Longitudinal analysis of microcirculatory parameters in gingival tissues after tooth extraction in patients with different risk profiles for wound healing disorders - a pilot study.

OBJECTIVES: We aimed to establish a risk profile for intraoral wound healing disorders based on measurements of microcirculation in gingival tissues. MATERIALS AND METHODS: Oxygen saturation (SO2) and blood flow in gingival tissues were measured with tissue spectrometry and laser doppler spectroscopy in 37 patients before/after tooth extractions. Patients were assigned to four groups: anamnestically and periodontally healthy patients (n = 7), anamnestically healthy but suffering from periodontitis (n = 10), anamnestically healthy but smoking and suffering from periodontitis (n = 10) and suffering from diabetes and periodontitis (n = 10). Measurements were performed at three different time points: Baseline measurement (T0), one day post extractionem (p.e.) (T1) and seven days p.e. (T2). RESULTS: Baseline SO2 values were higher in control patients (p = .038). This effect was most evident in comparison to smokers suffering from periodontitis (p = .042), followed by diabetics suffering from periodontitis (p = .09). An opposite trend was seen for blood flow. Patients suffering from periodontitis demonstrated higher blood flow values (p = .012). Five patients, which belonged to the group of smokers suffering from periodontitis, showed clinically a delayed wound healing. CONCLUSION: Differences in SO2 and blood flow of gingival tissue could be detected in different groups of patients with existing periodontitis compared to control patients. CLINICAL RELEVANCE: Lower baseline SO2 values could be a warning signal for possible wound healing disorders after oral surgery.

Possible implications of Ni(II) on oral IL-1ß-induced inflammatory processes.

OBJECTIVES: Nickel (Ni) is one of the main metal elements in orthodontic and prosthetic devices. Different effects of Ni are described ranging from an induction of local inflammation to allergy and cancerous/mutagenic properties. Inflammatory reactions are frequently observed in the oral cavity, but the interrelationship of Ni with those events is still unknown. Therefore, we focused on the impact of Ni on inflammation in vitro. METHODS: In accordance to previous immersion tests of our lab, human gingival fibroblasts (HGFs) (n=6) were exposed to a pro-inflammatory environment using interleukin-1 beta (IL-1ß) and additionally stimulated with different Ni(II) concentrations (400 and 4000ng/ml). At varying time points the expression of pro- and anti-inflammatory as well as matrix degeneration proteins, i.e. MMPs, were analyzed. Furthermore, proliferation assays, wound healing tests and the detection of NF-κB activation were conducted. Unstimulated HGFs served as control. RESULTS: Our experiments showed that low clinical average Ni(II) levels did not alter pro-inflammatory cytokines significantly compared to control (p>0.05). Instead, a 10-fold higher dose up-regulated these mediators significantly in a time-dependent manner (p<0.01). This was even more pronounced combining both Ni(II) concentrations with an inflammatory condition (p<0.001), MMP expressions were in line with our findings (p<0.001). The mRNA data were supported by proliferation and wound closure assays (p<0.001). However, the combination of both stimuli induced contradictory results. Analyzing NF-κB activation revealed that our results may be in part attributed to NF-κB. SIGNIFICANCE: Our in vitro study implicated that Ni(II) has various modifying effects on IL-1ß-induced inflammatory processes depending on the concentration.