Role of microliths in the aetiology of chronic submandibular sialadenitis: a clinicopathological investigation of 154 cases

Abstract

Inflammation possibly arises from ascending infection in a normal gland and exerts an obstructive and destructive effect on the parenchyma with the development of the related histological changes and a vicious circle involving further ascending infection. Normal glands contain microliths that possibly by localized obstruction cause atrophic foci that are reservoirs for ascending infection. Microliths and liths were unrelated: microliths were related to age as in normal glands whereas liths were related to duration of symptoms and appeared to be secondary to the sialadenitis. Many glands showed minimal changes, which raises the possibility of conservative treatment.

Retrograde Theory in Sialolithiasis Formation

“…15 Glandular inactivity, induced by parasympathectomy in cats, increases the incidence of microliths, mainly in the submandibular gland. 14 However, despite extensive investigation of microliths in the pathogenesis of sialolithiasis by Harrison et al, 16 several clinical and experimental considerations, such as the paucity of microliths within the parotid gland, cast doubts that microliths play a central role in the formation of sialolithiasis. These microliths might be just one of the components of the mucous part and/or mucous plugs (Figure 1) of the saliva.…”

Tenascin-C in Chronic Sclerosing Sialadenitis

“…All patients had given informed consent and the whole study was performed according to Helsinski II declaration. Five specimens of normal submandibular glands were selected from postmortem material used in previous investigations [4,7,8].…”

“…Cases of Grades 0 and 1 were grouped together as cases with ''no or localized fibrosis'', and cases with Grades 2 and 3 were grouped together as cases with ''widespread fibrosis'' [4,7].…”

“…In fact, CSS is associated with sialolithiasis in 29-83% of cases [3,4]. A major clinicopathologic study on CSS revealed that there was increasing fibrosis and duration of symptoms and that fibrosis was related to inflammation, atrophy, and sialolithiasis [4].…”

“…A major clinicopathologic study on CSS revealed that there was increasing fibrosis and duration of symptoms and that fibrosis was related to inflammation, atrophy, and sialolithiasis [4]. The processes involved in fibrosis of CSS remain poorly understood as only a small number of cases have been reported [5][6][7][8].…”