J. Ussmuller et K. Donath, Clinical, histopathological and immunohistochemical investigations of chronic sialectatic parotitis in children and juveniles, KLIN PADIAT, 211(3), 1999, pp. 165-171
Chronic sialectatic parotitis (CSP) causes problems in differential diagnos
is and therapy. CSP shows the typical clinical features of chronic recurren
t parotitis and will be investigated histopathologically only after ultimat
ive parotidectomy. The etiology and pathogenesis of these unspecific inflam
mations is still unknown. Therefore no causal therapy is available and a lo
t of different trials (sialogoga, gland massage, infrared light, antibiotic
s, antiphlogistics, Trasylol(R), duct occlusion, duct ligation, gland dener
vation, radiotherapy) are not successful in the-long run.
Material and method: The salivary gland registry of the University of Hambu
rg (1965-1996) contains 22 infants and juvenile patients showing very sever
e courses of CSP. These cases have been investigated clinical (ultrasound,
sialography), histopathological (paraffin embedded sections, histomorphomet
ry of the ectatic duct lumina) and immunohistochemical (CK-MNF, AKTIN, KiM4
) in a retrospective study to research the pathogenesis of CSP.
Results: Recurrent and always very dolent parotid swelling occurs between t
he age of 3 and 14 years for the first time. The courses vary from 3 months
until 25 years. Local findings as well as ultrasound and sialographic feat
ures allow no certain differentiation of chronic recurrent parotitis. Conse
rvative therapy fails in each case and leads to the necessity of surgical t
reatment. Histopathological three different stages of development can be ob
served: Initial stages show regular lobular architectonic structure of the
parotid gland parenchyme with duct ectasies surrounded by slight inflammati
on of lymphocytes and plasmacells. Advanced stages are characterized by an
increase of periductal inflammation and the appearance of lymphfollicels. N
early complete lymphatic transformation of the parenchyme with destruction
of the lobular formation dominates the terminal "immunologic" stage. Some c
ases show multiple myoepithelial islands within this lymphatic stroma typic
ally observed in benign lymphoepithelial lesions. Whether bacteria nor prim
ary obstructive changes can be observed. The histomorphometric analyses of
the average and maximal luminal duct diameters show marked increase of 39%
respectively 46% from advanced to terminal stages of CSP. Therefore the pat
hognomonic duct ectasies seem to depend on the progredient inflammation and
are not due to a hereditary malformation of the duct system. Immunohistoch
emical terminal stages show follicular lymphatic hyperplasia (KiM4) express
ing overshooting humoral immune reaction of MALT.
Conclusion: Concerning the pathogenesis CSP corresponds to a immunopatholog
ical disorder of MALT and seems to be a prestage of benign lymphoepithelial
lesion. Consequently important changes in the diagnosis and therapy of CSP
lead to early histopathological investigation to differentiate the stage o
f inflammation. In stage III conservative parotidectomy should be carried o
ut because spontaneous healing can nor be expected. In contrast initial cas
es should be treated at first by glucocorticoids and immunosuppressives.