crypts; fibrosis; and density of S-100(+) cells, CD20(+) cells, CD45RO(+) cells, lymphocytes and plasma cells, and cyclin D(1)(+) cells in surface epithelium, crypt epithelium, extrafollicular area, and follicles. In the RTTH group, follicle number and follicular area and circumference, S-100(+) cell density in crypt and surface epithelium, and CD20(+) cell density in crypt epithelium were higher than in the RT group. The other measures were lower in the RTTH group than in the RT group. In patients with RTTH, the increase in follicle number and S-100(+) cell density in surface epithelium and decrease in cyclin D(1)(+) cell density in surface epithelium were significant. The number of CD45RO(+) cells was unchanged, while S-100(+) cell density increased in surface epithelium; however, in the RTTH group, CD20(+) cell density, together with cyclin D(1)(+) cell density, decreased in surface epithelium when compared with the RT group. Also, there was a 50% decrease in cyclin D(1)(+) cell density in follicles, but CD20(+) cell density decreased minimally in follicles. In the RTTH group, the increase or decrease in the number of cyclin D(1)-expressing cells was parallel with the increase or decrease in the number of CD20(+) cells in the areas without follicles. Tonsil hypertrophy occurred with follicular hyperplasia and hypertrophy. There is a deficiency of proliferating active cells in response to mitogenic stimulation in RTTH. New follicles might have formed with B cells supplied from other sites because of the deficiency of proliferating active cells.

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