– Monoclonal activation markers (la, Tac, T9, and 4F2) were used to detect the degree of activation of mononuclear cells in the inflammatory infiltrates of oral lichen planus in situ. In addition the specimens were stained with the following monoclonal antibodies: T4, T8, T11, Ml, and pan‐B. T‐lymphocyte was the predominant cell type in the inflammatory infiltrates. According to the results of the activation marker analysis, the majority of the Tlymphocytes were resting. However, activated cytotoxic T8 and 4F2 T‐cells were located close to damaged basal cells; this finding may suggest that they are responsible for the damage and supports the claim that a cell‐mediated immune response participates actively in local pathogenetic mechanisms in oral lichen planus.

Oral mucosal lichen planus (OMLP) is a well recognized mucosal disease with unknown etiology. Considerable controversy exists as to whether OMLP is intrinsically premalignant, or if the disorder facilitates the development of oral mucosal squamous cell carcinoma (OMSCC) by external factors. The aim of the present study was to investigate the expression of c-erbB-2 protein in the keratinocytes of initial biopsies or oral mucosal disorders diagnosed as OMLP with no evidence of epithelial dysplasia, and to compare the results with the expression of c-erbB-2 protein in subsequent biopsies obtained from the same patients. These results were compared with the findings from control groups (patients with dysplasia with no evidence of OMLP, patients with OMSCC with no evidence of OMLP and normal oral mucosa). The expression of the c-erbB-2 protein was evaluated by immunohistochemical staining of the gene product with the avidin-biotin-complex method using paraffin-embedded tissues sections. Five of the initial biopsies from patients with OMLP expressed the c-erbB-2 protein and one did not. None of the OMLP cases that subsequently showed evidence of dysplasia expressed the c-erbB-2 protein, and of the three OMSCC specimens from the patients with OMLP, two were negative and one expressed c-erbB-2 protein. The specimens from the control groups all expressed the c-erbB-2 protein. The results indicated the probability of the absence of c-erbB-2 staining being an indication of a potential for neoplastic transformation in OMLP with dysplastic changes.

The concentration of lactoferrin (LF) in unstimulated mixed saliva in Sjogren's syndrome assayed by a double-antibody solid-phase radioimmunoassay was 16.28 * 3.05 pg/mg of protein (range 7.42-33.64) and differed significantly (P < 0.001) from that of normal control subjects matched for sex and age (2.82 * 0.80 pglmg of protein, range 0. 59-7.35). An unlabeled antibody-enzyme (peroxidase-antiperoxidase) method for labial salivary gland biopsies optimally fixed in Carnoy's fluid yielded strong staining of LF in intralobular and interlobular ducts, whereas only weak staining was observed in the serous secretory units of these mixed glands; this contrasted to the LF distribution in normal salivary glands. The results indicate that the

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