Abstract
Periodontitis patients are at risk of alveolar bone loss during orthodontic treatment. The aim of this study was to investigate whether intermittent parathyroid hormone (1–34) treatment (iPTH) could reduce alveolar bone loss during orthodontic tooth movement (OTM) in individuals with periodontitis and the underlying mechanism. A rat model of OTM in the context of periodontitis was established and alveolar bone loss was observed. The control, iPTH and iPTH + stattic groups received injections of vehicle, PTH and vehicle, or PTH and the signal transducer and activator of transcription 3 (STAT3) inhibitor stattic, respectively. iPTH prevented alveolar bone loss by enhancing osteogenesis and suppressing bone resorption in the alveolar bone during OTM in rats with periodontitis. This effect of iPTH was along with STAT3 activation and reduced by a local injection of stattic. iPTH promoted osteoblastic differentiation and might further regulate the Wnt/β-catenin pathway in a STAT3-dependent manner. The findings of this study suggest that iPTH might reduce alveolar bone loss during OTM in rats with periodontitis through STAT3/β-catenin crosstalk.
Highlights
There is an increasing number of periodontal patients seeking orthodontic treatment for improvements in function and aesthetics.[1]It has been found that appropriate orthodontic-periodontal combination therapies can improve periodontal conditions.[2,3] in patients with periodontitis (PD), there can be an increased risk of alveolar bone loss due to unfavourable orthodontic conditions, e.g., poor oral hygiene due to increased difficulty in tooth brushing and formation of biofilms[4] with higher periodontal pathogenicity leads to the recurrence of active PD and exacerbation of alveolar bone loss.[5]
This study aimed to investigate the effect of intermittent parathyroid hormone (1–34) treatment (iPTH) on alveolar Inhibition of signal transducer and activator of transcription 3 (STAT3) hindered the protective effect of daily PTH
Th and Compared with that in the PD group, the cementoenamel junction-alveolar bone crest (CEJ-ABC) distance in BMD; these results indicated that the protective effect of iPTH was the orthodontic tooth movement (OTM) + PD group was further exacerbated on day 7 and 14 reversed by stattic in the OTM + PD + PTH + S group
Summary
There is an increasing number of periodontal patients seeking orthodontic treatment for improvements in function and aesthetics.[1]It has been found that appropriate orthodontic-periodontal combination therapies can improve periodontal conditions.[2,3] in patients with periodontitis (PD), there can be an increased risk of alveolar bone loss due to unfavourable orthodontic conditions, e.g., poor oral hygiene due to increased difficulty in tooth brushing and formation of biofilms[4] with higher periodontal pathogenicity leads to the recurrence of active PD and exacerbation of alveolar bone loss.[5]. There is an increasing number of periodontal patients seeking orthodontic treatment for improvements in function and aesthetics.[1]. Intermittent parathyroid hormone (1–34) treatment (iPTH) has been used for treating postmenopausal osteoporosis and iPTH shows promising potential for regenerating alveolar bone and preventing alveolar bone loss in rats.[13,14,15,16,17,18] Clinical studies have shown the effectiveness of iPTH in improving periodontal indices in humans.[19,20] iPTH may be a pharmaceutical approach to prevent alveolar bone loss during orthodontic treatment in PD patients. The anabolic effect of iPTH relies on promoting osteogenesis and increasing osteoblastic cell numbers.[21] Several signalling pathways and cytokines have been proven to be involved in the mechanism by which iPTH regulates bone homoeostasis. Other PTHresponsive factors, such as the Notch ligand Jagged-1,25,26 cfos,[27,28] insulin-like growth factor-1,29,30 fibroblast growth factor 231 and interleukin (IL)-6 family cytokines,[32,33] contribute to the anabolic effect of PTH on bone homoeostasis
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