Major and Minor Salivary Glands

2016 ◽  
pp. 229-294 ◽  
Author(s):  
Silvana Di Palma ◽  
Roderick H. W. Simpson ◽  
Alena Skalova ◽  
Isabel Fonseca ◽  
Ilmo Leivo ◽  
...  
JMS SKIMS ◽  
2012 ◽  
Vol 15 (1) ◽  
pp. 76-77
Author(s):  
Mohd Athar ◽  
K S Sodhi ◽  
S Kala ◽  
R K Maurya ◽  
S Chauhan ◽  
...  

Adenoid cystic carcinoma is a relatively uncommon tumour of salivary, glands and is characterised by a prolonged clinical course and a fatal outcome. It was first described as `cylindroma' by Billroth in 1859. Half of these tumors occur in glandular tissues other than the major salivary glands; principally in the hard palate, but they can also arise in the tongue and minor salivary glands. Unusual locations include the external auditory canal, nasopharynx, lacrimal glands, breast, vulva, esophagus, cervix and Cowper glands. The long natural history of this tumor and its tendency for local recurrence are well known. JMS 2012;15(1):76-77.


2021 ◽  
Author(s):  
Stephan Ihrler ◽  
Abbas Agaimy ◽  
Orlando Guntinas‐Lichius ◽  
Christian J. Haas ◽  
Martin Mollenhauer ◽  
...  

2021 ◽  
Vol 17 (1) ◽  
Author(s):  
Eloá Borges Luna ◽  
Pâmella Pinho Montovani ◽  
Rafaela Elvira Rozza-de-Menezes ◽  
Karin Soares Cunha

AbstractIntroductionNeurofibromin, a protein encoded by theNF1gene, is mutated in neurofibromatosis 1, one of the most common genetic diseases. Oral manifestations are common and a high prevalence of hyposalivation was recently described in individuals with neurofibromatosis 1. Although neurofibromin is ubiquitously expressed, its expression levels vary depending on the tissue type and developmental stage of the organism. The role of neurofibromin in the development, morphology, and physiology of salivary glands is unknown and a detailed expression of neurofibromin in human normal salivary glands has never been investigated.AimTo investigate the expression levels and distribution of neurofibromin in acinar and ductal cells of major and minor salivary glands of adult individuals without NF1.Material and methodTen samples of morphologically normal major and minor salivary glands (three samples of each gland: parotid, submandibular and minor salivary; and one sample of sublingual gland) from individuals without neurofibromatosis 1 were selected to assess neurofibromin expression through immunohistochemistry. Immunoquantification was performed by a digital method.ResultsNeurofibromin was expressed in the cytoplasm of both serous and mucous acinar cells, as well as in ducts from all the samples of salivary glands. Staining intensity varied from mild to strong depending on the type of salivary gland and region (acini or ducts). Ducts had higher neurofibromin expression than acinar cells (p = 0.003). There was no statistical association between the expression of neurofibromin and the type of the salivary gland, considering acini (p = 0.09) or ducts (p = 0.50) of the four salivary glands (parotid, submandibular, minor salivary, and sublingual gland). Similar results were obtained comparing the acini (p = 0.35) and ducts (p = 0.50) of minor and major salivary glands. Besides, there was no correlation between the expression of neurofibromin and age (p = 0.08), and sex (p = 0.79) of the individuals, considering simultaneously the neurofibromin levels of acini and duct (n = 34).ConclusionNeurofibromin is expressed in the cytoplasm of serous and mucous acinar cells, and ductal cells of salivary glands, suggesting that this protein is important for salivary gland function.


2002 ◽  
Vol 110 (4) ◽  
pp. 316-321 ◽  
Author(s):  
Manoela Domingues Martins ◽  
Vera Cavalcanti De Araújo ◽  
Ricardo Raitz ◽  
Ney Soares de Araújo

Reumatismo ◽  
2016 ◽  
Vol 67 (3) ◽  
pp. 85 ◽  
Author(s):  
A. Alunno ◽  
V. Caneparo ◽  
F. Carubbi ◽  
O. Bistoni ◽  
S. Caterbi ◽  
...  

The interferon (IFN) signature, namely the overexpression of IFN-inducible genes is a crucial aspect in the pathogenesis of primary Sjögren’s syndrome (pSS). The IFN-inducible IFI16 protein, normally expressed in cell nuclei, may be overexpressed, mislocalized in the cytoplasm and secreted in the extracellular milieu in several autoimmune disorders including pSS. This leads to tolerance breaking to this self-protein and development of anti-IFI16 antibodies. The aim of this study was to identify pathogenic and clinical significance of IFI16 and anti-IFI16 autoantibodies in pSS. IFI16 and anti-IFI16 were assessed in the serum of 30 pSS patients and one-hundred healthy donors (HD) by ELISA. IFI16 was also evaluated in 5 minor salivary glands (MSGs) of pSS patients and 5 MSGs of non-pSS patients with sicca symptoms by immunohistochemistry. Normal MSGs do not constitutively express IFI16. Conversely, in pSS-MSGs a marked expression and cytoplasmic mislocalization of IFI16 by epithelial cells was observed with infiltrations in lymphocytes and peri/ intra-lesional endothelium. pSS patients display higher serum levels of both IFI16 and anti-IFI16 autoantibodies compared to HD. Our data suggest that IFI16 protein may be involved in the initiation and perpetuation of glandular inflammation occurring in pSS.


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