Looking Deeper Into Biopsies for Extraglandular Risks in Sjӧgren’s


Inquiring into the state of immune cells and messengers in salivary gland biopsies could reveal the risks for comorbidities of Sjӧgren syndrome such as lymphoma.

Carubbi F, Alunno A, Cipriani P. Is minor salivary gland biopsy more than a diagnostic tool in primary SjÓ§gren’s syndrome? Association between clinical, histopathological, and molecular features: A retrospective study. Semin Arthritis Rheum. 2014 May 15. pii: S0049-0172(14)00109-7. doi: 10.1016/j.semarthrit.2014.05.015. [Epub ahead of print]  

Salivary gland biopsies, the gold standard for diagnosing SjÓ§gren’s syndrome, coupled with advanced molecular analysis of immune cells and cytokines may reveal which patients are at risk for complications such as lymphoma, according to a new study from Italy.

At least one third of primary SjÓ§gren’s patients have extra-glandular manifestations such as musculoskeletal, skin, kidney, and lung problems, and 5% develop lymphoma, mainly mucosa-associated lymphoid tissue (MALT) non-Hodgkin lymphoma (NHL).

Use of immunofluorescence or molecular assays in conjunction with minor salivary gland (MSG) biopsy reveals distinct patterns of inflammation and immune cell infiltrates that could, if validated, be used to help identify patients at risk, these researchers say.

They studied biopsied MSG tissue from the lips of 104 primary SjÓ§gren’s patients and 40 controls. Half of the control patients had sicca symptoms (e.g, dry eye) but normal salivary glands and no clinical or serological features of SjÓ§gren’s. The rest had various grades of salivary gland inflammation. The majority of the patients were women in their 50s with extraglandular signs and symptoms.

Using advanced molecular imaging, the investigators looked for clusters of lymphocytes resembling “germinal centers” (CGs), cellular structures associated with NHL where specific B-cells are activated. These GC-like structures in minor salivary glands are also associated with a higher frequency of joint, skin, and lung problems.

They also looked for unique genetic, serological and cytokine profiles in patients with CGs, studying these with other clinical and laboratory findings, such as autoantibodies.

The researchers found severe inflammatory infiltrates in all the SjÓ§gren’s patients with CG-like structures, but in only around half of the controls with or without CGs.

SjÓ§gren’s patients with CGs had been diagnosed at a younger age, had more severe glandular involvement, higher levels of inflammatory cytokines, and key antibodies, as well as unique genetic sequences. If confirmed, this profile could paint a picture of risk for certain SjÓ§gren’s patients.


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