Assessment of heat provocation tests on the human gingiva: the effect of periodontal disease and smoking

Abstract

Periodontal inflammation is associated with morphological changes in the blood vessels which may influence the regulation of gingival blood flow (GBF). Our aim was to adapt the heat provocation test to the human gingiva to assess vascular reactivity in periodontal inflammation. Method: GBF was recorded by Laser Doppler Flowmetry before and after heat provocation in healthy volunteers (n = 50). Heat was generated either by warm saline or a halogen lamp. The latter method was also utilized for a heat test in non-smoking and smoking patients with periodontal inflammation. The circulatory parameters were correlated to the inflammatory marker, i.e. gingival crevicular fluid (GCF) production measured by Periotron. Results: Local application of heat caused a rapid, significant and transient increase in GBF regardless of the method used. The increase in the speed and not in the concentration of moving blood cells was responsible for increased GBF. Higher GCF values were correlated with increased peak flow, flux pulse amplitude and faster restoration of GBF after the test in non-smokers, but not in smokers. Conclusions: The heat test could be a valuable tool to check the vascular reactivity of gingival vessels. Moderate periodontal inflammation may facilitate gingival vascular responsiveness which can be suppressed by smoking.

Evidence of spreading vasodilation in the human gingiva evoked by nitric oxide

“…Vasodilation ends within 60 seconds in other tissues, contrary to our study, in which it was sustained for more than 10 minutes in the Nitro POHL group and lasted longer than the observation period (14 minutes) in the Nitromint group. The extended hyperaemia is in line with our other observations in the human gingiva, where hyperaemia after short‐time occlusion or after heat provocation lasted much longer than in other tissues, suggesting a high reactivity of the gingiva.…”

“…But extent of the vasodilatory effect was very similar to the previous data. In these studies, thermal provocation of the gingiva or post‐occlusive reactive hyperaemia test were applied in which NO has a significant role in the vasodilatory mechanism . These indicate that the locally released NO from nitroglycerin in this study could be close to the physiological levels.…”

To what extent does smoking affect gingival bleeding response to supragingival plaque? Site‐specific analyses in a population‐based study

“…The underlying mechanisms of smoking and its effect on gingival bleeding are somewhat unclear. There is limited evidence that tobacco smoke promotes gingival vasoconstriction in humans . There is some evidence of tobacco‐induced suppressed angiogenesis, where a reduced number of gingival vessels or vessels of smaller caliber have been found in smokers relative to non‐smokers .…”

Tobacco‐induced suppression of the vascular response to dental plaque

“…More recently, Molnar et al. have shown that the gingiva of smokers are less responsive to a heat provocation test, which assesses vascular reactivity, than nonsmokers, as measured by induction of gingival crevicular fluid (GCF) flow . Interestingly, the authors reported that, independent of periodontal disease classification, the volume of GCF produced is significantly lower in smokers compared with nonsmokers.…”