Upregulation of immunoreactivity of endothelin-1 and a-SMA in PDL microvasculature following acute tooth loading: an immunohistochemical study in the marmoset

Abstract

Objectives – To test the hypothesis that a continuous mechanical tooth load would elevate immunoreactivity of endothelin-1 (ET-1) and alpha-smooth muscle actin (a-SMA) in the periodontal ligament (PDL) microvasculature. Design – A randomized control study employing 1.5 h of loading to first molars. Setting and Sample Population – Orthodontic Research Laboratory, Dental School, Adelaide University. Four young adult, male marmoset monkeys were consecutively anaesthetized and treated. Experimental Variable – An external telescoping frame applied a jaw closing load (120–200 g) transmitted occlusally, via a rubber pad, to randomly assigned mandibular left or right first molars. Contralateral molars were used as controls. Outcome Measure – Undemineralized, midsagittal, mandibular molar slices, 150 lm thick were immunolabelled with ET-1 and a-SMA antibodies and examined in a confocal laser scanning microscope (CLSM) for vascular endothelium and smooth muscle immunolabelling. Results – Three categories of post-capillary-sized venule endothelial cell immunolabelling occurred: endothelium labelled solely with ET-1; endothelium labelled solely with a-SMA; endothelium labelled with both ET-1 and a-SMA. In endothelial cells, the a-SMA showed a moderate cytoplasmic distribution with dense peripheral concentration. Loading increased arteriole a-SMA actin labelling. Conclusion – Scattered expression of ET-1 is the default state in primate PDL endothelial cells. Increased antigenicity of endothelial cells to both ET-1 and a-SMA, and of arteriolar smooth muscle to a-SMA, is a response to shear and compression loads.