Sjogren's syndrome is an autoimmune disease characterized by inflammation and destruction of lacrimal and salivary glands. The development of the inflammation requires the migration of lymphocytes from the blood into these tissues. This migration involves multistep cascades with binding of lacrimal gland endothelial adhesion molecules to their ligands on circulating lymphocytes. We used nonobese diabetic mice, which develop autoimmune-mediated lacrimal gland inflammation, as an experimental model to define the adhesion molecules that control lymphocyte migration into inflamed lacrimal glands. We found that vascular endothelia in inflamed areas of lacrimal gland expressed vascular cell adhesion molecule (VCAM)-1 and the peripheral node addressin (PNAd), but not mucosal addressin cell adhesion molecule-1. Most lymphocytes in the inflamed glands expressed alpha(4) integrin, L-selectin, and lymphocyte function-associated antigen (LFA)-1. In vivo studies revealed that antibodies against VCAM-1, alpha(4) integrin, PNAd, L-selectin, or LFA-1 almost completely blocked lymphocyte migration from blood into inflamed lacrimal glands. There was no inhibition of migration by antibodies against mucosal addressin cell adhesion molecule-1 or alpha(4)beta(7) integrin. These results indicate that endothelial/lymphocyte adhesion cascades involving VCAM-1/alpha(4)beta(1) integrin, PNAd/L-selectin, and LFA-1 control the migration of lymphocytes into inflamed lacrimal gland. These adhesion molecules offer potential therapeutic targets to block the development of lacrimal gland inflammation and destruction.

The authors report two cases of cranial fasciitis occurring at prior craniotomy sites. They review the presentation and pathological features associated with cranial fasciitis and describe two unusual cases and their treatment. The first case is that of a 16-year-old girl who underwent suboccipital craniectomy for resection of medulloblastoma and 14 months later was found to have a 4-cm nontender mass at the incision site, with evidence of skull erosion on neuroimaging. Resection of the mass revealed cranial fasciitis. The patient later developed two more lesions in the cranial region, as well as lesions on the chest wall and abdomen consistent with nodular fasciitis; all of the lesions were resected. The second case is that of a 61-year-old man who underwent suboccipital craniectomy for hypertensive hemorrhage and 2 years later was found to have an enlarging mass at the incision site, causing compression of the cerebellum. The mass was resected and found to be consistent with cranial fasciitis. Cranial fasciitis is a rare, benign lesion of the cranial region. It is histologically identical to nodular fasciitis, a self-limiting fibroblastic process of the superficial and deep fascia. Although most cases of cranial fasciitis are reported to occur spontaneously in the very young, the two cases reported here involved older patients and lesions that developed at prior craniotomy sites in a delayed fashion, a phenomenon not previously reported. Interestingly, one patient exhibited lesions in other areas as well.

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