Chronic Sclerosing Sialadenitis of the Submandibular Gland is Mainly Due to a T Lymphocyte Immune Reaction

Abstract

The aim of our study was to investigate the role of immunopathological processes in the pathogenesis of chronic sclerosing sialadenitis of submandibular glands (Küttner tumor). For this purpose, biopsy specimens from submandibular glands of 22 patients with the histological diagnosis of chronic sclerosing sialadenitis were analyzed. Paraffin-embedded tissues were immunostained for T-lymphocyte subsets (CD3, CD4, CD8), cytotoxic T cells (granzyme B), B cells (CD20, Ki-B3), and macrophages (Ki-M1P). Polymerase chain reaction and capillary electrophoresis were used to detect rearrangements of the T-cell receptor gamma chain and the CDRIII region of the immunoglobulin heavy chain. In all cases, abundant cytotoxic T cells were found, especially in close association with ducts and acini. T-cell receptor gamma chain rearrangements showed a monoclonal pattern in 6 cases (27.3%), an oligoclonal pattern in 8 (36.4%), and a polyclonal pattern in 8 (36.4%). The B-cell reaction was less pronounced and largely restricted to lymph follicles. Molecular analysis of immunoglobulin heavy chain revealed a polyclonal rearrangement in 17 cases (77.3%). In conclusion, there is an intimate relationship between the T-cell-dominated inflammatory infiltrate and acinar and duct cells. This, together with the frequent demonstration of monoclonal and oligoclonal populations of cytotoxic T cells and their histopathological behavior, suggests that chronic sclerosing sialadenitis may be the result of an immune process triggered by intraductal agents.

Chronic Sclerosing Sialadenitis of the Parotid Gland

“…3,8 In the largest study on CSS, Seifert et al 9 showed that the findings in early and late CSS were similar to those in obstructive sialadenitis; however, the progression of the inflammatory process could not be explained by purely obstructive mechanisms. In a recent study to investigate the role of immunopathologic processes in the pathogenesis of CSS, Tiemann et al 10 found that there was an intimate relationship between the T cell-dominated inflammatory infiltrate and the acinar and duct cells, together with the frequent demonstration of monoclonal and oligoclonal populations of cytotoxic T cells and their histopathologic behavior. They concluded that CSS might be the result of an immune process triggered by intraductal agents.…”

Kuttner tumor

“…The effects of microliths (sialoliths), infectious agents, secretory dysfunctions, duct abnormalities, and immune processes have been considered (5,6,7,10).…”

“…Histopathology shows preservation of the lobular architecture, dense lymphoplasmatic infi ltration, periductal fi brosis, and loss of acini (5,14).…”

“…Chronic sclerosing sialadenitis has some characteristic features on fi ne-needle aspiration cytologic specimens: (1) relatively low cellularity and thus relative diffi culty in obtaining the cellular elements; (2) scattered ductal structures with paucity or absence of acini; (3) ducts intimately surrounded by collagen sheaths or lymphoid cells; (4) small isolated fragments of fi brous stroma; (5) moderate to large numbers of lymphoid cells that lack defi nitive atypia (5,11).…”

IgG4-LINKED SYSTEMIC DISEASE. MODERN OUTLOOK ON «OLD» DISEASE

“…Зачастую заболевание начи-нается остро, с высокой лихорадкой и лабораторными признаками воспаления. ХСС необходимо дифференци-ровать с БМ, БШ, лимфомами слюнных желез, саркоидо-зом, AL-амилоидозом, фиброгистиоцитарными опухоля-ми и неоплазмами [74][75][76][77][78][79][80][81]. ХСС считается редким заболе-ванием, однако этот факт может быть обусловлен сложно-стями диагностики, ведь на данный момент единствен-ным способом получения ткани ПЧСЖ является ее удале-ние -достаточно сложная и опасная операция.…”