2021
DOI: 10.1007/s00056-021-00311-4
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Assessment of salivary stress and pain biomarkers and their relation to self-reported pain intensity during orthodontic tooth movement: a longitudinal and prospective study

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Cited by 7 publications
(7 citation statements)
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“…However, they contradict the data of Chetan et al [ 39 ], who found that there is a statistically significant decrease in salivary cortisol levels in orthodontic patients 1 h and 4–6 weeks after the start of the treatment. Moreover, Canigur et al [ 40 ] showed that orthodontic tooth movement did not cause significant alterations in salivary pain and stress biomarkers.…”
Section: Discussionmentioning
confidence: 99%
“…However, they contradict the data of Chetan et al [ 39 ], who found that there is a statistically significant decrease in salivary cortisol levels in orthodontic patients 1 h and 4–6 weeks after the start of the treatment. Moreover, Canigur et al [ 40 ] showed that orthodontic tooth movement did not cause significant alterations in salivary pain and stress biomarkers.…”
Section: Discussionmentioning
confidence: 99%
“…However, this study used a short-lasting, high-intensity pain model, which may have resulted in a pain state that was too short-lasting to activate the autonomic nervous system (ANS), leading to sAA secretion [41]. Furthermore, orthodontic tooth removal did not cause significant changes in sAA in response to pain and stress in children [26]. Similarly, a study by Sadi et al failed to show any significant correlation between dental anxiety and sAA values [38].…”
Section: Salivary α-Amylasementioning
confidence: 99%
“…Additionally, Brockington et al suggested that a combination of increased oxytocin and reduced cortisol may reduce negative emotions and pain perception in children during hospitalization [25]. However, a study on orthodontic tooth procedures did not result in significant alterations in salivary cortisol levels [26].…”
Section: Cortisolmentioning
confidence: 99%
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“…In clinical relevance, SAA is a potentially cost‐effective biomarker of psychological stress that can be used to objectively assess the severity of pain for a patient (Christidis et al, 2020 ; Laurikainen et al, 1988 ; Nater & Rohleder, 2009 ; Nederfors & Dahlof, 1996 ; Nederfors et al, 1994 ; Speirs et al, 1974 ; van Stegeren et al, 2006 ). Regarding oral and periodontal diseases, SAA has been referenced for assessing pain perception and severity in many types of patients (Canigur Bavbek et al, 2021 ; Castillo‐Felipe et al, 2022 ; Cotoia et al, 2018 ; Vahedi et al, 2018 ; Vaswani et al, 2020 ; Wittwer et al, 2016 ; Yennurajalingam et al, 2018 ). Mechanistically, painful stimuli initially activate symptomatic systems to increase plasma epinephrine or norepinephrine secretions and subsequently increase SAA secretions in response to pain.…”
Section: Introductionmentioning
confidence: 99%