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Objectives Fibrous reactive hyperplasia (FRH) is a common fibrous lesion in the oral cavity. The disease characteristics of FRH, including the expression patterns of CD34, which is a well-known fibroblast marker, have not been investigated in detail. Therefore, in this study, we aimed to investigate the characteristics of FRH compared to those of the healthy mucosa, based on CD34 expression profiles. Methods CD34 expression was analyzed at the protein and mRNA levels using immunohistochemistry, quantitative polymerase chain reaction, and in situ hybridization (ISH). Results CD34 was not expressed in the lamina propria of the oral mucosa, but was commonly observed in submucosal fibroblasts. CD34-positive fibroblasts were commonly observed in FRH. A total of 17 out of 19 cases (89.5%) were CD34-positive. Furthermore, we identified a significant difference in the ratio of CD34-positive cells between the healthy and FRH tissues. Quantitative polymerase chain reaction showed that CD34 mRNA was expressed in all cases of FRH, and CD34 mRNA expression in FRH samples was found to be localized to spindle-shaped fibroblasts, as determined by ISH. A positive correlation was also found between the CD34 mRNA levels and the proportion of the CD34-positive cells. Conclusions These findings suggest that the increase in collagen synthesis in CD34-positive fibroblasts in the submucosa leads to the development of FRH. To our knowledge, this is the first report confirming the mRNA expression patterns of CD34 in FRH.

The anti-inflammatory activity of cyclic adenosine 3',5'-monophosphate (cAMP) alone or in combination with theophylline was examined in acute and chronic types of experimental inflammations in rats. cAMP suppressed carrageenin-induced edema by intraperitoneal, subcutaneous and oral administrations. In addition, cAMP inhibited the formation of carrageenin-induced granuloma. Systemic applications of cAMP also suppressed the leakage of circulating dye in rat skins induced by moderate thermal injury and by histamine and inorganic pyrophosphate, but they suppressed less effectively the leakage induced by exogenous bradykinin. Theophylline always augmented the suppressive effects of cAMP in these inflammations. A single intraperitoneal injection of cAMP alone or in combination with theophylline induced a slight, transient hyperglycemia and did not significantly alter the plasma level of corticoids. It seems unlikely that the anti-inflammatory action of cAMP is mediated solely by hyperglycemia or by increased production of corticosteroids.