Psychological stress exposure (PSE) is a major risk factor for neurological disorders, such as bipolar disorder, depression, and schizophrenia; 1 however, it is also associated with the etiopathogenesis of oral inflammatory conditions, including gingivitis, periodontitis, and aphthous stomatitis. 2 One explanation for this is that PSE increases blood cortisol levels, thereby compromising immune system activity and reducing monocyte and T-lymphocyte counts. 3,4 Moreover, PSE compromises wound healing by reducing the levels of cytokines, such as interleukin (IL)-1α, IL-6, and IL-8, and impairing inflammatory response. 5,6 Furthermore, elevated cortisol levels inhibit the proliferation, differentiation, and apoptosis of osteoblasts, 7 which might influence orthodontic therapy (OT) by either increasing or decreasing the amount of orthodontic tooth movement (OTM).Tooth movement has an inflammation-resembling nature that involves neural and immune processes. 8 A number of studies have assessed the impact of PSE on OT. [9][10][11][12][13][14] Results from a prospective clinical study showed that a reduction in PSE is associated with an improvement in the outcome of OT. 10 Moreover, in an experimental study, PSE in rats significantly increased OTM compared with unrestrained rats. 11 Conversely, Mirzakouchaki et al 13 showed that PSE
AbstractThe aim of the present study was to comprehensively review the influence of psychological stress exposure (PSE) on orthodontic therapy (OT). Original clinical and experimental studies were assessed. Quality assessment of experimental studies was performed using the Animal Research Reporting In Vivo Experiment (ARRIVE) guidelines. Six studies (2 clinical and 4 experimental) were included. One clinical study showed that PSE during OT significantly increases nickel release from orthodontic appliances into the saliva. In another study, maternal support was found to be an important predictor of the outcome of OT. In one experimental study, chronic PSE increased orthodontic tooth movement (OTM), and in two experimental studies, PSE decreased OTM. One study on rats reported that PSE is not a risk factor for orthodonticallyinduced root resorption during OTM. One experimental study showed a significantly higher number of osteoclasts in the bone on the side of OTM in restrained rats compared with unrestrained rats. One study showed decreased osteoclast counts in the bone during OTM under PSE. The lowest, highest, and mean ARRIVE scores (out of 20)for the experimental studies were 16, 18, and 16.75 ± 0.96, respectively. The role of PSE in clinical orthodontics remains unclear, most likely due to a lack of studies in humans. Further power-adjusted, well-designed, and randomized studies are needed.
K E Y W O R D Semotional stress, orthodontic therapy, psychological stress exposure, review, tooth movement