Mikulicz's disease (MD) has been considered part of primary Sjögren's syndrome (SS) since Morgan's report in 1953. However, MD shows a unique condition involving persistent swelling of the lachrymal and salivary glands characterized by good responsiveness to glucocorticoids, leading to the recovery of gland function. Recently, it has been revealed that MD patients show elevated serum immunoglobulin G4 (IgG4) concentrations and prominent infiltration of IgG4-positive plasma cells. The complications of MD include autoimmune pancreatitis, retroperotoneal fibrosis, tubulointerstitial nephritis, autoimmune hypophysitis, and Riedel's thyroiditis, all of which show IgG4 involvement in their pathogenesis. Thus, MD is a systemic IgG4-plasmacytic disease. On the other hand, Kuttner's tumor (KT) is chronic sclerosing sialadenitis that presents with asymmetrical firm swelling of the submandibular glands. Immunohistochemical analyses have revealed that a proportion of IgG4-positive plasma cells was also elevated in KT. MD and KT differ from SS and are thought to possibly form a singular systemic IgG4-related plasmacytic disease.

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Salivary gland pleomorphic adenoma (PA) has morphological diversity in tumor cell arrangements within its characteristic myxochondroid stroma, although it remains uncertain whether neoplastic myoepithelial or ductal cells are responsible for such diversity. To analyze the morphological and functional characteristics of the constituent cells of salivary gland PA, we investigated comparative expressions of p63 gene products (P63) as a myoepithelial/basal cell marker as well as those of cytokeratin 8 (CK8) as a duct epithelial cell marker through the use of double-immunohistochemical staining. Formalin-fixed, paraffin-embedded sections of 10 samples each of PA and normal salivary gland were examined. In normal salivary glands, P63-positive myoepithelial cells were distinguished from CK8-positive luminal cells of intercalated ducts. In PA, P63-positivity was observed in both luminal and basal cells of ductal structures, in spindle-shaped cells scattered in the myxoid stroma, and in peripheral cells of squamous-metaplastic foci, while CK8 was only positive in luminal cells of the ductal structures. Based on the simultaneous labeling of the two markers on same sections through double immunostaining, the ductal structures in PA were shown to be not functionally the same as normal ducts, and hence it is possible to consider that most of the PA cells shared myoepithelial phenotypes.

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Lipoma has been recognized to be one of the most common soft-tissue tumors in the oral region. This case report presents a heretofore undescribed intraoral lesion that resembled mature lipoma but also featured multiple non-lipomatous dendritic cell nodules immunopositive for S-100 protein. We demonstrate histological and immunohistochemical evidence of cellular transitions between non-lipogenic S-100 protein-positive dendrocytes and adipocytes. Although it is likely that this tumor comprises part of the spectrum of what has been referred to in the literature as lipoma, the presence of S-100 protein-positive dendritic cells as an integral component is quite unique and worthy of reporting.

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Chemical peeling is a treatment method that destroys the epidermis and/or dermis with subsequent regeneration of new epidermis and dermis using a peeling agent. Phenol is one peeling agent that has been extremely effective in obtaining a complete response for gingival leukoplakia. In this report, we describe three cases of gingival leukoplakia that were treated with phenol peel, and we discuss the effects and applicable cases. All patients consulted our hospital in 2003 and refused surgical treatment, including laser surgery, so we performed chemical peeling using a phenolalcohol method that was previously reported for gingival melanin pigmentation. All cases achieved a complete response without local anesthesia or hospitalization. No patient felt pain at the time of application or post-treatment. None of the cases had a local recurrence or malignant transformation for approximately 69 months after the application of phenol peel. The use of a phenol peel may also be indicated for leukoplakia with dysplasia or other epithelial lesions. However, additional clinical studies that closely follow treated patients and further basic studies are still needed.

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