Mechanisms of Atomization from Rotary Dental Instruments and Its Mitigation.

Since the onset of coronavirus disease 2019, the potential risk of dental procedural generated spray emissions (including aerosols and splatters), for severe acute respiratory syndrome coronavirus 2 transmission, has challenged care providers and policy makers alike. New studies have described the production and dissemination of sprays during simulated dental procedures, but findings lack generalizability beyond their measurements setting. This study aims to describe the fundamental mechanisms associated with spray production from rotary dental instrumentation with particular focus on what are currently considered high-risk components-namely, the production of small droplets that may remain suspended in the room environment for extended periods and the dispersal of high-velocity droplets resulting in formites at distant surfaces. Procedural sprays were parametrically studied with variables including rotation speed, burr-to-tooth contact, and coolant premisting modified and visualized using high-speed imaging and broadband or monochromatic laser light-sheet illumination. Droplet velocities were estimated and probability density maps for all laser illuminated sprays generated. The impact of varying the coolant parameters on heating during instrumentation was considered. Complex structured sprays were produced by water-cooled rotary instruments, which, in the worst case of an air turbine, included droplet projection speeds in excess of 12 m/s and the formation of millions of small droplets that may remain suspended. Elimination of premisting (mixing of coolant water and air prior to burr contact) resulted in a significant reduction in small droplets, but radial atomization may still occur and is modified by burr-to-tooth contact. Spatial probability distribution mapping identified a threshold for rotation speeds for radial atomization between 80,000 and 100,000 rpm. In this operatory mode, cutting efficiency is reduced but sufficient coolant effectiveness appears to be maintained. Multiple mechanisms for atomization of fluids from rotatory instrumentation exist, but parameters can be controlled to modify key spray characteristics during the current crisis.

11ß-HSD1 plays a critical role in trabecular bone loss associated with systemic glucocorticoid therapy.

BACKGROUND: Despite their efficacy in the treatment of chronic inflammation, the prolonged application of therapeutic glucocorticoids (GCs) is limited by significant systemic side effects including glucocorticoid-induced osteoporosis (GIOP). 11ß-Hydroxysteroid dehydrogenase type 1 (11ß-HSD1) is a bi-directional enzyme that primarily activates GCs in vivo, regulating tissue-specific exposure to active GC. We aimed to determine the contribution of 11ß-HSD1 to GIOP. METHODS: Wild type (WT) and 11ß-HSD1 knockout (KO) mice were treated with corticosterone (100 µg/ml, 0.66% ethanol) or vehicle (0.66% ethanol) in drinking water over 4 weeks (six animals per group). Bone parameters were assessed by micro-CT, sub-micron absorption tomography and serum markers of bone metabolism. Osteoblast and osteoclast gene expression was assessed by quantitative RT-PCR. RESULTS: Wild type mice receiving corticosterone developed marked trabecular bone loss with reduced bone volume to tissue volume (BV/TV), trabecular thickness (Tb.Th) and trabecular number (Tb.N). Histomorphometric analysis revealed a dramatic reduction in osteoblast numbers. This was matched by a significant reduction in the serum marker of osteoblast bone formation P1NP and gene expression of the osteoblast markers Alp and Bglap. In contrast, 11ß-HSD1 KO mice receiving corticosterone demonstrated almost complete protection from trabecular bone loss, with partial protection from the decrease in osteoblast numbers and markers of bone formation relative to WT counterparts receiving corticosterone. CONCLUSIONS: This study demonstrates that 11ß-HSD1 plays a critical role in GIOP, mediating GC suppression of anabolic bone formation and reduced bone volume secondary to a decrease in osteoblast numbers. This raises the intriguing possibility that therapeutic inhibitors of 11ß-HSD1 may be effective in preventing GIOP in patients receiving therapeutic steroids.