ABSTRACT
BACKGROUND: The mechanisms responsible for periodontal disease progression remain unclear. However, recent studies suggest that apoptosis may be one mechanism underlying the pathophysiology of periodontal disease progression. This pilot study is the 3 month follow-up of our published baseline study on the presence of apoptotic factors in serum, saliva, and gingival crevicular fluid (GCF) and their association with periodontal disease severity and activity. METHODS: GCF samples were obtained from 37 adult patients with chronic periodontitis (CP) and 7 healthy controls. Clinical measurements, including probing depth (PD), clinical attachment level (CAL), and radiographs, were used to evaluate data by sites and to classify patients into healthy, mild, and moderate/severe CP groups. Enzyme-linked immunosorbent assays were used to measure apoptosis or DNA fragmentation levels in GCF. Western immunoblotting was used to detect several apoptotic proteins, Fas, FasL, sFasL, and caspase-3 expression and its cleavage products in GCF. RESULTS: At the patient level clinical and apoptotic measurements change minimally over time. At the site level, DNA fragmentation levels increase with increasing PDs at 3 months and baseline. Apoptotic protein expression exhibits increasing trends with increasing PDs at baseline and 3 months. FasL and Active FasL show a high specificity and PPV; low sensitivity and NPV. Caspase-3 products (ProCas35K and Active Cas) show a high PPV with moderate to high specificity; low sensitivity and NPV. ProCas70K shows a high PPV with moderate to high sensitivity; low specificity and NPV. CONCLUSION: Factors associated with apoptosis show minimal changes in expression in periodontitis groups in comparison to a healthy group over a short time interval (3 months). However, at the site level, apoptotic factors (DNA fragmentation and apoptotic proteins) exhibit significant increases or increasing trends with increasing PDs at any time point examined (baseline or 3 months). Several of these apoptotic factors also exhibit a high sensitivity and high positive predictive value. Thus, apoptotic molecules may be helpful biomarkers of disease status at any point in time.
ABSTRACT
Acute changes in the diastolic pressure-volume relationship of the left ventricle. Europ. J. Cardiol., 4/Suppl., 105-120. The present study was designed to investigate acute changes in the passive length-tension relations of isolated heart muscle and acute alterations of the left ventricular diastolic pressure-volume relationship of patients. In isolated heart muscle a constant lengthening and shortening technique with computer curve fitting was used to characterize the entire passive length-tension relation. There was no change in passive elastivity following an increase in stimulation frequency or an increase in muscle stretching rate. During the transition from stimulated to nonstimulated contractions, there was a shift to the left in the passive length-tension relation, with a shorter muscle length at the same resting force. In 10 patients undergoing revascularization for preinfarction angina, 7 patients showed a significantly reduced left ventricular enddiastolic pressure at the same enddiastolic volume, together with an improvement in postoperative ejection fraction. In 6 patients who experienced a perioperative myocardial infarction, variable changes in the pressure volume relationship occurred. These presumably reflected the opposite effects of stiffening of infarcted muscle and cardiac dilatation secondary to heart failure. 26 patients with chronic coronary artery disease had ventriculograms before and after 0.4 mg sublingual nitroglycerin. 9 patients showed a significant shift downwards in their pressure-volume relation, with a decreased enddiastolic pressure at the same volume. 2 showed a shift upwards, while the remaining patients showed no measurable change. It is proposed that this latter shift in pressure-volume relationships is due to hemodynamic factors rather than to intrinsic changes in muscle stiffness. Theoretical calculations utilizing A SIMPLIFIED SPHERICAL MODEL of the ventricle suggest that the magnitude of the changes observed cannot be explained by stiffening of the muscle alone and is therefore probably due to hemodynamic factors.
