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Abstract: Metastasis to the mandibular condyle is rare, and such lesions should be identified by both clinical and pathological examinations. We experienced a case of adenocarcinoma occurring in the right mandibular condyle. A 65-year-old female with uterine cervical cancer showed condylar dysfunction. Imaging examinations revealed a tumor with bone destruction and a rapidly progressive course, while pathological examinations suggested metastasis originating from another site. Based on the clinical and pathological findings, the patient was diagnosed with condylar metastasis derived from the uterine cervix, in addition to a recurrence of uterine cervical cancer. [Copyright &y& Elsevier]

The article details a study which investigated if induction of systemic inflammation accelerates the development of Sjögren's syndrome (SS) in genetically susceptible mice. The study treated female mice with either Freund's incomplete adjuvant (IFA) or phosphate buffered saline (PBS). The mice were killed at different time points and underwent sialadenitis and salivary gland-infiltrating cells tests. It concluded that generalized inflammatory stimuli can accelerate the development of SS-like disease.

In the labial salivary glands (LSGs) of 16 primary and 18 secondary Sjögren's syndrome (SS) patients, infiltrating lymphocytes were histologically and immunohistochemically examined; also, the serum levels of rheumatoid factor, antinuclear antibodies, anti-DNA antibodies, anti-SS-A and anti-SS-B antibodies, and immunoglobulins (including IgG, IgM and IgA) were all assayed. An immunohistochemical analysis of the lymphocyte subsets in LSGs revealed that severe lymphocytic infiltration was frequently accompanied by marked B cell accumulation both in primary and secondary SS patients. Furthermore, local B cell accumulation was also closely associated with elevated levels of anti-SS-A and anti-SS-B antibodies and IgG, and this association was statistically significant in the group with primary SS but not in the group with secondary SS. Thus, local lymphocytic infiltration, especially B cell accumulation, in the salivary glands is suggested to be involved in serological abnormalities in primary SS, while complicated autoimmune diseases other than SS may also be involved in serological abnormalities in secondary SS. [ABSTRACT FROM AUTHOR]

Objective: This study was undertaken to determine whether induction of systemic inflammation accelerates the development of Sjögren's syndrome (SS) in genetically susceptible mice., Methods: Female (NZB x NZW)F1 mice were treated with either Freund's incomplete adjuvant (IFA) or phosphate buffered saline (PBS) at monthly intervals. Salivary gland function was monitored by measuring pilocarpine-induced saliva volume. Mice were killed at different time points and examined for sialadenitis and salivary gland-infiltrating cells. Sera were analyzed for autoantibodies to salivary gland antigens, nuclear antigens, and Ro60., Results: While IFA-treated mice had significantly decreased salivary secretion 7 weeks after the initial treatment, salivary secretion did not decrease in PBS-treated controls until 17 weeks. At 7 weeks, the severity of sialadenitis and the number of T and B cells infiltrating the salivary glands did not differ between the 2 groups. However, at this time point IFA-treated mice showed significantly higher frequencies of CD11clow, B220+, Ly6C+, mouse PDCA-1+ dendritic cells (DCs) in the salivary glands. While levels of autoantibodies did not differ between the 2 groups at early time points, by late time points IFA-treated mice had higher levels. The gland dysfunction observed in IFA-treated mice at earlier time points did not correlate with the severity of sialadenitis or levels of autoantibodies. Instead, it was associated with increased frequency of plasmacytoid DCs in the gland., Conclusion: Our data suggest that generalized inflammatory stimuli can accelerate the development of SS-like disease in (NZB x NZW)F1 mice, and that gland dysfunction in SS can develop prior to the generation of a robust adaptive autoimmune response.