BACKGROUND: Chronic sialectatic parotitis (CSP) is classified as a characteristic form of chronic recurrent parotitis the etiology and pathogenesis of which still remains unclear. The multiplicity of different therapeutic advices, especially the permanent failure of antibiotic treatment, underlines the lack of an appropriate causal therapy. CASE REPORT: Detailed histopathological investigations of an 41-year old woman were possible over a seven-year period. These follow-up observations enabled clarification of the histopathogenesis of CSP by means of immunohistochemistry. RESULTS: During the course and development of CSP different stages can be observed: The initial phase is characterised by mild infiltration of B-lymphocytes (CD20, CD45 R) and plasma cells in the environment of ectatic ducts. Progredient stages show neogenetic lymph follicles periductular as well as metaplasia of the ductal epithelium. Terminal phases of CSP are characterised by near-total lymphatic transformation of parenchyma, follicular lymphatic hyperplasia (KiM4) and myoepithelial proliferation. In this phase myoepithelial sialadenitis (MESA, i.e. benign lymphoepithelial lesion, possibly part of Sjögren's syndrome) develops. Beyond it low grade non-Hodgkin's lymphoma of the MALT-Type of the submandibular gland occurred finally. CONCLUSIONS: CSP presents as a precursor of MESA. Immunohistological detection of follicular dentritic network (KiM4) within extensive lymphatic hyperplasia periductular demonstrates overshooting humoral immune reaction of B-lymphocytes. Hence, CSP should be classified with regard to pathogenesis as an immunopathological disorder of the MALT system.
BACKGROUND:Chronic sialectatic parotitis (CSP) is classified as a characteristic form of chronic recurrent parotitis the etiology and pathogenesis of which still remains unclear. The multiplicity of different therapeutic advices, especially the permanent failure of antibiotic treatment, underlines the lack of an appropriate causal therapy. CASE REPORT: Detailed histopathological investigations of an 41-year old woman were possible over a seven-year period. These follow-up observations enabled clarification of the histopathogenesis of CSP by means of immunohistochemistry. RESULTS: During the course and development of CSP different stages can be observed: The initial phase is characterised by mild infiltration of B-lymphocytes (CD20, CD45 R) and plasma cells in the environment of ectatic ducts. Progredient stages show neogenetic lymph follicles periductular as well as metaplasia of the ductal epithelium. Terminal phases of CSP are characterised by near-total lymphatic transformation of parenchyma, follicular lymphatic hyperplasia (KiM4) and myoepithelial proliferation. In this phase myoepithelial sialadenitis (MESA, i.e. benign lymphoepithelial lesion, possibly part of Sjögren's syndrome) develops. Beyond it low grade non-Hodgkin's lymphoma of the MALT-Type of the submandibular gland occurred finally. CONCLUSIONS: CSP presents as a precursor of MESA. Immunohistological detection of follicular dentritic network (KiM4) within extensive lymphatic hyperplasia periductular demonstrates overshooting humoral immune reaction of B-lymphocytes. Hence, CSP should be classified with regard to pathogenesis as an immunopathological disorder of the MALT system.