There is increasing evidence of 11β-hydroxysteroid dehydrogenase (11β-HSD) isoforms playing a pivotal role in the pathogenesis of various metabolic, systemic and inflammatory diseases such as diabetes mellitus or ischemic and coronary heart disease. Additionally, bone affecting diseases such as rheumatoid arthritis or osteoporosis correlate with altered 11β-HSD expression patterns and glucocorticoid (GC)-action as described earlier. Interestingly, the pathogenesis of periodontitis is indeed frequently accompanied by the aforementioned systemic inflammatory comorbidities. The genomic response to inflammatory stimuli relies, besides on other mechanisms, on the activation of the glucocorticoid receptor (GR), which in turn represses or stimulates expression of diverse pro- and anti-inflammatory genes in order to regulate stress and inflammatory responses. To avoid or dampen unwanted systemic effects of GCs (e.g. cortisone, cortisol), this mechanism depends upon tissue-specific fine-tuning. Thus, transformation of GCs is mediated by specialised enzymes, which convert steroid hormones from their inactive to their active forms and vice versa. A key role is played by the two isoforms of 11β-HSD which catalyse the interconversion of active cortisol and inactive cortisone. The interaction and expression of both 11β-HSD isoforms is highly dynamic in various types of tissues, as they individually equilibrate local and systemic GC-concentrations and hence control transcription patterns under different physiological conditions. However, most studies targeting the expression patterns of 11β-HSD isoforms and GC-action in the clinical picture of periodontitis are restricted to mouse models. For the first time, the present study examines human gingival tissue of periodontitis patients and healthy controls with the use of quantitative Real-Time PCR (qRT-PCR) in order to test whether tissue-specific dysregulation of 11β-HSD isoforms contributes to the progression of periodontal disease. On the mRNA level, our results do not indicate dysregulation of 11β-HSD isoforms in cases and controls. However, regulation patterns of 11β-HSD isoforms in the clinical picture of peri-implantitis remain to be investigated in future studies as these enzymes constitute promising pharmaceutical targets to ameliorate disease progression and medical conditions of the oral cavity. Schlagwörter: Periodontitis, 11beta-hydroxysteroid dehydrogenase type 1, 11beta-hydroxysteroid dehydrogenase type 2, inflammation, glucocorticoids, cortisone