The mechanisms leading to the chronic cholecystitis are not settled [Citation[1]]. Chronic cholecystitis is associated with gallstones. However, there is no relation between number of gallstones and, severity of inflammation. Gross examination reveals variation in size of the gall bladder and variation in wall thickness. The key diagnostic light microscopic changes are fibrosis, mononuclear inflammatory infiltrates and metaplasia. The composition of the infiltrate varies from lymphocyte rich, to more involvement of plasma cells and macrophages. Penetration of bile through the epithelial layer may cause inflammation with abundant macrophages containing ceroid material. Dystrophic calcifications can occur and are associated with development of carcinomas [Citation[1]].
Gilloteaux and co-workers have for many years worked within this field and presented several important contributions. In previous studies the ultrastructure of the normal mucosa, ultrastructural observations regarding mucoid material and lipids have been outlined [Citation[2],Citation[3],Citation[4],Citation[5],Citation[6]]. It was early evident that alterations in the cholecystocytes were only identified with ultrastructural examinations. Light microscopic analyses did not give a high enough resolution.
In chronic cholecystitis a change in accumulation products in the apical part of the epithelial cells are seen. Accumulations of apparently normal mucous vesicles can be found. Sometimes changes in the secretory material are found, like variations in anionic components. Changes in cystic ultrastructure have been reported, as well as accumulations of lipids and mucolipids.
In the present study [Citation[7]] Gilloteaux and co-workers outline their experience with cases of chronic cholecystitis with limited or no lipid and mucolipid accumulations in the apical regions. The cholecystocytes have altered microvilli, mitochondrial damages in the apical regions. The cholecystocytes have altered microvilli, mitochondrial damages in the apical region, as well as mucous accumulation with aggregated, angulated lysosomes and liposomes with needleshaped crystals. Cell fragments were observed in the biliary sludge [Citation[7]].
Cell components being part of the biliary sludge can cause an instable situation and promoting development of gallstones. Thus, the authors have outlined support for the hypothesis that a prolonged, untreated cholecystitis could then cause malignant changes or cholesterolosis, as a basis for the clinical porcelain gallbladder [Citation[7]].
REFERENCES
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- Gilloteaux J, Pomerants B, Kelly TR. Human gallbladder mucosa ultrastructure evidence of intraepithelial nerve structures. Am J Anat. 1989; 184: 321–333. [PUBMED], [INFOTRIEVE]
- Oldham-Ott CK, Gilloteaux J. Comparative morphology of the gallbladder and the biliary tract in vertebrates: variation in structure, homologyin functions and gallstones. Microsc Res Tech. 1997; 38: 571–597. [PUBMED], [INFOTRIEVE], [CSA], [CROSSREF]
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